Upload
others
View
5
Download
0
Embed Size (px)
Citation preview
Daniel Steffens
MECHANISMS OF LOW BACK PAIN
Belo Horizonte
2015
Daniel Steffens
MECHANISMS OF LOW BACK PAIN
Belo Horizonte
2015
Tese apresentada ao Programa de
Pósgraduação em Ciências da
Reabilitação, da Escola de Educação
Física, Fisioterapia e Terapia Ocupacional
da Universidade Federal de Minas Gerais
como requisito à obtenção do título de
Doutor em Ciências da Reabilitação
Orientadora: Profª. Drª. Leani SM
Pereira
Co-Orientador: Prof. Dr. Chris Maher
Co-Orientadora: Profª. Drª. Jane Latimer
S817
2015
Steffens, Daniel
Mechanisms of low back pain. [manuscrito]/.Daniel Steffens – 2015.
245f., enc.: il.
Orientadora: Leani Souza Máximo Pereira
Co-orientador: Chris Maher
Co-orientadora: Jane Latimer
Tese (doutorado) – Universidade Federal de Minas Gerais, Escola de Educação Física,
Fisioterapia e Terapia Ocupacional.
1. Aptidão física - Teses. 2. Dor Lombar - Teses. 3. Incapacidade - Teses. I.
Pereira, Leani Souza Máximo. II. Maher, Chris. III. Latimer, Jale. IV. Universidade
Federal de Minas Gerais. Escola de Educação Física, Fisioterapia e Terapia
Ocupacional. V. Título.
CDU: 612.76 Ficha catalográfica elaborada pela equipe de bibliotecários da Biblioteca da Escola de Educação Física,
Fisioterapia e Terapia Ocupacional da Universidade Federal de Minas Gerais.
Supervisors’ Statement
As supervisors of Daniel Steffens’ doctoral work, we certify that we consider his thesis
“Mechanisms of Low Back Pain” to be suitable for examination.
Professor Leani de Souza Máximo Pereira
Universidade Federal de Minas Gerais Date: 01.01.2015
Professor Christopher Maher
The George Institute for Global Health Date: 01.01.2015
The University of Sydney
Professor Jane Latimer
The George Institute for Global Health Date: 01.01.2015
The University of Sydney
i
Candidate’s Statement
I, Daniel Steffens, hereby declare that this submission is my own work and that it
contains no material previously published or written by another person except where
acknowledged in the text. Nor does it contain material which has been accepted for the
award of another degree.
I, Daniel Steffens, understand that if I am awarded a higher degree for my thesis entitled
“Mechanisms of low back pain” being lodged herewith for examination, the thesis will
be lodged in the Universidade Federal de Minas Gerais and The University of Sydney
libraries and be available immediately for use. I agree that the University Librarian (or
in the case of a department, the Head of the Department) may supply a photocopy or
microform of the thesis to an individual for research or study or to a library.
Daniel Steffens
Date: 01.01.2015
ii
iii
iv
Acknowledgments
My thanks go firstly to my supervisors Prof Leani SM Pereira and Prof Chris G
Maher and my co-supervisor Prof Jane Latimer. Leani, all this could not be possible without
your persistence and dedication. Chris, you are the best supervisor I could have ever asked
for. Your competence, dedication, patience and sense of humour made this journey much
easier. You are truly an inspiration to all of us. Jane, your kindness and guidance allowed me
to always see the light at the end of the tunnel. You were a great co-supervisor for which I
have immense respect and admiration.
I would like to acknowledge my appreciation to the Universidade Federal de Minas
Gerais and The University of Sydney for establishing the Cotutelle agreement allowing me to
pursue my studies. I would also like to thank the George Institute for Global Health for
providing the modern infra-structure and support; and the Department of Physiotherapy from
the Universidade Federal de Minas Gerais for their support.
I am grateful to several people whose advice and support ensured that this thesis was
completed. I am indebted to all my co-authors, who played a major role in the construction of
each chapter of this thesis. In particular, I would like to thank Dr Mark Hancock for all his
support, dedication, mentorship, transparency and willingness to help. You are one of the
reasons I started my PhD.
To all my friends and colleagues, it is impossible to imagine these four years without
the BBQs, beers, laughs and advice. In particular, Zamba, Marcinha, Big Mike, Vinicius,
Tarci, Bruno, Tie, Patricia, Gustavo, Marina, Amabile, Saad, Aron, Matt and Richard. You
have made all the difference.
To all my family, Mum, Dad, brothers and sister, you all have contributed to this.
Mum, your unconditional support allowed me to choose my journey. Dad, I miss you and I
wish you were here to share this moment with me. Your son will finally become a Doctor.
You both were always there for me and I hope I have made you proud.
Finally, to the love of my life. Paula, thank you for your support, encouragement and
help at every single stage. This thesis is dedicated to you, the most important person in my
life.
v
Publications and Presentations
Parts of the work presented in this thesis have been published and/or presented in the
following forms:
Publications
Steffens D, Maher CG, Ferreira ML, Hancock MJ, Glass T, Latimer J. Clinicians’
views on factors that trigger a sudden onset of low back pain. European Spine Journal.
2014; 23:512-519.
Steffens D, Ferreira ML, Latimer J, Ferreira PH, Koes BK, Blyth F, Li Q, Maher CG.
What triggers an episode of low back pain? A case-crossover study. Arthritis Care &
Research. 2015; 67:403-410.
Steffens D, Maher CG, Li Q, Ferreira ML, Pereira LSM, Koes BK, Latimer J. Effect of
weather on back pain: results from a case-crossover study. Arthritis Care & Research.
2014; 66:1867-1872.
Steffens D, Hancock MJ, Maher CG, Williams C, Jensen TS, Latimer J. Does magnetic
resonance imaging predict future low back pain? A systematic review. European
Journal of Pain. 2014; 18:755-765.
Steffens D, Hancock MJ, Maher CG, Latimer J, Satchell R, Ferreira ML, Ferreira PH,
Partington M, Bouvier AL. Prognosis of chronic low back pain in patients presenting to
a private community-based group exercise program. European Spine Journal. 2014; 23:
113-119.
Steffens D, Hancock MJ, Pereira LSM, Kent PM, Latimer J, Maher CG. Do magnetic
resonance imaging findings identify patients with low back pain who respond better to
particular interventions? A systematic review. Submitted for publication to European
Journal of Pain on 28th
October 2014.
Steffens D, Maher CG, Ferreira ML, Hancock MJ, Pereira LSM, Williams CM, Latimer
J. Influence of clinician characteristics and operational factors on recruitment of
participants with low back pain: an observational study. Journal of Manipulative
Physiological Therapeutics. 2014; 38:151-158.
vi
Steffens D, Ferreira ML, Maher CG, Latimer J, Koes BW, Blyth FM, Ferreira PH.
Triggers for an episode of sudden onset low back pain: study protocol. BMC
Musculoskeletal Disorders. 2012; 24:13-17.
Presentations
Steffens D, Ferreira ML, Latimer J, Ferreira PH, Koes BK, Blyth F, Li Q, Maher CG.
What triggers an episode of low back pain? Results of a Case-crossover study. XIII
International Back Pain Forum. Campos do Jordão, Brazil, 2014.
Steffens D, Maher CG, Li Q, Ferreira ML, Pereira LSM, Koes BK, Latimer J. Could the
weather trigger an episode of acute low back pain? A case cross-over study. XIII
International Back Pain Forum. Campos do Jordão, Brazil, 2014.
Steffens D, Ferreira ML, Latimer J, Ferreira PH, Koes BK, Blyth F, Li Q, Maher CG.
What triggers an episode of low back pain? Results of a case-crossover study.
Australian Pain Society, 34th
Annual Meeting. Hobart, Australia, 2014.
Steffens D, Hancock MJ, Maher CG, Williams C, Jensen TS, Latimer J. Does magnetic
resonance imaging predict future low back pain? A systematic review. VIII Pain in
Europe. Florence, Italy, 2013.
Steffens D, Ferreira ML, Maher CG, Latimer J, Koes BW, Blyth FM, Ferreira PH. Does
the method of training of recruiting clinicians influence recruitment to a low back pain
case-crossover study. Primary Care Research on Back Pain - XII Odense International
Forum. Odense, Denmark, 2012.
Steffens D, Ferreira ML, Maher CG, Latimer J, Koes BW, Blyth F, Ferreira PH.
Clinician’s views on triggers for sudden onset low back pain. Primary Care Research
on Back Pain - XII Odense International Forum. Odense, Denmark, 2012.
Steffens D, Hancock MJ, Satchill R, Ferreira ML, Ferreira PH, Maher CG, Partington
M, Bouvier AL. Prognosis of patients with chronic low back pain presenting to a private
functional group exercise program. Australian Physiotherapy Association Biennial
Conference. Brisbane, Australia, 2011.
vii
Preface
This thesis is part of a Cotutelle Agreement between the Universidade Federal de
Minas Gerais and The University of Sydney made on 1 August 2011.
This thesis is arranged in Ten Chapters, written so that each chapter can be read
independently. The Universidade Federal de Minas Gerais and The University of Sydney
allow for published papers arising from the candidature to be included in the thesis.
Chapter One is an introduction to the thesis and provides an overview of the relevant
low back pain literature with a specific focus on aspects related to the mechanisms of back
pain.
Chapter Two is an observational study conducted to describe short- and long-term
factors that primary care clinicians consider important in triggering a sudden episode of acute
low back pain. This study is presented as published in the European Spine Journal.
Chapter Three is the protocol for the case-crossover study presented in Chapter
Four. This protocol is presented as published in BMC Musculoskeletal Disorders.
Chapter Four investigates the increase in risk of an episode of sudden onset, acute
low back pain associated with transient exposure to a range of physical (e.g manual tasks,
vigorous physical activity) and psychosocial factors (e.g. distraction/fatigue). The paper is
presented in the format required by Arthritis Care & Research where it has been accepted for
publication.
Chapter Five is a case-crossover study evaluating the influence of various weather
conditions on risk of an episode of sudden onset, acute low back pain. This study is presented
as published in Arthritis Care & Research.
Chapter Six is a systematic review investigating whether magnetic resonance
imaging findings of the lumbar spine predict future low back pain. This study is presented as
published in the European Journal of Pain.
Chapter Seven is an observational study investigating the prognosis and prognostic
factors for patients with chronic low back pain presenting to a private, community-based,
group exercise program. This study is presented as published in the European Spine Journal.
viii
Chapter Eight consists of a systematic review investigating if the presence of
magnetic resonance imaging findings at baseline identifies patients with low back pain who
respond better to particular interventions. The paper is presented in the format required by
European Journal of Pain where it was submitted for publication.
Chapter Nine is an observational study conducted to identify factors that influence
recruitment to a large observational study. The paper is presented in the format required by
Journal of Manipulative and Physiological Therapeutics where it has been accepted for
publication.
Finally, Chapter Ten consists of an overview, and discusses the clinical implications
and directions for further research.
Each chapter contains its own reference list. Appendices that were published as online
supplementary material are included at the end of the relevant chapter. Ethical approval was
obtained from the Human Research Ethics Committee of the University of Sydney for all
studies prior to commencement.
ix
Resumo
A dor lombar é um grande problema a nível mundial e está associada a
e levados custos socioeconômicos e de saúde para o indivíduo e para a sociedade. Nas
últimas décadas, apesar do número considerável de pesquisas sobre o tema, o avanço
na identificação de abordagens que forneçam resultados significativos no tratamento da
dor lombar ainda permanece limitado. A identificação ou a melhor compreensão dos
fatores de risco que aumentam a ocorrência da dor lombar, ou que estejam associados
com o prognóstico ou a resposta de tratamento, são cruciais para o desenvolvimento de
estratégias para sua prevenção. Os estudos desenvolvidos nesta tese focam na avaliação
dos mecanismos do desenvolvimento da dor lombar, em relação ao risco, prognóstico e a
resposta terapêutica.
Até o momento, evidências sobre as causas da dor lombar na população que
procura o atendimento em serviços de atenção primária à saúde permanecem limitadas.
Os profissionais que atuam em cuidados primários, que comumente atendem um grande
número desses pacientes, ainda não conseguem fornecer informações esclarecedoras
sobre as causas do aparecimento da dor lombar. O estudo observacional apresentado no
Capítulo Dois investigou os fatores de risco de curto e longo prazo que os profissionais
em cuidados primários acreditam ser responsáveis por desencadear um episódio súbito de
dor lombar aguda. Este estudo baseou-se nas opiniões de 103 profissionais em cuidados
de saúde primários que estavam recrutando participantes para um estudo caso-cruzado.
Os fatores de risco a curto e a longo prazo mais citados como responsáveis por
desencadear um episódio súbito de dor lombar aguda foram fatores biomecânicos
(89,3% e 54,2%, respectivamente) e características individuais, tais como episódios
anteriores de dor lombar (6,4%e 39,0%,respectivamente). Surpreendentemente, fatores
de risco psicológicos/psicossociais e genéticos não foram considerados por esses
profissionais, como importantes para desencadeamento de um episódio súbito de dor
lombar aguda, apesar da literatura atual considerar esses fatores como relevantes. Os
resultados apresentados no Capitulo 2 ajudará a informar aos profissionais de saúde do
setor primário sobre a importância de considerar esses fatores em programas de
prevenção e tratamento da dor lombar.
Uma melhor compreensão dos fatores que aumentam o risco de dor lombar é
crucial para o desenvolvimento de estratégias de prevenção. Estudos anteriores
concentraram-se em fatores de risco que não são modificáveis tais como a idade dos
x
indivíduos ou, envolvem hábitos de vida a longo prazo como o tabagismo. Um estudo
caso-cruzado para investigar quais os fatores de risco físicos e psicossociais que
estavam presentes no período mais próximo para o aparecimento de um episódio súbito
de dor lombar aguda foi realizado. Os Capítulos Três e Quatro descrevem o protocolo
e os resultados encontrados no estudo, respectivamente. Um total de 999 pacientes que
apresentaram um novo episódio de dor lombar aguda foram recrutados por meio de 300
clínicas de atenção primária á saúde em Sidney, Austrália. A exposição a fatores
desencadeadores físicos e psicossociais durante as duas horas que precederam o início da
dor foi comparada com as mesmas duas horas em dois períodos controles, de 24 e 48
horas antes do surgimento da dor. A exposição à tarefas manuais envolvendo má postura
(odds ratio 8,03; intervalo de confiança de 95%: 5,46 a 11,82), manuseio de objetos
longe do corpo (odds ratio 6,20; intervalo de confiança de 95%: 2,41 a 15,94),
manuseio de pessoas ou animais vivos (odds ratio 5,8; intervalo de confiança de 95%:
2,25 a 14,98) ou manuseio de carga instável, difícil de pegar ou segurar (odds ratio 5,13;
intervalo de confiança de 95%:2,40 a 10,93), bem como distrair-se durante uma tarefa
(odds ratio 25,0; intervalo deconfiança de 95%: 3,4 a 184,5), ou estar cansado (odds
ratio 3,7; intervalo de confiança de95%: 2,2 a 6,3), aumentou significativamente as
chances do surgimento de um novo episódio de dor lombar. O consumo de bebidas
alcoólicas (odds ratio 1,5; intervalo de confiança de 95%: 0,6 a 3,7) ou a realização de
atividade sexual (odds ratio 0,7; intervalo de confiança de 95%: 0,3 a 1,8), não
aumentaram o risco no surgimento de dor lombar. Estas associações não foram
moderadas por atividade física habitual, índice de massa corporal, episódios anteriores
de dor lombar, ou depressão e ansiedade. A idade dos indivíduos moderou o risco
associado à exposição à cargas pesadas (odds ratio para pessoas com idades entre
20, 40 ou 60 anos foram de 13,6, 6,0 e 2,7, respectivamente) e de atividade sexual (odds
ratio para pessoas com idades entre 20, 40 ou 60 anos foram 0,05, 0,41 e 3,21,
respectivamente). Este foi o primeiro estudo a usar o desenho caso-cruzado para avaliar a
associação entre exposições físicas e psicossociais e o risco do surgimento de dor lombar
aguda. Os resultados apresentados podem ser usados para auxiliar no desenvolvimento de
novas abordagens de prevenção dor lombar.
Existem muitos fatores responsáveis por desencadear um episódio de dor lombar.
Muitos pacientes com dor musculoesquelética comumente relatam que seus sintomas são
influenciados pelo clima, no entanto, até o momento esta associação não foi avaliada
xi
para a condição musculoesquelética mais comum, que é a dor lombar. O estudo relatado
no Capítulo Cinco teve como objetivo investigar a influência de diferentes condições
climáticas no risco de desencadeamento de um episódio de dor lombar aguda. Foi
realizado um estudo caso-cruzado envolvendo 993 pacientes que apresentaram-se à
clínicas de atenção primária a saúde em Sidney, Austrália. As informações clínicas e
demográficas de todos os participantes foram obtidas a partir de uma entrevista. Os
parâmetros meteorológicos foram obtidos por meio do Instituto Australiano de
Meteorologia. Utilizou-se o método analítico em pares (regressão logística condicional)
para o estudo caso-cruzado para contrastar o clima no momento em que os participantes
notaram pela primeira vez a dor lombar (janela caso) com o tempo, ao mesmo tempo,
uma semana e um mês antes (janelas controle). A maioria dos participantes eram do sexo
masculino (54,2%), com idade média de 45,2 anos. Temperatura, umidade relativa do ar,
pressão atmosférica, direção do vento e precipitação não mostraram associação com o
início de um novo episódio de dor lombar. Velocidade do vento (odds ratio 1,17;
intervalo de confiança de 95%: 1,04 a 1,32; p = 0,01; para um aumento de 11 km/h) e
rajada de vento (odds ratio 1,14; intervalo de confiança de 95%:1,02 a 1,28; p =
0,02; para um aumento de 14 km/h) aumentaram as chances para o surgimento da
dor. A maioria dos parâmetros climáticos não foram associados com o surgimento da dor
lombar. A velocidade do vento e da rajada do vento foram associadas a um pequeno
aumento no risco do surgimento de dor lombar, porém essa variável não é considerada
como sendo clinicamente importante.
A ressonância magnética tem sido muito utilizada pelos médicos para a
identificação de patologias responsáveis pela dor lombar. No entanto, a importância dos
achados na ressonância magnética permanece controversa, a evidência é limitada e
nenhuma revisão sistemática sobre este tema foi conduzida até o presente momento.
Portanto, a revisão sistemática apresentada no Capítulo Seis investigou se os achados
de ressonância magnética da coluna lombar podem prever o aparecimento de futuros
casos de dor lombar em pessoas com e sem dor lombar presente. As buscas foram
realizadas em três bancos de dados internacionais (MEDLINE, EMBASE e CINAHL) e
12 estudos de coorte prospectivos foram encontrados. Devido à heterogeneidade dos
estudos incluídos, a condução de uma meta-análise não foi possível. Não foram
identificadas associações consistentes entre os achados na ressonância magnética e dor
ou incapacidade. Três estudos relataram associações significativas para Modic changes
tipo 1 com dor (odds ratio 6,2; intervalo de confiança de 95%: 1,9 a 20,2),
xii
degeneração discal com incapacidade em amostras com a presença de dor lombar (odds
ratio 2,2; intervalo de confiança de 95%: 1,2 a 4,0) e hérnia de disco com dor em uma
amostra mista, com e sem dor lombar (odds ratio 0,2; intervalo de confiança de 95%: não
reportado; p = 0,01). Poucos estudos investigaram se a ressonância magnética pode
prever o aparecimento de novos casos de dor lombar. Embora três resultados
estatisticamente significativos tenham sido encontrados, esses estudos apenas fornecem
evidências limitadas. Há uma clara necessidade de envidar esforços, para que futuros
estudos sejam conduzidos adequadamente nesta área.
O prognóstico da dor lombar crônica é considerado desfavorável. Uma melhor
compreensão dos fatores prognósticos para os pacientes com dor lombar crônica poderia
ajudar os profissionais de saúde a tratar e educar os pacientes em relação a essa
disfunção. O estudo prospectivo apresentado no Capítulo Sete teve como objetivo
analisar o prognóstico e os fatores prognósticos para pacientes com dor lombar
crônica que se apresentaram a uma clinica de fisioterapia privada para realização de
exercícios em grupo. Este estudo baseou-se em um coorte de 118 pacientes consecutivos
com dor lombar crônica atendidos em uma clínica de atenção primária. Análises de
regressão linear múltipla foram realizadas para investigar se uma série de variáveis
prognósticas (por exemplo, número de episódios anteriores) podem prever dor e
incapacidade em 12 meses de acompanhamento. A maioria dos pacientes (95%), foram
acompanhados no decorrer dos 12 meses. Aos 3 e 6 meses de acompanhamento dos
pacientes, a intensidade da dor, o incômodo causado pela dor, incapacidade e função
apresentaram melhoras semelhantes. No entanto, de 6 a 12 meses, a incapacidade e a
função continuaram a melhorar, enquanto um progresso marginal foi observado no
incômodo causado pela dor e na intensidade da dor. Os modelos finais mostraram
evidências de uma associação entre a intensidade da dor avaliada na linha de base com
a intensidade da dor aos 12 meses; enquanto que a duração do episódio atual,
incapacidade avaliada na linha de base e nível educacional foram associados com a
incapacidade aos 12 meses. A maior parte da variância no resultado não foi explicada
pelos preditores investigados neste estudo. Nossos resultados sugerem que, na população
estudada, a previsão dos resultados aos 12 meses pode ser mais difícil, ou outros
preditores não investigados devam ser considerados.
Nos últimos anos, pouco ou nenhum progresso ocorreu na identificação de
estratégias de intervenção eficazes para a dor lombar. Este fato pode ser explicado pela
dificuldade na identificação de uma causa específica de dor lombar na maioria das
xiii
pessoas. Como resultado, uma única intervenção é oferecida para distintos grupos de
pacientes com causas de dor potencialmente diferentes. A ressonância magnética tem a
capacidade de revelar uma série de degenerações e outras anormalidades anatômicas que
acometem a coluna lombo-sacra. No entanto, pouco tem-se focado na identificação de
subgrupos baseados em possíveis causas patoanatômicas da dor lombar. Assim, a revisão
sistemática apresentada no Capítulo Oito investigou se a presença de achados de
ressonância magnética tem a capacidade de identificar pacientes com dor lombar que
respondem melhor a certas intervenções terapeuticas. Esta revisão conduziu buscas em
três bancos de dados (MEDLINE, EMBASE e CENTRAL) e incluiu ensaios clínicos
randomizados que investigaram achados na ressonância magnética como modificadores
do efeito de tratamento para pacientes com dor lombar ou ciática. Baseado nos resultados
de oito estudos que investigaram interações em 38 subgrupos para combinações de
diferentes achados de ressonância magnética, intervenções e resultados, apenas dois
subgrupos apresentaram uma interação significativa. Atualmente, existe uma
carência de estudos para determinar se os achados de uma ressonância magnética
podem modificar o efeito do tratamento para dor lombar ou ciática.
A dificuldade de recrutamento dos pacientes para participar em pesquisas na
atenção primária á saúde é um fator importante que impede a realização de estudos
contendo um adequado e representativo tamanho amostral. Há uma carência de estudos
que investigam quais seriam as barreiras e facilitadores para aumentar o recrutamento de
pacientes pelos profissionais para participar de estudos observacionais em cuidados
primários à saúde. O estudo final desta tese é apresentado no Capítulo Nove e teve como
objetivo investigar os fatores associados ao recrutamento de participantes para um estudo
observacional. O estudo incluiu uma amostra de 138 profissionais em cuidados
primários que identificaram 1.585 pacientes de outubro de 2011 a novembro de 2012.
Os dados foram analisados através de uma regressão binomial negativa multivariada para
determinar as associações de uma variedade de características clínicas e fatores
operacionais, como a taxa de recrutamento. Os profissionais em cuidados primários
recrutaram 951 participantes, a uma taxa de 0,99 participantes por mês. Dois fatores
operacionais (profissionais que escolheram receber treinamento pelo telefone e o número
de pacientes não elegíveis referidos ao estudo) e um fator de clínico (profissionais que
não eram membros de sua respectiva associação) foram associados com a taxa de
recrutamento. O tamanho amostral necessário para o estudo foi atingido dentro de um
prazo razoável. No entanto, os fatores operacionais e clínicos associados à taxa de
xiv
recrutamento parecem limitados.
Os estudos apresentados nesta tese contribuem para a melhor compreensão dos
mecanismos responsáveis pela dor lombar. Foi constatado que fatores de risco
biomecânicos e individuais foram considerados pelos profissionais em cuidados primários
como sendo fatores importantes para o desenvolvimento de dor lombar aguda e devem ser
investigados em estudos futuros. A exposição a uma variedade de fatores físicos e
psicossociais aumentou o risco de um episódio de dor lombar aguda e devem ser
considerados. Parâmetros meteorológicos têm pouco efeito no surgimento de um episódio
de dor lombar aguda. Apesar de a velocidade do vento e de rajadas de vento mostrarem ter
um efeito pequeno, a magnitude do aumento não foi clinicamente relevante. Esses
resultados contribuem para o conhecimento sobre os fatores de risco da dor lombar e
podem orientar futuras estratégias de prevenção. Poucos estudos investigaram a associação
entre os achados da ressonância magnética e dor lombar, portanto, futuros estudos nesta
área se fazem necessários. O prognóstico de pacientes com dor lombar crônica que se
apresentaram a uma clínica de fisioterapia privada para realização de exercícios em grupo
é favorável. Esta informação é importante tanto para profissionais da área da saúde quanto
para pacientes, uma vez que contribui para uma expectativa realista, podendo ser usado
para orientar a tomada de decisões sobre a necessidade de implementação de intervenções
adicionais. Além disso, a necessidade de estudos de alta qualidade, com tamanho amostral
adequados, investigando achados da ressonância magnética como modificadores de efeito
de tratamento é essencial para determinar a importância clínica destes resultados na dor
lombar e ciática. Finalmente, esta tese fornece evidências de que é possível recrutar um
grande número de participantes para estudos observacionais. No entanto, a identificação de
fatores que possam estimular o recrutamento ainda permanece obscura.
Palavras-chave: Dor Lombar. Fatores de Risco. Mecanismo. Incapacidade. Ressonância
Magnética.
xv
Abstract
Low back pain is a very common condition that presents a significant burden to
individuals and society, being one of the leading causes of disability globally. Despite
considerable research over the past decades, there has been limited progress in identifying
management approaches that provide large treatment effects. Progress in identifying effective
prevention strategies has been no better. The identification, or better understanding, of factors
that increase the risk for the development of back pain, or that are associated with prognosis
or response to treatment, is crucial for developing and refining prevention and management
strategies. The studies in this thesis focus on evaluating the mechanisms of low back pain in
relation to risk, prognosis and response to treatment.
There is limited information about the causes of low back pain in the general
population presenting to care. Primary care clinicians who commonly manage a large number
of these patients could provide valuable insights into what may be the most important causes
for low back pain. The observational study presented in Chapter Two investigated the short-
and long-term risk factors that primary care clinicians believe most likely to trigger a sudden
episode of acute low back pain. This study was based on the views of 103 primary care
clinicians recruiting patients for a large case-crossover study. The most endorsed short- and
long-term risk factors to trigger an episode of sudden acute low back pain were
biomechanical (89.3% and 54.2%, respectively) and traits of the individual such as previous
low back pain episodes (6.4% and 39.0%, respectively). Surprisingly,
psychological/psychosocial and genetic risk factors were not considered important risk
factors for an episode of low back pain. Primary care clinicians believe that biomechanical
and individual risk factors are the most important factors to trigger an episode of low back
pain. The reason why the current literature considers psychosocial and genetic risk factors
important and primary care clinicians do not should be further investigated. This information
will help inform low back pain management and prevention programs.
A better understanding of what factors increase the risk of back pain is crucial to the
development of prevention strategies. Previous studies have focused on factors that are either
not modifiable (e.g. age) or involve long-term exposure (e.g. smoking). To evaluate factors
more proximal to the pain onset, a case-crossover study investigating a range of physical and
psychosocial risk factors for an episode of sudden onset, acute back pain was conducted.
Chapter Three and Four describe the study protocol and the report of the study,
xvi
respectively. A total of 999 patients with a new episode of acute low back pain were recruited
from 300 primary care clinics in Sydney. Exposure to physical and psychosocial triggers
during the two hours preceding back pain onset was compared to that in the 2-hour periods 24
and 48 hours before the onset. Exposure to manual tasks involving awkward positioning
(odds ratio 8.03; 95% confidence interval 5.46 to 11.82), objects far from the body (odds
ratio 6.20; 95% confidence interval 2.41 to 15.94), handling of live people or animals (odds
ratio 5.8; 95% confidence interval 2.25 to 14.98) or a load that was unstable, unbalanced or
difficult to grasp or hold (odds ratio 5.13; 95% confidence interval 2.40 to 10.93); as well as
being distracted during a task (odds ratio 25.0; 95% confidence interval 3.4 to 184.5), or
being fatigued (odds ratio 3.7; 95% confidence interval 2.2 to 6.3) significantly increased the
odds of a new episode of back pain. Exposure to alcohol consumption (odds ratio 1.5; 95%
confidence interval 0.6 to 3.7) or sexual activity (odds ratio 0.7; 95% confidence interval 0.3
to 1.8) did not increase risk of back pain onset. These associations were not moderated by
habitual physical activity, body mass index, previous low back pain episodes, or depression
and anxiety. Age moderated the risk associated with exposure to heavy loads (odds ratios for
people aged 20, 40 or 60 years were 13.6, 6.0 and 2.7 respectively) and sexual activity (odds
ratios for people aged 20, 40 or 60 years were 0.05, 0.41 and 3.21 respectively). This is the
first study to use this robust design to evaluate the association of physical and psychosocial
exposures and low back pain onset. These results can inform the development of new
prevention approaches for back pain.
There are many factors believed to trigger an episode of low back pain. Many patients
with musculoskeletal pain commonly report that their symptoms are influenced by the
weather, but this issue has not been evaluated for the most common musculoskeletal
condition, back pain. The study reported in Chapter Five aimed to investigate the influence
of various weather conditions on risk of acute low back pain. A case-crossover study was
performed with 993 patients presenting to primary care in Sydney. All participants’
demographic and clinical information were obtained from an interview. Weather parameters
were obtained from the Australian Bureau of Meteorology. We used the pair-matched
analytic approach (conditional logistic regression) for the case-crossover design to contrast
the weather at the time when participants first noticed their back pain (case window) with the
weather at the same time one week and one month prior (control windows). Most participants
were male (54.2%), with mean age of 45.2 years. Temperature, relative humidity, air
pressure, wind direction and precipitation showed no association with onset of a new episode
xvii
of back pain. Higher wind speed (odds ratio 1.17; 95% CI 1.04 to 1.32; p=0.01; for an
increase of 11 km/h) and wind gust (odds ratio 1.14; 95% CI 1.02 to 1.28; p=0.02; for an
increase of 14 km/h) increased the odds of pain onset. Most weather parameters were not
associated with the onset of back pain. Higher wind speed and wind gust speed provided a
very small increase in risk of back pain onset that does not seem clinically important.
Magnetic resonance imaging has been increasingly used by clinicians in order to
identify pathology responsible for low back pain. However, the importance of findings on
magnetic resonance imaging remains controversial, the evidence is limited and no systematic
review on this topic has been conducted. Therefore, the systematic review presented in
Chapter Six investigated whether magnetic resonance imaging findings of the lumbar spine
predict future low back pain in different samples with and without low back pain. Searches
performed in three international databases (MEDLINE, EMBASE and CINAHL) located 12
prospective cohort studies. Due to heterogeneity of the included studies, pooling the data for
a meta-analysis was not possible. No consistent associations between findings on magnetic
resonance imaging and pain or disability were identified. Three studies reported significant
associations for Modic changes type 1 with pain (odds ratio 6.2; 95% confidence interval 1.9
to 20.2), disc degeneration with disability in samples with current LBP (odds ratio 2.2; 95%
confidence interval 1.2 to 4.0) and disc herniation with pain in a mixed sample (odds ratio
0.2; 95% confidence interval not provided; p = 0.01). Few studies have investigated if
magnetic resonance imaging findings predict future low back pain. Although there were three
statistically significant results, overall these studies only provide limited evidence. There is a
clear need for further appropriately designed research.
The prognosis for chronic low back pain is considered poor. Better understanding of
prognostic factors for patients with chronic low back pain may help clinicians to manage and
educate patients regarding their future health. The prospective study presented in Chapter
Seven aimed to examine the prognosis and prognostic factors for patients with chronic low
back pain who presented to a private, community-based, group exercise program. This study
was based on the data of a cohort of 118 consecutive patients with chronic low back pain in a
primary care setting. Multivariate linear regression analyses were performed to investigate
whether a range of prognostic variables (e.g. number of previous episodes) predict pain and
disability at 12 months follow up. Most of the patients (95%) were followed up at 12 months.
At 3 and 6 months, pain intensity, bothersomeness, disability and function improved
similarly, but from 6 to 12 months, disability and function continued to improve while only
xviii
small further changes in bothersomeness and pain intensity occurred. The final models
showed evidence of an association between baseline pain intensity and 12 months pain
outcomes; whereas duration of current episode, baseline disability and educational level
accounted for 12 months disability outcome. Most of the variance in outcome was not
explained by any of the predictors we investigated in this study. Our findings suggest that in
this population, predicting 12 month outcome may be more difficult or other predictors may
be more important.
There has been little or no progress in identifying effective intervention strategies for
low back pain. This lack of progress may be explained by the current inability to identify a
specific cause in most people. As a result, a single intervention is provided to heterogeneous
groups of patients with potentially different causes of their pain. Magnetic resonance imaging
can reveal a range of degenerative findings and anatomical abnormalities affecting the
lumbosacral spine. However, very little attention has focussed on identifying subgroups
based on possible patho-anatomical causes of low back pain. Thus, the systematic review
presented in Chapter Eight investigated if the presence of magnetic resonance imaging
findings identifies patients with low back pain who respond better to particular interventions.
This review conducted a sensitive search in three databases (MEDLINE, EMBASE and
CENTRAL) and included randomised controlled trials investigating findings on magnetic
resonance imaging as treatment effect modifiers for patients with low back pain or sciatica.
Based on data from eight published reports investigating 38 subgroup interactions for
combinations of different magnetic resonance imaging findings, interventions and outcomes,
two subgroups displayed a significant interaction. At present, there is a lack of studies to
determine whether magnetic resonance imaging features modify effect of treatment for low
back pain or sciatica.
Patient recruitment to research studies is often difficult. Problematic recruitment in
primary care is one major factor preventing the collection of large representative samples for
research. Studies investigating factors that enhance recruitment to observational studies in
primary care is lacking. The final study of this thesis is presented in Chapter Nine and aimed
to investigate factors associated with recruitment of participants to an observational study.
The study included a sample of 138 primary care clinicians that screened 1,585 patients from
October 2011 to November 2012. Multivariate negative binomial regression was used to
determine associations of a variety of clinician characteristics and operational factors with the
recruitment rate. Primary care clinicians recruited 951 participants at a rate of 0.99
xix
participants per month. Two operational factors (clinicians who chose to be trained by
telephone and number of ineligible patients referred) and one clinician factor (clinicians who
were not member of their association) were associated with recruitment rate. We reached our
target sample size in a reasonable time frame. However, the operational and clinician factors
associated with recruitment rate seem limited.
Overall, the studies described in this thesis have provided an important contribution to
better understanding the mechanisms of back pain. Firstly, biomechanical and individual risk
factors were considered by primary care clinicians’ to be important triggers for acute low
back pain and should be investigated further in future research. Secondly, exposure to a range
of physical and psychosocial triggers increased the risk of an acute low back pain episode.
Weather parameters have little effect on triggering an episode of acute low back pain. While
wind speed and wind gusts were shown to have a small effect the magnitude of the increase
was not clinically relevant. These results are important in increasing our knowledge about
risk factors for low back pain and guide future prevention strategies. A systematic review of
the literature found only a few studies on the association between findings of magnetic
resonance imaging and low back pain, and clearly more studies in this area are needed.
Thirdly, the prognosis of patients with chronic low back pain presenting to a private,
community-based, group exercise program is favourable. This information is important for
clinicians and patients as it helps with realistic expectation and can be used to guide decision
making regarding the need for additional interventions. In addition, the need for high quality,
adequately powered trials investigating magnetic resonance imaging findings as effect
modifiers is essential to determine the clinical importance of these findings in low back pain
and sciatica. Finally, this thesis provides evidence that it is reasonably easy to recruit large
number of participants to observational studies; however, the identification of consistent
factors that increase recruitment remains unclear.
Keywords: Low back pain. Risk Factors. Mechanism. Disability. Magnetic Resonance
Imaging.
xx
Table of Contents
Supervisors’ statement ................................................................................................................ i
Candidate’s statement ................................................................................................................ ii
Approval letter .......................................................................................................................... iii
Record ....................................................................................................................................... iv
Acknowledgements .................................................................................................................... v
Publications and presentations .................................................................................................. vi
Preface ..................................................................................................................................... viii
Abstract ...................................................................................................................................... x
Resumo (Abstract in Portuguese) ........................................................................................... xvi
Chapter One: Introduction ..................................................................................................... 26
1. Epidemiology of low back pain .................................................................................... 27
2. Economic burden of low back pain .............................................................................. 27
3. Definition and classification of low back pain ............................................................. 28
4. Mechanisms of low back pain ...................................................................................... 29
4.1 Risk factors .......................................................................................................... 29
4.1.1. Primary care clinician’s perception on risk factors for low back pain .. 30
4.1.2. Physical and psychosocial risk factors ................................................... 30
4.1.3. Environmental factors and low back pain .............................................. 31
4.1.4. Magnetic resonance imaging ................................................................. 32
4.2. Prognostic factors.................................................................................................. 32
4.2.1. Prognostic factors for chronic low back pain ........................................ 33
4.3. Subgroup of low back pain ................................................................................... 33
4.3.1. Magnetic resonance imaging subgrouping ............................................ 34
5. Recruitment for large observational studies of low back pain ...................................... 35
5.1. Factors that influence recruitment to observational studies .................................. 35
6. Aims of the thesis ......................................................................................................... 36
xxi
7. References ..................................................................................................................... 37
Chapter Two: Clinicians’ views on factors that trigger a sudden onset of low back pain ..... 46
Statement of authorship contribution ................................................................................ 47
Abstract ............................................................................................................................. 48
Introduction ....................................................................................................................... 48
Materials and methods ...................................................................................................... 49
Results ............................................................................................................................... 51
Discussion ......................................................................................................................... 52
Conclusions ....................................................................................................................... 53
References ......................................................................................................................... 53
Chapter Three: Triggers for an episode of sudden onset low back pain: study protocol ..... 56
Statement of authorship contribution ................................................................................ 57
Abstract ............................................................................................................................. 58
Background ....................................................................................................................... 58
Methods/Design ................................................................................................................ 59
Discussion ......................................................................................................................... 61
References ......................................................................................................................... 61
Additional file 1: Clinicians’ questionnaire ...................................................................... 63
Additional file 2: Study participants’ questionnaire ......................................................... 64
Chapter Four: What triggers an episode of acute low back pain? A case-crossover study . 79
Statement of authorship contribution ................................................................................ 80
Abstract ............................................................................................................................. 81
Introduction ....................................................................................................................... 81
Patients and methods ........................................................................................................ 81
Results ............................................................................................................................... 83
Discussion ......................................................................................................................... 86
References ......................................................................................................................... 88
xxii
Appendix Table 1 .............................................................................................................. 89
Appendix Table 2 .............................................................................................................. 91
Appendix Table 3 .............................................................................................................. 93
Appendix Table 4 .............................................................................................................. 95
Appendix 5 ........................................................................................................................ 97
Chapter Five: Effect of weather on back pain: Results from a case-crossover study ......... 112
Statement of authorship contribution .............................................................................. 113
Abstract ........................................................................................................................... 114
Introduction ..................................................................................................................... 114
Subjects and methods ...................................................................................................... 115
Results ............................................................................................................................. 116
Discussion ....................................................................................................................... 116
References ....................................................................................................................... 119
Chapter Six: Does magnetic resonance imaging predict future low back pain? A systematic
review ..................................................................................................................................... 120
Statement of authorship contribution .............................................................................. 121
Abstract ........................................................................................................................... 122
Introduction ..................................................................................................................... 122
Methods .......................................................................................................................... 123
Results ............................................................................................................................. 124
Discussion ....................................................................................................................... 130
Conclusions ..................................................................................................................... 131
References ....................................................................................................................... 131
Appendix S1 ................................................................................................................... 133
Appendix S2 ................................................................................................................... 134
Chapter Seven: Prognosis of chronic low back pain in patients presenting to a private
community-based group exercise program ............................................................................ 136
Statement of authorship contribution .............................................................................. 137
xxiii
Abstract ........................................................................................................................... 138
Introduction ..................................................................................................................... 138
Material and methods ...................................................................................................... 139
Results ............................................................................................................................. 140
Discussion ....................................................................................................................... 141
Conclusions ..................................................................................................................... 142
References ....................................................................................................................... 144
Chapter Eight: Do magnetic resonance imaging findings identify patients with low back
pain who respond better to particular interventions? A systematic review ........................... 145
Statement of authorship contribution .............................................................................. 146
Abstract ........................................................................................................................... 148
Introduction ..................................................................................................................... 149
Methods .......................................................................................................................... 151
Results ............................................................................................................................. 154
Discussion ....................................................................................................................... 159
Conclusions ..................................................................................................................... 162
References ....................................................................................................................... 163
Figure 1 ........................................................................................................................... 168
Table 1 ............................................................................................................................ 169
Table 2 ............................................................................................................................ 170
Table 3 ............................................................................................................................ 172
Appendix S1 ................................................................................................................... 175
Appendix S2 ................................................................................................................... 176
Appendix S3 ................................................................................................................... 177
Appendix S4 ................................................................................................................... 179
Chapter Nine: Clinician characteristics and operational factors have limited influence on
participant recruitment in primary care: Results from an observational study ...................... 183
Statement of authorship contribution .............................................................................. 184
xxiv
Abstract ........................................................................................................................... 185
Introduction ..................................................................................................................... 185
Methods .......................................................................................................................... 186
Results ............................................................................................................................. 188
Discussion ....................................................................................................................... 189
Conclusion ...................................................................................................................... 191
References ....................................................................................................................... 191
Chapter Ten: Conclusions .................................................................................................... 193
10.1. Aim ........................................................................................................................ 194
10.2. Overview of principal findings .............................................................................. 195
10.3. Implications and suggestions for future research .................................................. 196
10.3.1. Mechanism: Risk factors for low back pain .................................................. 196
10.3.2. Management: Prognosis and subgroups for low back pain ........................... 199
10.3.3. Factors influencing recruitment rate .............................................................. 200
10.4. References .............................................................................................................. 202
Appendix ............................................................................................................................... 205
Appendix A: Media coverage of Chapter Five ............................................................... 206
Appendix B: Curriculum Vitae ....................................................................................... 237
xxv
Chapter One
Introduction
26
1. Epidemiology of low back pain
Low back pain is an extremely common health problem that affects a large part of the
population during their lifetime (HOY et al., 2010; HOY et al., 2012). Until 10 years ago, it
was largely thought of as a problem of developed Western countries (VOLINN, 1997).
However, since that time an increasing number of studies have demonstrated that low back
pain is also a major problem in less developed countries (MARIETTE and MARIETTE,
2003; LOUW, MORRIS and GRIMMER-SOMERS, 2007; HOY, BROOKS et al., 2010;
BALAGUE et al., 2012). It is estimated that over one year, the incidence of people who have
a first-ever episode of low back pain ranged from 6.3% to 15.4%, and the one year incidence
of people who have any episode of low back pain (i.e., first-ever or recurrent) ranged from
1.5% to 36% (HOY, BROOKS et al., 2010). The highest prevalence of low back pain is
among females and people aged 40 to 80 years. The mean (SD) global prevalence of activity
limiting low back pain lasting for more than 1 day is estimated to be 11.9% (2.0) (HOY,
BAIN et al., 2012). Although low back pain is not a life threatening condition, it is the
leading cause of activity limitation and work absence throughout much of the world, and it
causes an enormous economic burden on individuals, families, communities, industry and
governments (THELIN, HOLMBERG and THELIN, 2008; FERREIRA et al., 2011;
MURRAY et al., 2012).
2. Economic burden of low back pain
The economic burden of low back pain is very large and appears to be rising. It is
estimated that the number of visits to allied health professionals exceeds 30 million per year
in the United States alone (ANDERSSON, 1999). This high frequency of annual visits leads
to both high direct and indirect costs (HOY et al., 2010). Direct costs includes resources
spent on assessing and treating low back pain, such as medications, assistive devices,
diagnostic tests, and may also include non-medical costs incurred by the patient and family
and other public resources (e.g. transportation). Indirect costs commonly include costs related
to employment and household productivity (EKMAN, JOHNELL and LIDGREN, 2005;
DAGENAIS, CARO and HALDEMAN, 2008).
In the United States, the economic burden for low back pain is estimated to be over
US$85 billion a year (DAGENAIS, CARO and HALDEMAN, 2008). In Australia AU$ 9.17
27
billion per annum is the total cost spent on care for low back pain (WALKER, MULLER and
GRANT, 2003). The total annual cost in Europe has been estimated, for instance, €6.4 billion
in the Netherlands (LAMBEEK et al., 2011), €6.6 billion in Switzerland (WIESER et al.,
2011), ₤12.3 billion in the United Kingdom (HOY, BROOKS et al., 2010) and €1.9 billion in
Sweden (EKMAN, JOHNELL and LIDGREN, 2005). Although the economic burden for low
back varies among countries, it is apparent that low back pain represents an enormous public
health problem worldwide.
3. Definition and classification of low back pain
Low back pain is defined as pain and discomfort, localised below the costal margin
and above the inferior gluteal folds, with or without leg pain (VAN TULDER et al., 2006).
Diagnostic triage is a simple and practical classification, which has gained international
acceptance, by dividing low back pain into three main categories: (i) serious spinal
pathologies; (ii) Nerve root pain (radicular pain)/spinal canal stenosis; and (iii) non-specific
low back pain (KOES et al., 2010).
Serious spinal pathologies include spinal tumours, vertebral infections, cauda equina
syndrome, vertebral fracture and inflammatory diseases such as ankylosing spondylitis
(CHOU et al., 2007). Only a minority of patients (less than 1%) with acute low back pain
presenting to primary care are diagnosed with a serious spinal pathology (HENSCHKE et al.,
2009). When serious spinal pathology is suspected as a cause of low back pain, further
diagnostic investigations are usually required. Guidelines recommend the use of red flags to
screen for serious pathology and to identify those patients that may need imaging and
laboratory test or specialist referral to establish a definitive diagnosis (MAHER et al., 2011).
Nerve root pain (radicular pain) or spinal canal stenosis represent approximately 5%
of the low back pain cases and are characterised by presentations where leg pain is dominant
(KONSTANTINOU and DUNN, 2008). In approximately 90% of the case of leg dominant
pain the condition is caused by a herniated disc with nerve root compression, but lumbar
canal or foraminal stenosis and (less often) tumours or cysts are other possible causes
(VALAT et al., 2010). While there are a range of definitions of sciatica, the key clinical
features that can help clinicians to distinguish it from nonspecific low back pain include
unilateral leg pain that is worse than the low back pain, pain radiating below the knee,
28
presence of numbness or pins and needles in a dermatomal distribution, positive results on a
straight leg raise test, and weakness or reflex changes, or both, in a myotomal distribution
(KOES, VAN TULDER and PEUL, 2007).
Non-specific low back pain is a term used synonymously with simple low back pain
or mechanical low back pain and is defined as low back pain not attributable to a
recognisable, known specific pathology (BALAGUE, MANNION et al., 2012). Due to the
inability to identify the source of pain, the vast majority of low back pain patients
(approximately 90%) fall into the non-specific low back pain category (HANCOCK et al.,
2007).
Low back pain is often classified in three stages (acute, sub-acute and chronic)
according to its duration and this provides some information to the clinician with regards to
treatment and prognosis. Acute low back pain is usually defined as an episode persisting for
less than 6 weeks; sub-acute low back pain as low back pain persisting between 6 to 12
weeks and chronic low back pain as low back pain persisting for 12 weeks or longer (VAN
TULDER, BECKER et al., 2006).
4. Mechanisms of low back pain
Low back pain may originate from many anatomical structures in the lumbar spine,
including bones, intervertebral discs, ligaments, muscles, neural structures and blood vessels
(DEYO and WEINSTEIN, 2001). However, the exact source of low back pain is often
difficult to identify using conventional tests available in primary care (ANDERSSON, 1999;
HANCOCK, MAHER et al., 2007). Research into risk factors for low back pain is often
challenging due to heterogeneity across research methods, case definitions and study
populations, it is clear that there are a number of environmental and individual factors that
influence the onset and course of low back pain (HOY, BROOKS et al., 2010).
4.1. Risk factors
Low back pain is a complex condition with many factors believed to contribute to its
onset (LATZA et al., 2000). Investigations into risk factors for low back pain is in a
developing stage when compared with other common conditions, such as cardiovascular
29
disease and cancer (MANEK and MACGREGOR, 2005). Broadly, the risk factors associated
with low back pain can be classified as individual, psychosocial, occupational, genetic and
biomechanical (HAMBERG-VAN REENEN et al., 2007; LANG et al., 2012; TAYLOR et
al., 2014). There are a reasonable number of recognised risk factors for low back pain,
however, most of these risk factors are not robust or replicable, and many are not modifiable
(TAYLOR, GOODE et al., 2014). Identifying factors that may increase the risk for or
predispose individuals to the development of back pain is critical in attempting to reduce the
prevalence and ultimately the social impact of this condition (RUBIN, 2007).
4.1.1. Primary care clinician’s perceptions on risk factors for low back pain
Risk factors for the development of low back pain in the general population who
present to primary health clinics are poorly understood (VAN TULDER, BECKER et al.,
2006), despite the high volume of patients seeking care (DEYO and PHILLIPS, 1996). One
reason for this is that most work up-to-date has focused on samples of specific occupational
groups or working conditions (BURDORF, NAAKTGEBOREN and DE GROOT, 1993;
MURTEZANI et al., 2011; FERGUSON et al., 2012; VANDERGRIFT et al., 2012).
Although studies conducted in occupational settings may reveal important risk factors for
work-related back pain, these risks may not be relevant to other populations, such as those
drawn from primary care. Primary care clinicians who frequently manage patients with low
back pain may provide an important understanding into the most common risk factors. The
identification of putative risk factors in primary care is essential to strengthen future research
and help inform low back pain prevention programs. Chapter Two presents the most likely
risk factors involving short and long-term exposure that primary care clinicians believe could
trigger a sudden episode of acute low back pain.
4.1.2. Physical and psychosocial risk factors
Many studies have attempted to identify and evaluate the contribution of multiple
different demographic, physical, socioeconomic, psychological, and occupational factors to
the development of back pain (VINDIGNI et al., 2005; RUBIN, 2007; TAYLOR, GOODE et
al., 2014). Known non-modifiable risk factors for low back pain include increasing age,
number of children, previous episode of low back pain and major scoliosis. Those that are
30
modifiable are poor health, obesity, smoking and prolonged sitting (VINDIGNI, WALKER et
al., 2005). However, there is a significant limitation in interpreting the literature on risk
factors for low back pain. Most of the recognised risk factors were assessed only in single or
small studies, with weak and non-reproducible evidence to support a definite association, are
not robust or replicable across studies, and were not modifiable (HURWITZ and
MORGENSTERN, 1997; KOPEC, SAYRE and ESDAILE, 2004; RUBIN, 2007; TAYLOR,
GOODE et al., 2014). Another problem with previous studies on risk factors for low back
pain is the focus on long-term exposure. Little is known about short-term exposure to
physical and psychological risk e.g. distraction while lifting. Modifying such risk factors may
be extremely important in preventing back pain recurrence.
One of the best designs to investigate transient risk factors is the case-crossover
design. This design is more efficient than cohort designs because it samples only cases and
may be less exposed to selection bias than case-control designs because cases provide their
own control data (MACLURE, 1991). One of the main advantages of the case-crossover
design is that each case serves as its own control. Consequently, case-crossover studies are
not confounded by time-invariant risk factors. Another advantage is that the case-crossover
design is immune to one of the main causes of bias in case-control studies: the selection of
control that is not representative of the population that produced the cases. A further
advantage is the ability to assess short-term reversible exposures (MACLURE, 1991;
MACLURE and MITTLEMAN, 2000). Chapter Three represents the published study
protocol of a case-crossover study investigating the association between an episode of sudden
onset, acute back pain with transient exposure to a range of physical and psychosocial factors.
The results of this study are described in Chapter Four.
4.1.3. Environmental factors and low back pain
There are an increasing number of studies examining the association between
environmental factors (e.g. temperature, humidity, air pressure, wind and precipitation) and
the onset of musculoskeletal conditions. Most of the efforts to measure climatic effects have
been directed at individuals with rheumatoid arthritis and chronic pain (JAMISON,
ANDERSON and SLATER, 1995; PATBERG and RASKER, 2004; ABASOLO et al.,
2013). Patients with musculoskeletal pain (e.g. low back pain) commonly report that certain
weather conditions influence their symptoms (SMEDSLUND et al., 2009). Despite the high
31
frequency with which this belief is reported, there are few robust studies that have
investigated this potential association (TENIAS et al., 2009; ABASOLO, TOBIAS et al.,
2013). Chapter Five investigates the influence of various weather conditions on risk of low
back pain.
4.1.4. Magnetic resonance imaging
Most low back pain sufferers, around 90%, are classified as having non-specific low
back pain (VAN TULDER, BECKER et al., 2006), reflecting the inability to identify a clear
anatomical source for the pain (WANG, VIDEMAN and BATTIE, 2012). If the source of
pain could be identified in at least some of these patients, then it is possible that more logical
and effective interventions could be found (HANCOCK, MAHER et al., 2007).
Magnetic resonance imaging is the preferred investigation for most spinal diseases
and is increasingly requested for people with low back pain (SHEEHAN, 2010). Various
abnormalities can be identified on lumbar magnetic resonance imaging, including disc
herniation, nerve root impingement, disc degeneration, and high intensity zone or annular tear
(ENDEAN, PALMER and COGGON, 2011). However, the importance of findings on
magnetic resonance imaging remains controversial (WASSENAAR et al., 2012). Many
studies have documented a high prevalence of disc abnormalities on imaging in
asymptomatic subjects (JARVIK et al., 2001). Magnetic resonance imaging findings in
currently asymptomatic people may represent markers of early pre-symptomatic disease that
is later characterized by episodes of pain and/or disability. Chapter Six reports on a
systematic review that sought to investigate whether magnetic resonance imaging findings of
the lumbar spine predict future low back pain in different samples with and without low back
pain.
4.2. Prognostic factors
Prognosis is a description of the course or prediction of the outcome of a health
condition over time (HAYDEN et al., 2010). Important to prognosis is consideration and
assessment of characteristics or factors that are associated with or determine the course of a
condition. Clinicians may use prognostic information to educate or inform the management
32
of their patients (CROFT, DUNN and RASPE, 2006). The likely prognosis of low back pain
varies according to the duration of symptoms. The prognosis for acute low back pain is
inconsistently reported, with estimates of recovery ranging from 39% to 90% (KOES, VAN
TULDER et al., 2010; DA et al., 2012). Patients presenting with a longer duration with low
back pain or with recurrent low back pain the prognosis may be less favourable (KOES, VAN
TULDER et al., 2010).
4.2.1. Prognostic factors for chronic low back pain
For those patients with symptoms persisting for longer than 3 months, approximately
one third will recover within 1-2 years after initial onset (VON KORFF et al., 1993; COSTA
LDA et al., 2009). According to a recent systematic review, the prognosis of patients
suffering from chronic pain is less favourable for those who have taken previous sick leave
for low back pain, have high disability levels or high pain intensity at onset of chronic low
back pain, have lower education, perceive themselves as having a high risk of persistent pain,
and were born outside Australia (COSTA LDA, MAHER et al., 2009). Patients presenting
for care in settings where these adverse prognostic factors are uncommon may have a more
favourable prognosis than widely reported. Until now no study has investigated the prognosis
of people with chronic low back pain attending a private, community-based, group exercise
program. Chapter Seven reports the prognosis and prognostic factors for this population.
4.3. Subgroups of low back pain
To date, there are clear trends in recent high quality randomised clinical trials, that
show that the sorts of interventions that primary care clinicians have to offer, on average,
have small (sometimes insignificant) to moderate effects (LITTLE et al., 2008; LAMB et al.,
2010), and often there is little or no difference between the effectiveness of different
interventions (CAIRNS, FOSTER and WRIGHT, 2006; JOHNSON et al., 2007). One
explanation for this lack of progress may be that a single intervention is usually provided to
heterogeneous groups of patients with potentially different causes of their pain. Many
clinicians and researchers believe that there are subgroups of people with spinal pain who
respond differently to treatment and have different prognosis (KENT, KEATING and
BUCHBINDER, 2009). The Identification of subgroups of low back pain patients has been
33
identified as a key research priority in the field (COSTA LDA et al., 2013), which may lead
to improve low back pain patient’s outcome.
Two recent reviews have investigated subgrouping of low back pain treatment. Most
previous research in this area has focussed on identifying clinical and psychosocial variables
associated with patients who respond better to different interventions (KENT, MJOSUND
and PETERSEN, 2010; KENT and KJAER, 2012). However, very little attention has
focussed on identifying subgroups based on possible patho-anatomical causes of low back
pain.
4.3.1. Magnetic resonance imaging subgrouping
There has been considerable interest in magnetic resonance imaging subgrouping
recently (KJAER et al., 2006). Modic changes were first described by Modic et al. 1988
(MODIC et al., 1988; MODIC and ROSS, 2007), who identified three types (Type I, II and
III). Based on the histological studies, Type I was characterised by fissured endplates and
vascular granulation tissue adjacent to the endplate, whereas Type II was characterised as
disruption of the endplates as well as fatty degeneration of the adjacent bone marrow
(MODIC et al., 1988). Type III appeared to involve sclerosis of the bone marrow as seen on
radiographs (MODIC, MASARYK et al., 1988). Up to date, one review has investigated if
Modic changes constitute a specific subgroup of low back pain (JENSEN and LEBOEUF-
YDE, 2011). However, the inclusion of single subgroup designs (e.g. studies including all
people with Modic changes and no people without Modic changes) prevents a robust
evaluation of whether effect modification occurred in this subgroup (KENT et al., 2010).
If subgroups of patients, based on magnetic resonance imaging findings, who respond
best to specific interventions could be identified, the potential exists to significantly improve
patient outcomes and healthcare system efficiency. Chapter Eight reports on a systematic
review that sought to investigate if the presence of magnetic resonance imaging findings
identifies patients with low back pain who respond better to particular interventions.
34
5. Recruitment for large observational studies of low back pain
There is a need for large-scale well-designed studies evaluating risk factors for low
back pain. Universally, research studies need sufficient participants to ensure statistical
power and validity, but recruitment remains problematic (FAIRHURST and DOWRICK,
1996). Participant recruitment is considered the most difficult aspect of the research process
(BLANTON et al., 2006; BOWER, WILSON and MATHERS, 2007). Previous research has
reported that problems with recruitment are a major reason for the failure of research studies,
leading to wasted research funding (HUNNINGHAKE, DARBY and PROBSTFIELD, 1987).
One major challenge to collecting large quality samples of data is efficient recruitment of
participants to a study (SPAAR et al., 2009).
5.1. Factors that influence recruitment to observational studies
There are many factors that could potentially contribute to successful recruit
participants to an observational study. Previous research has examined methods to increase
the participation of both patients and healthcare professionals to primary care studies, with
much of the research to date focused on randomised controlled trials (RENDELL, MERRITT
and GEDDES, 2007; ROLLMAN et al., 2008). There is limited evidence available to inform
researchers about factors that can influence recruitment to observational studies conducted in
primary care (HAYWARD et al., 2013). To improve the availability of information on
participant recruitment to observational studies, Chapter Nine of this thesis investigates
factors that influence recruitment to an observational study for low back pain.
35
6. Aims of the thesis
The specific aims of this thesis were to:
1. Describe the short and long-term factors that primary care clinicians consider
important in triggering a sudden episode of acute low back pain (Chapter 2)
2. Investigate the increase in risk of an episode of sudden onset, acute back pain
associated with transient exposure to a range of physical and psychosocial factors
(Chapter 3 and 4).
3. Investigate the influence of various weather conditions on risk of low back pain
(Chapter 5).
4. Systematically review whether magnetic resonance imaging findings of the lumbar
spine predict future low back pain in different samples with and without low back
pain (Chapter 6).
5. Examine the prognosis and prognostic factors for patients with chronic low back pain
presenting to a private, community-based, group exercise program (Chapter 7).
6. Investigate if the presence of magnetic resonance imaging findings identifies patients
with low back pain who respond better to particular interventions (Chapter 8).
7. Identify factors that influence recruitment to an observational study (Chapter 9).
36
7. References
ABASOLO, L., A. TOBIAS, L. LEON, L. CARMONA, J. L. FERNANDEZ-RUEDA, A. B.
RODRIGUEZ, B. FERNANDEZ-GUTIERREZ and J. A. JOVER, Weather conditions may
worsen symptoms in rheumatoid arthritis patients: the possible effect of temperature.
Reumatol Clin, 9, 4, p. 226-228, 2013.
ANDERSSON, G. B., Epidemiological features of chronic low-back pain. Lancet, 354,
9178, p. 581-585, 1999.
BALAGUE, F., A. F. MANNION, F. PELLISE and C. CEDRASCHI, Non-specific low back
pain. Lancet, 379, 9814, p. 482-491, 2012.
BLANTON, S., D. M. MORRIS, M. G. PRETTYMAN, K. MCCULLOCH, S. REDMOND,
K. E. LIGHT and S. L. WOLF, Lessons learned in participant recruitment and retention: the
EXCITE trial. Phys Ther, 86, 11, p. 1520-1533, 2006.
BOWER, P., S. WILSON and N. MATHERS, Short report: how often do UK primary care
trials face recruitment delays? Fam Pract, 24, 6, p. 601-603, 2007.
BURDORF, A., B. NAAKTGEBOREN and H. C. DE GROOT, Occupational risk factors for
low back pain among sedentary workers. J Occup Med, 35, 12, p. 1213-1220, 1993.
CAIRNS, M. C., N. E. FOSTER and C. WRIGHT, Randomized controlled trial of specific
spinal stabilization exercises and conventional physiotherapy for recurrent low back pain.
Spine (Phila Pa 1976), 31, 19, p. E670-681, 2006.
CHOU, R., A. QASEEM, V. SNOW, D. CASEY, J. T. CROSS, JR., P. SHEKELLE and D.
K. OWENS, Diagnosis and treatment of low back pain: a joint clinical practice guideline
from the American College of Physicians and the American Pain Society. Ann Intern Med,
147, 7, p. 478-491, 2007.
COSTA LDA, C., B. W. KOES, G. PRANSKY, J. BORKAN, C. G. MAHER and R. J.
SMEETS, Primary care research priorities in low back pain: an update. Spine (Phila Pa
1976), 38, 2, p. 148-156, 2013.
COSTA LDA, C., C. G. MAHER, J. H. MCAULEY, M. J. HANCOCK, R. D. HERBERT,
K. M. REFSHAUGE and N. HENSCHKE, Prognosis for patients with chronic low back
pain: inception cohort study. BMJ, 339, p. b3829, 2009.
CROFT, P. R., K. M. DUNN and H. RASPE, Course and prognosis of back pain in primary
care: the epidemiological perspective. Pain, 122, 1-2, p. 1-3, 2006.
37
DA, C. M. C. L., C. G. MAHER, M. J. HANCOCK, J. H. MCAULEY, R. D. HERBERT and
L. O. COSTA, The prognosis of acute and persistent low-back pain: a meta-analysis. CMAJ,
184, 11, p. E613-624, 2012.
DAGENAIS, S., J. CARO and S. HALDEMAN, A systematic review of low back pain cost
of illness studies in the United States and internationally. Spine J, 8, 1, p. 8-20, 2008.
DEYO, R. A. and W. R. PHILLIPS, Low back pain. A primary care challenge. Spine (Phila
Pa 1976), 21, 24, p. 2826-2832, 1996.
DEYO, R. A. and J. N. WEINSTEIN, Low back pain. N Engl J Med, 344, 5, p. 363-370,
2001.
EKMAN, M., O. JOHNELL and L. LIDGREN, The economic cost of low back pain in
Sweden in 2001. Acta Orthop, 76, 2, p. 275-284, 2005.
ENDEAN, A., K. T. PALMER and D. COGGON, Potential of magnetic resonance imaging
findings to refine case definition for mechanical low back pain in epidemiological studies: a
systematic review. Spine (Phila Pa 1976), 36, 2, p. 160-169, 2011.
FAIRHURST, K. and C. DOWRICK, Problems with recruitment in a randomized controlled
trial of counselling in general practice: causes and implications. J Health Serv Res Policy, 1,
2, p. 77-80, 1996.
FERGUSON, S. A., W. G. ALLREAD, D. L. BURR, C. HEANEY and W. S. MARRAS,
Biomechanical, psychosocial and individual risk factors predicting low back functional
impairment among furniture distribution employees. Clin Biomech (Bristol, Avon), 27, 2, p.
117-123, 2012.
FERREIRA, G. D., M. C. SILVA, A. J. ROMBALDI, E. D. WREGE, F. V. SIQUEIRA and
P. C. HALLAL, Prevalence and associated factors of back pain in adults from southern
Brazil: a population-based study. Rev Bras Fisioter, 15, 1, p. 31-36, 2011.
HAMBERG-VAN REENEN, H. H., G. A. ARIENS, B. M. BLATTER, W. VAN
MECHELEN and P. M. BONGERS, A systematic review of the relation between physical
capacity and future low back and neck/shoulder pain. Pain, 130, 1-2, p. 93-107, 2007.
HANCOCK, M. J., C. G. MAHER, J. LATIMER, M. F. SPINDLER, J. H. MCAULEY, M.
LASLETT and N. BOGDUK, Systematic review of tests to identify the disc, SIJ or facet joint
as the source of low back pain. Eur Spine J, 16, 10, p. 1539-1550, 2007.
HAYDEN, J. A., K. M. DUNN, D. A. VAN DER WINDT and W. S. SHAW, What is the
prognosis of back pain? Best Pract Res Clin Rheumatol, 24, 2, p. 167-179, 2010.
38
HAYWARD, R. A., M. PORCHERET, C. D. MALLEN and E. THOMAS, Recruiting
patients and collecting data for an observational study using computerised record pop-up
prompts: the PROG-RES study. Prim Health Care Res Dev, 14, 1, p. 21-28, 2013.
HENSCHKE, N., C. G. MAHER, K. M. REFSHAUGE, R. D. HERBERT, R. G.
CUMMING, J. BLEASEL, J. YORK, A. DAS and J. H. MCAULEY, Prevalence of and
screening for serious spinal pathology in patients presenting to primary care settings with
acute low back pain. Arthritis Rheum, 60, 10, p. 3072-3080, 2009.
HOY, D., C. BAIN, G. WILLIAMS, L. MARCH, P. BROOKS, F. BLYTH, A. WOOLF, T.
VOS and R. BUCHBINDER, A systematic review of the global prevalence of low back pain.
Arthritis Rheum, 64, 6, p. 2028-2037, 2012.
HOY, D., P. BROOKS, F. BLYTH and R. BUCHBINDER, The Epidemiology of low back
pain. Best Pract Res Clin Rheumatol, 24, 6, p. 769-781, 2010.
HOY, D., L. MARCH, P. BROOKS, A. WOOLF, F. BLYTH, T. VOS and R.
BUCHBINDER, Measuring the global burden of low back pain. Best Pract Res Clin
Rheumatol, 24, 2, p. 155-165, 2010.
HUNNINGHAKE, D. B., C. A. DARBY and J. L. PROBSTFIELD, Recruitment experience
in clinical trials: literature summary and annotated bibliography. Control Clin Trials, 8, 4
Suppl, p. 6S-30S, 1987.
HURWITZ, E. L. and H. MORGENSTERN, Correlates of back problems and back-related
disability in the United States. J Clin Epidemiol, 50, 6, p. 669-681, 1997.
JAMISON, R. N., K. O. ANDERSON and M. A. SLATER, Weather changes and pain:
perceived influence of local climate on pain complaint in chronic pain patients. Pain, 61, 2, p.
309-315, 1995.
JARVIK, J. J., W. HOLLINGWORTH, P. HEAGERTY, D. R. HAYNOR and R. A. DEYO,
The Longitudinal Assessment of Imaging and Disability of the Back (LAIDBack) Study:
baseline data. Spine (Phila Pa 1976), 26, 10, p. 1158-1166, 2001.
JENSEN, R. K. and C. LEBOEUF-YDE, Is the presence of modic changes associated with
the outcomes of different treatments? A systematic critical review. BMC Musculoskelet
Disord, 12, p. 183, 2011.
JOHNSON, R. E., G. T. JONES, N. J. WILES, C. CHADDOCK, R. G. POTTER, C.
ROBERTS, D. P. SYMMONS, P. J. WATSON, D. J. TORGERSON and G. J.
MACFARLANE, Active exercise, education, and cognitive behavioral therapy for persistent
disabling low back pain: a randomized controlled trial. Spine (Phila Pa 1976), 32, 15, p.
1578-1585, 2007.
39
KENT, P., M. HANCOCK, D. H. PETERSEN and H. L. MJOSUND, Clinimetrics corner:
choosing appropriate study designs for particular questions about treatment subgroups. J
Man Manip Ther, 18, 3, p. 147-152, 2010.
KENT, P. and P. KJAER, The efficacy of targeted interventions for modifiable psychosocial
risk factors of persistent nonspecific low back pain - a systematic review. Man Ther, 17, 5,
p. 385-401, 2012.
KENT, P., H. L. MJOSUND and D. H. PETERSEN, Does targeting manual therapy and/or
exercise improve patient outcomes in nonspecific low back pain? A systematic review. BMC
Med, 8, p. 22, 2010.
KENT, P. M., J. L. KEATING and R. BUCHBINDER, Searching for a conceptual
framework for nonspecific low back pain. Man Ther, 14, 4, p. 387-396, 2009.
KJAER, P., L. KORSHOLM, T. BENDIX, J. S. SORENSEN and C. LEBOEUF-YDE,
Modic changes and their associations with clinical findings. Eur Spine J, 15, 9, p. 1312-
1319, 2006.
KOES, B. W., M. VAN TULDER, C. W. LIN, L. G. MACEDO, J. MCAULEY and C.
MAHER, An updated overview of clinical guidelines for the management of non-specific
low back pain in primary care. Eur Spine J, 19, 12, p. 2075-2094, 2010.
KOES, B. W., M. W. VAN TULDER and W. C. PEUL, Diagnosis and treatment of sciatica.
BMJ, 334, 7607, p. 1313-1317, 2007.
KONSTANTINOU, K. and K. M. DUNN, Sciatica: review of epidemiological studies and
prevalence estimates. Spine (Phila Pa 1976), 33, 22, p. 2464-2472, 2008.
KOPEC, J. A., E. C. SAYRE and J. M. ESDAILE, Predictors of back pain in a general
population cohort. Spine (Phila Pa 1976), 29, 1, p. 70-77; discussion 77-78, 2004.
LAMB, S. E., Z. HANSEN, R. LALL, E. CASTELNUOVO, E. J. WITHERS, V. NICHOLS,
R. POTTER and M. R. UNDERWOOD, Group cognitive behavioural treatment for low-back
pain in primary care: a randomised controlled trial and cost-effectiveness analysis. Lancet,
375, 9718, p. 916-923, 2010.
LAMBEEK, L. C., M. W. VAN TULDER, I. C. SWINKELS, L. L. KOPPES, J. R. ANEMA
and W. VAN MECHELEN, The trend in total cost of back pain in The Netherlands in the
period 2002 to 2007. Spine (Phila Pa 1976), 36, 13, p. 1050-1058, 2011.
LANG, J., E. OCHSMANN, T. KRAUS and J. W. LANG, Psychosocial work stressors as
antecedents of musculoskeletal problems: a systematic review and meta-analysis of stability-
adjusted longitudinal studies. Soc Sci Med, 75, 7, p. 1163-1174, 2012.
40
LATZA, U., W. KARMAUS, T. STURMER, M. STEINER, A. NETH and U. REHDER,
Cohort study of occupational risk factors of low back pain in construction workers. Occup
Environ Med, 57, 1, p. 28-34, 2000.
LITTLE, P., G. LEWITH, F. WEBLEY, M. EVANS, A. BEATTIE, K. MIDDLETON, J.
BARNETT, K. BALLARD, F. OXFORD, P. SMITH, L. YARDLEY, S. HOLLINGHURST
and D. SHARP, Randomised controlled trial of Alexander technique lessons, exercise, and
massage (ATEAM) for chronic and recurrent back pain. BMJ, 337, p. a884, 2008.
LOUW, Q. A., L. D. MORRIS and K. GRIMMER-SOMERS, The prevalence of low back
pain in Africa: a systematic review. BMC Musculoskelet Disord, 8, p. 105, 2007.
MACLURE, M., The case-crossover design: a method for studying transient effects on the
risk of acute events. Am J Epidemiol, 133, 2, p. 144-153, 1991.
MACLURE, M. and M. A. MITTLEMAN, Should we use a case-crossover design? Annu
Rev Public Health, 21, p. 193-221, 2000.
MAHER, C., WILLIAMS C, LIN C and L. J., Managing low back pain in primary care. Aust
Prescr, 34, p. 128-132, 2011.
MANEK, N. J. and A. J. MACGREGOR, Epidemiology of back disorders: prevalence, risk
factors, and prognosis. Curr Opin Rheumatol, 17, 2, p. 134-140, 2005.
MARIETTE, S. and X. MARIETTE, Low back pain in rural Tibet. Lancet, 361, 9369, p.
1654, 2003.
MODIC, M. T., T. J. MASARYK, J. S. ROSS and J. R. CARTER, Imaging of degenerative
disk disease. Radiology, 168, 1, p. 177-186, 1988.
MODIC, M. T. and J. S. ROSS, Lumbar degenerative disk disease. Radiology, 245, 1, p. 43-
61, 2007.
MODIC, M. T., P. M. STEINBERG, J. S. ROSS, T. J. MASARYK and J. R. CARTER,
Degenerative disk disease: assessment of changes in vertebral body marrow with MR
imaging. Radiology, 166, 1 Pt 1, p. 193-199, 1988.
MURRAY, C. J., T. VOS, R. LOZANO, M. NAGHAVI, A. D. FLAXMAN, C. MICHAUD,
M. EZZATI, K. SHIBUYA, J. A. SALOMON, S. ABDALLA, V. ABOYANS, J.
ABRAHAM, I. ACKERMAN, R. AGGARWAL, S. Y. AHN, M. K. ALI, M. ALVARADO,
H. R. ANDERSON, L. M. ANDERSON, K. G. ANDREWS, C. ATKINSON, L. M.
BADDOUR, A. N. BAHALIM, S. BARKER-COLLO, L. H. BARRERO, D. H. BARTELS,
M. G. BASANEZ, A. BAXTER, M. L. BELL, E. J. BENJAMIN, D. BENNETT, E.
BERNABE, K. BHALLA, B. BHANDARI, B. BIKBOV, A. BIN ABDULHAK, G.
BIRBECK, J. A. BLACK, H. BLENCOWE, J. D. BLORE, F. BLYTH, I. BOLLIGER, A.
41
BONAVENTURE, S. BOUFOUS, R. BOURNE, M. BOUSSINESQ, T. BRAITHWAITE, C.
BRAYNE, L. BRIDGETT, S. BROOKER, P. BROOKS, T. S. BRUGHA, C. BRYAN-
HANCOCK, C. BUCELLO, R. BUCHBINDER, G. BUCKLE, C. M. BUDKE, M. BURCH,
P. BURNEY, R. BURSTEIN, B. CALABRIA, B. CAMPBELL, C. E. CANTER, H.
CARABIN, J. CARAPETIS, L. CARMONA, C. CELLA, F. CHARLSON, H. CHEN, A. T.
CHENG, D. CHOU, S. S. CHUGH, L. E. COFFENG, S. D. COLAN, S. COLQUHOUN, K.
E. COLSON, J. CONDON, M. D. CONNOR, L. T. COOPER, M. CORRIERE, M.
CORTINOVIS, K. C. DE VACCARO, W. COUSER, B. C. COWIE, M. H. CRIQUI, M.
CROSS, K. C. DABHADKAR, M. DAHIYA, N. DAHODWALA, J. DAMSERE-DERRY,
G. DANAEI, A. DAVIS, D. DE LEO, L. DEGENHARDT, R. DELLAVALLE, A.
DELOSSANTOS, J. DENENBERG, S. DERRETT, D. C. DES JARLAIS, S. D.
DHARMARATNE, M. DHERANI, C. DIAZ-TORNE, H. DOLK, E. R. DORSEY, T.
DRISCOLL, H. DUBER, B. EBEL, K. EDMOND, A. ELBAZ, S. E. ALI, H. ERSKINE, P.
J. ERWIN, P. ESPINDOLA, S. E. EWOIGBOKHAN, F. FARZADFAR, V. FEIGIN, D. T.
FELSON, A. FERRARI, C. P. FERRI, E. M. FEVRE, M. M. FINUCANE, S. FLAXMAN,
L. FLOOD, K. FOREMAN, M. H. FOROUZANFAR, F. G. FOWKES, M. FRANSEN, M.
K. FREEMAN, B. J. GABBE, S. E. GABRIEL, E. GAKIDOU, H. A. GANATRA, B.
GARCIA, F. GASPARI, R. F. GILLUM, G. GMEL, D. GONZALEZ-MEDINA, R.
GOSSELIN, R. GRAINGER, B. GRANT, J. GROEGER, F. GUILLEMIN, D. GUNNELL,
R. GUPTA, J. HAAGSMA, H. HAGAN, Y. A. HALASA, W. HALL, D. HARING, J. M.
HARO, J. E. HARRISON, R. HAVMOELLER, R. J. HAY, H. HIGASHI, C. HILL, B.
HOEN, H. HOFFMAN, P. J. HOTEZ, D. HOY, J. J. HUANG, S. E. IBEANUSI, K. H.
JACOBSEN, S. L. JAMES, D. JARVIS, R. JASRASARIA, S. JAYARAMAN, N. JOHNS, J.
B. JONAS, G. KARTHIKEYAN, N. KASSEBAUM, N. KAWAKAMI, A. KEREN, J. P.
KHOO, C. H. KING, L. M. KNOWLTON, O. KOBUSINGYE, A. KORANTENG, R.
KRISHNAMURTHI, F. LADEN, R. LALLOO, L. L. LASLETT, T. LATHLEAN, J. L.
LEASHER, Y. Y. LEE, J. LEIGH, D. LEVINSON, S. S. LIM, E. LIMB, J. K. LIN, M.
LIPNICK, S. E. LIPSHULTZ, W. LIU, M. LOANE, S. L. OHNO, R. LYONS, J.
MABWEIJANO, M. F. MACINTYRE, R. MALEKZADEH, L. MALLINGER, S.
MANIVANNAN, W. MARCENES, L. MARCH, D. J. MARGOLIS, G. B. MARKS, R.
MARKS, A. MATSUMORI, R. MATZOPOULOS, B. M. MAYOSI, J. H. MCANULTY, M.
M. MCDERMOTT, N. MCGILL, J. MCGRATH, M. E. MEDINA-MORA, M. MELTZER,
G. A. MENSAH, T. R. MERRIMAN, A. C. MEYER, V. MIGLIOLI, M. MILLER, T. R.
MILLER, P. B. MITCHELL, C. MOCK, A. O. MOCUMBI, T. E. MOFFITT, A. A.
42
MOKDAD, L. MONASTA, M. MONTICO, M. MORADI-LAKEH, A. MORAN, L.
MORAWSKA, R. MORI, M. E. MURDOCH, M. K. MWANIKI, K. NAIDOO, M. N. NAIR,
L. NALDI, K. M. NARAYAN, P. K. NELSON, R. G. NELSON, M. C. NEVITT, C. R.
NEWTON, S. NOLTE, P. NORMAN, R. NORMAN, M. O'DONNELL, S. O'HANLON, C.
OLIVES, S. B. OMER, K. ORTBLAD, R. OSBORNE, D. OZGEDIZ, A. PAGE, B.
PAHARI, J. D. PANDIAN, A. P. RIVERO, S. B. PATTEN, N. PEARCE, R. P. PADILLA,
F. PEREZ-RUIZ, N. PERICO, K. PESUDOVS, D. PHILLIPS, M. R. PHILLIPS, K.
PIERCE, S. PION, G. V. POLANCZYK, S. POLINDER, C. A. POPE, 3RD, S. POPOVA, E.
PORRINI, F. POURMALEK, M. PRINCE, R. L. PULLAN, K. D. RAMAIAH, D.
RANGANATHAN, H. RAZAVI, M. REGAN, J. T. REHM, D. B. REIN, G. REMUZZI, K.
RICHARDSON, F. P. RIVARA, T. ROBERTS, C. ROBINSON, F. R. DE LEON, L.
RONFANI, R. ROOM, L. C. ROSENFELD, L. RUSHTON, R. L. SACCO, S. SAHA, U.
SAMPSON, L. SANCHEZ-RIERA, E. SANMAN, D. C. SCHWEBEL, J. G. SCOTT, M.
SEGUI-GOMEZ, S. SHAHRAZ, D. S. SHEPARD, H. SHIN, R. SHIVAKOTI, D. SINGH,
G. M. SINGH, J. A. SINGH, J. SINGLETON, D. A. SLEET, K. SLIWA, E. SMITH, J. L.
SMITH, N. J. STAPELBERG, A. STEER, T. STEINER, W. A. STOLK, L. J. STOVNER, C.
SUDFELD, S. SYED, G. TAMBURLINI, M. TAVAKKOLI, H. R. TAYLOR, J. A.
TAYLOR, W. J. TAYLOR, B. THOMAS, W. M. THOMSON, G. D. THURSTON, I. M.
TLEYJEH, M. TONELLI, J. A. TOWBIN, T. TRUELSEN, M. K. TSILIMBARIS, C.
UBEDA, E. A. UNDURRAGA, M. J. VAN DER WERF, J. VAN OS, M. S. VAVILALA, N.
VENKETASUBRAMANIAN, M. WANG, W. WANG, K. WATT, D. J. WEATHERALL,
M. A. WEINSTOCK, R. WEINTRAUB, M. G. WEISSKOPF, M. M. WEISSMAN, R. A.
WHITE, H. WHITEFORD, N. WIEBE, S. T. WIERSMA, J. D. WILKINSON, H. C.
WILLIAMS, S. R. WILLIAMS, E. WITT, F. WOLFE, A. D. WOOLF, S. WULF, P. H.
YEH, A. K. ZAIDI, Z. J. ZHENG, D. ZONIES, A. D. LOPEZ, M. A. ALMAZROA and Z.
A. MEMISH, Disability-adjusted life years (DALYs) for 291 diseases and injuries in 21
regions, 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010.
Lancet, 380, 9859, p. 2197-2223, 2012.
MURTEZANI, A., Z. IBRAIMI, S. SLLAMNIKU, T. OSMANI and S. SHERIFI, Prevalence
and risk factors for low back pain in industrial workers. Folia Med (Plovdiv), 53, 3, p. 68-74,
2011.
PATBERG, W. R. and J. J. RASKER, Weather effects in rheumatoid arthritis: from
controversy to consensus. A review. J Rheumatol, 31, 7, p. 1327-1334, 2004.
43
RENDELL, J. M., R. D. MERRITT and J. R. GEDDES, Incentives and disincentives to
participation by clinicians in randomised controlled trials. Cochrane Database Syst Rev, 2,
p. MR000021, 2007.
ROLLMAN, B. L., G. S. FISCHER, F. ZHU and B. H. BELNAP, Comparison of electronic
physician prompts versus waitroom case-finding on clinical trial enrollment. J Gen Intern
Med, 23, 4, p. 447-450, 2008.
RUBIN, D. I., Epidemiology and risk factors for spine pain. Neurol Clin, 25, 2, p. 353-371,
2007.
SHEEHAN, N. J., Magnetic resonance imaging for low back pain: indications and
limitations. Ann Rheum Dis, 69, 1, p. 7-11, 2010.
SMEDSLUND, G., P. MOWINCKEL, T. HEIBERG, T. K. KVIEN and K. B. HAGEN,
Does the weather really matter? A cohort study of influences of weather and solar conditions
on daily variations of joint pain in patients with rheumatoid arthritis. Arthritis Rheum, 61, 9,
p. 1243-1247, 2009.
SPAAR, A., M. FREY, A. TURK, W. KARRER and M. A. PUHAN, Recruitment barriers in
a randomized controlled trial from the physicians' perspective: a postal survey. BMC Med
Res Methodol, 9, p. 14, 2009.
TAYLOR, J. B., A. P. GOODE, S. Z. GEORGE and C. E. COOK, Incidence and risk factors
for first-time incident low back pain: a systematic review and meta-analysis. Spine J, p.
2014.
TENIAS, J. M., M. ESTARLICH, V. FUENTES-LEONARTE, C. INIGUEZ and F.
BALLESTER, Short-term relationship between meteorological variables and hip fractures: an
analysis carried out in a health area of the Autonomous Region of Valencia, Spain (1996-
2005). Bone, 45, 4, p. 794-798, 2009.
THELIN, A., S. HOLMBERG and N. THELIN, Functioning in neck and low back pain from
a 12-year perspective: a prospective population-based study. J Rehabil Med, 40, 7, p. 555-
561, 2008.
VALAT, J. P., S. GENEVAY, M. MARTY, S. ROZENBERG and B. KOES, Sciatica. Best
Pract Res Clin Rheumatol, 24, 2, p. 241-252, 2010.
VAN TULDER, M., A. BECKER, T. BEKKERING, A. BREEN, M. T. DEL REAL, A.
HUTCHINSON, B. KOES, E. LAERUM and A. MALMIVAARA, Chapter 3. European
guidelines for the management of acute nonspecific low back pain in primary care. Eur
Spine J, 15 Suppl 2, p. S169-191, 2006.
44
VANDERGRIFT, J. L., J. E. GOLD, A. HANLON and L. PUNNETT, Physical and
psychosocial ergonomic risk factors for low back pain in automobile manufacturing workers.
Occup Environ Med, 69, 1, p. 29-34, 2012.
VINDIGNI, D., B. F. WALKER, J. R. JAMISON, C. DA COSTA, L. PARKINSON and S.
BLUNDEN, Low back pain risk factors in a large rural Australian Aboriginal community. An
opportunity for managing co-morbidities? Chiropr Osteopat, 13, p. 21, 2005.
VOLINN, E., The epidemiology of low back pain in the rest of the world. A review of
surveys in low- and middle-income countries. Spine (Phila Pa 1976), 22, 15, p. 1747-1754,
1997.
VON KORFF, M., R. A. DEYO, D. CHERKIN and W. BARLOW, Back pain in primary
care. Outcomes at 1 year. Spine (Phila Pa 1976), 18, 7, p. 855-862, 1993.
WALKER, B. F., R. MULLER and W. D. GRANT, Low back pain in Australian adults: the
economic burden. Asia Pac J Public Health, 15, 2, p. 79-87, 2003.
WANG, Y., T. VIDEMAN and M. C. BATTIE, ISSLS prize winner: Lumbar vertebral
endplate lesions: associations with disc degeneration and back pain history. Spine (Phila Pa
1976), 37, 17, p. 1490-1496, 2012.
WASSENAAR, M., R. M. VAN RIJN, M. W. VAN TULDER, A. P. VERHAGEN, D. A.
VAN DER WINDT, B. W. KOES, M. R. DE BOER, A. Z. GINAI and R. W. OSTELO,
Magnetic resonance imaging for diagnosing lumbar spinal pathology in adult patients with
low back pain or sciatica: a diagnostic systematic review. Eur Spine J, 21, 2, p. 220-227,
2012.
WIESER, S., B. HORISBERGER, S. SCHMIDHAUSER, C. EISENRING, U. BRUGGER,
A. RUCKSTUHL, J. DIETRICH, A. F. MANNION, A. ELFERING, O. TAMCAN and U.
MULLER, Cost of low back pain in Switzerland in 2005. Eur J Health Econ, 12, 5, p. 455-
467, 2011.
45
Chapter Two
Clinicians’ views on factors that trigger a sudden onset of low back pain
Chapter Two is published as:
Steffens D, Maher CG, Ferreira ML, Hancock MJ, Glass T, Latimer J. Clinicians’ views on
factors that trigger a sudden onset of low back pain. European Spine Journal. 2014; 23:512-
519.
46
Statement from co-authors confirming authorship contribution of the PhD candidate
As co-authors of the paper “Clinicians’ views on factors that trigger a sudden onset of low
back pain”, we confirm that Daniel Steffens has made the following contributions:
Conception and design of the research
Data collection
Analysis and interpretation of the findings
Writing of the manuscript and critical appraisal of the content
Christopher G Maher Date: 01.01.2015
Manuela L Ferreira Date: 01.01.2015
Mark J Hancock Date: 01.01.2015
Timothy Glass Date: 01.01.2015
Jane Latimer Date: 01.01.2015
47
ORIGINAL ARTICLE
Clinicians’ views on factors that trigger a sudden onsetof low back pain
Daniel Steffens • Chris G. Maher • Manuela L. Ferreira •
Mark J. Hancock • Timothy Glass • Jane Latimer
Received: 8 August 2013 / Revised: 24 November 2013 / Accepted: 24 November 2013 / Published online: 8 December 2013
� Springer-Verlag Berlin Heidelberg 2013
Abstract
Purpose Little is known about what triggers an episode of
low back pain (LBP) in those presenting to primary care.
Previous studies of risk factors have focused on specific
occupational settings and work conditions. No study has
asked primary care clinicians to consider what triggers an
episode of sudden-onset LBP in patients presenting to them
for care. The purpose of this study, therefore, was to
describe the short- and long-term factors that primary care
clinicians consider important in triggering a sudden epi-
sode of acute LBP.
Methods One hundred and thirty-one primary care clini-
cians who were recruiting patients with LBP to a large
observational study were invited to participate. A ques-
tionnaire was designed to obtain information about the
clinician’s characteristics, profession and clinical experi-
ence. We also asked clinicians to nominate the five short-
and five long-term exposure factors, most likely to trigger a
sudden episode of acute LBP, based on their experience.
Descriptive statistics and frequency distributions were used
to describe clinician’s characteristics and the frequencies of
the main risk factor categories were reported.
Results Based on the views of 103 primary care clini-
cians, biomechanical risk factors appear to be the most
important short-term triggers (endorsed by 89.3 % of cli-
nicians) and long-term triggers (endorsed by 54.2 % of
clinicians) for a sudden episode of acute LBP. Individual
risk factors were endorsed by 39 % of clinicians as
important long-term triggers, while only 6.4 % of clini-
cians considered them important short-term triggers. Other
risk factors, such as psychological/psychosocial and
genetic factors, were not commonly endorsed as risk fac-
tors for an episode of LBP by primary care clinicians.
Conclusions This study shows that primary care clini-
cians believe that biomechanical risk factors are the most
important short-term triggers, while biomechanical and
individual risk factors are the most important long-term
triggers for a sudden onset of LBP. However, other risk
factors, such as psychological/psychosocial and genetic,
were not commonly endorsed as risk factors for an episode
of LBP by primary care clinicians. Results of this study are
based on primary care clinicians’ views and further
investigation is needed to test the validity of these sug-
gested risk factors.
Keywords Low back pain � Primary care � Risk factors �Observational � Epidemiology
Introduction
Low back pain (LBP) is the most common musculoskeletal
condition affecting approximately 80 % of the adult
D. Steffens � C. G. Maher � M. L. Ferreira � J. Latimer
Musculoskeletal Division, The George Institute for Global
Health, Sydney Medical School, The University of Sydney,
Level 13, 321 Kent Street, Sydney, NSW 2000, Australia
D. Steffens (&)
Musculoskeletal Division, The George Institute for Global
Health, Sydney Medical School, The University of Sydney,
Missenden Road, PO Box M201, Sydney, NSW 2050, Australia
e-mail: [email protected]
M. J. Hancock
Discipline of Physiotherapy, Faculty of Human Sciences,
Macquarie University, 2 Technology Place, Macquarie Park,
Sydney, NSW 2113, Australia
T. Glass
Warwick Medical School, University of Warwick,
Coventry CV4 7AL, UK
123
Eur Spine J (2014) 23:512–519
DOI 10.1007/s00586-013-3120-y
48
population at least once during their lifetime [1, 2]. LBP
troubles are the fifth most frequent reason for a visit to a
primary health care clinician in the USA and the seventh
most frequent reason in Australia [3, 4]. In Australia back
pain is the health condition that carries the greatest burden
when considering lives lived with disability [5]. The global
burden of the condition is enormous and includes high
costs with medical care, loss of productivity and indemnity
payments [6]. Despite this, investigation into risk factors
for LBP is in a developing stage when compared with other
common conditions such as cardiovascular disease and
cancer [7]. A better understanding of factors that trigger an
episode of LBP may provide important insights into the
prevention and management of this condition.
LBP is a complex condition with many factors believed
to contribute to its onset [8]. These factors can be aggre-
gated into a smaller number of categories [9] including
biomechanical factors (regular lifting, exposure to vibra-
tion, physically demanding jobs, bending and twisting,
pushing and pulling heavy loads, awkward posture) [2, 7–
20], psychological/psychosocial factors (job satisfaction,
local support in the workplace, depression, job control,
stress) [2, 7, 9, 16, 19–25] and individual risk factors
(sedentary lifestyle, age, smoking, gender, obesity, poor
general health, marital status, pregnancy) [2, 7, 9, 12, 13,
20, 21, 23, 26–31]. Past studies have investigated many of
these factors and their relationship to LBP. A few studies
have also investigated genetic risk factors [7, 29, 32].
Interestingly, only a small number of studies have exam-
ined risk factors across all four risk factor categories.
While there are many studies of risk factors for LBP [9,
33, 34], most knowledge stems from studies focused on
specific occupational groups and working conditions [8–
10, 12–19, 23]. Although studies conducted in occupational
settings may reveal important risk factors for work-related
back pain, these risks may not be relevant to other popu-
lations such as those drawn from primary care. In addition,
previous studies of LBP have been criticised as being too
narrowly focused on only one or perhaps two of the cate-
gories of individual, biomechanical, psychological/psy-
chosocial and genetic aspects of the problem [12].
Little is known about the causes of LBP in the general
population who present to primary care. The starting point
in evaluating risk factors for LBP in primary care is the
identification of putative risk factors that need to be
investigated. Interviewing primary care clinicians who
frequently manage patients with LBP can provide insight
into what may be the most common triggers for this con-
dition. The aim of this study, therefore, was to describe the
most likely risk factors involving short- and long-term
exposure that primary care clinicians believe could trigger
a sudden episode of acute LBP.
Materials and methods
Data for this study were provided by clinicians recruiting
participants to the TRIGGERS case crossover study [35].
TRIGGERS is an observational study and was designed
to quantify the transient increase in risk of a sudden
episode of LBP associated with acute exposure to a
range of common physical and psychological factors
[35].
Study sample
Participants in the study were 131 primary care clinicians
(physiotherapists and chiropractors) who were recruiting
patients for the TRIGGERS study from October 2011 to
November 2012 in NSW, Australia.
Recruitment
Clinicians were contacted and invited to participate by
e-mail. In the e-mail, we attached the invitation letter,
consent form and a one-page questionnaire. The invitation
letter consisted of a brief explanation of the study methods
and aims. Clinicians who consented to participate were
instructed to answer the one-page questionnaire based on
their clinical experience and send it back to the research
team. Clinicians who had not responded within 2 weeks
were contacted by a study researcher and again invited to
participate. Ethical approval for the study was granted by
the University of Sydney Human Research Ethics
Committee.
Data collection
A one-page self-administered questionnaire was designed
to obtain information about the clinician’s characteristics
(gender, age and address), profession (physiotherapist or
chiropractor) and clinical experience (years as practising
clinician and years managing LBP). Two items were used
to measure their beliefs about triggers for LBP. These
were:
1. Based on your clinical experience, list what you
consider to be the five most likely factors involving
short-term exposure that are triggers for a sudden
episode of acute low back pain?
2. Based on your clinical experience, list what you
consider to be the five most likely factors involving
long-term exposure that increase the risk of a sudden
episode of acute low back pain?
All questionnaires were returned by e-mail and the
answers entered in the study database.
Eur Spine J (2014) 23:512–519 513
123
49
Risk factors categories
We developed descriptive categories to code the free text
responses based upon published risk factor studies. A
search from the earliest record to January 2013 was
undertaken on PubMed to identify relevant studies using
the following keywords: low back pain, backache, lum-
bago, risk factors, causality, aetiology and epidemiology.
Abstracts were retrieved and examined. Reported risk
factors were extracted and entered into a table. Figure 1
describes the categories we developed including main
category (or aggregate label) and the sub-categories
(Table 1).
Coding short- and long-term risk factors
Two researchers individually coded the free text answers
about short- and long-term exposures that may be a
trigger for a sudden episode of acute LBP. The free text
responses were first coded into five main categories
(Fig. 1):
1. Individual risk factors
2. Biomechanical risk factors
3. Psychological/psychosocial risk factors
4. Genetic risk factors
5. Other risk factors
Fig. 1 Diagram of risk factors for low back pain
514 Eur Spine J (2014) 23:512–519
123
50
The same researchers then coded the free text responses
into sub-categories. Each nominated risk factor was only
classified once into a main category and a sub-category
(e.g. 1: Smoking was first categorised as an ‘‘individual
risk factor’’ and then sub-categorised into ‘‘smoking’’. e.g.
2: Golf was first categorised as a ‘‘biomechanical risk
factor’’ and then sub-categorised into ‘‘sport injuries’’). In
case of disagreement, a third researcher was consulted and
a decision was made by consensus.
Statistical analysis
To check the reliability of the coding of free text data, we
compared the independent coding of the two researchers.
Inter-rater reliability was expressed using percentage exact
agreement and Cohen’s kappa [36] for the main categories
and sub-categories.
Descriptive statistics and frequency distributions were
calculated to describe the characteristics of the clinicians
and the frequencies that the main risk factor categories
were reported (individual, biomechanical, psychological/
psychosocial, genetic and other risk factors).
The clinicians’ endorsement of various categories of
triggers (main categories and sub-categories) was exam-
ined using the Chi-squared (v2) statistic. All analyses were
performed using the statistical package SPSS for Windows
version 21 (SPSS, Inc., Chicago, IL) with a significance
level set at 0.05.
Results
Of the 131 clinicians invited to participate in the study, 103
(79 %) completed the questionnaire. The characteristics of
the participating clinicians are described in Table 2. The
mean age was 43 years (range 23–65), clinical experience
managing LBP was 18 years (range 1–40) and slightly
more were male (55 %).
In general, the reliability between the two independent
researchers who coded the short- and long-term risk factor
categories was very good (Table 2). The observed agree-
ment ranged from 89 to 99 % and the inter-rater reliability
ranged from substantial (j = 0.71) to almost perfect
agreement (j = 0.95) [36].
Short- and long-term main categories risk factors
Table 3 lists the frequency of endorsement of the main
short- and long-term risk factor categories. Based on the
views of 103 primary care clinicians, biomechanical risk
factors appear to be the most important short-term triggers
(endorsed by 89.3 % of clinicians) and long-term triggers
(endorsed by 54.2 % of clinicians) for a sudden episode of
acute LBP. Individual risk factors were endorsed by 39 %
of clinicians as important long-term triggers, while only
6.4 % of clinicians considered them important short-term
triggers. Only one clinician reported genetics (0.2 %) as a
long-term risk factor for acute LBP. Chi-square tests con-
firmed a significant difference in proportions of the main
short- and long-term risk factor categories (v2 = 180.70,
p \ 0.001). While biomechanical factors were considered
the most important short- and long-term risk factors,
individual factors were endorsed far more commonly as
long-term risk factors.
Table 1 Clinicians’ characteristics (n = 103)
Characteristics n (%) or mean ± SD
Gender (male) 56 (55 %)
Age (years) 43 ± 10
Profession
Physiotherapist 102 (99 %)
Chiropractor 1 (1 %)
Current position
Principal/owner 45 (44 %)
Clinician/senior clinician 58 (56 %)
Clinical experience (years) 19 ± 10
Clinical experience managing LBP (years) 18 ± 9
Table 2 Reliability between researchers A and B
Risk factors categories Observed agreement (%) ja
Short-term main categories 99 0.95
Short-term sub-categories 96 0.89
Long-term main categories 94 0.88
Long-term sub-categories 89 0.71
a Interpretation: 0.01–0.20 slight agreement; 0.21–0.40 fair agree-
ment; 0.41–0.60 moderate agreement; 0.61–0.80 substantial agree-
ment; 0.81–0.99 almost perfect agreement [36]
Table 3 Frequency of main risk factors stratified by short and long
term
Main categories risk factors Short terma Long terma
N % N %
Individual 33 6.4 201 39
Biomechanical 460 89.3 279 54.2
Psychological/psychosocial 3 0.6 16 3.1
Genetic 0 0.0 1 0.2
Other risk factors 9 1.7 8 1.6
Missing data 10 1.9 10 1.9
Total 515 100 515 100
a v2 = 180.70, p \ 0.001
Eur Spine J (2014) 23:512–519 515
123
51
Short- and long-term sub-categories risk factors
Table 4 lists the frequency of endorsement of short- and
long-term sub-category risk factors for acute LBP. Lifting
(17.5 %) was the most frequently endorsed short-term sub-
category risk factor, followed by prolonged sitting (9.1 %)
and physical trauma (8.9 %). For long-term sub-category
risk factors, prolonged sitting (13.4 %) was most frequently
endorsed followed by lifting (10.9 %) and physical inactiv-
ity (9.1 %). Similarly to the analysis of the main categories,
the Chi-square test (v2 = 360.456, p \ 0.001) suggested
that there was a difference between short- and long-term sub-
category risk factors. Obvious sub-category differences
included physical trauma and physical inactivity for short
and long term; physical trauma was endorsed more fre-
quently as a short-term risk factor, while inactivity was
endorsed more commonly as a long-term risk factor.
Discussion
Statement of principal findings
Based on the opinions of 103 primary care clinicians, the
most important main short- and long-term risk factors to
trigger an episode of sudden acute LBP are biomechanical
(89.3 and 54.2 %, respectively) and individual risk factors
(6.4 and 39 %, respectively). Surprisingly, other risk factors,
such as psychological/psychosocial and genetic factors,
were not commonly endorsed as risk factors for an episode of
LBP by primary care clinicians. Some of the most frequently
reported short- and long-term sub-categories to trigger a
sudden episode of acute LBP are lifting (17.5 and 10.9 %,
respectively) and prolonged sitting (9.1 and 13.4 %,
respectively).
Strengths and weaknesses of the study
We were able to interview a considerable number of
experienced primary care clinicians currently treating
patients with LBP. In addition, we identified a range of
factors that are considered triggers involving short- and
long-term exposures. The reliability between the two
independent researchers who coded the short- and long-
term risk factor categories was very good with the inter-
rater reliability ranging from substantial to almost perfect
agreement [36]. However, the results of the study are based
on primary care clinicians’ views and further investigation
is needed to test the validity of these suggested risk factors.
Comparison to others studies
To our knowledge, this is the first observational study that
has interviewed primary care clinicians to determine their
views on short- and long-term triggers for a sudden episode
of acute LBP in the general population. Most of the pre-
vious studies on risk factors for LBP tended to focus on
specific triggers and included samples from occupational
settings. There is a research focus on biomechanical [2, 7–
20], psychological/psychosocial [2, 7, 9, 16, 19–25] and
Table 4 Frequency of risk factor sub-categories stratified by short
and long term
Risk factors sub-categories Short terma Long terma
N % N %
Lifting 90 17.5 56 10.9
Prolonged sitting 47 9.1 69 13.4
Physical trauma 46 8.9 3 0.6
Bending 41 8.0 24 4.7
Unaccustomed activity 38 7.4 2 0.4
Other biomechanical risk factors 27 5.2 28 5.4
Sport injuries 24 4.7 9 1.7
Gardening 20 3.9 2 0.4
Bending and twisting 17 3.3 6 1.2
Twisting 14 2.7 4 0.8
Coughing/sneezing 12 2.3 1 0.2
Lifting and twisting 12 2.3 0 0.0
Lifting and bending 12 2.3 8 1.6
Driving 11 2.1 15 2.9
Bending and twisting while lifting 10 1.9 2 0.4
Sudden movements 8 1.6 1 0.2
Other risk factors 9 1.7 8 1.6
Prolonged standing 6 1.2 16 3.1
Unexpected load 6 1.2 0 0.0
Repetitive movements 5 1.0 8 1.6
Other individual risk factors 4 0.8 30 5.8
Pulling/pushing 5 1.0 2 0.4
Pregnancy/childbirth 3 0.6 13 2.5
Previous LBP episodes 2 0.4 15 2.9
Diminished trunk muscle strength and
fatigability
2 0.4 22 4.3
Spine/pelvis/lower limb impairment 2 0.4 23 4.5
Sedentary work 2 0.4 14 2.7
Stress 2 0.4 9 1.7
Overweight 1 0.2 25 4.9
Spine/pelvis/lower limb pathology 1 0.2 11 2.1
Physical inactivity 0 0.0 47 9.1
Less frequent risk factorsb 26 5.0 32 6.2
Missing data 10 1.9 10 1.9
Total 515 100 515 100
Bold top five short and long risk factor sub-categoriesa v2 = 360.456, p \ 0.001b Risk factors with a grouped frequency count B5 were combined
516 Eur Spine J (2014) 23:512–519
123
52
individual risk factors [2, 7, 9, 12, 13, 20, 21, 23, 26–31]
for LBP; however, only a few studies investigated risk
factors from all domains together [7].
Findings from our study suggest that the views of cli-
nicians are as variable as in the evidence found in the
literature. Our study found that biomechanical risk factors,
such as lifting, prolonged sitting and bending, were con-
sidered by primary care clinicians to be important risk
factors for the onset of LBP, in accordance with previous
studies [10, 15, 26, 37]. On the other hand, individual risk
factors, such as physical inactivity, have only weak support
in the literature as a risk factor for developing LBP [27,
29]. This is in contrast to the study clinicians who con-
sidered physical inactivity as a common long-term risk
factor for LBP. Although psychological/psychosocial and
genetic risk factors did not appear to be endorsed strongly
by the primary care clinicians interviewed in this study,
there is strong evidence in the literature suggesting the
opposite [12, 22, 37]. However, this inconsistency between
the present study and the literature may be due to the dif-
ferent settings in which the studies were performed and/or
clinician’s lack of awareness about the importance of
psychological risk factors. Psychological/psychosocial
factors may be more important in occupational settings
than in primary care. Conversely, individual risk factors
may be more important in primary care settings than
occupational settings.
Meaning of the study: possible mechanisms
and implications for clinicians
Based on the opinion of primary care clinicians, the most
likely short-term risk factors for triggering an episode of
LBP are, by far, the biomechanical risk factors and the
most likely causes involving long-term exposure are indi-
vidual and biomechanical risk factors. This is somewhat
inconsistent with the literature [27, 29]. The reasons why
experienced clinicians think such factors are important may
be due to the fact that they are seeing a general sample of
the population, while previous studies tend to focus on
occupational settings. One other reason may be that pri-
mary care clinicians have limited expertise in assessing
psychosocial/psychological and genetic factors as likely
triggers for an onset of LBP.
A better understanding of the most endorsed risk factors
for LBP in primary care will help clinicians to improve
patient treatment and also provide important advice in
prevention of future LBP episodes.
Unanswered questions and future research
Future studies should investigate risk factors for LBP in
samples of the general population and simultaneously
investigate all main categories of risk factors found to
trigger an episode of LBP (individual, biomechanical,
psychosocial/psychological, genetic and others risk fac-
tors). There is also a need to investigate the combination of
two or more risk factors. Previous studies have confirmed
that a combination of two or more risk factors (i.e. poor
posture, repetitive lifting and high job strain) are com-
monly identified in the same individual [23]. Increasing our
understanding of what triggers an episode of LBP will
enable us to design better prevention programs. Future
research could involve the modification of endorsed trig-
gers in a clinical trial to determine the effectiveness in
reducing future episodes of LBP. In addition, there is a
need to determine whether psychological/psychosocial
features are important risk factors in the primary care set-
ting using rigorous prospective cohort designs.
Conclusions
Based on primary care clinicians’ opinion, biomechanical
risk factors are the most important short-term triggers,
while biomechanical and individual risk factors are the
most important long-term triggers for sudden-onset LBP.
Psychological/psychosocial and genetic risk factors were
not considered important risk factors by primary care cli-
nicians. Findings from this study should be further inves-
tigated to better understand short- and long-term exposures
that are triggers for an acute sudden episode of LBP. This
information will help inform LBP prevention programs.
Conflict of interest None.
References
1. Britt H, Miller G, Knox S, Charles J, Pan Y, Henderson J,
Baryram C, Valenti L, Ng A, O’Halloran J (2005) General
practice activity in Australia 2004–2005. General practice series
No. 18. Australian Institute of Health and Welfare, Canberra
2. Rubin DI (2007) Epidemiology and risk factors for spine pain.
Neurol Clin 25(2):353–371. doi:10.1016/j.ncl.2007.01.004
3. Williams C, Maher C, Hancock M, McAuley J, McLachlan A,
Britt H, Fahridin S, Harrison C, Latimer J (2010) Low back pain
and best practice care: a survey of general practice physicians.
JAMA 170(3):271–277
4. Deyo R (1998) Low-back pain. Sci Am 279(2):48–53
5. Murray CJ, Vos T, Lozano R, Naghavi M, Flaxman AD, Michaud
C, Ezzati M, Shibuya K, Salomon JA, Abdalla S, Aboyans V,
Abraham J, Ackerman I, Aggarwal R, Ahn SY, Ali MK, Alva-
rado M, Anderson HR, Anderson LM, Andrews KG, Atkinson C,
Baddour LM, Bahalim AN, Barker-Collo S, Barrero LH, Bartels
DH, Basanez MG, Baxter A, Bell ML, Benjamin EJ, Bennett D,
Bernabe E, Bhalla K, Bhandari B, Bikbov B, Bin Abdulhak A,
Birbeck G, Black JA, Blencowe H, Blore JD, Blyth F, Bolliger I,
Bonaventure A, Boufous S, Bourne R, Boussinesq M, Braithwaite
T, Brayne C, Bridgett L, Brooker S, Brooks P, Brugha TS, Bryan-
Eur Spine J (2014) 23:512–519 517
123
53
Hancock C, Bucello C, Buchbinder R, Buckle G, Budke CM,
Burch M, Burney P, Burstein R, Calabria B, Campbell B, Canter
CE, Carabin H, Carapetis J, Carmona L, Cella C, Charlson F,
Chen H, Cheng AT, Chou D, Chugh SS, Coffeng LE, Colan SD,
Colquhoun S, Colson KE, Condon J, Connor MD, Cooper LT,
Corriere M, Cortinovis M, de Vaccaro KC, Couser W, Cowie BC,
Criqui MH, Cross M, Dabhadkar KC, Dahiya M, Dahodwala N,
Damsere-Derry J, Danaei G, Davis A, De Leo D, Degenhardt L,
Dellavalle R, Delossantos A, Denenberg J, Derrett S, Des Jarlais
DC, Dharmaratne SD, Dherani M, Diaz-Torne C, Dolk H, Dorsey
ER, Driscoll T, Duber H, Ebel B, Edmond K, Elbaz A, Ali SE,
Erskine H, Erwin PJ, Espindola P, Ewoigbokhan SE, Farzadfar F,
Feigin V, Felson DT, Ferrari A, Ferri CP, Fevre EM, Finucane
MM, Flaxman S, Flood L, Foreman K, Forouzanfar MH, Fowkes
FG, Fransen M, Freeman MK, Gabbe BJ, Gabriel SE, Gakidou E,
Ganatra HA, Garcia B, Gaspari F, Gillum RF, Gmel G, Gonzalez-
Medina D, Gosselin R, Grainger R, Grant B, Groeger J, Guille-
min F, Gunnell D, Gupta R, Haagsma J, Hagan H, Halasa YA,
Hall W, Haring D, Haro JM, Harrison JE, Havmoeller R, Hay RJ,
Higashi H, Hill C, Hoen B, Hoffman H, Hotez PJ, Hoy D, Huang
JJ, Ibeanusi SE, Jacobsen KH, James SL, Jarvis D, Jasrasaria R,
Jayaraman S, Johns N, Jonas JB, Karthikeyan G, Kassebaum N,
Kawakami N, Keren A, Khoo JP, King CH, Knowlton LM,
Kobusingye O, Koranteng A, Krishnamurthi R, Laden F, Lalloo
R, Laslett LL, Lathlean T, Leasher JL, Lee YY, Leigh J, Lev-
inson D, Lim SS, Limb E, Lin JK, Lipnick M, Lipshultz SE, Liu
W, Loane M, Ohno SL, Lyons R, Mabweijano J, MacIntyre MF,
Malekzadeh R, Mallinger L, Manivannan S, Marcenes W, March
L, Margolis DJ, Marks GB, Marks R, Matsumori A, Matzopoulos
R, Mayosi BM, McAnulty JH, McDermott MM, McGill N,
McGrath J, Medina-Mora ME, Meltzer M, Mensah GA, Merri-
man TR, Meyer AC, Miglioli V, Miller M, Miller TR, Mitchell
PB, Mock C, Mocumbi AO, Moffitt TE, Mokdad AA, Monasta L,
Montico M, Moradi-Lakeh M, Moran A, Morawska L, Mori R,
Murdoch ME, Mwaniki MK, Naidoo K, Nair MN, Naldi L,
Narayan KM, Nelson PK, Nelson RG, Nevitt MC, Newton CR,
Nolte S, Norman P, Norman R, O’Donnell M, O’Hanlon S,
Olives C, Omer SB, Ortblad K, Osborne R, Ozgediz D, Page A,
Pahari B, Pandian JD, Rivero AP, Patten SB, Pearce N, Padilla
RP, Perez-Ruiz F, Perico N, Pesudovs K, Phillips D, Phillips MR,
Pierce K, Pion S, Polanczyk GV, Polinder S, Pope CA, 3rd,
Popova S, Porrini E, Pourmalek F, Prince M, Pullan RL, Ramaiah
KD, Ranganathan D, Razavi H, Regan M, Rehm JT, Rein DB,
Remuzzi G, Richardson K, Rivara FP, Roberts T, Robinson C, De
Leon FR, Ronfani L, Room R, Rosenfeld LC, Rushton L, Sacco
RL, Saha S, Sampson U, Sanchez-Riera L, Sanman E, Schwebel
DC, Scott JG, Segui-Gomez M, Shahraz S, Shepard DS, Shin H,
Shivakoti R, Singh D, Singh GM, Singh JA, Singleton J, Sleet
DA, Sliwa K, Smith E, Smith JL, Stapelberg NJ, Steer A, Steiner
T, Stolk WA, Stovner LJ, Sudfeld C, Syed S, Tamburlini G,
Tavakkoli M, Taylor HR, Taylor JA, Taylor WJ, Thomas B,
Thomson WM, Thurston GD, Tleyjeh IM, Tonelli M, Towbin JA,
Truelsen T, Tsilimbaris MK, Ubeda C, Undurraga EA, van der
Werf MJ, van Os J, Vavilala MS, Venketasubramanian N, Wang
M, Wang W, Watt K, Weatherall DJ, Weinstock MA, Weintraub
R, Weisskopf MG, Weissman MM, White RA, Whiteford H,
Wiebe N, Wiersma ST, Wilkinson JD, Williams HC, Williams
SR, Witt E, Wolfe F, Woolf AD, Wulf S, Yeh PH, Zaidi AK,
Zheng ZJ, Zonies D, Lopez AD, AlMazroa MA, Memish ZA
(2012) Disability-adjusted life years (DALYs) for 291 diseases
and injuries in 21 regions, 1990–2010: a systematic analysis for
the Global Burden of Disease Study 2010. Lancet 380
(9859):2197–2223. doi:10.1016/s0140-6736(12)61689-4
6. Hoy D, March L, Brooks P, Woolf A, Blyth F, Vos T, Buchbinder
R (2010) Measuring the global burden of low back pain. Best
Pract Res Clin Rheumatol 24:155–165
7. Manek NJ, MacGregor AJ (2005) Epidemiology of back disor-
ders: prevalence, risk factors, and prognosis. Curr Opin Rheu-
matol 17:134–140
8. Latza U, Karmaus W, Sturmer T, Steiner M, Neth A, Rehder U
(2000) Cohort study of occupational risk factors of low back pain
in construction workers. Occup Environ Med 57:28–34
9. Ferguson S, Allread W, Burr D, Heaney C, Marras W (2012)
Biomechanical, psychosocial and individual risk factors predict-
ing low back functional impairment among furniture distribution
employees. Clin Biomech 27:117–123
10. Burdorf A, Naaktgeboren B, de Groot HCWM (1993) Occupa-
tional risk factors for low back pain among sedentary workers.
J Occup Med 35(12):1213–1220
11. Frymoyer JW, Pope MH, Clements JH, Wilder DG, MacPherson
B, Ashikaga T, Vermont B (1983) Risk factors in low-back pain:
An epidemiological survey. J B Join Surg 65-A(2):213–218
12. Kerr MS, Frank JW, Shannon HS, Norman RWK, Wells RP,
Neumann WP (2001) Biomechanical and psychosocial risk fac-
tors for low back pain at work. Am J Pub Health 91(7):
1069–1075
13. Lee P, Helewa A, Goldsmith CH, Smythe HA, Stitt LW (2000)
Low back pain: prevalence and risk factors in an industrial set-
ting. J Rheumatol 28(2):346–351
14. Marras W, Lavender S, Leurgans S, Fathallah F, Ferguson S,
Allread W, Rajulu S (1995) Biomechanical risk factors for
occupationally related low back disorders. Ergonomics 38(2):
377–410
15. Murtezani A, Ibraimi Z, Sllamniku S, Osmani T, Sherifi S (2011)
Prevalence and risk factors for low back pain in industrial
workers. Folia Med 53(3):68–74
16. Nieuwenhuyse AV, Fatkhutdinova L, Verbeke G, Pirenne D,
Johannik K, Somville PR, Mairiaux P, Moens GF, Masschelein R
(2004) Risk factors for first-ever low back pain among workers in
their first employment. Occup Med 54:513–519
17. Smedley J, Egger P, Cooper C, Coggon D (1995) Manual han-
dling activities and risk of low back pain in nurses. Occup
Environ Med 52:160–163
18. Troup JDG (1984) Causes, prediction and prevention of back pain
at work. Scand J Work Environ Health 10:419–428
19. Vandergrift JL, Gold JE, Hanlon A, Punnett L (2012) Physical and
psychosocial ergonomic risk factors for low back pain in automo-
bile manufacturing workers. Occup Environ Med 69:29–34
20. Vindigni D, Walker BF, Jamison JR, Da Costa C, Parkinson L,
Blunden S (2005) Low back pain risk factors in a large rural
Australian Aboriginal community. An opportunity for managing
co-morbidities? Chiropr Osteopathy 13(1):21
21. Griffith LE, Shannon HS, Wells RP, Walter SD, Cole DC, Cote P,
Frank J, Hogg-Johnson S, Langlois LE (2012) Individual par-
ticipant data meta-analysis of mechanical workplace risk factors
and low back pain. Am J Public Health 102:309–318
22. Hoogendoorn WE, van Poppel MNM, Bongers PM, Koes BW,
Bouter LM (2000) Systematic review of psychosocial factors at
work and private life as risk factors for back pain. Spine
25(16):2114–2125
23. Janwantanakul P, Sitthipornvorakul E, Paksaichol A (2012) Risk
factors for the onset of nonspecific low back pain in office
workers: a systematic review of prospective cohort studies.
J Manip Physiol Ther 35:568–577
24. Linton SJ (2000) A review of psychological risk factors in back
and neck pain. Spine 25(9):1148–1156
25. Ramond A, Bouton C, Richard I, Roquelaure Y, Baufreton C,
Legrand E, Huez J (2011) Psychosocial risk factors for chronic
low back pain in primary care—a systematic review. Fam Pract
28:12–21
26. Adams M, Mannion AF, Dolan P (1999) Personal risk factors for
first-time low back pain. Spine 24(23):2497–2505
518 Eur Spine J (2014) 23:512–519
123
54
27. Chen S, Liu M, Cook J, Bass S, Lo SK (2009) Sedentary lifestyle
as a risk factor for low back pain: a systematic review. Int Arch
Occup Environ Health 82:797–806
28. Leboeuf-Yde C (2000) Body weight and low back pain: a sys-
tematic literature review of 56 journal articles reporting on 65
epidemiologic studies. Spine 25(2):226–237
29. Leboeuf-Yde C (2004) Back pain—individual and genetic fac-
tors. J Electromyogr Kinesiol 14:129–133
30. Reisbord LS, Greenland S (1985) Factors associated with self-
reported back-pain prevalence: a population-based study.
J Chronic Dis 38(8):691–702
31. Wang S, Dezinno P, Maranets I, Berman M, Caldwell-Andrews
AA, Kain ZN (2004) Low back pain during pregnancy: preva-
lence, risk factors, and outcomes. Am Coll Obstet Gynecol
104(1):65–70
32. Livshits G, Popham M, Malkin I, Sambrook PN, MacGregor AJ,
Spector T, Williams FMK (2011) Lumbar disc degeneration and
genetic factors are the main risk factors for low back pain in
women: the UK Twin Spine Study. Ann Rheum Dis
70:1740–1745
33. Ferguson SA, Marras WS (1997) A literature review of low back
disorder surveillance measures and risk factors. Clin Biomech
12(4):211–226
34. Davis K, Heaney C (2000) The relationship between psychosocial
work characteristics and low back pain: underlying methodo-
logical issues. Clin Biomech 15(6):389–406
35. Steffens D, Ferreira ML, Maher CG, Latimer J, Koes BW, Blyth
FM, Ferreira PH (2012) Triggers for an episode of sudden onset
low back pain: study protocol. BMC Musculoskelet Disord
13(1):7. doi:10.1186/1471-2474-13-7
36. Viera AJ, Garrett JM (2005) Understanding interobserver
agreement: the kappa statistic. Fam Med 37(5):360–363
37. Hoy D, Brooks P, Blyth F, Buchbinder R (2010) The epidemi-
ology of low back pain. Best Pract Res Clin Rheumatol
24:769–781
Eur Spine J (2014) 23:512–519 519
123
55
Chapter Three
Triggers for an episode of sudden onset low back pain: study protocol
Chapter Three is published as:
Steffens D, Ferreira ML, Maher CG, Latimer J, Koes BW, Blyth FM, Ferreira PH. Triggers
for an episode of sudden onset low back pain: study protocol. BMC Musculoskeletal
Disorders. 2012; 24:13-17.
56
Statement from co-authors confirming authorship contribution of the PhD candidate
As co-authors of the paper “Triggers for an episode of sudden onset low back pain: study
protocol”, we confirm that Daniel Steffens has made the following contributions:
Conception and design of the research
Writing of the manuscript and critical appraisal of the content
Manuela L Ferreira Date: 01.01.2015
Christopher G Maher Date: 01.01.2015
Jane Latimer Date: 01.01.2015
Bart W Koes Date: 01.01.2015
Fiona M Blyth Date: 01.01.2015
Paulo H Ferreira Date: 01.01.2015
57
STUDY PROTOCOL Open Access
Triggers for an episode of sudden onset low backpain: study protocolDaniel Steffens1, Manuela L Ferreira1, Christopher G Maher1*, Jane Latimer1, Bart W Koes2, Fiona M Blyth3 andPaulo H Ferreira4
Abstract
Background: Most research on risk factors for low back pain has focused on long term exposures rather thanfactors immediately preceding the onset of low back pain. The aim of this study is to quantify the transientincrease in risk of a sudden episode of low back pain associated with acute exposure to a range of commonphysical and psychological factors.
Methods/design: This study uses a case-crossover design. One thousand adults with a sudden onset of low backpain presenting to primary care clinicians will be recruited. Basic demographic and clinical information includingexposure to putative triggers will be collected using a questionnaire. These triggers include exposure to hazardousmanual tasks, physical activity, a slip/trip or fall, consumption of alcohol, sexual activity, being distracted, and beingfatigued or tired. Exposures in the case window (0-2 hours from the time when participants first notice their backpain) will be compared to exposures in two control time-windows (one 24-26 hours and another 48-50 hoursbefore the case window).
Discussion: The completion of this study will provide the first-research based estimates of the increase in risk of asudden episode of acute low back pain associated with transient exposure to a range of common factors thoughtto trigger low back pain.
BackgroundNearly 4 million people in Australia suffer from backpain at any one time [1], with total treatment costsexceeding $1 billion a year [2]. In the US, the figure isan astonishing US$32 billion a year [3]. Back complaintsare the seventh most common condition in patientsconsulting general practitioners in Australia, and themost common musculoskeletal condition [4]. It is alsothe most common health problem for which an imagingtest is ordered by a general practitioner [4].A potential solution to managing the problem of low
back pain is the identification and control of modifiablerisk factors. This approach is appealing and seeminglylogical and there are notable examples where such anapproach has provided major improvements in publichealth. For back pain this approach has not yet been
fruitful: Cochrane reviews of workplace interventions[5], insoles [6] and lumbar supports [7] have failed tosupport these traditional back pain preventionapproaches. Prevention strategies have to date been lar-gely based on controlling long-term exposure to riskfactors, for example, modifying seats to control vibrationin truck drivers. However it is likely that the full poten-tial of prevention will not be reached unless we alsoconsider commonly occurring, modifiable risk factorsthat happen just before the onset of back pain. In thisregard we see our proposed research as complementaryto, rather than in conflict with, research evaluating longterm risk factors.The existence of short term risk factors or ‘triggers’ is
consistent with the time course of back pain. It is wellestablished that most people will experience low backpain in their lifetime [8], that pain is typically recurrent[9] and that episodes are usually of sudden onset [10].For example research conducted by our group demon-strated that in an inception cohort of 969 subjects, 82%reported that their onset of low back pain was sudden
* Correspondence: [email protected] division, The George Institute for Global Health, SydneyMedical School, The University of Sydney, PO Box M201, Missenden Road,Sydney, New South Wales 2050, AustraliaFull list of author information is available at the end of the article
Steffens et al. BMC Musculoskeletal Disorders 2012, 13:7http://www.biomedcentral.com/1471-2474/13/7
© 2012 Steffens et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative CommonsAttribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction inany medium, provided the original work is properly cited.
58
[10]. This pattern of low back pain suggests that ratherthan solely looking at long term exposure to risk factorsit would be instructive to also look closely at eventsoccurring immediately prior to the episode to identifymodifiable triggers to the episode. This information isroutinely sought by health practitioners when a patientwith low back pain seeks care. The treating cliniciancommonly asks the patient what activity they were per-forming just prior to the onset of pain, in essence, “wasthe episode triggered by something unusual that hap-pened just before?” The scientific method best suited toanswer this question is the case-crossover design [11].We will use the case-crossover design to provide the
first accurate estimates of the transient increase in riskof low back pain associated with transient exposure tovarious triggers. It is possible that we will identify sev-eral factors that are not modifiable but this informationwill be extremely important to our understanding andexplanation of the causes of low back pain.
Study Aims1) To quantify the transient increase in risk of an epi-sode of sudden onset, acute, low back pain associatedwith exposure to a range of common physical and psy-chological factors listed in Table 1.2) To determine if habitual physical activity moderates
the transient increase in risk of an episode of suddenonset, acute, low back pain associated with exposure tothe physical and psychological factors listed above.
Methods/DesignThe study will use the case-crossover design. The case-crossover design enables quantification of the risk asso-ciated with transient exposures [12]. It is more efficientthan cohort designs because it samples only cases, andmay be less exposed to selection bias than case-controldesigns because cases provide their own control data.
Cases will be identified from patients presenting to pri-mary care seeking treatment for an episode of suddenonset, acute, low back pain. In the case crossover designthe time of the onset of low back pain is identified andthen data are obtained on exposure to a series of possi-ble risk factors in the two hour period prior to theonset of low back pain (case window). Additional dataare obtained on exposures to the same set of possiblerisk factors in an earlier period (24-26 and 48-50 hoursprior to the case window) that did not precede an epi-sode of low back pain (these are referred to as the con-trol windows).The study has been approved by the Human Research
Ethics Committee at the University of Sydney (protocolnumber 05-2011/13742) and has received funding fromAustralia’s National Health and Medical Research Coun-cil (application ID APP1003608).
Study ParticipantsOne thousand consecutive patients (study participants)presenting to primary care clinicians (general medicalpractitioners, physiotherapists, chiropractors and phar-macists) for treatment of an episode of sudden onset,acute, low back pain will be recruited in Sydney, Austra-lia. Primary care clinicians will be trained individually orin small groups on the study methods and procedures.Study participants must be 18 years of age (or older) toparticipate.To be eligible to enter the study participants must
meet the criteria below:
▪ Comprehends spoken English;▪ Primary complaint of pain in the area between the12th rib and buttock crease, with or without leg pain;▪ Pain at least moderate intensity during the first 24hours of the episode (assessed using a modified ver-sion of item 7 of the SF36);
Table 1 Factors that may trigger an episode of low back pain to be evaluated in the study
Physical Factors Hazardous manual tasks:
- tasks involving heavy loads;
- tasks involving awkward postures;
- tasks involving objects that could not be positioned close to the body;
- tasks involving live people or animals;
- tasks involving loads that are unstable, unbalanced or difficult to grasp or hold;
Vigorous physical activity
Moderate physical activity
A slip/trip or fall
Consumption of alcohol
Sexual activity
Psychological Being distracted
Factors Being fatigued or tired
Steffens et al. BMC Musculoskeletal Disorders 2012, 13:7http://www.biomedcentral.com/1471-2474/13/7
Page 2 of 5
59
▪ Presentation for treatment within 7 days from thetime of pain onset;▪ Not have known or suspected serious spinalpathology (eg metastatic, inflammatory or infectivediseases of spine, cauda equina syndrome, spinalfracture);
An episode of acute low back pain will be defined asan episode preceded by a period of at least one monthwithout low back pain where the participant was notconsulting a health care practitioner or continuing withmedication for their low back pain (in accordance withthe De Vet et al. [13] definition of an ‘episode’ of acutelow back pain). A sudden onset episode of low backpain will be defined as pain of at least moderate inten-sity that developed over the first 24 hours (assessedusing a modified version of item 7 of the SF36).To describe further the cohort of study clinicians, we
will collect descriptive data, including the clinician’s age,contact details, current position and past clinical experi-ence. Secondly, we are collecting information regardingwhat clinicians in general consider as possible triggersfor a new episode of back pain. Based on their clinicalexperience, they are asked to list the five most likelytriggers for a sudden onset episode of low back pain.They will consider both (i) short term and (ii) long termexposures (see additional file 1). These data will be usedto inform the categorisation of putative risk factors inthe analyses of our participant data, and to assesswhether opinions of the study participants regardingpossible triggers for their low back pain are analogouswith their clinicians’ perceptions.
Participant recruitmentPatients seeking care for acute low back pain that fulfilthe inclusion criteria and agreeing to participate will bereferred to the study and their details (screening formand consent form) will be sent by fax to the study office.A study researcher will receive the fax and contact theparticipant as soon as possible to perform the studyinterview. Patients not able to answer the study ques-tionnaire in seven days from the time their clinicianreferred them to the study will be excluded.Prior to the study interview, the researchers will dou-
ble-check the eligibility criteria and explain the natureof the study to the participant. Participants are able towithdrawn from the study at any time.
Study interviewThe interview is divided into two parts. In the first partwe will collect basic demographic and clinical data andin the second part, we will collect information on puta-tive triggers (see additional file 2). We will record thedate and time when the patient first noticed their back
pain. Where possible, using a diary, calendar and/orsmartphone, we will then ask them to recall what theywere doing in the three days leading up to the onset oftheir back pain and also on the day of their back pain.Following this we will ask about exposure to the pre-
viously mentioned putative triggers. Where subjectsrespond affirmatively we collect detailed information onthe trigger, time and duration in free text. We will alsoask the study participant to consider what they thinkmay have triggered their LBP and similarly recorddetailed information on the nominated trigger, time andduration in free text.When asking the study participant about exposure to
specific triggers we have developed a script to lead theinterview (see additional file 2).
BlindingClinicians and study participants will be blinded to thecase and control periods. The study questionnaire isdesigned to investigate exposure to triggers over alonger time period than will be used in the analysis sothat participants in the trial remain blind to the dura-tion of the case and control windows. For example par-ticipants will be asked about their exposures for threedays preceding their back pain and also on the day oftheir back pain. A random sample of telephone calls willbe audited and the congruency of the log and telephonecall checked by the investigators. Data entry into thedatabase will be conducted by a separate person whowill be blinded to all putative risk factors. Blinding maybe less important in case-crossover designs than case-control studies because in the case-crossover design par-ticipants report exposure to triggers in both the case andcontrol windows. Recall bias can only occur if there isdifferential mis-reporting in the case and control win-dows. In our opinion this is unlikely.
Statistical analysisThe analyses follows standard methods for stratifiedanalyses [12] with the individual subject the stratifyingvariable in a case-crossover design. The estimates ofrelative risk are based on the ratio of the observed fre-quency of exposure to each of the transient triggers dur-ing the case period, to the expected frequency ofexposure during the two control periods. This is knownas a matched-pair interval approach where contrasts aremade between a pair of case control periods contributedby the same subject. In our proposed study there will betwo matched-pair intervals.To analyse the matched-pair interval data we will use
standard methods for case-control data (Mantel-Haens-zel estimator). Instead of having concordant and discor-dant pairs of subjects, the pairs will consist of twointervals for each subject, a case period (2 hours prior
Steffens et al. BMC Musculoskeletal Disorders 2012, 13:7http://www.biomedcentral.com/1471-2474/13/7
Page 3 of 5
60
to the event) and a control period (24-26 hours prior tothe event). A subject’s pair of intervals will either beconcordant or discordant with respect to each of thetriggers nominated on the item list. Ninety-five percentconfidence intervals will be computed by exact methodsbased on the binomial distribution. Comparison withthe first control period will form the primary analyses.Secondary analyses will be performed as describedabove but using the second control period (48-50 hoursprior to the event) as the control data for the matched-pair interval.
Sample sizeThe study was designed to be adequately powered forthe primary analysis, which involves estimation of therisk associated with transient exposure to the differenttypes of triggers. We calculated the sample size neces-sary for a paired case-control study using the proceduresdescribed by Dupont [14]. This showed that in a con-ventional paired case-control design with alpha set at0.05 we would need a sample of 1,000 cases to providean 80% probability of detecting an odds ratio of 1.5 orgreater across the plausible range of exposure preva-lence’s in control windows (0.2 to 0.8) and plausiblerange of correlations between exposure in case and con-trol windows (0.0 to 0.5).
DiscussionThis case cross-over study will provide the first-researchbased estimates of the transient increase in risk of asudden onset, acute, episode of low back pain associatedwith transient exposures to a range of physical and psy-chological factors. We anticipate that we will identifyseveral modifiable factors that are triggers for an episodeof low back pain. This information will be invaluable indesigning future prevention strategies, and enabling clin-icians to give evidence based advice to patients keen toavoid future episodes of low back pain.Recall bias is a major limitation of retrospective stu-
dies. Participants may under or overestimate the usualfrequency of exposures to the time of the injury (casewindow). They may also under or overestimate exposurein the case control windows because of memory lapse ordifficulty in estimating exposure. In this study, partici-pants must have presented for care within seven days ofthe onset of the injury to facilitate recall of activities. Inaddition, our questionnaire asks participants to useprompts such as referring to their agenda, calendar and/or smartphones to stimulate their memory of the activ-ities they performed in the days prior to the onset oftheir low back pain.The completion of this trial is expected by early 2014.
Additional material
Additional file 1: Clinicians’ questionnaire. Questionnaire to beapplied to describe further the cohort of study clinicians.
Additional file 2: Study Participants’ Questionnaire. Questionnaire tobe applied to the study participants.
AcknowledgementsThe TRIGGERS study team includes Anurina Das. We would like toacknowledge the valuable contribution of Qiang Li to the study statisticalanalysis plan. The National Health and Medical Research Council (NHMRC),Australia, provides funding for this study.
Author details1Musculoskeletal division, The George Institute for Global Health, SydneyMedical School, The University of Sydney, PO Box M201, Missenden Road,Sydney, New South Wales 2050, Australia. 2Department of General Practice,Erasmus MC, PO Box 2040, 3000 CA Rotterdam, The Netherlands. 3Centre forEducation and Research on Ageing, The University of Sydney, C 22 -Concord Hospital, Sydney, New South Wales 2006, Australia. 4Discipline ofPhysiotherapy, Faculty of Health Sciences, The University of Sydney, PO Box170, Lidcombe 1825, Syndey, New South Wales, Australia.
Authors’ contributionsCGM, JL, MLF, BWK, FMB and PHF are the principal investigators - togetherthey conceived and designed the trial and procured funding. DS and MLFdrafted the first version of the manuscript. All authors contributed to thewriting of the manuscript. All authors read and approved the final version ofthe manuscript.
Competing interestsThe authors declare that they have no competing interests. Prof Maher andA/Prof Latimer’s fellowships are funded by the Australian Research Council.
Received: 24 December 2011 Accepted: 24 January 2012Published: 24 January 2012
References1. Australian Institute of Health and Welfare: Arthritis and musculoskeletal
conditions in Australia. Canberra: Australian Institute of Health and Welfare;2005.
2. Walker B, Muller R, Grant W: Low back pain in Australian adults: theeconomic burden. Asia Pac J Public Health 2003, 15(2):79-87.
3. Agency for Healthcare Research and Quality: Total Expenses and PercentDistribution for Selected Conditions by Type of Service: United States.Medical Expenditure Panel Survey Household Component Data; 2005.
4. Britt H, Miller G, Knox S, Charles J, Pan Y, Henderson J, Baryram C, Valenti L,Ng A, O’Halloran J: General practice activity in Australia 2004-2005.Canberra: Australian Institute of Health and Welfare; 2005.
5. Van Oostrom S, Driessen M, de Vet H, Franche R, Schonstein E, Loisel P, VanMechelen W, Anema J: Workplace interventions for preventing workdisability. Cochrane Database of Systematic Reviews 2009.
6. Sahar T, Cohen MJ, Ne’eman V, Kandel L, Odebiyi D, Lev I, Brezis M,Lahad A: Insoles for prevention and treatment of back pain. CochraneDatabase of Systematic Reviews 2007, , 4: CD005275.
7. Van Duijvenbode I, Jellema P, Van Poppel MN, Van Tulder MW: Lumbarsupports for prevention and treatment of low back pain. CochraneDatabase of Systematic Reviews 2008, 2.
8. Waddell G: The Back Pain Revolution. Edinburgh: Churchill Livingstone;, 22004.
9. Von Korff M, Saunders K: The course of back pain in primary care. Spine1996, 21(24):2833-2839.
10. Henschke N, Maher CG, Refshauge KM: A systematic review identifies fivered flags to screen for vertebral fracture in patients with low back pain.J Clin Epidemiol 2008, 61(2):110-118.
11. Maclure M, Mittleman M: Should we use a case-crossover design? AnnuRev Public Health 2000, 21:193-221.
Steffens et al. BMC Musculoskeletal Disorders 2012, 13:7http://www.biomedcentral.com/1471-2474/13/7
Page 4 of 5
61
12. Maclure M: The case-crossover design: a method for studying transienteffects on the risk of acute events. Am J Epidemiol 1991, 133:144-153.
13. de vet H, Heymans M, Dunn K, Pope D, van der Beek A, Macfarlane G,Bouter L, Croft P: Episodes of low back pain. A proposal for uniformdefinitions to be used in research. Spine 2002, 27(21):2409-2416.
14. Dupont W: Power calculations for matched case-control studies.Biometrics 1988, 44:1157-1168.
Pre-publication historyThe pre-publication history for this paper can be accessed here:http://www.biomedcentral.com/1471-2474/13/7/prepub
doi:10.1186/1471-2474-13-7Cite this article as: Steffens et al.: Triggers for an episode of suddenonset low back pain: study protocol. BMC Musculoskeletal Disorders 201213:7.
Submit your next manuscript to BioMed Centraland take full advantage of:
• Convenient online submission
• Thorough peer review
• No space constraints or color figure charges
• Immediate publication on acceptance
• Inclusion in PubMed, CAS, Scopus and Google Scholar
• Research which is freely available for redistribution
Submit your manuscript at www.biomedcentral.com/submit
Steffens et al. BMC Musculoskeletal Disorders 2012, 13:7http://www.biomedcentral.com/1471-2474/13/7
Page 5 of 5
62
Name: ___________________________________________________________________
Gender: □ Female □ Male Date of Birth: _____________________________
Address: ________________________________________________________________
Phone:_____________________________ FAX: ________________________________
Email:_____________________________
Profession (tick one)
physiotherapist medical practitioner pharmacist
Current Position:__________________________________________________________________
Clinical experience
Years as practicing clinician _______________________________
Years managing low back pain ______________________________
1. Based on your clinical experience, list what you consider to be the five most likely
factors involving short term exposure that are triggers for a sudden episode of acute
low back pain? (E.g. in my clinical experience, running 15km on the road with poor shoes
can trigger an episode of shin splints).
1)________________________________________________________________________
2)________________________________________________________________________
3)________________________________________________________________________
4)________________________________________________________________________
5)________________________________________________________________________
2. Based on your clinical experience, list what you consider to be the five most likely
factors involving long term exposure that increase the risk of a sudden episode of
acute low back pain (e.g. in my clinical experience working with a ‘poke neck’ posture
increases the risk of neck pain and headaches).
1)________________________________________________________________________
2)________________________________________________________________________
3)________________________________________________________________________
4)________________________________________________________________________
5)________________________________________________________________________
Additional file 1 – Clinicians’ Questionnaire
63
Triggers Specific Questions Tick the boxes where the participant reports pain on the mannequin below:
Height (cm): ______________________ Weight (Kg): _____________________
How much back pain have you had during the first 24 hours of this episode? [1]
None Very mild Mild Moderate Severe Very Severe
During the first 24 hours of this episode how much did back pain interfere with your
normal work (including both work outside the home and housework)? [1]
Not at all A little bit Moderately Quite a bit Extremely
How tense or anxious have you felt in the past week? Circle one. [2]
0 1 2 3 4 5 6 7 8 9 10
Appendix 5. Study Questionnaire
Calm and
relaxed
As
tense/anxious
as I’ve ever
felt
64
Physical Activity [3]
1. In the last week, how many times have you walked continuously, for at least 10 minutes, for
recreation, exercise or to get to or from places? ______times;
And in the week before your low back pain started? ______times.
What do you estimate was the total time that you spent walking in this way in the last week?
______hours ______minutes;
And in the week before your low back pain started? ______ hours ______minutes.
2. In the last week, how many times did you do any vigorous physical activity which made
you breathe harder or puff and pant? (e.g. jogging, cycling, aerobics, competitive
tennis)______times;
And in the week before your low back pain started? ______times.
What do you estimate was the total time that you spent doing this vigorous physical activity in
the last week? ______hours ______minutes;
And in the week before your low back pain started? ______ hours ______minutes.
3. In the last week, how many times did you do any moderate physical activities that you have
not already mentioned? (e.g. gentle swimming, social tennis, golf)______times;
And in the week before your low back pain started? ______times.
What do you estimate was the total time that you spent doing these activities in the last week?
______hours ______minutes;
And in the week before your back pain started? ______ hours ______minutes.
4. Was your level of physical activity last week typical for you? Yes No
65
Triggers Exposure
Please write the date and time you first noticed your low back pain on the table below:
Day Fri Sat Sun Mon Tues Wed Thurs Fri Sat Sun
Date
Time
I am going to ask you to recall what you were doing in the three days leading up to
your back pain and also on the day of your back pain. To help your memory I
would like you to sit down with your diary and smartphone. To help make sure we
have the right days I want you to tell me the day, weather and a key thing you did
on each day.
Example: Tuesday: cold and wet; visited parents
Day of back pain: _______________________________________________________
Day before: ____________________________________________________________
2 days earlier: __________________________________________________________
3 days earlier: __________________________________________________________
66
1a. MANUAL TASKS …
HEAVY LOADS [4]
Day
If yes, precisely describe manual task (type of task,
load, duration and time). e.g. Lifted 50 large boxes,
one at a time, (~15kg each box – perceived as heavy)
from the floor and placed them on a bench at waist
height. 8:00am - 20min.
The first group of questions is
about manual tasks. Manual tasks
include lifting, lowering, pushing,
carrying or otherwise moving,
holding or restraining any person,
animal or item.
Firstly we are interested in manual
tasks involving HEAVY LOADS.
So on the day of your back pain did
you engage in any manual tasks
involving a heavy load?
That was the (restate their
description of the day).
Now what about the day before….
That was the (restate their
description of the day).
OK now two days back That was
the (restate their description of the
day).
OK finally three days back That was
the (restate their description of the
day)
Day of back
pain
Yes No
Day before
Yes No
2 days earlier
Yes No
3 days earlier
Yes No
67
1b. MANUAL TASKS…
AWKWARD POSTURE [4] Day
If yes, precisely describe manual task and posture (type
of task, load, duration, time & body position). e.g. knelt
down while gardening. 2:00pm – 40min.
Now I want you to think about
manual tasks involving an
AWKWARD POSTURE.
So on the day of your back pain did
you engage in any manual tasks
involving an awkward position?
That was the (restate their
description of the day).
Now what about the day before….
That was the (restate their
description of the day).
OK now two days back That was the
(restate their description of the day).
OK finally three days back That was
the (restate their description of the
day)
Day of back
pain
Yes No
Day before
Yes No
2 days
earlier
Yes No
3 days
earlier
Yes No
68
1c. MANUAL TASKS…
AN OBJECT THAT COULD
NOT BE POSITIONED CLOSE
TO THE BODY [4]
Day
If yes, precisely describe manual task and posture (type
of task, load, duration, time and body position). e.g.
Lifted large box (~7Kg – perceived as light) out of the
car boot and placed it on the floor. 11:00am – 10 sec.
Now I want you to think about
manual tasks involving AN
OBJECT THAT COULD NOT BE
POSITIONED CLOSE TO THE
BODY.
So on the day of your back pain did
you engage in any manual tasks
involving an object that could not
be positioned close to the body?
That was the (restate their
description of the day).
Now what about the day before….
That was the (restate their
description of the day).
OK now two days back That was the
(restate their description of the day).
OK finally three days back That was
the (restate their description of the
day)
Day of back
pain
Yes No
Day before
Yes No
2 days
earlier
Yes No
3 days
earlier
Yes No
69
1d. MANUAL TASKS…
LIVE PEOPLE OR ANIMALS [4] Day
If yes, precisely describe manual task and posture (type
of task, load, duration, time and body position). e.g.
Lifted 2 year-old child (~12kg – perceived as moderate)
from the floor onto the bed. 8:00pm once. Lifted and
carried baby (5 kg perceived as light), 3 to 4 times from
one room to another. 8:10pm – 30min
Now I want you to think about
manual tasks involving LIVE
PEOPLE OR ANIMALS.
So on the day of your back pain did
you engage in any manual tasks
involving live people or animals?
That was the (restate their description
of the day).
Now what about the day before….
That was the (restate their description
of the day).
OK now two days back…
That was the (restate their description
of the day).
OK finally three days back…
That was the (restate their description
of the day)
Day of back
pain
Yes No
Day before
Yes No
2 days
earlier
Yes No
3 days
earlier
Yes No
70
1e. MANUAL TASKS…
A LOAD THAT WAS
UNSTABLE, UNBALANCED OR
DIFFICULT TO GRASP OR
HOLD [4]
Day
If yes, precisely describe manual task and posture (type
of task, load, duration, time and body position). e.g.
lifted a 4 meter extension ladder (~12 Kg – perceived as
moderate) from the car roof racks, carried to garage
and hung on wall. 3:00pm - 5min.
Now I want you to think about
manual tasks involving A LOAD
THAT WAS UNSTABLE,
UNBALANCED OR DIFFICULT
TO GRASP OR HOLD.
So on the day of your back pain did
you engage in any manual tasks
involving a load that was unstable,
unbalanced or difficult to grasp or
hold?
That was the (restate their
description of the day).
Now what about the day before….
That was the (restate their
description of the day).
OK now two days back…
That was the (restate their
description of the day).
OK finally three days back…
That was the (restate their
description of the day)
Day of back
pain
Yes No
Day before
Yes No
2 days
earlier
Yes No
3 days
earlier
Yes No
71
2a. VIGOROUS
PHYSICAL ACTIVITY Day
If yes, precisely describe activity/task, time and
duration. e.g. ran 10km at fast pace (5 mins per km)
10:00am - 50min.
The next questions are about
VIGOROUS PHYSICAL
ACTIVITY. This could be sports or
hobbies, paid or volunteer work,
work outside the home and
housework.
Examples of vigorous physical
activity include: running, rope
skipping, axe chopping, using heavy
tools, canoeing and truck driving.
So on the day of your back pain did
you engage in any manual tasks
involving VIGOROUS PHYSICAL
ACTIVITIES?
That was the (restate their
description of the day).
Now what about the day before…
That was the (restate their
description of the day).
OK now two days back… That was
the (restate their description of the
day).
OK finally three days back… That
was the (restate their description of
the day)
Day of back
pain
Yes No
Day before
Yes No
2 days
earlier
Yes No
3 days
earlier
Yes No
72
2b. MODERATE
PHYSICAL ACTIVITY Day
If yes, precisely describe activity/task, time and
duration. e.g. Mowed the lawn. 11:00am -12:00 pm.
The next questions are about
MODERATE PHYSICAL
ACTIVITY. This could be sports or
hobbies, paid or volunteer work,
work outside the home and
housework.
Examples of moderate physical
activity include: leisure cycling,
fishing, general home repairs, music
playing, golf, surfing and painting.
So on the day of your back pain did
you engage in any manual tasks
involving MODERATE
PHYSICAL ACTIVITIES?
That was the (restate their
description of the day).
Now what about the day before….
That was the (restate their
description of the day).
OK now two days back… That was
the (restate their description of the
day).
OK finally three days back… That
was the (restate their description of
the day).
Day of back
pain
Yes No
Day before
Yes No
2 days
earlier
Yes No
3 days
earlier
Yes No
73
3. SLIP, TRIP OR FALL [5] Day
If yes, precisely describe incident and time. e.g.
Descending stairs, missed bottom step and jarred back.
8:30am – one occasion.
Now I want you to think about SLIP,
TRIP OR FALL.
So on the day of your back pain did
you have a slip, trip or fall? That
was the (restate their description of
the day).
Now what about the day before….
That was the (restate their
description of the day).
OK now two days back…
That was the (restate their
description of the day).
OK finally three days back….
That was the (restate their
description of the day)
Day of back
pain
Yes No
Day before
Yes No
2 days
earlier
Yes No
3 days
earlier
Yes No
74
4. CONSUMED ALCOHOL [6] Day
If yes, specify amount (refer to standard drink table at
the end of booklet), time and duration. E.g. 2x red wine
glasses (180ml). 8:20pm – 1h.
Now I want you to think about
ALCOHOL CONSUMPTION.
So on the day of your back pain did
you consume alcohol? That was the
(restate their description of the day).
Now what about the day before….
That was the (restate their
description of the day).
OK now two days back… That was
the (restate their description of the
day).
OK finally three days back… That
was the (restate their description of
the day)
Day of back
pain
Yes No
Day before
Yes No
2 days
earlier
Yes No
3 days
earlier
Yes No
5. SEXUAL ACTIVITY [7] Day If yes, specify time. E.g. 11:00pm
Now I want you to think about
SEXUAL ACTIVITY. So on the
day of your back pain did you
engage in sexual activity? That was
the (restate their description of the
day).
Now what about the day before….
That was the (restate their
description of the day).
OK now two days back… That was
the (restate their description of the
day).
OK finally three days back… That
was the (restate their description of
the day)
Day of back
pain
Yes No
Day before
Yes No
2 days
earlier
Yes No
3 days
earlier
Yes No
75
6. DISTRACTION [8] Day
If yes, specify time and duration, distraction and task.
e.g. Distracted by child crying while lifting a box from
car boot and it slipped from his/her hands. 8:30am –
one occasion.
Now I want you to think about being
DISTRACTED.
So on the day of your back pain were
you DISTRACTED for any reason
while engaged in a task or activity?
That was the (restate their
description of the day).
Now what about the day before….
That was the (restate their
description of the day).
OK now two days back… That was
the (restate their description of the
day).
OK finally three days back… That
was the (restate their description of
the day)
Day of back
pain
Yes No
Day before
Yes No
2 days
earlier
Yes No
3 days
earlier
Yes No
7. FATIGUE OR TIREDNESS [9] Day
If yes, specify time and duration. e.g. Disrupted and
poor sleep the night before as youngest child kept
waking due to earache. 3:00am – 24h.
Now I want you to think about
feeling FATIGUED or TIRED. So
on the day of your back pain did you
feel FATIGUED OR TIRED? That
was the (restate their description of
the day).
Now what about the day before….
That was the (restate their
description of the day).
OK now two days back… That was
the (restate their description of the
day).
OK finally three days back… That
was the (restate their description of
the day)
Day of back
pain
Yes No
Day before
Yes No
2 days
earlier
Yes No
3 days
earlier
Yes No
76
8. What do you think may have triggered your low back pain? (Record what the patient thinks may have
triggered his/her episode of back pain. eg. Bent down once to pick up newspaper from lawn. 7:00am -
immediately).
___________________________________________________________________________________________
____________________________________________________________________________________________
____________________________________________________________________________________________
____________________________________________________________________________________________
____________________________________________________________________________________________
So on the day of your back pain did you
do the activity described above? That
was the (restate their description of the
day).
Now what about the day before…. That
was the (restate their description of the
day).
OK now two days back… That was the
(restate their description of the day).
OK finally three days back… That was
the (restate their description of the day)
Day of back pain
Yes No
Day before
Yes No
2 days earlier
Yes No
3 days earlier
Yes No
77
Reference
1. Ware J, Sherbourne C: The MOS 36-item short-form health survey (SF-36). 1.
Conceptual framework and item selection. Medical Care 1992, 30:473-483.
2. Linton S, Hellsing A, Bergstrom G: Exercise for workers with musculoskeletal
pain: does enhancing compliance decrease pain? J Occup Med 1996, 6(3):177-190.
3. Armstrong T, Bauman A, Davies J: Physical activity patterns of Australian Adults.
In. Edited by Welfare AIoHa. Canberra; 2000.
4. Australian Safety Compensation Council: National code of practice for the
prevention of musculoskeletal disorders from performing manual tasks at work.
In. Canberra; 2007.
5. Verma S, Lombardi D, Chang W, Courtney T, Huang Y, Brennan M, Mittleman M,
Ware J, Perry M: Rushing, distraction, walking on contaminated floors and risk
of slipping in limited-service restaurants: a case--crossover study. Occupational &
Environmental Medicine 2010, 68(8):575-581.
6. Vinson DC, Mabe N, Leonard LL, Alexander J, Becker J, Boyer J, Moll J: Alcohol
and injury. A case-crossover study. Arch Fam Med 1995, 4(6):505-511.
7. Dahabreh IJ, Paulus JK, Dahabreh IJ, Paulus JK: Association of episodic physical
and sexual activity with triggering of acute cardiac events: systematic review and
meta-analysis. JAMA, 305(12):1225-1233.
8. Sorock G, Lombardi D, Peng D, Hauser R, Eisen E, Herrick R, Mittleman M: Glove
use and the relative risk of acute hand injury: a case-crossover study. Journal of
Occupational & Environmental Hygiene 2004, 1(3):182-190.
9. Chen S, Fong P, Lin S, Chang C, Chan C: A case-crossover study on transient risk
factors of work-related eye injuries. Occupational & Environmental Medicine
2009, 66(8):517-522.
78
Chapter Four
What triggers an episode of low back pain? A case-crossover study
Chapter Four is published as:
Steffens D, Ferreira ML, Latimer J, Ferreira PH, Koes BK, Blyth F, Li Q, Maher CG. What
triggers an episode of low back pain? A case-crossover study. Arthritis Care & Research.
2015; 67:403-410.
79
Statement from co-authors confirming authorship contribution of the PhD candidate
As co-authors of the paper “What triggers an episode of low back pain? A case-crossover
study”, we confirm that Daniel Steffens has made the following contributions:
Conception and design of the research
Data collection
Analysis and interpretation of the findings
Writing of the manuscript and critical appraisal of the content
Manuela L Ferreira Date: 01.01.2015
Jane Latimer Date: 01.01.2015
Paulo H Ferreira Date: 01.01.2015
Bart W Koes Date: 01.01.2015
Fiona Blyth Date: 01.01.2015
Qiang Li Date: 01.01.2015
Christopher G Maher Date: 01.01.2015
80
What Triggers an Episode of Acute Low BackPain? A Case–Crossover StudyDANIEL STEFFENS,1 MANUELA L. FERREIRA,2 JANE LATIMER,2 PAULO H. FERREIRA,2
BART W. KOES,3 FIONA BLYTH,2 QIANG LI,2 AND CHRISTOPHER G. MAHER2
Objective. To investigate a range of transient risk factors for an episode of sudden-onset, acute low back pain (LBP).Methods. This case–crossover study recruited 999 subjects with a new episode of acute LBP between October 2011 andNovember 2012 from 300 primary care clinics in Sydney, Australia. Each participant was asked to report exposure to 12putative triggers over the 96 hours preceding the onset of back pain. Conditional logistic regression was used to estimateodds ratios (ORs) expressing the magnitude of increased risk with exposure to each trigger.Results. Exposure to a range of physical and psychosocial triggers significantly increased the risk of a new onset of LBP;ORs ranged from 2.7 (moderate or vigorous physical activity) to 25.0 (distracted during an activity or task). Agemoderated the effect of exposure to heavy loads and sexual activity. The ORs for heavy loads for people ages 20, 40, or60 years were 13.6, 6.0, and 2.7, respectively. The risk of developing back pain was greatest between 7:00 AM and noon.Conclusion. Transient exposure to a number of modifiable physical and psychosocial triggers substantially increasesrisk for a new episode of LBP. Triggers previously evaluated in occupational injury studies, but never in LBP, have beenshown to significantly increase risk. These results aid our understanding of the causes of LBP and can inform thedevelopment of new prevention approaches.
INTRODUCTION
Back pain affects approximately 10% of the world’s pop-ulation at any point in time (1–3). When disease burden ismeasured by disability-adjusted life years, back pain is oneof the 10 leading causes of disease burden globally. Backpain is, however, unique among this list of 10 diseasesbecause there has been little or no progress in identifyingeffective prevention strategies (4–6).
Understanding what modifiable factors increase the riskof back pain is a crucial first step in prevention. Existingresearch has focused on factors that are not modifiable(e.g., age) or involve long-term exposure (e.g., smoking),
whereas the role of modifiable factors more proximal to theonset of back pain is yet to be investigated. Controllingexposure to these factors may be extremely important inpreventing back pain.
The case–crossover design provides an ideal method forquantifying the increased risk due to transient exposure totriggers (7,8). In this design a person acts as their owncontrol and hence the potential for between-person con-founding is reduced. This perfect matching is important inback pain research as it eliminates potential effects ofunmeasured confounders such as genetic and lifestyle in-fluences (9). The TRIGGERS study for low back pain aimedto investigate a number of transient physical and psycho-social risk factors for an episode of sudden-onset, acutelow back pain (LBP). Physical factors included heavyloads; awkward positioning; handling of objects far fromthe body; handling people or animals and unstable load-ing; a slip, trip, or fall; engagement in moderate or vigorousphysical activity; and sexual activity. Psychosocial factorsincluded alcohol consumption and being distracted andfatigued.
PATIENTS AND METHODS
Study design. The TRIGGERS study employed a case–crossover design to quantify the risk associated with tran-sient exposure to modifiable triggers for back pain. Trig-
Supported by the National Health and Medical ResearchCouncil of Australia.
1Daniel Steffens, BPT: The University of Sydney, Sydney,Australia, and Federal University of Minas Gerais, MinasGerais, Brazil; 2Manuela L. Ferreira, PhD, Jane Latimer,PhD, Paulo H. Ferreira, PhD, Fiona Blyth, PhD, Qiang Li,PhD, Christopher G. Maher, PhD: The George Institute forGlobal Health, The University of Sydney, Sydney, Australia;3Bart W. Koes, PhD: Erasmus Medical Center, Rotterdam,The Netherlands.
Address correspondence to Manuela L. Ferreira, PhD,The George Institute for Global Health, Sydney MedicalSchool, The University of Sydney, PO Box M201 MissendenRoad, Sydney, 2015, New South Wales, Australia. E-mail:[email protected].
Submitted for publication August 21, 2014; accepted inrevised form December 9, 2014.
Arthritis Care & ResearchVol. 67, No. 3, March 2015, pp 403–410DOI 10.1002/acr.22533© 2015, American College of Rheumatology
ORIGINAL ARTICLE
403
81
gers from the list of hazardous tasks provided in a nationalcode of practice were included (10). Additionally a num-ber of factors that had been previously identified as trig-gers in occupational injury studies (11–14), but never eval-uated in the area of back pain, were included. Theexposure to each trigger during the 2 hours preceding theonset of back pain (case window) was compared to expo-sure in two 2-hour periods ending 24 and 48 hours beforethe onset of back pain (control windows). The study wasapproved by the Human Research Ethics Committee of theUniversity of Sydney (protocol number 05-2011/13742). Adetailed protocol has been previously published (15).
Participants. A total of 999 consecutive patients, age�18 years and with a new episode of acute back pain, wererecruited from 300 primary care clinics in New SouthWales, Australia between October 2011 and November2012. A new episode of back pain was defined as a primarycomplaint of pain between the 12th rib and the buttockcrease, with or without leg pain, causing the patient toseek health care or take medication and preceded by aperiod of at least 1 month without back pain (16). Patientsneeded to present to primary care within 7 days from painonset and report pain of at least moderate intensity inthe first 24 hours of the current episode (measured usingitem 7 of the Short Form 36 questionnaire). This inclusionmeans that we did not study patients with an insidiousonset, a less common presentation for nonspecific backpain that would be less suited to study with a case–crossover design (17). Patients were excluded from thestudy if they presented with known or suspected seriousspinal pathology (e.g., metastatic, inflammatory, or infec-tive diseases of the spine). All participants gave writteninformed consent for participation.
Study interview. Participants were interviewed byphone within 7 days following referral to the study.Trained research staff used an interview script to collectsociodemographic and clinical characteristics of the backpain episode as well as data on exposure to a variety ofpossible triggers. The interview script was piloted on 20
subjects with back pain and adjustments made to improveclarity and participant recall.
During the interview, participants were asked to identifythe date and time of pain onset with the assistance ofrecommended recall aids such as a diary, calendar, and/orsmartphone. Each participant was then asked to reportexposure, including its time and duration, to each of the 12putative triggers in the 96 hours preceding the onset ofback pain. For example, for questions about manual tasksinvolving a heavy load would be as follows: so on the dayof your back pain did you engage in any manual tasksinvolving a heavy load? That was the . . . (the interviewerwould restate the participant’s description of the day, i.e.,that was the quite warm day you went to church). Nowwhat about the day before . . . (the interviewer would re-state the description of that day, i.e., the windy day whenyou did your weekly shopping). What about two daysback. That was the . . . (the interviewer would restate thedescription of that day, i.e., the day you visited your par-ents and it rained all day). Participants, clinicians, andinterviewers were blinded to the time and length of thepredetermined case and control windows.
Physical triggers included manual tasks (heavy loads,awkward positioning, handling of objects far from thebody, and handling people or animals and unstable load-ing); a slip, trip, or fall; engagement in moderate or vigor-ous physical activity; and sexual activity. Physical activi-ties were coded as moderate or vigorous physical activityconsidering their energy cost (18). Psychosocial triggersincluded alcohol consumption and being distracted or fa-tigued. Recruiting clinicians were not aware of the specifictriggers evaluated in the study. Although data were ob-tained for exposure to the 12 putative triggers over the 96hours prior to back pain onset, the primary analysis onlyused data for the 2-hour period immediately preceding theback pain onset and for the two 2-hour periods ending 24and 48 hours before the pain onset.
Participants were also questioned regarding their habit-ual physical activity. This was assessed using the ActiveAustralia questionnaire, which estimates the total numberof hours of light, moderate, and vigorous physical activityperformed by the participant in the past week (19). For thepurpose of this study, the questionnaire was modified toinclude the recall period of interest, i.e., the week beforethe onset of back pain. Supplementary Appendix A, avail-able in the online version of this article at http://onlinelibrary.wiley.com/doi/10.1002/acr.22533/abstract, pre-sents the study questionnaire.
Statistical analysis. The frequency of exposure to eachtrigger was calculated for the case window (2 hours priorto onset of back pain) and 2 control windows (24–26 hoursand 48–50 hours prior to onset of back pain, respectively).A frequency distribution graph of pain onset by time ofday (in hours) was calculated. Conditional logistic regres-sion models were constructed to quantify the risk of backpain onset associated with each trigger, where each par-ticipant represented a matched set of data for case andcontrol exposures (20). Odds ratios (ORs) and 95% confi-dence intervals (95% CIs) were derived comparing expo-
Significance & Innovations● Back pain is the leading cause of disability glob-
ally, yet there has been little or no progress inidentifying effective prevention strategies.
● To date, no studies have examined the role ofexposure to transient risk factors in triggering anepisode of acute low back pain.
● The results of this study demonstrate for the firsttime that brief exposure to a range of physical andpsychosocial factors can considerably increase therisk of an episode of acute back pain.
● These results will have significant clinical andpolicy implications for the control of a disease thatis a major problem worldwide.
404 Steffens et al
82
sure in the case window with each of 2 control windows.Conditional logistic regression was also used to assessvalidity of the control windows by comparing their expo-sure data. Secondary analyses evaluated interaction be-tween exposure to triggers and habitual physical activity,age, body mass index (BMI), number of previous LBPepisodes, depression, and anxiety scores.
It is plausible that physical and psychosocial factorscould cause an episode of back pain that does not becomeapparent in the 2 hours after the participant was exposed.Therefore, sensitivity analyses were conducted using caseand control windows of 4- and 6-hour duration. Sensitiv-ity analyses using case and control windows of 1-hourduration were also performed. STATA 12 software wasused for all analyses.
Sample size. The study was designed to be adequatelypowered for the primary analysis, which involves estima-tion of the risk associated with transient exposure to thedifferent types of triggers by comparing exposures in thecase window to the first control window. We calculatedthe sample size necessary for a paired case–control studyusing the procedures described by Dupont (21). Samplesize was estimated using procedures for a paired case–control design (21). With alpha set at 0.05, a sample of1,000 cases would provide an 80% probability of detectingan OR of 1.5 or greater across the plausible range of expo-sure prevalence in control windows (0.2–0.8) and theplausible range of correlations between exposure in caseand control windows (0.0–0.5).
RESULTS
Primary care clinicians referred 1,639 patients with a newepisode of back pain, with 999 being interviewed andcontributing data to the study (Figure 1).
Patterns of pain onset. The mean � SD duration of theepisode was 4.9 � 2.7 days, with a mean � SD timebetween pain onset and presentation to primary care of2.0 � 2.1 days, and 1.9 � 2.0 days from presentation tointerview (Table 1). Approximately half the participants(49.5%) reported having severe pain in the first 24 hours of
Figure 1. Study recruitment flow chart. LBP � low back pain.
Table 1. Characteristics of the participants (n � 999)*
Characteristics Value
Age, years 45.3 � 13.4Male sex 541 (54.2)Height, cm 172.4 � 10.4Weight, kg 78.9 � 18.1†Body mass index, kg/m2‡ 26.4 � 5.2†Duration of current episode, days 4.9 � 2.7Number of previous episodes 5.9 � 14.0Days to seek care 3.0 � 2.1Days from presentation to health care and
interview2.0 � 2.0
Days of reduced activity 2.3 � 2.2Pain scores (0–10) 5.3 � 2.1Currently taking medication 452 (45.3)Currently employed 836 (83.7)Workers compensation 89 (8.9)If in paid employment, what is done for a
livingNot employed 163 (16.3)Clerical/administrative worker 103 (10.3)Community/personal service worker 47 (4.7)Laborer 30 (3.0)Machinery operator/driver 27 (2.7)Manager 159 (15.9)Professional 341 (34.1)Sales worker 52 (5.2)Technician/trade worker 77 (7.7)
Pain location§Upper back 59 (5.9)Lower back 999 (100)Left thigh (back) 97 (9.7)Left leg (back) 44 (4.40)Right thigh (back) 107 (10.7)Right leg (back) 48 (4.8)Right thigh (front) 29 (2.9)Right leg (front) 11 (1.1)Left thigh (front) 27 (2.7)Left leg (front) 8 (0.8)
Pain severity in first 24 hoursModerate 373 (37.3)Severe 494 (49.5)Very severe 132 (13.2)
Pain interfering with work in first 24 hoursNot at all 21 (2.1)A little bit 101 (10.1)Moderately 250 (25.0)Quite a bit 389 (38.9)Extremely 238 (23.8)
Habitual physical activity in last week¶Sedentary 542 (54.3)Insufficient activity 164 (16.4)Sufficient activity 293 (29.3)
Habitual physical activity during weekbefore
Sedentary 360 (36.0)Insufficient activity 174 (17.4)Sufficient activity 465 (46.6)
Tense/anxious scores 4.0 � 2.6Depression scores 2.7 � 2.7
* Values are the number (percentage) or the mean � SD.† N � 998.‡ Body mass index � weight in kilograms divided by the square ofthe height in meters.§ Pain location was assessed using a pain mannequin provided tothe participant by the referring clinician.¶ Habitual physical activity: moderate activity time � (2 � vigorousactivity time). Sedentary (zero), insufficient activity (�1 to �149),and sufficient activity (�150).
Triggers for Low Back Pain 405
83
the current episode, and 87.8% reported that pain inter-fered at least moderately with daily activities. Morningswere the most frequent time of day for back pain onset,with 35.2% of participants (n � 352) reporting pain onsetbetween 7:00 AM and 10:00 AM (Figure 2). Only 3.7% ofparticipants (n � 37) reported pain onset between mid-night and 5:00 AM, with a large increase in reports from6:00 AM.
Exposure to potential triggers. Exposure to all physicaltriggers was more frequent in the case window than in the
2 control windows (Table 2). The highest exposure in thecase window was to manual tasks involving an awkwardposture (27.4% of case windows; 7% for first control win-dow and 5.4% for second control window), followed bymanual tasks involving heavy loads (17.9% in case win-dows; 6.4% and 5.9% in the first and second controlwindows, respectively). A total of 37 participants reportedbeing exposed to a slip, trip, or fall in the 2 hours beforepain onset, compared to only 1 participant in the firstcontrol window and none in the second control window.This suggests a strong association between this trigger and
Figure 2. Frequency of back pain onset by time of day for 999 participants.Panel shows the percentage of episodes that commenced in each 1-hour timeepoch across the day.
Table 2. Exposure frequency and ORs for each trigger: primary analysis (2-hour window)*
Triggers
Case window(0–2 hours)
no. (%)
First control window(24–26 hours)
no. (%)
Second control window(48–50 hours)
no. (%) OR (95% CI)† P
Physical factorsManual tasks involving…
Heavy loads 179 (17.9) 64 (6.4) 59 (5.9) 5.0 (3.3–7.4) � 0.001Awkward posture 274 (27.4) 70 (7.0) 54 (5.4) 8.0 (5.5–11.8) � 0.001Objects not close to the body 40 (4.0) 14 (1.4) 10 (1.0) 6.2 (2.4–15.9) � 0.001People or animals 86 (8.6) 62 (6.2) 63 (6.3) 5.8 (2.3–15.0) � 0.001Unstable, unbalanced,
difficult to grasp52 (5.2) 19 (1.9) 13 (1.3) 5.1 (2.4–10.9) � 0.001
Moderate or vigorous physicalactivity
225 (22.5) 129 (12.9) 112 (11.2) 2.7 (2.0–3.6) � 0.001
Vigorous physical activity only 105 (10.5) 44 (4.4) 38 (3.8) 3.9 (2.4–6.3) � 0.001Slip/trip/fall‡ 37 (3.7) 1 (0.1) 0 (0.0) – –Sexual activity 8 (0.8) 11 (1.1) 11 (1.1) 0.7 (0.3–1.8) 0.49
Psychosocial factorsConsumption of alcohol 13 (1.3) 9 (0.9) 12 (1.2) 1.5 (0.6–3.7) 0.37Distracted during an activity
or task30 (3.0) 6 (0.6) 8 (0.8) 25.0 (3.4–184.5) 0.002
Fatigued/tired 118 (11.8) 69 (6.9) 60 (6.0) 3.7 (2.2–6.3) � 0.001
* Results of the primary analyses based on case and control windows of 2 hours duration. OR � odds ratio; 95% CI � 95% confidence interval.† For the primary analysis, ORs and 95% CIs were derived by comparing exposure in the case window (0–2 hours) to exposure in the first controlwindow (24–26 hours).‡ Due to small frequencies of exposure in the control windows, this trigger could not be included in the conditional logistic regression analyses.
406 Steffens et al
84
onset of back pain; however, exposure frequencies werevery small in the control windows and slip, trip, or fallcould not be sensibly included in the regression analyses.
Exposure frequency for being fatigued and tired washigher in the case window (11.8%) than control windows(6.90% and 6.00% in the first and second control win-dows, respectively). However, for sexual activity and al-cohol consumption, exposure frequency was similaracross case and control windows (Table 2).
Association of exposure and risk of back pain. Allphysical triggers included in the analysis were stronglyassociated with an increased risk of back pain (Table 2).Exposure to manual tasks involving awkward positioningwas associated with 8.0 (95% CI 5.5–11.8) times greaterodds of the onset of back pain. Likewise, the OR associatedwith exposure to manual tasks involving objects not closeto the body was 6.2 (95% CI 2.4–16.0), 5.80 (95% CI2.3–15.0) for manual tasks involving people or animals,
and 5.1 (95% CI 2.4–10.9) for manual tasks involvingunstable or unbalanced objects. Being exposed to physicalactivity of at least moderate intensity (i.e., participantsreporting being exposed to either moderate or vigorousphysical activity) increased the odds of developing backpain in the following 2 hours by 2.7 (95% CI 2.0–3.6)when compared to no exposure to physical activity. Theodds increased further when participants were exposed tovigorous physical activity (i.e., only participants reportingbeing exposed to vigorous physical activity) compared tono physical activity (OR 3.9, 95% CI 2.4–6.3).
Among the psychosocial triggers, being distracted dur-ing a task or activity (OR 25.0, 95% CI 3.4–184.5) orfatigued (OR 3.7, 95% CI 2.2–6.3) increased significantlythe odds of a new onset of back pain, but alcohol consump-tion and sexual activity showed no association with onsetof back pain.
No significant change in OR estimates was observedwhen window duration was increased to 4 hours (Supple-
Table 3. Influence of time of onset on risk: ORs for back pain that developed in the morning versus later in the day*
Triggers
Time of onset, 7 AM to 12 PM
(n � 441)Time of onset, 1 PM to 6 AM
(n � 558) Interactionanalysis,
P†OR (95% CI) P OR (95% CI) P
Physical factorsManual tasks involving
Heavy loads 5.3 (2.70–10.4) � 0.0001 4.8 (2.9–7.9) � 0.0001 0.813Awkward posture 13.4 (6.5–27.4) � 0.0001 6.0 (3.8–9.5) � 0.0001 0.066Objects not close to the body 7.5 (1.7–32.8) 0.007 5.3 (1.6–18.3) 0.008 0.728People/animals 7.0 (1.59–30.8) 0.01 5.0 (1.5–17.3) 0.011 0.733Unstable/unbalanced/difficult to grasp 9.5 (2.2–40.8) 0.002 3.7 (1.5–9.0) 0.005 0.276
Moderate or vigorous physical activity 1.9 (1.2–3.0) 0.008 3.3 (2.2–5.0) � 0.0001 0.072Vigorous physical activity 2.5 (1.2–5.2) 0.014 5.2 (2.7–9.9) � 0.0001 0.144Slip/trip/fall‡Sexual activity 1.0 (0.4–2.9) 1.0 0.3 (0.0–2.2) 0.215 0.263
Psychosocial factorsConsumption of alcohol – – 1.5 (0.6–3.7) 0.374 –Distracted during an activity or task 12.0 (1.6–92.3) 0.017Fatigued/tired 4.5 (1.9–10.9) 0.001 3.3 (1.8–6.4) � 0.0001 0.591
* Results of post hoc analyses based on case and control windows of 2-hours’ duration. OR � odds ratio; 95% CI � 95% confidence interval.† Interaction test between risk factors (7:00 AM to 12:00 PM and 1:00 PM to 6:00 AM).‡ Due to small frequencies of exposure, this trigger could not be included in the conditional logistic regression analyses.
Table 4. ORs for combined triggers: secondary analysis (2-hour window)*
Combined Triggers
Case window(0–2 hours)
no. (%)
First control window(24–26 hours)
no. (%)
Second control window(48–50 hours)
no. (%)OR
(95% CI)† P
Heavy loads � awkward posture 89 (8.9) 22 (2.2) 11 (1.1) 6.2 (3.4–11.1) � 0.0001Heavy loads � unstable/unbalanced/
difficult to grasp43 (4.3) 15 (1.5) 8 (0.8) 5.0 (2.2–11.3) � 0.0001
Heavy loads � fatigued 23 (2.3) 6 (0.6) 3 (0.3) 5.3 (1.8–15.3) 0.002Heavy loads � object not close to
body25 (2.5) 12 (1.2) 6 (0.6) 3.2 (1.3–7.9) 0.014
Moderate or vigorous physicalactivity � fatigued
24 (2.4) 4 (0.4) 5 (0.5) 7.7 (2.3–25.5) 0.001
* OR � odds ratio; 95% CI � 95% confidence interval.† ORs describe the increase in odds of an episode of low back pain when exposed to the combined trigger compared to not being exposed to thecombined trigger.
Triggers for Low Back Pain 407
85
mentary Table 1, available in the online version of thisarticle at http://onlinelibrary.wiley.com/doi/10.1002/acr.22533/abstract) or 6 hours (Supplementary Table 2, avail-able in the online version of this article at http://onlinelibrary.wiley.com/doi/10.1002/acr.22533/abstract). TheOR estimates observed when window duration was de-creased to 1 hour (Supplementary Table 3, available in theonline version of this article at http://onlinelibrary.wiley.com/doi/10.1002/acr.22533/abstract) were similar to theprimary analysis (window duration of 2 hours) (Table 2).
Interactions. No interaction was observed between ex-posure to any trigger and habitual participation in physicalactivity, BMI, number of previous LBP episodes, depres-sion, and anxiety score with P values greater than 0.05 forall triggers (Supplementary Table 4, available in the onlineversion of this article at http://onlinelibrary.wiley.com/doi/10.1002/acr.22533/abstract). However, age moderatedthe effect of exposure to manual tasks involving heavyloads (P � 0.01) and sexual activity (P � 0.04). To illus-trate the moderating effect of age on exposure to these 2triggers, we used the coefficients from the regression mod-els to calculate the ORs for a subject age 20, 40, or 60 years.For manual tasks involving heavy loads these were asfollows: at 20 years: OR 13.6, 95% CI 5.4–34.5, P � 0.01;at 40 years: OR 6.0, 95% CI 3.8–9.5, P � 0.01; and at 60years: OR 2.7, 95% CI 1.5–4.7, P � 0.01). For sexualactivity these were as follows: at 20 years: OR 0.05, 95% CI0.03–0.97, P � 0.04; at 40 years: OR 0.41, 95% CI 0.12–1.43, P � 0.16; and at 60 years: OR 3.21, 95% CI 0.57–18.22, P � 0.19).
Given the unexpected diurnal pattern of pain onsetobserved in our study, with more episodes commencingin the morning, exploratory post hoc analyses were con-ducted to evaluate if the back was more vulnerable totriggers in the morning. We evaluated the risk associatedwith being exposed to triggers in the period between7:00 AM and 12:00 PM to that between 1:00 PM and 6:00 AM.While there was no statistically significant interaction be-tween time of exposure and risk of developing back pain,when compared to the afternoon or night, exposure toawkward posture (OR 13.4, 95% CI 6.5–27.4) and manualtasks involving unstable loading (OR 9.5, 95% CI 2.2–40.8)in the morning was more strongly associated with risk ofback pain onset (Table 3). Unfortunately our study lackedsufficient power to resolve this issue.
Multiple triggers. A theory-driven approach was ad-opted to select combinations of triggers that would in-crease the risk of back pain onset. Five combinationswere chosen by consensus among investigators as follows:1) manual tasks involving heavy loads and awkward pos-ture; 2) manual tasks involving heavy loads and loads thatare unstable, unbalanced, or difficult to grasp; 3) manualtasks involving heavy loads and being fatigued; 4) manualtasks involving heavy loads and objects far from the body;and 5) being engaged in moderate or vigorous physicalactivity and feeling fatigued (Table 4). These analyses werenot prespecified in the study protocol. Manual tasks in-volving heavy loads associated with awkward posture in-
creased the odds of developing back pain by 6.2 (95% CI3.4–11.1, P � 0.00001) and by 5.3 (95% CI 1.8–15.3, P �0.002) if associated with feeling fatigued when comparedto no exposure. Similarly, engaging in physical activityseems to increase further the risk of back pain if associatedwith feeling fatigued or tired (OR 7.7, 95% CI 2.3–25.5,P � 0.001).
DISCUSSION
To date, back pain risk studies have only examined long-term exposure to factors such as smoking and inactivity(22). Our study adds to the knowledge of risk of back painby demonstrating for the first time that brief exposure to arange of modifiable physical and psychosocial factors in-creases the risk of an episode of back pain. The ORs for thetriggers we evaluated ranged from 2.7 to 25.0, confirmingthat short-term exposure may substantially increase risk ofback pain. Older age decreased the risk associated withmanual tasks involving heavy loads and increased the riskin those exposed to sexual activity. Habitual physical ac-tivity, age, BMI, previous number of LBP episodes, depres-sion, and anxiety scores did not significantly change therisk associated with exposure to the other investigatedtriggers. Notably, we also demonstrated that the onset ofback pain is not evenly distributed across the day, withmornings being the most frequent time of day for back painonset.
A major strength of our study was the large representa-tive sample of patients with a moderate to severe episodeof back pain recruited at inception. Moreover, the self-matching in case–crossover designs addresses some of theimportant limitations of previous risk studies in the backpain field (23,24). Self-matching eliminates potential ef-fects of unmeasured confounders, such as genetic andlifestyle factors, and minimizes selection bias (9). A poten-tial limitation of case–crossover studies is the potential forrecall bias, especially if the recall period is long; however,in our study the mean time between episode onset andinterview was only 5 days. Further, in an attempt to max-imize recall, participants were asked to link the day ofonset of back pain and each of the 3 previous control daysto significant events using a calendar and/or personal di-ary. If participants were more likely to remember what hadhappened during the case window than in the controlwindows (i.e., differential recall bias), the effect of a triggerwould be overestimated. To minimize this potential prob-lem research assistants and participants were blinded tothe case and control windows. We also acknowledge thatfor some people recall may have been difficult, so ourinterview script asked participants to refer to their diary/smartphone and to nominate key aspects of each day.Participants were also blinded to the time and length of thecase and control windows and were asked to describe theirengagement in each trigger over a period of 96 hours.These strategies have been used successfully in othercase–crossover studies and suggest that participants are asable to recall data on the preceding 2 days as they are onthe day of the event (25). Furthermore, the analysis of thestudy did not control for time-variant confounders beyond
408 Steffens et al
86
the triggers included in the study. We acknowledge, there-fore, that additional time-variant confounders may haveinfluenced our study findings.
A recent systematic review has identified multiple psy-chosocial and physically related risk factors for LBP (26).No consistent risk factor emerged as predictive of first-timeLBP, although prior LBP was a consistent predictor offuture incident LBP. However, many of the risk factorsinvestigated are not robust or replicable, and many are notmodifiable. Our results demonstrate that the onset of backpain may be triggered by brief exposure to physical andpsychological factors. Past research has linked long-termexposure to physical risk factors, such as heavy loads andawkward posture, and future occurrence of back pain withthe accumulation of exposure over time holding strongerassociations (23). Our results provide the first accurateestimates to confirm that even brief exposure to thesephysical factors may trigger moderate to severe back pain.The importance of psychosocial factors has also been high-lighted as our results have identified that transient expo-sure to stress and fatigue triples the odds of developingimmediate back pain, whereas distraction increases theodds by a factor of 25.
Results from our interaction analysis suggested that agemoderates the effect of exposure to manual tasks involvingheavy loads. Interestingly, the odds associated with man-ual tasks involving heavy loads at age 60 years is morethan 5 times smaller than at age 20 years. While previousstudies have reported the association between long-termexposure to heavy loads and LBP (23), this is the first studythat demonstrates a decrease in risk with age. One poten-tial reason for this may be that older people have learnedto lift correctly or are more careful when handling heavyloads. Future research is required to evaluate this hypoth-esis.
There is little published information about the time ofonset of back pain. Biomechanists have theorized that therisk of back pain may be higher in the morning as inter-vertebral discs imbibe fluid overnight, leaving them moresusceptible to stresses when loaded (27,28). Sprains andstrains (an injury category that includes back pain) havebeen previously associated with a similar diurnal patternto our study with �40% of sprains and strains occurringfrom 8:00 AM to 11:00 AM (29). The strong diurnal patternfor back pain onset would suggest that the morning may bea key time to intervene in order to prevent back pain. Thisapproach was adopted in a sham controlled trial (30) thatshowed that advising patients with persistent LBP to re-strict lumbar flexion in the morning was effective in re-ducing pain. Unfortunately, our post hoc analyses pro-vided imprecise estimates of the effect of time of exposureon the triggers evaluated in the study. Nonetheless theOR point estimates for morning exposure (i.e., 7:00 AM to12:00 PM) to manual tasks involving awkward posture andthose involving unstable, unbalanced, and difficult tograsp objects were meaningfully different to the point es-timates for exposure at other times. While larger studiesare still clearly required, our study provides preliminaryevidence that both the nature of the trigger and the time ofday of exposure to the trigger may influence the risk ofdeveloping back pain.
The challenge for future research is to develop and eval-uate prevention programs that aim to reduce exposure tothe triggers identified in this study by thoughtfully con-sidering each trigger. Exposure to triggers such as manualtasks involving heavy loads could be completely avoidedby redesigning the workplace so workers are no longerrequired to lift heavy loads. Exposure to other triggerscould be reduced by education, for example, throughpopulation-based public health messaging or onsite train-ing of workers. Some triggers such as slips, trips, and fallsare probably more difficult to avoid, but we would notethat there are successful falls prevention strategies di-rected at the elderly, suggesting that even these triggers arepotentially avoidable. It may not be sensible to aim toavoid the trigger “moderate or vigorous physical activity”because, while transient exposure increases the risk ofLBP, long-term exposure has many health benefits againstmany chronic diseases.
We acknowledge that changing human behavior is farfrom simple; however, the burden of back pain around theglobe does provide a compelling case that somethingshould be done. For example, the burden of disease dueto road traffic injury is far less than that for back pain,yet many countries devote considerable resources to con-trolling behaviors that increase the risk of road crashes.For example, mobile phone use has been shown in case–crossover studies to increase the risk for road crashes,which has led to media campaigns to change driver be-havior.
An important unanswered question from our study iswhether long-term exposure to risk factors, such assmoking and driving, moderate the risk associated withtransient exposure to the triggers we studied. We alsoacknowledge that our secondary analyses evaluatingwhether attributes of the person (such as BMI and habitualphysical activity) moderate the risk of developing lowback pain, were underpowered, and we would encouragelarger studies to evaluate this important issue. Future re-search directed at determining how best to modify thetriggers identified in this study, and whether incorporatingthis knowledge into prevention programs leads to reducedepisodes of LBP, should be also conducted. Moreover, wedid not collect data on the place of occurrence of LBP.Future studies could investigate whether the trigger stud-ied occurred in the work place, during sport, or at home.
Our results have significant clinical and policy implica-tions for the control of a disease that is a major problemglobally. We offer robust estimates for the increase in riskof back pain following exposure to modifiable physicaland psychosocial triggers. Future research should evaluatethe success of programs that modify the triggers identifiedin this study in preventing episodes of back pain.
AUTHOR CONTRIBUTIONSAll authors were involved in drafting the article or revising
it critically for important intellectual content, and all authorsapproved the final version to be submitted for publication.Dr. M. Ferreira had full access to all of the data in the study andtakes responsibility for the integrity of the data and the accuracyof the data analysis.Study conception and design. Steffens, M. Ferreira, Latimer,P. Ferreira, Koes, Blyth, Li, Maher.
Triggers for Low Back Pain 409
87
Acquisition of data. Steffens, M. Ferreira, Latimer, Blyth, Li,Maher.Analysis and interpretation of data. Steffens, M. Ferreira,Latimer, P. Ferreira, Koes, Blyth, Li, Maher.
REFERENCES
1. Murray CJ, Lopez AD. Measuring the global burden of disease.New Engl J Med 2013;369:448–57.
2. Murray CJ, Vos T, Lozano R, Naghavi M, Flaxman AD,Michaud C, et al. Disability-adjusted life years (DALYs) for291 diseases and injuries in 21 regions, 1990-2010: a system-atic analysis for the Global Burden of Disease Study 2010.Lancet 2013;380:2197–223.
3. Vos T, Flaxman AD, Naghavi M, Lozano R, Michaud C, EzzatiM, et al. Years lived with disability (YLDs) for 1160 sequelaeof 289 diseases and injuries 1990-2010: a systematic analysisfor the Global Burden of Disease Study 2010. Lancet 2013;380:2163–96.
4. Deyo RA. Treatments for back pain: can we get past trivialeffects? [letter]. Ann Intern Med 2004;141:957–8.
5. Jellema P, van Tulder MW, van Poppel MN, Nachemson AL,Bouter LM. Lumbar supports for prevention and treatment oflow back pain: a systematic review within the framework ofthe Cochrane Back Review Group. Spine 2001;26:377–86.
6. Sahar T, Cohen M, Ne’eman V, Kandel L, Odebiyi D, Lev I,et al. Insoles for prevention and treatment of back pain.Cochrane Database Syst Review 2007;4:CD005275.
7. Maclure M. The case-crossover design: a method for studyingtransient effects on the risk of acute events. Am J Epidemiol1991;133:144–53.
8. Maclure M, Mittlemann MA. Should we use a case-crossoverdesign? Ann Rev Public Health 2000;21:193–221.
9. Mittleman MA, Mostofsky E. Exchangeability in the case-crossover design. Int J Epidemiol 2014;43:1645–55.
10. Australian Safety and Compensation Council. National codeof practice for the prevention of musculoskeletal disordersfrom performing manual tasks at work. Canberra: Common-wealth of Australia; 2007.
11. Sorock GS, Lombardi DA, Hauser R, Eisen EA, Herrick RF,Mittleman MA. A case-crossover study of transient risk fac-tors for occupational acute hand injury. J Occup Environ Med2004;61:305–11.
12. Verma SK, Lombardi DA, Chang WR, Courtney TK, HuangYH, Brennan MJ, et al. Rushing, distraction, walking on con-taminated floors and risk of slipping in limited-servicerestaurants: a case–crossover study. Occup Environ Med2011;68:575–81.
13. Vinson DC, Mabe N, Leonard LL, Alexander J, Becker J, BoyerJ, et al. Alcohol and injury: a case-crossover study. Arch FamMed 1995;4:505–11.
14. Chen SY, Fong PC, Lin SF, Chang CH, Chan CC. A case-crossover study on transient risk factors of work-related eyeinjuries. Occup Environ Med 2009;66:517–22.
15. Steffens D, Ferreira ML, Maher CG, Latimer J, Koes BW, BlythFM, et al. Triggers for an episode of sudden onset low backpain: study protocol. BMC Musculoskelet Disord 2012;13:7.
16. De Vet H, Heymans M, Dunn K, Pope D, van der Beek A,Macfarlane G, et al. Episodes of low back pain: a proposal for
uniform definitions to be used in research. Spine 2002;27:2409–16.
17. Henschke N, Maher CG, Refshauge KM, Herbert RD, Cum-ming RG, Bleasel J, et al. Prevalence of and screening forserious spinal pathology in patients presenting to primarycare settings with acute low back pain. Arthritis Rheum 2009;60:3072–80.
18. Ainsworth BE, Haskell WL, Herrmann SD, Meckes N, BassettDR Jr, Tudor-Locke C, et al. 2011 compendium of physicalactivities: a second update of codes and MET values. Med SciSports Exerc 2011;43:1575–81.
19. Armstrong T, Bauman A, Davies J. Physical activity patternsof Australian adults. Canberra: Australian Institute of Healthand Welfare; 2000.
20. Mittleman MA, Maclure M, Robins JM. Control samplingstrategies for case-crossover studies: an assessment of relativeefficiency. Am J Epidemiol 1995;142:91–8.
21. Dupont WD. Power calculations for matched case controlstudies. Biometrics 1988;44:1157–68.
22. Gatchel RJ, Polatin PB, Mayer TG. The dominant role ofpsychosocial risk factors in the development of chronic lowback pain disability. Spine 1995;20:2702–9.
23. Heneweer H, Staes F, Aufdemkampe G, van Rijn M, VanheesL. Physical activity and low back pain: a systematic review ofrecent literature. Euro Spine J 2011;20:826–45.
24. Hoogendoorn WE, van Poppel MN, Bongers PM, Koes BW,Bouter LM. Systematic review of psychosocial factors at workand private life as risk factors for back pain. Spine (Phila Pa1976) 2000;25:2114–25.
25. Broderick CR, Herbert RD, Latimer J, Barnes C, Curtin JA,Mathieu E, et al. Association between physical activity andrisk of bleeding in children with hemophilia. JAMA 2012;308:1452–9.
26. Taylor JB, Goode AP, George SZ, Cook CE. Incidence and riskfactors for first-time incident low back pain: a systematicreview and meta-analysis. Spine J 2014;14:2299–319.
27. Adams M, Dolan P, Hutton W. Diurnal variations in thestresses on the lumbar spine. Spine (Phila Pa 1976) 1987;12:130–7.
28. Adams M, Dolan P, Hutton W, Porter R. Diurnal changes inspinal mechanics and their clinical significance. J Bone JointSurg Br 1990;72:266–70.
29. Choi B, Levitsky M, Lloyd R, Stones I. Patterns and riskfactors for sprains and strain in Ontario, Canada 1990: ananalysis of the Workplace Health and Safety Agency database. J Occup Environ Med 1996;38:379–89.
30. Snook S, Webster B, McGorry R, Fogleman M, McCann K. Thereduction of chronic nonspecific low back pain through thecontrol of early morning lumbar flexion: a randomized con-trolled trial. Spine (Phila Pa 1976) 1998;23:2601–7.
31. Ware J, Sherbourne C. The MOS 36-item short-form healthsurvey (SF-36). 1. Conceptual framework and item selection.Med Care 1992;30:473–83.
32. Linton S, Hellsing A, Bergstrom G. Exercise for workers withmusculoskeletal pain: does enhancing compliance decreasepain? J Occup Med 1996;6:177–90.
33. Dahabreh IJ, Paulus JK. Association of episodic physical andsexual activity with triggering of acute cardiac events: system-atic review and meta-analysis. JAMA 2011;305:1225–33.
410 Steffens et al
88
Ap
pen
dix
Ta
ble
1.
Exp
osu
re f
req
uen
cy a
nd
od
ds
rati
os
for
each
tri
gger
- s
en
siti
vit
y a
nal
ysi
s (4
ho
ur
win
do
w)
Tri
gg
ers
Ca
se W
ind
ow
(0-4
ho
urs
), N
o. (%
)
Fir
st C
on
tro
l W
ind
ow
(2
4-
28
ho
urs
), N
o.
(%)
Sec
on
d C
on
tro
l W
ind
ow
(48
-52
ho
urs
), N
o.
(%)
Od
ds
Ra
tio
(9
5%
CI)
P
Ph
ysi
cal
fact
ors
M
anual
task
s in
vo
lvin
g
Hea
vy l
oad
s 2
02
(2
0.2
) 7
9 (
7.9
) 6
7 (
6.7
) 5
.0 (
3.4
to 7
.3)
<0
.00
01
Aw
kw
ard
po
sture
2
90
(2
9.0
) 8
2 (
8.2
) 6
1 (
6.1
) 7
.3 (
5.1
to 1
0.5
) <
0.0
001
Obje
cts
no
t cl
ose
to
the
bo
dy
4
4 (
4.4
) 1
9 (
1.9
) 1
3 (
1.3
) 4
.1 (
1.9
to 8
.9)
<0
.00
01
Liv
e p
eop
le/
anim
als
92
(9
.2)
71
(7.1
) 6
5 (
6.5
) 3
.1 (
1.5
to 6
.3)
0.0
02
Unst
able
/ u
nb
alan
ce/
dif
ficult
to
gra
sp o
r ho
ld
61
(6
.1)
22
(2.2
) 1
6 (
1.6
) 4
.9 (
2.5
to 9
.7)
<0
.00
01
M
od
erat
e o
r vig
oro
us
ph
ysi
cal
act
ivit
y
25
0 (
25
.0)
16
0 (
16
.0)
14
2 (
14
.2)
2.2
(1
.7 t
o 2
.9)
<0
.00
01
V
igo
rous
ph
ysi
cal
acti
vit
y o
nly
1
13
(1
1.3
) 5
9 (
5.9
) 4
7 (
4.7
) 2
.6 (
1.7
to 3
.8)
<0
.00
01
S
lip
/ tr
ip/
fall
*
38
(3
.8)
1 (
0.1
) 0
(0
.0)
--
--
S
exual
act
ivit
y
11
(1
.1)
19
(1.9
) 1
3 (
1.3
) 0
.6 (
0.3
to 1
.2)
0.1
36
Psy
cho
soci
al f
acto
rs
C
onsu
mp
tio
n o
f al
coho
l 1
9 (
1.9
) 1
5 (
1.5
) 1
6 (
1.6
) 1
.3 (
0.6
to 2
.8)
0.4
51
D
istr
acte
d d
uri
ng a
n a
ctiv
ity o
r ta
sk
31
(3
.1)
6 (
0.6
) 9
(0
.9)
26
.0 (
3.5
to
19
1.6
) 0
.00
1
F
atig
ued
/ ti
red
1
32
(1
3.2
) 7
8 (
7.8
) 6
9 (
6.9
) 3
.8 (
2.3
to 6
.4)
<0
.00
01
Res
ult
s o
f se
nsi
tivit
y a
nal
yse
s b
ased
on c
ase
and
co
ntr
ol
win
do
ws
of
4 h
ours
dura
tio
n.
89
*D
ue
to s
mal
l fr
equen
cies
of
exp
osu
re i
n t
he
contr
ol
win
do
ws,
this
tri
gger
co
uld
no
t b
e in
clud
ed i
n c
ond
itio
nal
lo
gis
tic
regre
ssio
n a
nal
yse
s.
90
Ap
pen
dix
Ta
ble
2.
Exp
osu
re f
req
uen
cy a
nd
od
ds
rati
os
for
each
tri
gger
s -
sensi
tivit
y a
nal
ysi
s (6
ho
ur
win
do
w)
Tri
gg
ers
Ca
se W
ind
ow
(0-4
ho
urs
), N
o. (%
)
Fir
st C
on
tro
l W
ind
ow
(2
4-2
8
ho
urs
), N
o.
(%)
Sec
on
d C
on
tro
l W
ind
ow
(48
-52
ho
urs
), N
o.
(%)
Od
ds
Ra
tio
(9
5%
CI)
P
Ph
ysi
cal
fact
ors
M
anual
task
s in
vo
lvin
g
Hea
vy l
oad
s 2
10
(2
1.0
) 8
8 (
8.8
) 7
2 (
7.2
) 4
.4 (
3.1
to 6
.3)
<0
.00
01
Aw
kw
ard
po
sture
3
01
(3
0.1
) 8
6 (
8.6
) 6
3 (
6.3
) 7
.1 (
5.0
to 1
0.2
) <
0.0
001
Obje
cts
no
t cl
ose
to
the
bo
dy
4
4 (
4.4
) 2
1 (
2.1
) 1
3 (
1.3
) 3
.3 (
1.6
to 6
.7)
0.0
01
Liv
e p
eop
le/
anim
als
97
(9.7
) 7
4 (
7.4
) 7
2 (
7.2
) 3
.3 (
1.6
to 6
.7)
0.0
01
Unst
able
/ u
nb
alan
ce/
dif
ficult
to
gra
sp o
r ho
ld
64
(6.4
) 2
5 (
2.5
) 1
6 (
1.6
) 4
.0 (
2.2
to 7
.4)
<0
.00
01
M
od
erat
e o
r vig
oro
us
ph
ysi
cal
act
ivit
y
26
3 (
26
.3)
17
3 (
17
.3)
15
3 (
15
.3)
2.1
(1
.6 t
o 2
.8)
<0
.00
01
V
igo
rous
ph
ysi
cal
acti
vit
y o
nly
1
19
(1
1.9
) 6
4 (
6.4
) 5
3 (
5.3
) 2
.5 (
1.7
to 3
.7)
<0
.00
01
S
lip
/ tr
ip/
fall
*
38
(3.8
) 1
(0
.1)
0 (
0.0
) --
--
S
exual
act
ivit
y
13
(1.3
) 2
2 (
2.2
) 1
9 (
1.9
) 0
.6 (
0.3
to 1
.2)
0.1
22
Psy
cho
soci
al f
acto
rs
C
onsu
mp
tio
n o
f al
coho
l 2
2 (
2.2
) 2
0 (
2.0
) 2
1 (
2.1
) 1
.1 (
0.6
to 2
.3)
0.7
24
D
istr
acte
d d
uri
ng a
n a
ctiv
ity o
r ta
sk
31
(3.1
) 6
(0
.6)
9 (
0.9
) 2
6.0
(3
.5 t
o 1
91
.6)
0.0
01
F
atig
ued
/ ti
red
1
38
(1
3.8
) 8
7 (
8.7
) 7
5 (
7.5
) 3
.2 (
2.0
to 5
.1)
<0
.00
01
91
Res
ult
s o
f se
nsi
tivit
y a
nal
yse
s b
ased
on c
ase
and
co
ntr
ol
win
do
ws
of
6 h
ours
dura
tio
n.
*D
ue
to s
mal
l fr
equen
cies
of
exp
osu
re i
n t
he
contr
ol
win
do
ws,
this
tri
gger
co
uld
no
t b
e i
ncl
ud
ed i
n c
ond
itio
nal
lo
gis
tic
regre
ssio
n a
nal
yse
s.
92
Ap
pen
dix
Ta
ble
3.
Inte
ract
ion a
nal
ysi
s b
etw
een b
aseli
ne
vari
able
s an
d p
hysi
cal
and
psy
cho
logic
al f
acto
rs
Ph
ysic
al
fact
ors
Ha
bit
ua
l p
hy
sica
l
act
ivit
y*
Ag
e*
BM
I*
Pre
vio
us
epis
od
es*
D
epre
ssio
n*
A
nxie
ty*
OR
(9
5%
CI)
P
O
R (
95
% C
I)
P
OR
(9
5%
CI)
P
O
R (
95
% C
I)
P
OR
(9
5%
CI)
P
O
R (
95
% C
I)
P
Hea
vy l
oad
s 0
.95
(0
.75
-1.2
0)
0.6
7
0.5
9 (
0.3
9-0
.88
) 0
.01
1.3
8 (
0.8
2-2
.30
) 0
.22
0.9
3 (
0.7
8-1
.10
) 0
.40
0.8
9 (
0.5
8-1
.37
) 0
.59
0.9
1 (
0.5
6-1
.48
) 0
.71
Aw
kw
ard
po
sture
1
.21
(0
.81
-1.7
9)
0.3
6
1.1
3 (
0.7
6-1
.68
) 0
.53
1.0
8 (
0.7
3-1
.60
) 0
.69
1.0
1 (
0.9
1-1
.13
) 0
.82
0.8
3 (
0.5
4-1
.26
) 0
.38
0.8
1 (
0.5
1-1
.28
) 0
.36
Ob
ject
s no
t cl
ose
to
the
bo
dy
1.4
8 (
0.4
4-4
.99
) 0
.53
0.2
4 (
0.0
5-1
.17
) 0
.08
1.2
0 (
0.4
6-3
.10
) 0
.71
1.2
4 (
0.7
8-1
.98
) 0
.36
0.4
0 (
0.1
5-1
.12
) 0
.08
0.7
0 (
0.2
3-2
.17
) 0
.54
Liv
e p
eop
le/
anim
als
0.3
6 (
0.0
9-1
.47
) 0
.15
0.8
5 (
0.2
9-2
.47
) 0
.76
0.7
9 (
0.2
2-2
.80
) 0
.71
0.7
7 (
0.5
0-1
.18
) 0
.23
0.4
0 (
0.1
1-1
.50
) 0
.17
0.6
4 (
0.1
5-2
.77
) 0
.55
Unst
able
/ u
nb
alan
ce/
dif
ficult
to
gra
sp o
r ho
ld
0.8
9 (
0.5
7-1
.39
) 0
.62
0.4
2 (
0.1
4-1
.24
) 0
.12
4.0
6 (
0.8
2-
20
.06)
0.0
9
0.8
5 (
0.6
2-1
.17
) 0
.33
0.6
3 (
0.2
8-1
.42
) 0
.27
0.7
5 (
0.3
1-1
.82
) 0
.52
Vig
oro
us
ph
ysi
cal
acti
vit
y
1.0
3 (
0.7
3-1
.45
) 0
.86
0.5
6 (
0.3
0-1
.02
) 0
.06
1.9
6 (
0.9
9-3
.87
) 0
.05
0.9
2 (
0.7
4-1
.15
) 0
.48
0.9
5 (
0.5
5-1
.64
) 0
.86
1.3
7 (
0.7
3-2
.58
) 0
.33
Mo
der
ate
physi
cal
acti
vit
y
0.8
9 (
0.6
9-1
.16
) 0
.40
0.8
7 (
0.5
9-1
.29
) 0
.48
0.9
8 (
0.6
9-1
.40
) 0
.92
1.1
4 (
0.9
2-1
.41
) 0
.23
0.7
9 (
0.5
2-1
.20
) 0
.27
0.8
0 (
0.5
2-1
.24
) 0
.33
Sli
p/
trip
/ fa
ll
--
--
--
--
--
--
--
--
--
--
--
--
Co
nsu
mp
tio
n o
f al
coho
l 1
.14
(0
.37
-3.5
0)
0.8
2
1.1
6 (
0.5
4-2
.47
) 0
.71
0.8
6 (
0.3
1-2
.42
) 0
.78
0.9
0 (
0.4
2-1
.91
) 0
.78
2.1
3 (
0.4
6-9
.79
) 0
.33
1.1
5 (
0.3
5-3
.82
) 0
.81
Sex
ual
act
ivit
y
0.8
9 (
0.0
8-9
.93
) 0
.93
3.8
2 (
1.0
0-1
4.5
2)
0.0
4
1.0
0 (
0.2
9-3
.39
) 1
.00
1.1
8 (
0.8
3-1
.66
) 0
.36
1.2
1 (
0.4
4-3
.31
) 0
.71
0.6
7 (
0.2
3-1
.94
) 0
.46
Psy
ch
olo
gic
al
fact
ors
Dis
trac
ted
0
.52
(0
.14
-1.9
0)
0.3
2
0.5
0 (
0.0
6-4
.33
) 0
.53
--
--
0.8
5 (
0.1
8-4
.07
) 0
.84
--
--
0.1
6 (
0.0
1-5
.41
) 0
.31
93
Fat
igued
/ ti
red
1
.29
(0
.66
-2.5
5)
0.4
6
0.9
9 (
0.5
8-1
.71
) 0
.99
0.9
2 (
0.5
4-1
.58
) 0
.77
0.8
6 (
0.7
0-1
.06
) 0
.16
1.2
3 (
0.6
9-2
.20
) 0
.49
0.9
3 (
0.5
0-1
.73
) 0
.83
*E
nte
red
as
conti
nuo
us
var
iab
les,
incr
ease
fo
r 1
SD
. H
abit
ual
ph
ysi
cal
acti
vit
y=
35
0**;
Ag
e=1
3;
BM
I=5
; N
um
ber
of
pre
vio
us
epis
od
es=
5;
Dep
ress
ion
=3
; A
nxie
ty=
3.
** H
PA
: H
abit
ual
ph
ysi
cal
acti
vit
y i
s no
t no
rmal
dis
trib
ute
d a
nd
we
use
d I
QR
=3
50
min
s.
Bo
ld=
p<
0.0
5.
94
Ap
pen
dix
Ta
ble
4.
Exp
osu
re f
req
uen
cy a
nd
od
ds
rati
os
for
each
tri
gger
- s
eco
nd
ary a
naly
sis
(1ho
ur
win
do
w)
Tri
gg
ers
Ca
se w
ind
ow
(0-1
ho
urs
),
No
. (%
)
Fir
st c
on
tro
l w
ind
ow
(24
-25
ho
urs
),
No
. (%
)
Sec
on
d c
on
tro
l w
ind
ow
(48
-49
ho
urs
),
No
. (%
)
Od
ds
Ra
tio
(9
5%
CI)
†
P
Ph
ysi
cal
fact
ors
M
anual
task
s in
vo
lvin
g
Hea
vy l
oad
s 1
66
(1
6.6
) 5
2 (
5.2
) 5
0 (
5.0
) 6
.2 (
3.9
to 9
.7)
<0
.00
01
Aw
kw
ard
po
sture
2
59
(2
5.9
) 6
5 (
6.5
) 4
7 (
4.7
) 7
.9 (
5.4
to 1
1.8
) <
0.0
001
Obje
cts
no
t cl
ose
to
the
bo
dy
3
5 (
3.5
) 1
3 (
1.3
)
9 (
0.9
) 6
.5 (
2.3
to 1
8.6
) <
0.0
001
Liv
e p
eop
le o
r an
imal
s 7
3 (
7.3
) 5
5 (
5.5
) 5
5 (
5.5
) 5
.5 (
1.9
to 1
6.0
) 0
.00
2
Unst
able
/ u
nb
alan
ced
/ d
iffi
cult
to
gra
sp o
r ho
ld l
oad
s 4
9 (
4.9
) 1
6 (
1.6
) 1
2 (
1.2
) 7
.6 (
3.0
to 1
9.3
) <
0.0
001
M
od
erat
e o
r vig
oro
us
ph
ysi
cal
act
ivit
y
20
4 (
20
.4)
10
7 (
10
.7)
87
(8.7
) 2
.9 (
2.1
to 4
.0)
<0
.00
01
V
igo
rous
ph
ysi
cal
acti
vit
y o
nly
9
6 (
9.6
) 3
7 (
3.7
) 2
8 (
2.8
) 4
.3 (
2.6
to 7
.2)
<0
.00
01
S
lip
/ tr
ip/
fall
*
34
(3.4
) 1
(0
.1)
0 (
0.0
) --
--
S
exual
act
ivit
y
5 (
0.5
) 8
(0
.8)
9 (
0.9
) 0
.6 (
0.2
to 1
.9)
0.4
10
Psy
cho
soci
al f
acto
rs
C
onsu
mp
tio
n o
f al
coho
l 1
1 (
1.1
) 9
(0
.9)
9 (
0.9
) 1
.2 (
0.5
to 3
.0)
0.6
55
D
istr
acte
d d
uri
ng a
n a
ctiv
ity o
r ta
sk
26
(2.6
) 6
(0
.6)
8 (
0.8
) 2
1.0
(2
.8 t
o 1
56
.10
0
.00
3
95
F
atig
ued
/ ti
red
1
08
(1
0.8
) 6
3 (
6.3
) 5
7 (
5.7
) 3
.4 (
2.0
to 5
.6)
<0
.00
01
Res
ult
s o
f th
e se
cond
ary a
naly
ses
bas
ed o
n c
ase
and
co
ntr
ol
win
do
ws
of
1 h
our
dura
tio
n.
*D
ue
to s
mal
l fr
equen
cies
of
exp
osu
re i
n t
he
contr
ol
win
do
ws,
this
tri
gger
co
uld
no
t b
e in
clud
ed i
n t
he
cond
itio
nal
lo
gis
tic
regre
ssio
n a
nal
yse
s.
†O
dd
s ra
tio
s an
d 9
5%
co
nfi
dence
inte
rval
wer
e d
eriv
ed c
om
par
ing e
xp
osu
re i
n t
he
case
win
do
w (
0-1
ho
urs
) w
ith t
he
con
tro
l w
ind
ow
1 (
24
-25
ho
urs
).
96
Triggers Specific Questions Tick the boxes where the participant reports pain on the mannequin below:
Height (cm): ______________________ Weight (Kg): _____________________
How much back pain have you had during the first 24 hours of this episode? [1]
None Very mild Mild Moderate Severe Very Severe
During the first 24 hours of this episode how much did back pain interfere with your
normal work (including both work outside the home and housework)? [1]
Not at all A little bit Moderately Quite a bit Extremely
How tense or anxious have you felt in the past week? Circle one. [2]
0 1 2 3 4 5 6 7 8 9 10
Appendix 5. Study Questionnaire
Calm and
relaxed
As
tense/anxious
as I’ve ever
felt
97
Physical Activity [3]
1. In the last week, how many times have you walked continuously, for at least 10 minutes, for
recreation, exercise or to get to or from places? ______times;
And in the week before your low back pain started? ______times.
What do you estimate was the total time that you spent walking in this way in the last week?
______hours ______minutes;
And in the week before your low back pain started? ______ hours ______minutes.
2. In the last week, how many times did you do any vigorous physical activity which made
you breathe harder or puff and pant? (e.g. jogging, cycling, aerobics, competitive
tennis)______times;
And in the week before your low back pain started? ______times.
What do you estimate was the total time that you spent doing this vigorous physical activity in
the last week? ______hours ______minutes;
And in the week before your low back pain started? ______ hours ______minutes.
3. In the last week, how many times did you do any moderate physical activities that you have
not already mentioned? (e.g. gentle swimming, social tennis, golf)______times;
And in the week before your low back pain started? ______times.
What do you estimate was the total time that you spent doing these activities in the last week?
______hours ______minutes;
And in the week before your back pain started? ______ hours ______minutes.
4. Was your level of physical activity last week typical for you? Yes No
98
Triggers Exposure
Please write the date and time you first noticed your low back pain on the table below:
Day Fri Sat Sun Mon Tues Wed Thurs Fri Sat Sun
Date
Time
I am going to ask you to recall what you were doing in the three days leading up to
your back pain and also on the day of your back pain. To help your memory I
would like you to sit down with your diary and smartphone. To help make sure we
have the right days I want you to tell me the day, weather and a key thing you did
on each day.
Example: Tuesday: cold and wet; visited parents
Day of back pain: _______________________________________________________
Day before: ____________________________________________________________
2 days earlier: __________________________________________________________
3 days earlier: __________________________________________________________
99
1a. MANUAL TASKS …
HEAVY LOADS [4]
Day
If yes, precisely describe manual task (type of task,
load, duration and time). e.g. Lifted 50 large boxes,
one at a time, (~15kg each box – perceived as heavy)
from the floor and placed them on a bench at waist
height. 8:00am - 20min.
The first group of questions is
about manual tasks. Manual tasks
include lifting, lowering, pushing,
carrying or otherwise moving,
holding or restraining any person,
animal or item.
Firstly we are interested in manual
tasks involving HEAVY LOADS.
So on the day of your back pain did
you engage in any manual tasks
involving a heavy load?
That was the (restate their
description of the day).
Now what about the day before….
That was the (restate their
description of the day).
OK now two days back That was
the (restate their description of the
day).
OK finally three days back That was
the (restate their description of the
day)
Day of back
pain
Yes No
Day before
Yes No
2 days earlier
Yes No
3 days earlier
Yes No
100
1b. MANUAL TASKS…
AWKWARD POSTURE [4] Day
If yes, precisely describe manual task and posture (type
of task, load, duration, time & body position). e.g. knelt
down while gardening. 2:00pm – 40min.
Now I want you to think about
manual tasks involving an
AWKWARD POSTURE. So on the day of your back pain did
you engage in any manual tasks
involving an awkward position?
That was the (restate their
description of the day).
Now what about the day before….
That was the (restate their
description of the day).
OK now two days back That was the
(restate their description of the day).
OK finally three days back That was
the (restate their description of the
day)
Day of back
pain
Yes No
Day before
Yes No
2 days
earlier
Yes No
3 days
earlier
Yes No
101
1c. MANUAL TASKS…
AN OBJECT THAT COULD
NOT BE POSITIONED CLOSE
TO THE BODY [4]
Day
If yes, precisely describe manual task and posture (type
of task, load, duration, time and body position). e.g.
Lifted large box (~7Kg – perceived as light) out of the
car boot and placed it on the floor. 11:00am – 10 sec.
Now I want you to think about
manual tasks involving AN
OBJECT THAT COULD NOT BE
POSITIONED CLOSE TO THE
BODY.
So on the day of your back pain did
you engage in any manual tasks
involving an object that could not
be positioned close to the body?
That was the (restate their
description of the day).
Now what about the day before….
That was the (restate their
description of the day).
OK now two days back That was the
(restate their description of the day).
OK finally three days back That was
the (restate their description of the
day)
Day of back
pain
Yes No
Day before
Yes No
2 days
earlier
Yes No
3 days
earlier
Yes No
102
1d. MANUAL TASKS…
LIVE PEOPLE OR ANIMALS [4] Day
If yes, precisely describe manual task and posture (type
of task, load, duration, time and body position). e.g.
Lifted 2 year-old child (~12kg – perceived as moderate)
from the floor onto the bed. 8:00pm once. Lifted and
carried baby (5 kg perceived as light), 3 to 4 times from
one room to another. 8:10pm – 30min
Now I want you to think about
manual tasks involving LIVE
PEOPLE OR ANIMALS.
So on the day of your back pain did
you engage in any manual tasks
involving live people or animals?
That was the (restate their description
of the day).
Now what about the day before….
That was the (restate their description
of the day).
OK now two days back…
That was the (restate their description
of the day).
OK finally three days back…
That was the (restate their description
of the day)
Day of back
pain
Yes No
Day before
Yes No
2 days
earlier
Yes No
3 days
earlier
Yes No
103
1e. MANUAL TASKS…
A LOAD THAT WAS
UNSTABLE, UNBALANCED OR
DIFFICULT TO GRASP OR
HOLD [4]
Day
If yes, precisely describe manual task and posture (type
of task, load, duration, time and body position). e.g.
lifted a 4 meter extension ladder (~12 Kg – perceived as
moderate) from the car roof racks, carried to garage
and hung on wall. 3:00pm - 5min.
Now I want you to think about
manual tasks involving A LOAD
THAT WAS UNSTABLE,
UNBALANCED OR DIFFICULT
TO GRASP OR HOLD.
So on the day of your back pain did
you engage in any manual tasks
involving a load that was unstable,
unbalanced or difficult to grasp or
hold?
That was the (restate their
description of the day).
Now what about the day before….
That was the (restate their
description of the day).
OK now two days back…
That was the (restate their
description of the day).
OK finally three days back…
That was the (restate their
description of the day)
Day of back
pain
Yes No
Day before
Yes No
2 days
earlier
Yes No
3 days
earlier
Yes No
104
2a. VIGOROUS
PHYSICAL ACTIVITY Day
If yes, precisely describe activity/task, time and
duration. e.g. ran 10km at fast pace (5 mins per km)
10:00am - 50min.
The next questions are about
VIGOROUS PHYSICAL
ACTIVITY. This could be sports or
hobbies, paid or volunteer work,
work outside the home and
housework.
Examples of vigorous physical
activity include: running, rope
skipping, axe chopping, using heavy
tools, canoeing and truck driving.
So on the day of your back pain did
you engage in any manual tasks
involving VIGOROUS PHYSICAL
ACTIVITIES?
That was the (restate their
description of the day).
Now what about the day before…
That was the (restate their
description of the day).
OK now two days back… That was
the (restate their description of the
day).
OK finally three days back… That
was the (restate their description of
the day)
Day of back
pain
Yes No
Day before
Yes No
2 days
earlier
Yes No
3 days
earlier
Yes No
105
2b. MODERATE
PHYSICAL ACTIVITY Day
If yes, precisely describe activity/task, time and
duration. e.g. Mowed the lawn. 11:00am -12:00 pm.
The next questions are about
MODERATE PHYSICAL
ACTIVITY. This could be sports or
hobbies, paid or volunteer work,
work outside the home and
housework.
Examples of moderate physical
activity include: leisure cycling,
fishing, general home repairs, music
playing, golf, surfing and painting.
So on the day of your back pain did
you engage in any manual tasks
involving MODERATE
PHYSICAL ACTIVITIES?
That was the (restate their
description of the day).
Now what about the day before….
That was the (restate their
description of the day).
OK now two days back… That was
the (restate their description of the
day).
OK finally three days back… That
was the (restate their description of
the day).
Day of back
pain
Yes No
Day before
Yes No
2 days
earlier
Yes No
3 days
earlier
Yes No
106
3. SLIP, TRIP OR FALL [5] Day
If yes, precisely describe incident and time. e.g.
Descending stairs, missed bottom step and jarred back.
8:30am – one occasion.
Now I want you to think about SLIP,
TRIP OR FALL.
So on the day of your back pain did
you have a slip, trip or fall? That
was the (restate their description of
the day).
Now what about the day before….
That was the (restate their
description of the day).
OK now two days back…
That was the (restate their
description of the day).
OK finally three days back….
That was the (restate their
description of the day)
Day of back
pain
Yes No
Day before
Yes No
2 days
earlier
Yes No
3 days
earlier
Yes No
107
4. CONSUMED ALCOHOL [6] Day
If yes, specify amount (refer to standard drink table at
the end of booklet), time and duration. E.g. 2x red wine
glasses (180ml). 8:20pm – 1h.
Now I want you to think about
ALCOHOL CONSUMPTION.
So on the day of your back pain did
you consume alcohol? That was the
(restate their description of the day).
Now what about the day before….
That was the (restate their
description of the day).
OK now two days back… That was
the (restate their description of the
day).
OK finally three days back… That
was the (restate their description of
the day)
Day of back
pain
Yes No
Day before
Yes No
2 days
earlier
Yes No
3 days
earlier
Yes No
5. SEXUAL ACTIVITY [7] Day If yes, specify time. E.g. 11:00pm
Now I want you to think about
SEXUAL ACTIVITY. So on the
day of your back pain did you
engage in sexual activity? That was
the (restate their description of the
day).
Now what about the day before….
That was the (restate their
description of the day).
OK now two days back… That was
the (restate their description of the
day).
OK finally three days back… That
was the (restate their description of
the day)
Day of back
pain
Yes No
Day before
Yes No
2 days
earlier
Yes No
3 days
earlier
Yes No
108
6. DISTRACTION [8] Day
If yes, specify time and duration, distraction and task.
e.g. Distracted by child crying while lifting a box from
car boot and it slipped from his/her hands. 8:30am –
one occasion.
Now I want you to think about being
DISTRACTED.
So on the day of your back pain were
you DISTRACTED for any reason
while engaged in a task or activity?
That was the (restate their
description of the day).
Now what about the day before….
That was the (restate their
description of the day).
OK now two days back… That was
the (restate their description of the
day).
OK finally three days back… That
was the (restate their description of
the day)
Day of back
pain
Yes No
Day before
Yes No
2 days
earlier
Yes No
3 days
earlier
Yes No
7. FATIGUE OR TIREDNESS [9] Day
If yes, specify time and duration. e.g. Disrupted and
poor sleep the night before as youngest child kept
waking due to earache. 3:00am – 24h.
Now I want you to think about
feeling FATIGUED or TIRED. So
on the day of your back pain did you
feel FATIGUED OR TIRED? That
was the (restate their description of
the day).
Now what about the day before….
That was the (restate their
description of the day).
OK now two days back… That was
the (restate their description of the
day).
OK finally three days back… That
was the (restate their description of
the day)
Day of back
pain
Yes No
Day before
Yes No
2 days
earlier
Yes No
3 days
earlier
Yes No
109
8. What do you think may have triggered your low back pain? (Record what the patient thinks may have
triggered his/her episode of back pain. eg. Bent down once to pick up newspaper from lawn. 7:00am -
immediately).
___________________________________________________________________________________________
____________________________________________________________________________________________
____________________________________________________________________________________________
____________________________________________________________________________________________
____________________________________________________________________________________________
So on the day of your back pain did you
do the activity described above? That
was the (restate their description of the
day).
Now what about the day before…. That
was the (restate their description of the
day).
OK now two days back… That was the
(restate their description of the day).
OK finally three days back… That was
the (restate their description of the day)
Day of back pain
Yes No
Day before
Yes No
2 days earlier
Yes No
3 days earlier
Yes No
110
Reference
1. Ware J, Sherbourne C: The MOS 36-item short-form health survey (SF-36). 1.
Conceptual framework and item selection. Medical Care 1992, 30:473-483.
2. Linton S, Hellsing A, Bergstrom G: Exercise for workers with musculoskeletal
pain: does enhancing compliance decrease pain? J Occup Med 1996, 6(3):177-190.
3. Armstrong T, Bauman A, Davies J: Physical activity patterns of Australian Adults.
In. Edited by Welfare AIoHa. Canberra; 2000.
4. Australian Safety Compensation Council: National code of practice for the
prevention of musculoskeletal disorders from performing manual tasks at work.
In. Canberra; 2007.
5. Verma S, Lombardi D, Chang W, Courtney T, Huang Y, Brennan M, Mittleman M,
Ware J, Perry M: Rushing, distraction, walking on contaminated floors and risk
of slipping in limited-service restaurants: a case--crossover study. Occupational &
Environmental Medicine 2010, 68(8):575-581.
6. Vinson DC, Mabe N, Leonard LL, Alexander J, Becker J, Boyer J, Moll J: Alcohol
and injury. A case-crossover study. Arch Fam Med 1995, 4(6):505-511.
7. Dahabreh IJ, Paulus JK, Dahabreh IJ, Paulus JK: Association of episodic physical
and sexual activity with triggering of acute cardiac events: systematic review and
meta-analysis. JAMA, 305(12):1225-1233.
8. Sorock G, Lombardi D, Peng D, Hauser R, Eisen E, Herrick R, Mittleman M: Glove
use and the relative risk of acute hand injury: a case-crossover study. Journal of
Occupational & Environmental Hygiene 2004, 1(3):182-190.
9. Chen S, Fong P, Lin S, Chang C, Chan C: A case-crossover study on transient risk
factors of work-related eye injuries. Occupational & Environmental Medicine
2009, 66(8):517-522.
111
Chapter Five
Effect of weather on back pain: results from a case-crossover study
Chapter Five is published as:
Steffens D, Maher CG, Li Q, Ferreira ML, Pereira LSM, Koes BK, Latimer J. Effect of
weather on back pain: results from a case-crossover study. Arthritis Care & Research. 2014;
66:1867-1872.
112
Statement from co-authors confirming authorship contribution of the PhD candidate
As co-authors of the paper “Effect of weather on back pain: results from a case-crossover
study”, we confirm that Daniel Steffens has made the following contributions:
Conception and design of the research
Data collection
Analysis and interpretation of the findings
Writing of the manuscript and critical appraisal of the content
Christopher G Maher Date: 01.01.2015
Qiang Li Date: 01.01.2015
Manuela L Ferreira Date: 01.01.2015
Leani SM Pereira Date: 01.01.2015
Bart W Koes Date: 01.01.2015
Jane Latimer Date: 01.01.2015
113
Effect of Weather on Back Pain: Results From aCase-Crossover StudyDANIEL STEFFENS,1 CHRIS G. MAHER,2 QIANG LI,2 MANUELA L. FERREIRA,2
LEANI S. M. PEREIRA,3 BART W. KOES,4 AND JANE LATIMER2
Objective. To investigate the influence of various weather conditions on risk of low back pain.Methods. We conducted a case-crossover study in primary care clinics in Sydney, Australia. A total of 993 consecutivepatients with a sudden, acute episode of back pain were recruited from October 2011 to November 2012. Following thepain onset, demographic and clinical data about the back pain episode were obtained for each participant during aninterview. Weather parameters (temperature, relative humidity, air pressure, wind speed, wind gust, wind direction, andprecipitation) were obtained from the Australian Bureau of Meteorology for the entire study period. Weather exposuresin the case window (time when participants first noticed their back pain) were compared to exposures in 2 control timewindows (same time duration, 1 week and 1 month before the case window).Results. Temperature, relative humidity, air pressure, wind direction, and precipitation showed no association withonset of back pain. Higher wind speed (odds ratio [OR] 1.17 [95% confidence interval (95% CI) 1.04–1.32], P � 0.01 foran increase of 11 km/hour) and wind gust (OR 1.14 [95% CI 1.02–1.28], P � 0.02 for an increase of 14 km/hour) increasedthe odds of pain onset.Conclusion. Weather parameters that have been linked to musculoskeletal pain such as temperature, relative humidity,air pressure, and precipitation do not increase the risk of a low back pain episode. Higher wind speed and wind gustspeed provided a small increase in risk of back pain, and although this reached statistical significance, the magnitude ofthe increase was not clinically important.
INTRODUCTION
Patients with musculoskeletal pain commonly report thatcertain weather conditions influence their symptoms, thepain from rheumatoid arthritis being a clear example ofthis (1–3). Previous studies have reported that cold orhumid weather conditions (4,5) and changes in weatherconditions (6) negatively influence symptoms in patientsexperiencing chronic pain. Despite the high frequency
with which this belief is reported, there are few robuststudies that have investigated this potential association.The key problems are that study participants are notblinded to the study hypotheses, the studies have no con-trol period, and data are mainly based on subjective recallof both weather and symptoms.
It is a methodological challenge to assess the effect of theweather on pain onset using traditional study designs. Toour knowledge, only 2 studies have assessed whether as-pects of the weather influence musculoskeletal pain usinga case-crossover methodology (3,7). The case-crossover ap-proach was specifically designed to study exposures, suchas the weather, that have a short induction time and tran-sient effect. With this design, it would be possible toevaluate the increased risk associated with aspects of theweather by comparing exposure to meteorological vari-ables at the time of the pain onset or exacerbation (definedas the case window) and in earlier periods when the per-son was pain free (defined as the control windows) (8).
Subsequent to completing a case-crossover study evalu-ating physical and psychosocial triggers for an episode oflow back pain (LBP), we became aware of the limited dataon weather and musculoskeletal pain. We took the oppor-tunity to link back pain data from the original data set andhistorical weather data obtained from meteorological re-
1Daniel Steffens, BPhty: The George Institute for GlobalHealth, Sydney Medical School, and The University of Syd-ney, Sydney, New South Wales, Australia, and Federal Uni-versity of Minas Gerais, Minas Gerais, Brazil; 2Chris G.Maher, PhD, Qiang Li, MBiostat, Manuela L. Ferreira, PhD,Jane Latimer, PhD: The George Institute for Global Health,Sydney Medical School, and The University of Sydney, Syd-ney, New South Wales, Australia; 3Leani S. M. Pereira, PhD:Federal University of Minas Gerais, Minas Gerais, Brazil;4Bart W. Koes, PhD: Erasmus MC, University Medical Cen-ter Rotterdam, Rotterdam, The Netherlands.
Address correspondence to Daniel Steffens, BPhty, TheGeorge Institute for Global Health, Sydney Medical School,The University of Sydney, PO Box M201, Missenden Road,Sydney, 2050, New South Wales, Australia. E-mail:[email protected].
Submitted for publication March 19, 2014; accepted inrevised form May 27, 2014.
Arthritis Care & ResearchVol. 66, No. 12, December 2014, pp 1867–1872DOI 10.1002/acr.22378© 2014, American College of Rheumatology
ORIGINAL ARTICLE
1867
114
cords. The aim of this study was to quantify the transientincrease in risk of sudden onset of acute LBP associatedwith the following weather parameters: temperature (°C),relative humidity (%), air pressure (hPa), wind speed (km/hour), wind gust (km/hour), wind direction (degrees true),and precipitation (mm).
SUBJECTS AND METHODS
The present study is a reanalysis of original case-crossoverstudy data (9) linked to historical weather data obtainedfrom meteorological records. Since the present study wasconceived after completion of the original case-crossoverstudy (9), the weather exposure data and back pain historydata are independent, and participants and staff wereblinded to the study hypotheses during data collection.Ethical approval for the study was granted by the Univer-sity of Sydney Human Research Ethics Committee (proto-col 05-2011/13742).
Study participants. Consecutive patients presenting toprimary care clinicians (general medical practitioners,physiotherapists, chiropractors, and pharmacists) for treat-ment of an episode of sudden-onset, acute LBP were re-cruited in Sydney, Australia, from October 2011 to No-vember 2012. To be eligible to enter the study, participantsmust have met the following criteria: 1) comprehends spo-ken English; 2) primary symptom of pain in the area be-tween the 12th rib and buttock crease, with or without legpain; 3) pain of at least moderate intensity during the first24 hours of the episode (assessed using a modified versionof item 7 of the Short Form 36 [SF-36]); 4) presentation fortreatment within 7 days from the time of pain onset; and 5)no known or suspected serious spinal pathology (e.g., met-astatic, inflammatory, or infective diseases of the spine;cauda equina syndrome; spinal fracture). A sudden-onsetepisode of LBP was defined as pain of at least moderateintensity that developed over the first 24 hours (assessedusing a modified version of item 7 of the SF-36) (10).
Participant interview. Basic demographic and clinicaldata were collected by telephone interview (9). Only thosepatients who were interviewed within 14 days from the
onset of their LBP were included. In total, 993 people withLBP participated. All participants were ages �18 years.
Meteorological data. Sydney is the state capital of NewSouth Wales and the most populous city in Australia. Ithas a temperate climate with warm summers and mildwinters, and rainfall spread throughout the year. Meteoro-logical data were obtained from the Australian Bureau ofMeteorology for the entire study period from 5 weathermonitoring stations in Sydney (www.bom.gov.au). Theweather stations were located in 3 main regions: SydneyCentral (Sydney Airport-066037), Sydney North West(Penrith Lakes-067113 and Badgerys Creek-067108), andSydney South West (Mount Annan-068257 and CamdenAirport-068192). Two weather stations (Penrith Lakes andMount Annan) did not provide data on air pressure; there-fore, air pressure data were used from 2 neighboringweather stations (Badgerys Creek and Camden Airport).For each participant enrolled in the study, we used datafrom the weather station closest to the region where theylived. The following hourly weather parameters were ob-tained: temperature (°C), relative humidity (%), air pres-sure (hPa), wind speed (sustained wind speed averagedover 10 minutes leading up to the time of the observation;km/hour), wind gust (short burst of high-speed windaveraged over 3 seconds leading up to the time of theobservation; km/hour), wind direction (direction wherethe wind is coming from; degrees true), and precipitation(mm).
Study design. To determine whether there is an associ-ation between weather parameters and LBP onset, we useda case-crossover design. This design compares exposure toweather parameters at the time of back pain onset (definedas the case window) with exposure at the same time 1week and 1 month prior to the pain onset (defined ascontrol windows 1 and 2, respectively) for each partici-pant. The time periods for exposure were defined as fol-lows: 1) within 1 hour (average value at 1 hour immedi-ately before the pain onset), 2) at 24 hours (average value at24 hours immediately before the pain onset), and 3) aver-age value within 24 hours (average value from 0–24 hoursimmediately before the pain onset).
To determine whether change in the weather parametersis associated with LBP onset, we computed a change scoreusing this formula: average value over 0–24 hours imme-diately prior to the pain onset minus average value over25–48 hours immediately prior to the pain onset for eachparticipant.
Statistical analysis. First, a descriptive analysis wasperformed. Characteristics of the study subjects and dis-tribution of weather parameters were reported. Second,the analysis followed standard methods for stratified ana-lyses. In the case-crossover design, the individual subjectis the stratifying variable (8,11). We used the matched-pairanalytical approach (conditional logistic regression) tocontrast exposures (meteorological variables) for the caseperiod with exposures for the control period. For eachsubject, 1 case period was matched to 2 control periods
Significance & Innovations● Patients with musculoskeletal pain commonly re-
port that their symptoms are influenced by theweather, but this issue has not been evaluated inrobust research or for the most common musculo-skeletal condition, back pain.
● There was no association between temperature,relative humidity, air pressure, wind direction,and precipitation and risk of back pain.
● Higher wind speeds slightly increased the odds ofback pain onset, but the effect is not important.
1868 Steffens et al
115
exactly 1 week and 1 month before the date and time of thepain onset (11). Odds ratios (ORs) and 95% confidenceintervals (95% CIs) were derived comparing exposure inthe case window with each of the 2 control windows. Allweather parameters were treated as continuous variablesand we calculated the OR associated with a 1-SD increasein the weather parameter. The analyses were performedusing Stata, version 12 (12).
RESULTS
Primary care clinicians screened 1,639 consecutive pa-tients from October 2011 to November 2012, where 993met the inclusion criteria and consented to enter the study.The characteristics of the study participants are shown inTable 1. The mean � SD age was 45.2 � 13.4 years. Mostparticipants were male (54.2%) and professional workers(34.2%), and had a mean � SD number of previous epi-sodes of back pain of 5.9 � 14.0.
During the study period of 13 months, the mean weatherparameters were 1.4 mm of precipitation (range 0.0–115.4),temperature of 16.7°C (range �0.7 to 37.5), relative humid-ity of 71.6% (range 6.0–100.0%), wind speed of 11.2 km/hour (range 0.0–74.0), wind gust of 16.2 km/hour (range0.0–100.0), wind direction of 164.6 degrees true (range360.0 to 0.0), and 1,017.3 hPa of air pressure (range 994.7–1,035.8) (Table 2).
Descriptive data for the meteorological parameters in thecase and control windows are shown in Table 3. Estimatesof fixed parameters from conditional logistic regressionmodels for each weather parameter are also shown inTable 3. Only 2 of the 28 analyses were significant: windspeed 24 hours prior to onset (OR 1.17 [95% CI 1.04–1.32],P � 0.01 for an increase of 11 km/hour) and wind gust 24hours prior to onset (OR 1.14 [95% CI 1.02–1.28], P � 0.02for an increase of 14 km/hour) increased the risk of backpain. None of the other weather parameters investigatedwas associated with back pain onset.
DISCUSSION
This study provides the first evaluation of the influence ofthe weather on the most common musculoskeletal condi-tion, back pain. Contrary to popular belief, weather param-eters, such as temperature, precipitation, air pressure,wind direction, and humidity, were not associated withthe onset of back pain. Unexpectedly, heavier wind speed24 hours prior to an episode increased the risk of backpain, but the magnitude of the effect was very small andunlikely to be clinically important. Additionally, we didnot adjust the critical P value for multiple comparisons; ifthis was done, the obtained P values of 0.01 and 0.02 forwind parameters would no longer be statistically signifi-cant.
The use of a case-crossover design is a strength of thisstudy. In case-crossover studies, cases act as their owncontrols; consequently, case-crossover studies are not con-founded by time-invariant risk factors, since exposure in-formation is collected from the same individual (11). Thetiming and nature of our study allowed us to avoid some of
the potential problems associated with the case-crossoverdesign. We avoided the problems associated with recall,since exposure data were objectively measured and ob-tained independently of the back pain data. Since bothparticipants and assessors were blinded to the study hy-potheses, we avoided bias associated with people’s beliefsabout weather and pain. Lastly, we enrolled a large andwell-defined cohort of consecutive patients from primarycare clinics.
This study has some limitations that should be takeninto account. First, our data did not include potentiallyimportant individual data, such as time spent outdoors,characteristics of housing or work, and air conditioning,which could modify a participant’s vulnerability toweather conditions. Second, we used meteorological dataobtained from 3 main regions in Sydney and assumed thatthe LBP onset occurred in the individual while in a regionclose to their home. This may have introduced misclassi-fication for some patients’ exposure. The effect of thisnondifferential bias would be to change the present find-ings toward the null (13). Using data from 3 distinctweather regions, however, helped minimize the spatialvariations in the weather parameters that exist within re-gions (14). Third, participants’ time of back pain onset wasbased on their recall, which is a potential limitation ofretrospective studies. Therefore, participants were askedto use their diary, calendar, or smartphone to help recallthe onset time. Also, to avoid time recall bias, interviewswere performed as soon as possible after the onset of backpain, with the mean � SD time between pain onset andpresentation to primary care of 3.0 � 2.1 days and frompresentation to interview of 1.9 � 1.9 days.
There is little published research investigating the effectof the weather on musculoskeletal pain. Of the 2 previouscase-crossover studies, one found no effect of relative hu-midity, pressure, rain, and hours of sun and cloud coveron symptoms of rheumatoid arthritis (3), while the otherfound that higher wind speed slightly increased the risk ofhip fracture (7), but only in a subgroup of participants.Typically, the research cited to support a relationshipbetween weather and LBP uses very weak designs. Forexample, many studies simply survey patients about theiropinion on the effect of weather on their symptoms (4–6).Sometimes the belief that weather affects musculoskeletalpain is supported by reviews of studies that report higherprevalence of musculoskeletal pain in studies conductedin cooler settings; however, there are other between-studyfactors that also could have contributed to this finding(15). At present, there is no evidence derived from robustresearch that supports the widespread belief that theweather affects musculoskeletal pain. There is, however,some evidence for other health conditions. Previous case-crossover studies have shown that exposure to lower tem-peratures increases the risk of myocardial infarction (16),whereas higher temperatures and lower pressures lead toan increase in risk of headaches (17).
Our study provides clear evidence that weather does nothave an important effect on LBP onset. Only a trivialincrease in the risk was observed with higher wind speed24 hours prior to the onset of pain in this population ofAustralian adults. One possible explanation for the lack of
Influence of Weather on Back Pain 1869
116
Table 1. Characteristics of the participants*
SydneyCentral
(n � 666)
SydneyNorth West(n � 256)
SydneySouth West
(n � 71)Overall
(n � 993)
Male sex 356 (53.5) 138 (53.9) 44 (61.9) 538 (54.2)Age, mean � SD years 45.0 � 14.2 45.3 � 11.8 47.2 � 11.6 45.2 � 13.4Height, mean � SD cm 172.9 � 10.3 170.6 � 9.9 173.9 � 12.2 172.4 � 10.4Weight, mean � SD kg 78.8 � 17.7† 78.7 � 19.4 80.2 � 17.7 78.8 � 18.1‡BMI, mean � SD kg/m2 26.2 � 5.0† 26.9 � 5.9 26.4 � 4.4 26.4 � 5.2‡Duration of current episode, mean � SD days 5.1 � 2.7 4.5 � 2.8 4.9 � 2.9 4.9 � 2.7No. of previous episodes, mean � SD 6.3 � 15.9 4.7 � 7.7 6.2 � 12.6 5.9 � 14.0Days to seek care, mean � SD 3.0 � 2.1 2.7 � 2.1 2.9 � 2.0 3.0 � 2.1Days of reduced activity, mean � SD 2.4 � 2.2 1.9 � 1.9 3.0 � 2.3 2.3 � 2.2Depression status, mean � SD 2.7 � 2.6 2.7 � 2.8 2.9 � 2.8 2.7 � 2.7Pain, mean � SD 5.1 � 2.1 5.7 � 2.1 5.4 � 2.1 5.3 � 2.1GPES, mean � SD 1.8 � 1.8 1.7 � 1.7 1.7 � 1.9 1.8 � 1.8Tense/anxious, mean � SD 4.0 � 2.5 4.1 � 2.7 4.1 � 2.6 4.0 � 2.5Presence of leg pain 64 (9.6) 27 (10.5) 10 (14.1) 101 (10.2)Compensation 47 (7.1) 26 (10.2) 15 (21.1) 88 (8.9)Medication 320 (48.1) 98 (38.3) 32 (45.1) 450 (45.3)What do you do for a living?
Not employed 124 (18.6) 29 (11.3) 9 (12.7) 162 (16.3)Clerical and administrative worker 69 (10.4) 30 (11.7) 4 (5.6) 103 (10.4)Community and personal service worker 31 (4.7) 15 (5.9) 1 (1.4) 47 (4.7)Laborer 13 (2.0) 10 (3.9) 7 (9.9) 30 (3.0)Machinery operator and driver 14 (2.1) 10 (3.9) 3 (4.2) 27 (2.7)Manager 106 (15.9) 39 (15.2) 11 (15.5) 156 (15.7)Professional 234 (35.1) 83 (32.4) 23 (32.4) 340 (34.2)Sales worker 33 (5.0) 17 (6.6) 2 (2.8) 52 (5.2)Technician and trade worker 42 (6.3) 23 (9.0) 11 (15.5) 76 (7.7)
Pain location§Upper back 39 (5.9) 18 (7.0) 2 (2.8) 59 (5.9)Lower back 666 (100.0) 256 (100.0) 71 (100.0) 993 (100.0)Left thigh (back) 65 (9.8) 19 (7.4) 11 (75.5) 95 (9.6)Left leg (back) 22 (3.3) 15 (5.9) 5 (7.0) 42 (4.2)Right thigh (back) 72 (10.8) 23 (9.0) 12 (16.9) 107 (10.8)Right leg (back) 31 (4.7) 12 (4.7) 5 (7.0) 48 (4.8)Right thigh (front) 20 (3.0) 8 (3.1) 1 (1.4) 29 (2.9)Right leg (front) 8 (1.2) 3 (1.2) 0 (0.0) 11 (1.1)Left thigh (front) 20 (3.0) 3 (1.2) 3 (4.2) 26 (2.6)Left leg (front) 5 (0.8) 2 (0.8) 0 (0.0) 7 (0.7)
Pain severityModerate 251 (37.7) 98 (38.3) 22 (31.0) 371 (37.4)Severe 328 (49.3) 127 (49.6) 36 (50.7) 491 (49.5)Very severe 87 (13.1) 31 (12.1) 13 (18.3) 131 (13.2)
Pain interfering workNot at all 16 (2.4) 5 (2.0) 0 (0.0) 21 (2.1)A little bit 75 (11.3) 24 (9.4) 2 (2.8) 101 (10.2)Moderately 161 (24.2) 72 (28.1) 15 (21.1) 248 (25.0)Quite a bit 259 (38.9) 97 (37.9) 30 (42.3) 386 (38.9)Extremely 155 (23.3) 58 (22.7) 24 (33.8) 237 (23.9)
Habitual physical activity in the last week¶Sedentary 346 (51.9) 149 (58.2) 43 (60.5) 538 (54.2)Insufficient activity 114 (17.1) 34 (13.2) 15 (21.1) 163 (16.4)Sufficient activity 206 (30.9) 73 (28.5) 13 (18.3) 292 (29.4)
Habitual physical activity in the week before¶Sedentary 212 (31.8) 112 (43.7) 33 (46.5) 357 (35.9)Insufficient activity 122 (18.3) 41 (16.0) 11 (15.5) 174 (17.5)Sufficient activity 332 (49.8) 103 (40.2) 27 (38.0) 462 (45.5)
* Values are the number (percentage) unless indicated otherwise. BMI � body mass index; GPES � Global Perceived Effect Score.† N � 665.‡ N � 992.§ Pain location was assessed using a pain manikin provided to participants by the referring clinician.¶ Habitual physical activity � moderate activity time � (2 � vigorous activity time). Sedentary � 0 minutes, insufficient activity � �1 to �149minutes, and sufficient activity � �150 minutes.
1870 Steffens et al
117
effect in our results may be the temperate climate of theSydney region where the study was conducted. Regions
with more extreme weather conditions may present a dif-ferent result, but further research is needed. Interestingly,
Table 2. Features of weather parameters in 3 Sydney conurbations from October 2011 to November 2012
Sydney Central Sydney South West Sydney North West
Mean � SD* Min Max Mean � SD* Min Max Mean � SD* Min Max
Precipitation, mm 1.4 � 4.9 0.0 75.4 1.5 � 5.9 0.0 115.4 1.3 � 5.0 0.0 80.0Temperature, °C 17.9 � 4.6 6.0 37.5 16.8 � 6.0 1.1 37.1 15.5 � 6.1 �0.7 37.4Relative humidity, % 65.8 � 18.0 6.0 100.0 75.2 � 23.1 11.0 100.0 73.8 � 21.0 10.0 99.0Wind speed, km/hour 19.9 � 9.9 0.0 74.0 6.9 � 5.9 0.0 50.0 7.0 � 5.3 0.0 33.0Wind gust, km/hour 25.6 � 12.9 0.0 100.0 11.0 � 9.2 0.0 74.0 12.0 � 9.0 0.0 61.0Wind direction, degrees true 190.9 � 106.0 0.0 360.0 163.1 � 111.3 0.0 360.0 139.6 � 108.1 0.0 360.0Air pressure, hPa 1,017.2 � 6.4 994.7 1,035.3 1,017.3 � 6.5 995.6 1,035.7 1,017.3 � 6.6 995.0 1,035.8
* Values are the mean � SD of hourly measures for the study period.
Table 3. Exposure and estimates of fixed parameters for included weather conditions (n � 993)*
Case window(onset day)
Control window1 (1 week ago)
Control window2 (1 month ago) OR (95% CI)† P 1 SD†
Precipitation, mmWithin 1 hour‡ 1.12 � 4.36 1.24 � 5.45 1.21 � 4.75 0.98 (0.89–1.07) 0.59 5At 24 hours§ 1.14 � 5.02 1.20 � 4.56 1.25 � 4.89 0.98 (0.89–1.09) 0.76 5Average value over 24 hours¶ 1.20 � 3.42 1.36 � 4.15 1.35 � 3.77 0.95 (0.87–1.05) 0.32 4Change from 0–24 to 25–48 hours# 0.15 � 4.05 �0.23 � 4.58 0.03 � 4.90 1.08 (1.00–1.18) 0.05 4
Temperature, °CWithin 1 hour‡ 17.72 � 5.36 17.64 � 5.44 17.26 � 5.72 1.05 (0.90–1.22) 0.52 5At 24 hours§ 17.65 � 5.46 17.61 � 5.52 17.21 � 5.56 1.03 (0.88–1.19) 0.75 5Average value over 24 hours¶ 16.91 � 4.28 16.95 � 4.33 16.55 � 4.60 0.96 (0.82–1.13) 0.63 4Change from 0–24 to 25–48 hours# �0.03 � 2.32 �0.13 � 2.17 �0.17 � 2.12 1.04 (0.96–1.13) 0.30 2
Relative humidity, %Within 1 hour‡ 62.92 � 20.74 63.94 � 20.36 64.84 � 20.53 0.91 (0.81–1.03) 0.14 21At 24 hours§ 63.29 � 21.05 64.16 � 20.99 64.32 � 20.72 0.93 (0.82–1.04) 0.20 21Average value over 24 hours¶ 66.36 � 14.37 67.27 � 13.90 67.78 � 13.96 0.92 (0.83–1.01) 0.09 14Change from 0–24 to 25–48 hours# 0.67 � 12.19 0.72 � 11.88 0.38 � 11.55 1.00 (0.91–1.09) 0.93 12
Wind speed, km/hourWithin 1 hour‡ 16.56 � 10.37 16.55 � 10.78 16.32 � 10.67 1.00 (0.89–1.13) 0.99 11At 24 hours§ 17.26 � 10.90 16.30 � 10.60 16.45 � 11.04 1.17 (1.04–1.32) 0.01 11Average value over 24 hours¶ 16.11 � 8.38 15.77 � 8.44 15.74 � 8.82 1.09 (0.96–1.23) 0.19 8Change from 0–24 to 25–48 hours# �0.15 � 6.14 �0.10 � 5.89 �0.68 � 6.19 0.99 (0.91–1.08) 0.85 6
Wind gust, km/hourWithin 1 hour‡ 22.41 � 13.16 22.53 � 13.92 22.05 � 13.53 0.99 (0.88–1.11) 0.81 14At 24 hours§ 23.22 � 13.88 22.08 � 13.43 22.38 � 14.20 1.14 (1.02–1.28) 0.02 14Average value over 24 hours¶ 21.54 � 10.24 21.16 � 10.39 21.14 � 11.00 1.07 (0.95–1.20) 0.26 10Change from 0–24 to 25–48 hours# �0.16 � 8.43 �0.16 � 8.08 �0.96 � 8.49 1.00 (0.92–1.09) 1.00 8
Wind direction, degrees trueWithin 1 hour‡ 186.01 � 107.96 182.36 � 107.00 194.28 � 104.60 1.05 (0.95–1.16) 0.39 107At 24 hours§ 191.75 � 102.40 194.45 � 106.80 189.42 � 108.09 0.97 (0.87–1.07) 0.51 107Average value over 24 hours¶ 186.67 � 59.92 184.78 � 59.87 187.39 � 59.66 1.05 (0.94–1.18) 0.36 60Change from 0–24 to 25–48 hours# �0.06 � 53.94 0.25 � 54.38 0.79 � 55.69 0.99 (0.91–1.08) 0.90 54
Air pressure, hPaWithin 1 hour‡ 1,017.65 � 6.49 1,017.26 � 6.53 1,017.34 � 6.40 1.06 (0.98–1.16) 0.16 6At 24 hours§ 1,017.62 � 6.39 1,017.23 � 6.31 1,017.29 � 6.49 1.07 (0.98–1.17) 0.14 6Average value over 24 hours¶ 1,017.61 � 6.03 1,017.12 � 6.08 1,017.23 � 6.04 1.09 (1.00–1.19) 0.06 6Change from 0–24 to 25–48 hours# �0.13 � 4.85 0.09 � 4.91 0.08 � 4.63 0.95 (0.86–1.04) 0.28 5
* Values are the mean � SD unless indicated otherwise. OR � odds ratio; 95% CI � 95% confidence interval.† Per 1-SD increase.‡ Exposure defined as the value at 1 hour immediately before the pain onset.§ Exposure defined as the value at 24 hours immediately before the pain onset.¶ Exposure defined as the average value from 0–24 hours immediately before the pain onset.# Exposure defined as the average value from 0–24 hours immediately before the pain onset minus the average value from 25–48 hours the day beforepain onset.
Influence of Weather on Back Pain 1871
118
the popular belief about temperature, precipitation, airpressure, wind direction, and humidity and their associa-tion with back pain seems to be stronger than the datawould support. It should be noted, however, that theremay be musculoskeletal conditions other than LBP thatmay be affected by weather parameters, and this is animportant area for further research.
Further studies are needed to confirm our findings inwider populations and also to determine whether there isa subgroup of people in whom weather is more stronglyassociated with back pain onset. Case-crossover designscould be conducted in other musculoskeletal pain condi-tions. The importance of indoor temperatures, character-istics of housing or work, and air conditioning use shouldbe taken into account, since if a majority of the eventsoccur within the home, the results obtained in relation tometeorological variables may be biased toward the nullvalue. The small association found with higher windspeed may be better explained in regions where summerand winter are generally relatively extreme, rather than themoderate hot and cold of temperate regions.
In addition, co-exposure to multiple triggers (e.g., phys-ical and meteorological factors) may increase risk of backpain more than simple exposure to one meteorologicaltrigger. We are unaware of any study that has investigatedthis for musculoskeletal conditions. Additionally, usingthe case-crossover design to investigate whether exposureto weather parameters is associated with pain exacerbationor flares, in a sample of people with chronic back pain,may provide useful explanations for disease etiology andhow to improve quality of life.
In conclusion, this study shows that common weatherparameters previously believed to influence musculoskel-etal pain do not increase the risk of an episode of LBP. Thisstudy did, however, find a weak association between ex-posure to higher wind speed, wind gust, and back painonset, but the magnitude of this effect was small andtherefore not clinically important.
ACKNOWLEDGMENTSThe authors would like to thank all of the clinicians whoparticipated in the TRIGGERS for low back pain study.
AUTHOR CONTRIBUTIONS
All authors were involved in drafting the article or revising itcritically for important intellectual content, and all authors ap-proved the final version to be published. Mr. Steffens had fullaccess to all of the data in the study and takes responsibility forthe integrity of the data and the accuracy of the data analysis.Study conception and design. Steffens, Maher, Li, Ferreira,Pereira, Koes, Latimer.Acquisition of data. Steffens, Maher, Li, Ferreira, Pereira, Koes,Latimer.
Analysis and interpretation of data. Steffens, Maher, Li, Ferreira,Pereira, Koes, Latimer.
REFERENCES
1. Patberg WR, Rasker JJ. Weather effects in rheumatoid arthritis:from controversy to consensus. A review. J Rheumatol 2004;31:1327–34.
2. Smedslund G, Mowinckel P, Heiberg T, Kvien TK, Hagen KB.Does the weather really matter? A cohort study of influencesof weather and solar conditions on daily variations of jointpain in patients with rheumatoid arthritis. Arthritis Rheum2009;61:1243–7.
3. Abasolo L, Tobias A, Leon L, Carmona L, Fernandez-Rueda JL,Rodriguez AB, et al. Weather conditions may worsen symp-toms in rheumatoid arthritis patients: the possible effect oftemperature. Reumatol Clin 2013;9:226–8.
4. Shutty MS Jr, Cundiff G, DeGood DE. Pain complaint and theweather: weather sensitivity and symptom complaints inchronic pain patients. Pain 1992;49:199–204.
5. Jamison RN, Anderson KO, Slater MA. Weather changes andpain: perceived influence of local climate on pain complaintin chronic pain patients. Pain 1995;61:309–15.
6. Roth-Isigkeit A, Thyen U, Stoven H, Schwarzenberger J,Schmucker P. Pain among children and adolescents: restric-tions in daily living and triggering factors. Pediatrics 2005;115:e152–62.
7. Tenias JM, Estarlich M, Fuentes-Leonarte V, Iniguez C, Ball-ester F. Short-term relationship between meteorological vari-ables and hip fractures: an analysis carried out in a health areaof the Autonomous Region of Valencia, Spain (1996-2005).Bone 2009;45:794–8.
8. Maclure M. The case-crossover design: a method for studyingtransient effects on the risk of acute events. Am J Epidemiol1991;133:144–53.
9. Steffens D, Ferreira ML, Maher CG, Latimer J, Koes BW, BlythFM, et al. Triggers for an episode of sudden onset low backpain: study protocol. BMC Musculoskelet Disord 2012;13:7.
10. De Vet HC, Heymans MW, Dunn KM, Pope DP, van der BeekAJ, Macfarlane GJ, et al. Episodes of low back pain: a proposalfor uniform definitions to be used in research. Spine 2002;27:2409–16.
11. Mittleman MA, Maclure M, Robins JM. Control samplingstrategies for case-crossover studies: an assessment of relativeefficiency. Am J Epidemiol 1995;142:91–8.
12. StataCorp. Stata statistical software. College Station (TX):StataCorp; 2013.
13. Tsuchihashi Y, Yorifuji T, Takao S, Suzuki E, Mori S, Doi H,et al. Environmental factors and seasonal influenza onset inOkayama city, Japan: case-crossover study. Acta MedOkayama 2011;65:97–103.
14. Vaneckova P, Bambrick H. Cause-specific hospital admissionson hot days in Sydney, Australia. PloS One 2013;8:e55459.
15. Pienimaki T. Cold exposure and musculoskeletal disordersand diseases: a review. Int J Circumpolar Health 2002;61:173–82.
16. Madrigano J, Mittleman MA, Baccarelli A, Goldberg R, MellyS, von Klot S, et al. Temperature, myocardial infarction, andmortality: effect modification by individual- and area-levelcharacteristics. Epidemiology 2013;24:439–46.
17. Mukamal KJ, Wellenius GA, Suh HH, Mittleman MA.Weather and air pollution as triggers of severe headaches.Neurology 2009;72:922–7.
1872 Steffens et al
119
Chapter Six
Does magnetic resonance imaging predict future low back pain? A systematic review
Chapter Six is published as:
Steffens D, Hancock MJ, Maher CG, Williams C, Jensen TS, Latimer J. Does magnetic
resonance imaging predict future low back pain? A systematic review. European Journal of
Pain. 2014; 18:755-765.
120
Statement from co-authors confirming authorship contribution of the PhD candidate
As co-authors of the paper “Does magnetic resonance imaging predict future low back pain?
A systematic review”, we confirm that Daniel Steffens has made the following contributions:
Data extraction, analysis and interpretation of the findings
Writing of the manuscript and critical appraisal of the content
Mark J Hancock Date: 01.01.2015
Christopher G Maher Date: 01.01.2015
Ciaran Williams Date: 01.01.2015
Tue S Jensen Date: 01.01.2015
Jane Latimer Date: 01.01.2015
121
REVIEW ARTICLE
Does magnetic resonance imaging predict future low backpain? A systematic reviewD. Steffens1, M.J. Hancock2, C.G. Maher1, C. Williams3, T.S. Jensen4,5, J. Latimer1
1 The George Institute for Global Health, Sydney Medical School, The University of Sydney, Australia
2 Discipline of Physiotherapy, Faculty of Human Sciences, Macquarie University, Sydney, Australia
3 Active Physiotherapy Newtown, Sydney, Australia
4 Research Department, The Spine Centre of Southern Denmark, Middelfart, Denmark
5 Institute of Regional Health Services Research, Faculty of Health Sciences, University of Southern Denmark, Odense, Denmark
CorrespondenceDaniel Steffens
E-mail: [email protected]
Funding sourcesNone.
Conflict of interestNone declared.
Accepted for publication22 October 2013
doi:10.1002/j.1532-2149.2013.00427.x
Abstract
Background and Objective: Magnetic resonance imaging (MRI) has thepotential to identify pathology responsible for low back pain (LBP).However, the importance of findings on MRI remains controversial. Weaimed to systematically review whether MRI findings of the lumbar spinepredict future LBP in different samples with and without LBP.Databases and Data Treatment: MEDLINE, CINAHL and EMBASEdatabases were searched. Included were prospective cohort studies investi-gating the relationship between baseline MRI abnormalities of the lumbarspine and clinically important LBP outcome at follow-up. We excludedcohorts with specific diseases as the cause of their LBP. Associationsbetween MRI findings and LBP pain outcomes were extracted from eligiblestudies.Results: A total of 12 studies met the inclusion criteria. Six studiespresented data on participants with current LBP; one included a samplewith no current LBP, three included a sample with no history of LBP andtwo included mixed samples. Due to small sample size, poor overallquality and the heterogeneity between studies in terms of participants,MRI findings and clinical outcomes investigated, it was not possible topool findings. No consistent associations between MRI findings and out-comes were identified. Single studies reported significant associations forModic changes type 1 with pain, disc degeneration with disability insamples with current LBP and disc herniation with pain in a mixedsample.Conclusions: The limited number, heterogeneity and overall qualityof the studies do not permit definite conclusions on the association ofMRI findings of the lumbar spine with future LBP (PROSPERO:CRD42012002342).
1. Introduction
Despite the enormous costs of low back pain (LBP)and thousands of clinical trials, little progress has beenmade in the management of LBP with most treat-ments having only small effects (Deyo, 2004; Kelleret al., 2007). Limited understanding of the aetiology of
LBP is likely to be a major contributor to the lack ofprogress in management. After excluding people withnerve root pain and serious pathologies (e.g., fractureand cancer), around 90–95% of LBP sufferers are clas-sified as having non-specific low back pain (NSLBP)reflecting the inability to identify a clear source for thepain (van Tulder et al., 2006). If the source of pain
© 2013 European Pain Federation - EFIC® Eur J Pain •• (2013) ••–•• 1
122
could be identified in at least some of these patientsthen it is possible that more targeted and effectivetreatments could be found.
Magnetic resonance imaging (MRI) has the poten-tial to identify pathology responsible for LBP(Schwarzer et al., 1995); however, the importance offindings on MRI remains controversial (Modic andRoss, 2007). Previous studies reveal high rates ofabnormalities on MRI in people without LBP (Bodenet al., 1990; Boos et al., 1995, 2000; Jarvik et al.,2001). Consequently, it can be difficult to determinewhether abnormalities seen on MRI are truly thecause of LBP since morphological changes arecommon in asymptomatic subjects. The lack of awidely accepted gold standard test contributes to thedifficulty in assessing the diagnostic accuracy of MRIfindings (Hancock et al., 2012).
The presence of pathology on MRI in peoplewithout LBP does not necessarily mean MRI findingsare not important to the aetiology of LBP (Hancocket al., 2012). In many other health conditions (e.g.,cardiovascular disease), pathology (e.g., atherosclero-sis) exists in people without current symptoms;however, this pathology has been shown to be veryimportant to the aetiology of the disorder (Duncanet al., 2007). MRI findings in currently asymptomaticpeople may represent markers of early pre-symptomatic disease that is later characterized by epi-sodes of pain and/or disability.
Most previous research investigating the associationbetween MRI and LBP has been cross sectional. Thesestudies provide only weak evidence of the importance
or otherwise of MRI findings to the development orcourse of LBP (Endean et al., 2011). Longitudinalstudies provide the possibility to investigate if MRIfindings are associated with important outcomes suchas the development of future LBP in currently asymp-tomatic people or the course of LBP in people withcurrent LBP. We are unaware of any previous system-atic review of prospective longitudinal studies investi-gating the association between MRI findings of thelumbar spine and future LBP. Therefore, the specificreview questions were:(1) Do MRI findings predict future LBP in people withno history of LBP?(2) Do MRI findings predict future LBP in people withno current LBP, but a previous history of LBP?(3) Do MRI findings predict the course of LBP inpeople with current LBP?(4) Do MRI findings predict future LBP in a mixedsample of participants with and without current LBP?
2. Methods
A review protocol was specified in advance and registeredon PROSPERO: International prospective register of sys-tematic reviews (http://www.crd.york.ac.uk/PROSPERO/display_record.asp?ID=CRD42012002342).
2.1 Search strategy
A systematic search of the literature from the earliest recordto the first week of May 2012 was undertaken using a highlysensitive search strategy suggested by the Cochrane BackReview Group together with a strategy for searchingMEDLINE for prognosis studies. We combined text and,where appropriate, Medical Subject Headings terms for LBP,back pain or backache; and inception, survival, life tables, logrank, prospective or follow-up studies; and magnetic reso-nance imaging. The complete search strategies from all data-bases are included in Supporting Information Appendix S1.We identified relevant studies by electronic searches ofgeneral biomedical and science databases (MEDLINE,CINAHL and EMBASE), as well as examined the referencelists of identified papers. A final list of included studies wassent to experts in the field who reviewed the list for possibleomissions. This search had no language restrictions.
2.2 Study selection
To be included, studies were required to meet all of thefollowing criteria:(a) Prospective cohort study. This included secondary analy-sis of randomized controlled trials (RCTs), but only wherethe treatment provided was conservative, or data on theconservative arm were presented separately to the surgicalarm.
Databases• We identified relevant studies by conducting
electronic searches of MEDLINE, CINAHL andEMBASE, and by examining the reference lists ofidentified papers.
What does this study add?• No consistent associations were identified across
multiple studies.• Only Modic changes and disc degeneration at
baseline predicted poor outcome from low backpain at follow-up in single studies.
• The importance of magnetic resonance imaging(MRI) findings in predicting clinical outcomes isunclear due to the limited number and quality ofstudies and the heterogeneity between studies interms of the participants, MRI findings and clini-cal outcomes investigated.
MRI predicting future LBP D. Steffens et al.
© 2013 European Pain Federation - EFIC®2 Eur J Pain •• (2013) ••–••
123
(b) Participants underwent baseline MRI reporting anyabnormality of the lumbar spine (e.g., but not limited to discdegeneration, disc herniation, facet joint arthropathy, Modicchanges, high intensity zone).(c) Reported a clinically important LBP outcome atfollow-up (e.g., pain, disability or a global measure ofrecovery).(d) The association between MRI findings (baseline orchange) and LBP outcomes (or sufficient raw data to calcu-late a measure of association) was reported. Simply reportinga p-value was insufficient to meet this criterion.
We excluded studies that included patients with specificdiseases such as tumours, fractures, inflammatory arthritisand cauda equina syndrome, but not sciatica. One reviewerscreened the titles and abstracts to exclude clearly irrelevantarticles. For each potentially eligible study, the full articlewas obtained and independently assessed for inclusion bytwo review authors (D.S., M.J.H., C.G.M., J.L., C.W. orT.S.J.). Any discrepancies were resolved by discussion.
2.3 Data extraction
2.3.1 Study characteristics
Data extraction was completed independently by tworeviewers. Included studies were categorized into four maingroups: (1) sample with current LBP; (2) mixed sample ofpeople with and without current LBP; (3) sample with nocurrent LBP, but previous LBP; and (4) sample with nohistory of LBP. Data were extracted from the selected studiesregarding number of subjects, sample source, age, follow-upduration, MRI findings, clinical outcomes and strength ofassociation between MRI finding and clinical outcome.When sufficient raw data were available, odds ratios (OR)and 95% confidence intervals (95% CI) were calculated.
2.3.2 Methodological quality
The methodological quality of each of the studies wasassessed independently by two reviewers (D.S., M.J.H.,C.G.M., J.L., C.W. or T.S.J.) using a standardized checklist ofpre-defined criteria (Pengel et al., 2003; Costa et al., 2012).The checklist is a modified version based on theoretical con-siderations and methodological aspects described by Altman(2001). These criteria comprised (1) definition of studysample (description of participant source and inclusion andexclusion criteria); (2) representative sample of the targetsample (participants selected by random selection or as con-secutive cases); (3) follow-up rate >80% (outcome data wereavailable for at least 80% of participants at 3-monthfollow-up or later); (4) adequate follow-up time (at least oneprognostic outcome was followed up at 3 months or later);(5) interpretable prognostic outcomes available (raw data,percentages, survival rates or continuous outcome reported);and (6) blinding (assessor unaware of at least one prognosticfactor, used to predict prognostic outcome, at the time prog-nostic outcome was measured). Disagreements among the
reviewers were discussed and resolved during a consensusmeeting. Each criteria was scored positive ‘Yes’ or negative‘No’. A positive score indicates sufficient information and apositive assessment. The same criteria have been used inprevious systematic reviews on the prognosis of acute LBP(Pengel et al., 2003; Costa et al., 2012). Methodologicalquality was not an inclusion criterion.
2.4 Analysis
Our intention was to pool results, but due to the heterogene-ity between the studies in terms of the participants, MRIfindings and clinical outcomes, it was not possible or appro-priate to pool findings. The results are presented descriptively.
Studies of participants with current LBP were used toinvestigate if MRI findings predicted the course of LBP.Studies of participants with no current LBP were used toassess if MRI findings were risk factors for future LBP.
3. Results
3.1 Selection of studies
Our search identified 6666 citations (2304 MEDLINE,265 CINAHL, 4635 EMBASE) after removing all dupli-cates (n = 538). After review of title and abstract, 6608records were excluded. Five additional studies thatmet the inclusion criteria were identified after consul-tation with experts in the field, resulting in a total of63 full-text articles eligible for assessment. Whenreviewing full-text articles for the 63 articles, a further23 were excluded as they were not prospectivestudies, 16 did not assess a LBP outcome at follow-up,8 did not present an association between MRI findingsand LBP outcome (or provide raw data to enable cal-culation of this) and 4 did not perform MRI at base-line. A table of excluded full-text articles and theprimary reason for exclusion is included in SupportingInformation Appendix S2. Therefore, 13 studies metall the inclusion criteria (Borenstein et al., 2001;Elfering et al., 2002; Carragee et al., 2005, 2006a,b;Jarvik et al., 2005; Modic et al., 2005; Kleinstucket al., 2006; McNee et al., 2011; Hellum et al., 2012;Jensen et al., 2012; Keller et al., 2012) (Fig. 1). Forone study, results from the same cohort were identi-fied in two different publications (Carragee et al.,2006a,b), but only the published report with the fullresults was included in our analysis (Carragee et al.,2006a). Consequently, the methodological quality andresults are based on 12 studies.
3.2 Methodological quality
Most studies defined the study sample (91.5%). Onlyfour studies (33%) described methods for assembling a
D. Steffens et al. MRI predicting future LBP
© 2013 European Pain Federation - EFIC® Eur J Pain •• (2013) ••–•• 3
124
representative sample of the target sample. Ninestudies (75%) had a follow-up of at least 80% and allstudies had a follow-up for at least one prognosticoutcome at 3 months or longer and quantified progno-sis. Eleven studies used blinded assessment (91.5%).Data for individual studies are presented in Table 1.
3.3 Study characteristics
A comprehensive description of each study is providedin Table 2. Six studies included a sample of currentLBP (Modic et al., 2005; Kleinstuck et al., 2006;McNee et al., 2011; Hellum et al., 2012; Jensen et al.,
2012; Keller et al., 2012); two included a mixedsample of people with and without LBP (Carrageeet al., 2005, 2006a), one included a sample with nocurrent LBP, but previous LBP symptoms (Jarvik et al.,2005), and three studies included a sample of patientswith no history of LBP (Boos et al., 2000; Borensteinet al., 2001; Elfering et al., 2002).
The samples were recruited from primary healthcare (Elfering et al., 2002; Jarvik et al., 2005;Kleinstuck et al., 2006), secondary health care (Booset al., 2000; Carragee et al., 2005, 2006a; Modic et al.,2005; McNee et al., 2011; Hellum et al., 2012; Jensenet al., 2012; Keller et al., 2012) or volunteers from thecommunity (Borenstein et al., 2001). The majority ofthe studies focused largely or completely on men andwomen of working age, but some also included olderparticipants (ranging from 18 to 84 years old). Thefollow-up period ranged from 12 to 84 months.
3.4 Association of MRI findings withclinical outcomes
Due to the heterogeneity of samples, MRI findings andclinical outcomes, it was not possible to combine theresults of the studies included. The findings of all 12included studies are presented in Tables 3 and Figs. 2and 3.
ORs and 95% CI were calculated from the extractedraw data for the following studies (Boos et al., 2000;Elfering et al., 2002; Carragee et al., 2006a; McNeeet al., 2011; Hellum et al., 2012; Jensen et al., 2012).
Records identified through searches
MEDLINE = 2304CINAHL = 265EMBASE = 4635
(n = 7204)
Records screened after duplicates removed
(n = 6666)
Full-text articles assessed for eligibility
(n = 63)
Studies included -12 different cohorts
(n = 13)
Duplicate records excluded(n = 538)
Records excluded• Not related to low back pain;• Ineligible designs;• No MRI at baseline.
(n = 6608)
Records excluded• 23 not a prospective study;• 8 no association between
MRI findings and LBP outcome;
• 16 no LBP outcome at follow-up;
• 4 no MRI at baseline.(n = 51)
Full-text articles identified by
experts in the field (n = 5)
Figure 1 Flowchart of search strategy.
Table 1 Methodological quality assessment of included studies.
Study
Definition of
study samplea
Representative
sampleb
Follow-up rate
>80%c
Follow-up >3
monthsd
Outcomes
reportede
Blinded
outcomef
Borenstein et al., 2001 Yes No No Yes Yes Yes
Carragee et al., 2006a Yes Yes Yes Yes Yes Yes
Carragee et al., 2005 Yes Yes Yes Yes Yes Yes
Elfering et al., 2002 No No Yes Yes Yes No
Jarvik et al., 2005 Yes Yes Yes Yes Yes No
Keller et al., 2012 Yes No No Yes Yes Yes
McNee et al., 2011 Yes Yes No Yes Yes Yes
Jensen et al., 2012 Yes No Yes Yes Yes Yes
Kleinstuck et al., 2006 Yes No Yes Yes Yes Yes
Modic et al., 2005 Yes No Yes Yes Yes Yes
Boos et al., 2000 Yes No Yes Yes Yes Yes
Hellum et al., 2012 Yes No Yes Yes Yes Yes
aDescription of participant source and inclusion and exclusion criteria.bParticipants selected by random selection or as consecutive cases.cOutcome data were available for at least 80% of participants at 3-month follow-up or later.dAt least one prognostic outcome was followed up at 3 months or later.eRaw data, percentages, survival rates or continuous outcome reported.fAssessor unaware of at least one prognostic factor, used to predict prognostic outcome, at time prognostic outcome was measured.
MRI predicting future LBP D. Steffens et al.
© 2013 European Pain Federation - EFIC®4 Eur J Pain •• (2013) ••–••
125
Tab
le2
Ind
ivid
uals
tud
ych
arac
teri
stic
s.
Stud
ySa
mp
leso
urce
Mea
nag
e
(ran
ge)
MR
Ifind
ings
MR
Isco
ring
(thr
esho
ld)
Clin
ical
outc
omes
Out
com
esc
orin
g
(thr
esho
ld)
Follo
w-u
p,
dur
atio
n(%
)
Pop
ulat
ion
with
curr
ent
LBP
Kelle
ret
al.,
2012
269
pat
ient
sre
ferr
edto
univ
ersi
ty
spin
ecl
inic
49.7
(20–
60)
Mod
icch
ange
sty
pe
1Ye
s/N
o(p
rese
nt)
Patie
ntgl
obal
imp
ress
ion
of
imp
rove
men
t(P
GI-I
)
1–7
(≥3
not
reco
vere
d)
12m
onth
s(4
0%)
Mod
icch
ange
sty
pe
2Ye
s/N
o(p
rese
nt)
Patie
ntgl
obal
imp
ress
ion
of
imp
rove
men
t(P
GI-I
)
1–7
(≥3
not
reco
vere
d)
Hel
lum
etal
.,
2012
66tr
ialp
artic
ipan
tsre
crui
ted
from
univ
ersi
tyho
spita
ls(o
nly
par
ticip
ants
inco
nser
vativ
e
grou
p)
41.5
(?)
Mod
icch
ange
sty
pe
1Ye
s/N
o(p
rese
nt)
Dis
abili
ty(O
DI)
0–10
0(≥
15p
oint
s)12
mon
ths
(100
%)
Mod
icch
ange
sty
pe
2Ye
s/N
o(p
rese
nt)
Dis
cd
egen
erat
ion
(hei
ght
red
uctio
n)
%re
duc
tion
(≥40
%)
Dis
cd
egen
erat
ion
(sig
nali
nten
sity
)G
rad
ed1
to4
(>3)
Face
tjo
int
arth
opat
hyN
oor
slig
htto
≥mod
erat
e(≥
mod
erat
e)
Hig
h-in
tens
ityzo
neYe
s/N
o(p
rese
nt)
McN
eeet
al.,
2011
323
pat
ient
sof
hosp
italr
adio
logy
dep
artm
ent
?(20
–64)
Num
ber
ofM
RIa
bno
rmal
ities
0to
4(a
llle
vels
)Pa
in>1
4d
ays
pas
t4
wee
ksYe
s/N
o(?
)22
.2m
onth
s(m
ean)
(74%
)D
isc
deg
ener
atio
n?
(pre
sent
)D
isab
ility
pas
t4
wee
ks(R
M)
0–24
(≥11
poi
nts)
Jens
enet
al.,
2012
96p
atie
nts
ofsp
ecia
list
outp
atie
nt
spin
ecl
inic
46(2
1–60
)M
odic
chan
ges
typ
e1
Yes/
No
(pre
sent
)Pa
in(N
PR
S)0–
10(n
oim
pro
vem
ent,
chan
gesc
ore
≤0)
14m
onth
s(1
00%)
Mod
icch
ange
sty
pe
1(c
hang
ein
size
)
Size
0–4
(incr
ease
)
Klei
nstu
cket
al.,
2006
53p
artic
ipan
tsre
crui
ted
from
loca
lmed
iaad
vert
isem
ents
44(?
)H
igh
inte
nsity
zone
Yes/
No
(pre
sent
)Pa
inla
st2
wee
ks(V
AS)
0–10
(NA
)12
mon
ths
(90%
)
Dis
cb
ulge
Yes/
No
(pre
sent
)D
isab
ility
(RM
)0–
24(N
A)
Dis
cd
egen
erat
ion
Gra
ded
5–25
(>16
)
Mod
icch
ange
typ
e1
and
typ
e2
Gra
ded
0–15
(?)
Mod
icet
al.,
2005
246
pat
ient
sno
n-re
spon
der
sto
a
pre
oper
ativ
ein
tens
ive
cons
erva
tive
in-/o
utp
atie
nt
trea
tmen
tp
rogr
amm
e
43(?
)C
anal
sten
osis
?(p
rese
nt)
Dis
abili
ty(R
M)
0–24
(<50
%im
pro
vem
ent)
24m
onth
s(8
0%)
Ner
vero
otco
mp
ress
ion
?(p
rese
nt)
Dis
che
rnia
tion
?(p
rese
nt)
Pop
ulat
ions
ofp
eop
lew
ithan
dw
ithou
tcu
rren
tLB
P
Car
rage
eet
al.,
2006
a
200
pat
ient
sfr
omun
iver
sity
hosp
ital
39.4
(?)
Dis
cd
egen
erat
ion
Gra
ded
1–5
(gra
de
≥3)
Pain
(NP
RS)
0–10
(≥6
for
≥1w
eek)
60m
onth
s(1
00%)
End
pla
tech
ange
sM
ildto
seve
re(>
mod
erat
e)
Can
alst
enos
isM
ildto
seve
re(>
mod
erat
e)D
isab
ility
(OD
I)0–
100
(?)
Car
rage
eet
al.,
2005
100
pat
ient
sfr
omun
iver
sity
hosp
ital
42(?
)D
isc
hern
iatio
nYe
s/N
o(p
rese
nt)
Pain
(rem
issi
on)
Yes/
No
(6m
onth
s)63
mon
ths
(mea
n)
(100
%)
Pop
ulat
ion
with
nocu
rren
tLB
P,b
utp
revi
ous
LBP
Jarv
iket
al.,
2005
148
Vet
eran
sA
ffai
rsou
tpat
ient
s54
(36–
71)
Dis
che
rnia
tion
Pro
trus
ion
orex
trus
ion
(pre
sent
)Pa
in(P
FI)
1–6
(pai
n>2
oran
yof
the
othe
rth
ree
sym
pto
ms
as>1
)
36m
onth
s(8
8%)
Ner
vero
otco
ntac
tC
onta
ct/d
evia
tion/
com
pre
ssio
n
(pre
sent
)
Can
alst
enos
isM
ildto
seve
re(>
mod
erat
e)
Pop
ulat
ions
with
nohi
stor
yof
LBP
Elfe
ring
etal
.,
2002
41tr
aum
ap
atie
nts
pre
sent
ing
toa
univ
ersi
tycl
inic
?(2
0–50
)D
isc
deg
ener
atio
n(c
hang
e)Sa
me
orw
orse
(wor
seni
ng)
Pain
(NQ
)D
ays
with
pai
nla
stm
onth
(>8)
62m
onth
s(m
ean)
(100
%)
Boo
set
al.,
2000
46p
atie
nts
ofa
univ
ersi
tycl
inic
?(?)
Dis
che
rnia
tion
Yes/
No
(pre
sent
)Pa
in(N
Q)
Day
sw
ithp
ain
last
mon
th
(>8)
62m
onth
s(m
ean)
(100
%)N
erve
root
cont
act
Con
tact
/dev
iatio
n/co
mp
ress
ion
(pre
sent
)
Dis
cd
egen
erat
ion
Gra
de
1to
5(p
rese
nt)
Bor
enst
ein
etal
.,
2001
67vo
lunt
eers
recr
uite
dth
roug
h
adve
rtis
ing
orb
yw
ord
ofm
onth
42(?
)M
RIa
bno
rmal
ities
(cha
nge)
?(w
orse
ning
)Pa
in(o
rdin
alsc
ale)
0–5
(?)
84m
onth
s(7
5%)
?,no
tre
por
ted
;LB
P,lo
wb
ack
pai
n;M
RI,
mag
netic
reso
nanc
eim
agin
g;N
A,n
otap
plic
able
(con
tinuo
usou
tcom
e);N
PR
S,nu
mer
ical
pai
nra
ting
scal
e;N
Q,N
ord
icq
uest
ionn
aire
;OD
I,O
swes
try
dis
abili
tyq
uest
ionn
aire
;PFI
,pai
nfr
eque
ncy
ind
ex;P
GI-I
,pat
ient
glob
alim
pre
ssio
nof
imp
rove
men
tsc
ale;
RM
,Rol
and
Mor
ris
dis
abili
tyq
uest
ionn
aire
;VA
S,vi
sual
anal
ogue
scor
es.
D. Steffens et al. MRI predicting future LBP
© 2013 European Pain Federation - EFIC® Eur J Pain •• (2013) ••–•• 5
126
Table 3 Association between presence of MRI findings and poor clinical outcome.
MRI findings present Study Clinical outcome (follow-up duration) OR (95% CI) unless indicated
Populations with current LBPModic changes type 1 Jensen et al., 2012 Pain (14 months) 6.2 (1.9–20.2)Modic changes type 1 (change in size) Jensen et al., 2012 Pain (14 months) 1.0 (0.4–2.4)Modic changes type 1 Keller et al., 2012 Impression of improvement (12 months) 1.1 (0.5–2.7)a
Modic changes type 1 Hellum et al., 2012 Disability (12 months) 1.4 (0.5–4.1)Modic changes type 2 Hellum et al., 2012 Disability (12 months) 0.5 (0.2–1.4)Modic changes type 2 Keller et al., 2012 Impression of improvement (12 months) 1.4 (0.7–2.6)a
Modic changes type 1 or type 2 Hellum et al., 2012 Disability (12 months) 0.3 (0.1–1.6)Modic changes type 1 and type 2 Kleinstuck et al., 2006 Pain (12 months) −2 (p = 0.1)b
Modic changes type 1 and type 2 Hellum et al., 2012 Disability (12 months) 1.0 (0.3–3.3)Modic changes type 1 and type2 Kleinstuck et al., 2006 Disability (12 months) 0.4 (p = 0.2)b
Disc degeneration McNee et al., 2011 Pain (22.2 months, mean) 1.6 (0.9–2.8)Disc degeneration Kleinstuck et al., 2006 Pain (12 months) −1 (p = 0.4)b
Disc degeneration McNee et al., 2011 Disability (22.2 months, mean) 2.2 (1.2–4.0)Disc degeneration Kleinstuck et al., 2006 Disability (12 months) −0.8 (p = 0.1)b
Disc degeneration (height reduction) Hellum et al., 2012 Disability (12 months) 0.7 (0.2–2.1)Disc degeneration (signal intensity) Hellum et al., 2012 Disability (12 months) 0.7 (0.2–3.0)High-intensity zone Kleinstuck et al., 2006 Pain (12 months) −2 (p = 0.1)b
High-intensity zone Hellum et al., 2012 Disability (27 months) 1.5 (0.5–4.5)High-intensity zone Kleinstuck et al., 2006 Disability (12 months) 0.3 (p = 0.5)b
Disc bulge Kleinstuck et al., 2006 Pain (12 months) 1 (p = 0.4)b
Disc bulge Kleinstuck et al., 2006 Disability (12 months) 0.8 (p = 0.1)b
Facet joint arthopathy (≥moderate) Hellum et al., 2012 Disability (27 months) 0.7 (0.2–3.0)Disc herniation Modic et al., 2005 Disability (24 months) 0.4 (0.2–0.7)Canal stenosis Modic et al., 2005 Disability (24 months) 2.4 (0.9–6.7)Nerve root compression Modic et al., 2005 Disability (24 months) 0.8 (0.4–1.5)≥1 MRI abnormality McNee et al., 2011 Pain (22.2 months, mean) 0.7 (0.3–1.6)≥2 MRI abnormalities McNee et al., 2011 Pain (22.2 months, mean) 0.8 (0.4–1.8)≥3 MRI abnormality McNee et al., 2011 Pain(22.2 months, mean) 1.0 (0.4–2.2)≥1 MRI abnormality McNee et al., 2011 Disability (22.2 months, mean) 1.2 (0.5–2.9)≥2 MRI abnormalities McNee et al., 2011 Disability (22.2 months, mean) 1.3 (0.5–3.2)≥3 MRI abnormality McNee et al., 2011 Disability (22.2 months, mean) 1.5 (0.6–3.7)Populations of people with and without current LBPDisc degeneration (grade 5) Carragee et al., 2006a Pain (60 months) 4.4 (p = 0.08)c
Disc degeneration (graded ≥3) Carragee et al., 2006a Disability (60 months) 1.0 (0.4–2.3)Canal stenosis Carragee et al., 2006a Pain (60 months) 2.9 (p = 0.09)c
Canal stenosis (≥moderate) Carragee et al., 2006a Disability (60 months) 2.1 (0.8–5.1)Endplate changes (≥moderate) Carragee et al., 2006a Pain (60 months) 2.5 (p = 0.1)c
Disc herniation Carragee et al., 2005 Pain (63 months, mean) 0.2 (p = 0.01)c
Population with no current LBP, but previous LBPDisc herniation (extrusion) Jarvik et al., 2005 Pain (36 months) 1.2 (0.4–3.4)a
Disc herniation (protrusion) Jarvik et al., 2005 Pain (36 months) 0.5 (0.3–0.9)a
Nerve root contact Jarvik et al., 2005 Pain (36 months) 2.2 (0.6–8.0)a
Canal stenosis (>moderate) Jarvik et al., 2005 Pain (36 months) 1.9 (0.8–4.8)a
Populations with no history of LBPDisc degeneration Boos et al., 2000 Pain (62 months, mean) 2.1 (0.1–26.9)Disc degeneration (change) Elfering et al., 2002 Pain (62 months, mean) 4.8 (0.3–69.3)Disc herniation Boos et al., 2000 Pain (62 months, mean) 0.7 (0.1–9.3)Nerve root contact Boos et al., 2000 Pain (62 months, mean) 8.8 (0.6–117.2)MRI abnormalities (change) Borenstein et al., 2001 Pain (84 months) 3.5d
Odds ratios greater than 1 indicate greater odds of poor outcome in those with MRI feature than those without. LBP, low back pain; MRI, magnetic
resonance imaging.aHazard ratios (95% confidence interval). Hazard ratios greater than 1 indicate greater incidence of outcome in those with MRI feature than those without.
A positive association was defined as CI limits above 1.bβ (p-value) positive values indicate that the presence of the given MRI finding at baseline was associated with a poorer outcome.cOdds ratios (p-value), no confidence interval reported.dRelative risk (no confidence interval provided). Relative risk greater than 1 indicates that the poor outcome is more likely to develop in people with the
MRI feature.
MRI predicting future LBP D. Steffens et al.
© 2013 European Pain Federation - EFIC®6 Eur J Pain •• (2013) ••–••
127
3.4.1 Current LBP
Six studies investigated the association between MRIfindings and a range of clinical outcomes in a samplewith current LBP [five with chronic LBP (Kleinstucket al., 2006; McNee et al., 2011; Hellum et al., 2012;Jensen et al., 2012; Keller et al., 2012) and one withacute LBP (Modic et al., 2005)]. Of the six studies, fourreported on associations of Modic changes [type 1(Kleinstuck et al., 2006; Jensen et al., 2012) and/ortype 2 (Kleinstuck et al., 2006; Hellum et al., 2012;Keller et al., 2012)], three on disc degeneration(Kleinstuck et al., 2006; McNee et al., 2011; Hellumet al., 2012), two on high-intensity zone (HIZ)(Kleinstuck et al., 2006; Hellum et al., 2012) and onlyone reported on each of disc bulge (Kleinstuck et al.,2006), disc herniation (Modic et al., 2005), canalstenosis (Modic et al., 2005), facet joint arthropathy(Hellum et al., 2012), the number of MRI abnormali-ties (≥ 1 to ≥ 3) (McNee et al., 2011) and nerve rootcompression (Modic et al., 2005).
The association of Modic changes with LBP(Kleinstuck et al., 2006; Jensen et al., 2012; Kelleret al., 2012) and with disability (Kleinstuck et al.,2006; Hellum et al., 2012; Keller et al., 2012) wasinvestigated by four studies. Jensen et al. (2012)investigated 96 patients recruited from a specializedoutpatient spine clinic. This sample was drawn froman RCT that reported no effect of treatment, andreported a significant association of Modic change type1 with worsening of LBP intensity (OR = 6.2; 95%
CI = 1.9–20.2) over a 14-month period. There was noassociation between the change in size of Modic type 1changes and change in LBP intensity (OR = 1.0; 95%CI = 0.4–2.4), dichotomized into improvement(decrease in LBP intensity) or no improvement (nochange or increase of LBP intensity). Hellum et al.(2012) reported data from a randomized trial con-ducted at five hospitals. One hundred and fifty-fivepatients were randomized to receive either conserva-tive treatment or disc replacement surgery. In the con-servatively treated group (n = 66), neither type 1 ortype 2 Modic changes (OR = 0.3; 95% CI = 0.1–1.6)nor type 1 or type 2 Modic changes (OR = 1.0; 95%CI = 0.3–3.3) were significantly associated with dis-ability. Kleinstuck et al. (2006) investigated a total of53 patients who participated in a randomized clinicaltrial of active therapy for chronic LBP. Baseline end-plate changes (defined as Modic changes type 1 andtype 2) were not significantly associated with painintensity or disability at 12-month follow-up.
Only one study reported recovery rate at follow-up(Keller et al., 2012) in a sample of patients withcurrent LBP (n = 269). After 1 year, 40% of patientsrated themselves as recovered. Neither type 1 Modicchanges [hazard ratio (HR) = 1.1; 95% CI = 0.5–2.7]nor type 2 Modic changes (HR = 1.4; 95% CI = 0.7–2.6) were significantly associated with not recoveringover 12 months.
Disc degeneration was reported in three studies(Kleinstuck et al., 2006; McNee et al., 2011; Hellumet al., 2012). McNee et al. (2011) investigated 323
MRI findings present Outcome (time) MRI+ / -
Outcome+ / -
Odds ratio (95% CI) OR (95% CI)
Modic changes type 1 Jensen et al., 2012 Pain (14 months) 74 / 22 47 / 49 6.2 (1.9–20.2)Modic changes type 1 (change in size) Jensen et al., 2012 Pain (14 months) ? / ? ? / ? 1.0 (0.4–2.4)Modic changes type 1 Hellum et al., 2012 Disability (12 months) 44 / 22 31 / 35 1.4 (0.5–4.1)Modic changes type 2 Hellum et al., 2012 Disability (12 months) 44 / 22 31 / 35 0.5 (0.2–1.4)Modic changes type 1 or 2 Hellum et al., 2012 Disability (12 months) 9 / 59 31 / 37 0.3 (0.1–1.6)Modic changes type 1 and 2 Hellum et al., 2012 Disability (12 months) 53 / 13 30 / 36 1.0 (0.3–3.3)Disc degeneration McNee et al., 2011 Pain (22.2 months, mean) 11 / 13 85 / 155 1.6 (0.9–2.8)Disc degeneration McNee et al., 2011 Disability (22.2 months, mean) 11 / 130 70 / 170 2.2 (1.2–4.0)Disc degeneration (height reduction) Hellum et al., 2012 Disability (12 months) 20 / 45 30 / 35 0.7 (0.2–2.1)Disc degeneration (signal intensity) Hellum et al., 2012 Disability (12months) 10 / 55 30 / 35 0.7 (0.2–3.0)High intensity zone Hellum et al., 2012 Disability (27 months) 42 / 23 30 / 35 1.5 (0.5–4.5)Facet joint arthopathy (≥moderate) Hellum et al., 2012 Disability (27 months) 10 / 55 30 / 35 0.7 (0.2–3.0)Disc herniation Modic et al., 2005 Disability (24 months) ? / ? ? / ? 0.4 (0.2–0.7)Canal stenosis Modic et al., 2005 Disability (24 months) ? / ? ? / ? 2.4 (0.9–6.7)Nerve root compression Modic et al., 2005 Disability (24 months) ? / ? ? / ? 0.8 (0.4–1.5)≥1 MRI abnormality McNee et al., 2011 Pain (22.2 months, mean) 208 / 32 85 / 155 0.7 (0.3–1.6)≥2 MRI abnormalities McNee et al., 2011 Pain (22.2 months, mean) 173 / 32 75 / 130 0.8 (0.4–1.8)≥3 MRI abnormality McNee et al., 2011 Pain (22.2 months, mean) 106 / 32 56 / 82 1.0 (0.4–2.2)≥1 MRI abnormality McNee et al., 2011 Disability (22.2 months, mean) 208 / 32 70 / 170 1.2 (0.5–2.9)≥2 MRI abnormalities McNee et al., 2011 Disability (22.2 months, mean) 173 / 32 61 / 144 1.3 (0.5–3.2)≥3 MRI abnormality McNee et al., 2011 Disability (22.2 months, mean) 106 / 32 44 / 94 1.5 (0.6–3.7)
0.1 0.2 0.5 1 2 5 10
Study
Number of events
Figure 2 Forest plot presenting association
between magnetic resonance imaging (MRI)
findings and low back pain (LBP) outcomes on
a sample with current LBP.
MRI finding present Outcome (time) MRI+ / -
Outcome+ / -
Odds ratio (95% CI) OR (95% CI)
Disc degeneration Boos et al., 2000 Pain (62 months, mean) 15 / 15 3 / 27 2.1 (0.1–26.9)Disc degeneration (change) Elfering et al., 2002 Pain (62 months, mean) 19 / 21 3 / 32 4.8 (0.3–69.3)Disc herniation Boos et al., 2000 Pain (62 months, mean) 22 / 8 3 / 27 0.7 (0.1–9.3)Nerve root contact Boos et al., 2000 Pain (62 months, mean) 7 / 23 3 / 27 8.8 (0.6–117.2)
Sample with mixed LBP
Sample with no history of LBP
Study
Disc degeneration (graded ≥3) Carragee et al, 2006a Pain (60 months) 153 / 47 44 / 156 1.0 (0.4–2.3)Canal stenosis (≥moderate) Carragee et al, 2006a Pain (60 months) 26 / 174 44 / 156 2.1 (0.8–5.1)
0.01 0.1 1 10 100
Number of events
Figure 3 Forest plot presenting association
between magnetic resonance imaging (MRI)
findings and low back pain (LBP) outcomes.
D. Steffens et al. MRI predicting future LBP
© 2013 European Pain Federation - EFIC® Eur J Pain •• (2013) ••–•• 7
128
patients with mechanical LBP, and found positiveassociations between disc degeneration with LBP(OR = 1.6; 95% CI = 0.9–2.8) and disability (OR = 2.2;95% CI = 1.2–4.0). In the study by Kleinstuck et al.(2006), disc degeneration was not associated withpain, or disability at 12-month follow-up. Hellumet al. (2012) found no association between baselinefindings of disc degeneration (signal intensity) and12-month disability in participants treated conserva-tively (OR = 0.7; 95% CI = 0.2–3.0). Similarly, discdegeneration (height reduction) was not associatedwith 12-month disability (OR = 0.7; 95% CI = 0.2–2.1).
One study investigated the association between thenumber of MRI abnormalities (≥ 1 to ≥ 3) at baselineand future LBP and disability (McNee et al., 2011).Neither one nor more MRI abnormalities were associ-ated with pain or disability at follow-up.
Kleinstuck et al. (2006) found no associationbetween the presence of baseline disc bulge and HIZwith LBP or disability outcomes. Hellum et al. (2012)also investigated the association between HIZ and dis-ability. HIZ in the conservatively treated group(OR = 1.5; 95% CI = 0.5–4.5) was not significantlyassociated with disability at 12 months.
Disc herniation, severe canal stenosis and nerve rootcompression were investigated in one study (Modicet al., 2005). A total of 246 patients were randomizedto either the early information arm of the study, withMRI results provided within 48 h, or the second armof the study, where both patients and physicians wereblinded to MRI results. Disability at 24-monthfollow-up occurred 0.4 times (95% CI = 0.2–0.7) asoften among patients with disc herniation at baselineas among patients without disc herniation. Severecanal stenosis (OR = 2.4; 95% CI = 0.9–6.7) and nerveroot compression (OR = 0.8; 95% CI = 0.4–1.5) werenot significant predictors of future disability.
Similarly, Hellum et al. (2012) reported that base-line findings of facet joint arthropathy did not predictdisability at 12 months (OR = 0.7; 95% CI = 0.2–3.0)in the conservatively treated group.
3.4.2 Mixed samples (sample with and withoutcurrent LBP)
Two studies investigated a mixed sample (subjectswithout or mild LBP symptoms and/or with chronicnon-lumbar pain), reporting associations between discdegeneration, endplate changes, canal stenosis(Carragee et al., 2006a) and disc herniation (Carrageeet al., 2005) with disability (Carragee et al., 2006a)and LBP (Carragee et al., 2005, 2006a) outcomes.
Carragee et al. (2006a) investigated 200 patientsfrom a University Hospital and found that none of thebaseline MRI findings significantly predicted seriousLBP episodes nor disability after 60 months. Grade 5disc degeneration (OR = 4.40; p = 0.08), moderate/severe endplate changes (OR = 2.5; p = 0.1) and canalstenosis (OR = 2.9; p = 0.09) were weakly, but not sig-nificantly, associated with serious LBP episodes.Another study by Carragee et al. (2005) reported thatthe presence of disc herniation was associated withpain (OR = 0.2; p = 0.01) at follow-up, in 100 patientsfrom a University Hospital.
3.4.3 No current LBP, but previous LBP
One study investigated the association between base-line MRI findings and LBP in 128 Veterans Affairspatients who were initially asymptomatic (Jarviket al., 2005). Baseline MRI findings of nerve rootcontact (HR = 2.2; 95% CI = 0.6–8.0) and centralspinal stenosis (HR = 1.9; 95% CI = 0.8–4.8) producednon-significant HRs for future new LBP. The studyfound that having a disc herniation (protrusion)(HR = 0.5; 95% CI = 0.3–0.9) reduced the likelihoodof future LBP, whereas a disc herniation (extrusion)(HR = 1.2; 95% CI = 0.4–3.4) did not predict futurenew LBP episodes.
3.4.4 No history of LBP
Three studies provided estimates of the associationbetween MRI findings [disc degeneration (Boos et al.,2000; Elfering et al., 2002), disc herniation (Booset al., 2000), neural compromise (Boos et al., 2000)and worsening abnormalities on MRI (Borensteinet al., 2001)] with future LBP in a sample of asymp-tomatic individuals with no history of LBP.
Borenstein et al. (2001) followed up 50 subjects for84 months and reported a relative risk that LBP woulddevelop in individuals with worsening abnormalitieson MRI scans of 3.5 (no CIs or p-values reported).
Disc degeneration was investigated by two studies.Elfering et al. (2002) reported the association betweendisc degeneration and LBP after 60 months in 41patients. There was no significant association with LBPin those with disc degeneration (OR = 4.8; 95%CI = 0.3–69.3), although the very wide CIs indicatelack of statistical power. Boos et al. (2000) investigated46 asymptomatic individuals and did not find a signifi-cant association between disc degeneration and LBP(OR = 2.1; 95% CI = 0.1–26.9). Similarly, disc hernia-tion and neural compromise were not predictors of
MRI predicting future LBP D. Steffens et al.
© 2013 European Pain Federation - EFIC®8 Eur J Pain •• (2013) ••–••
129
LBP (OR = 0.7; 95% CI = 0.1–9.3 and OR = 8.8; 95%CI = 0.6–117.2, respectively).
4. Discussion
4.1 Statement of principal findings
Twelve studies met the inclusion criteria and wereincluded. Six studies investigated participants withcurrent LBP, two investigated mixed samples includingpeople with and without LBP, one included a samplewith no current LBP, but previous LBP symptoms, andthree studies included a sample of participants with nohistory of LBP. No consistent associations were iden-tified across multiple studies. Single studies reportedsignificant associations for Modic changes type 1(OR = 6.2; 95% CI = 1.9–20.2) with pain, and discdegeneration with disability (OR = 2.2; 95% CI = 1.2–4.0) in samples with current LBP, and disc herniation(OR = 0.2; p = 0.01) with pain in a mixed sample withand without LBP.
This systematic review reveals that there are rela-tively few studies that have investigated MRI findingsas predictors of future LBP. Not only are there fewstudies, but these studies are mostly small (number ofparticipants ranging from 41 to 323) and investigatedifferent MRI findings in a range of different samples(i.e., current LBP, no current LBP or mixed) and usedifferent outcome measures. As a result, it is not pos-sible to draw firm conclusions about the ability of MRIfindings to predict future LBP. Some MRI findingswere statistically associated with future LBP in singlestudies, but comparable studies were not identified toenable confirmation of these findings. The smallsample size of most studies meant that some poten-tially clinically important associations may have beenmissed. It remains unclear whether the MRI findingshave important associations with LBP outcomes orwhether no important associations truly exist.
4.2 Strengths and weaknesses of the study
To our knowledge, this is the first systematic review tosummarize the available evidence of MRI findings pre-dicting future LBP. We used a very sensitive searchstrategy previously used in other high-quality LBPprognosis studies (Pengel et al., 2003; Costa et al.,2012) and MRI systematic reviews (Chou et al., 2011;Endean et al., 2011), making it very likely that alleligible studies were included in our review. We alsoconsulted experts in the field to reduce the risk ofmissing any important articles. A limitation of thepresent study is the heterogeneity of the studies
reviewed particularly the different samples, MRI find-ings investigated and clinical outcomes. For thisreason, we were unable to pool study results. Somestudies included participants from RCTs (Modic et al.,2005; Kleinstuck et al., 2006; Hellum et al., 2012;Jensen et al., 2012) and it is not possible to determinehow the interventions may have impacted on the out-comes. The association between MRI finding andoutcome may vary as a result of confounding due totreatment. The association between MRI findings andoutcomes in a sample that underwent surgery(Hellum et al., 2012) were not reported in this review.Another factor that could have influenced the resultsof the included studies was that most studies used adifferent MRI protocol, sequences and training of MRIreaders. The current review only investigated MRIfindings and does not provide evidence on the value ofplain radiographs or computed tomography scans inpredicting future LBP.
4.3 Comparison with other studies
One previous systematic review has investigated thecross-sectional association of vertebral endplate signalchanges (Modic changes) with current NSLBP (Jensenet al., 2008). A relatively strong association betweenvertebral signal changes and NSLBP was found in 7 of10 studies with ORs ranging from 2.0 to 19.9. In oursearch, we chose to include articles that investigatedthe association of a variety of baseline MRI findings(i.e., disc degeneration, HIZ, herniation) with pain anddisability outcomes in a range of different samples.Furthermore, despite other systematic reviews in thisfield including cross-sectional studies, we chose toexclude these studies as they cannot logically deter-mine if baseline MRI findings predict future LBP.
4.4 Meaning of the study
While single studies reported significant associationsfor Modic changes type 1, disc herniation and discdegeneration for future LBP, there remains consider-able uncertainty about the importance of MRI find-ings. Definitive conclusions are not possible as theavailable studies typically enrolled small non-representative samples and the results were inconsis-tent between studies. Perhaps the only clear result toemerge from this review is that there is a paucity ofhigh-quality studies in this important area. Thisabsence of evidence is in contrast with the rapidlyincreasing use of MRI in patients with LBP (Chouet al., 2012).
D. Steffens et al. MRI predicting future LBP
© 2013 European Pain Federation - EFIC® Eur J Pain •• (2013) ••–•• 9
130
Many of the MRI findings are truly continuous mea-sures with different degrees of severity. Despite this,included studies tend to dichotomize these (i.e.,present or no present). This may result in loss ofimportant data, and therefore, more research isneeded to investigate if the relationships are linear orif important thresholds exist.
4.5 Recommendations for future research
Further large, high-quality studies are clearly neededto help determine the clinical meaningfulness of MRIfindings in relation to LBP. Additionally, a number offactors related to reporting of included studies could beimproved. Firstly, all of the included studies had somemethodological shortcomings. Future studies shoulddescribe the selection of participants in more detail.Assessment and reporting of clinical outcomes was notwell standardized. For example, pain intensity wasmeasured in nine studies with four different scales.Standardized methods for reporting outcomes, basedon published recommendations, would greatlyimprove future studies (Bombardier, 2000). The use ofa standardized MRI protocol, same sequences andtraining of MRI readers is also highly recommended.
The investigation of association between MRI find-ings and clinical outcomes is complicated. All reviewedstudies focused on the association between a singleimaging findings and pain and/or disability. Futurestudies should investigate which MRI findings typicallyoccur together and whether clusters of findings aremore predictive of outcome than single findings.
5. Conclusion
This review shows that there are few (heterogeneous)longitudinal studies that have investigated the associa-tion of lumbar spine MRI findings and LBP outcomes,which indicates the need for further research.
Acknowledgement
We thank Prof Jeffrey Jarvik for reviewing included studiesand suggesting possible additional studies.
Author contributions
D.S. designed and managed the study, planned analysis,drafted manuscript, extracted and analysed data. M.J.H.designed and managed the study, planned analysis, extractedand analysed data. C.G.M. designed and managed the study,extracted data and edited the manuscript. C.W., T.S.J. and
J.L. designed the study, extracted data and edited the manu-script. All authors approved the final version.
References
Altman, D.G. (2001). Systematic reviews of evaluations of prognosticvariables. BMJ 323, 224–228.
Boden, S.D., Davis, D.O., Dina, T.S., Patronas, N.J., Wiesel, S.W. (1990).Abnormal magnetic-resonance scans of the lumbar spine in asymptom-atic subjects. A prospective investigation. J Bone Joint Surg 72, 403–408.
Bombardier, C. (2000). Outcome assessments in the evaluation of treat-ment of spinal disorders: Summary and general recommendations.Spine 25, 3100–3103.
Boos, N., Rieder, R., Schade, V., Spratt, K.F., Semmer, N., Aebi, M. (1995).The diagnostic accuracy of magnetic resonance imaging, work percep-tion, and psychosocial factors in identifying symptomatic disc hernia-tions. Spine 20, 2613–2625.
Boos, N., Semmer, N., Elfering, A., Schade, V., Gal, I., Zanetti, M., Kissling,R., Buchegger, N., Hodler, J., Main, C.J. (2000). Natural history ofindividuals with asymptomatic disc abnormalities in magnetic reso-nance imaging: Predictors of low back pain-related medical monsulta-tion and work incapacity. Spine 25, 1484–1492.
Borenstein, D.G., O’Mara, J.W.J., Boden, S.D., Lauerman, W.C., Jacobson,A., Platenberg, C., Schellinger, D., Wiesel, S.W. (2001). The value ofmagnetic resonance imaging of the lumbar spine to predict low-backpain in asymptomatic subjects: A seven-year follow-up study. J BoneJoint Surg 83, 1306–1311.
Carragee, E., Alamin, T., Cheng, I., Franklin, T., Hurwitz, E. (2006a). Doesminor trauma cause serious low back illness? Spine 31, 2942–2949.
Carragee, E., Alamin, T., Cheng, I., Franklin, T., van den Haak, E.,Hurwitz, E. (2006b). Are first-time episodes of serious LBP associatedwith new MRI findings? Spine J 6, 624–635.
Carragee, E.J., Alamin, T.F., Miller, J.L., Carragee, J.M. (2005). Disco-graphic, MRI and psychosocial determinants of low back pain disabilityand remission: A prospective study in subjects with benign persistentback pain. Spine J 5, 24–35.
Chou, D., Samartzis, D., Bellabarba, C., Patel, A., Luk, K.D.K., Kisser,J.M.S., Skelly, A.C. (2011). Degenerative magnetic resonance imagingchanges in patients with chronic low back pain: A systematic review.Spine 36, S43–S53.
Chou, R., Deyo, R., Jarvik, J. (2012). Appropriate use of lumbar imagingfor evaluation of low back pain. Radiol Clin North Am 50, 569–585.
Costa, L.C.M., Maher, C.G., Hancock, M.J., McAuley, J.H., Herbert, R.D.,Costa, L.O.P. (2012). The prognosis of acute and persistent low-backpain: A meta-analysis. CMAJ 184, 613–624.
Deyo, R.A. (2004). Treatments for back pain: Can we get past trivialeffect? Ann Intern Med 141, 957–958.
Duncan, R., Peat, G., Thomas, E., Hay, E., McCall, I., Croft, P. (2007).Symptoms and radiographic osteoarthritis: Not as discordant as they aremade out to be? Ann Rheum Dis 66, 86–91.
Elfering, A., Semmer, N., Birkhofer, D., Zanetti, M., Hodler, J., Boos, N.(2002). Risk factors for lumbar disc degeneration: A 5-year prospectiveMRI study in asymptomatic individuals. Spine 27, 125–134.
Endean, A., Palmer, K.T., Coggon, D. (2011). Potential of magnetic reso-nance imaging findings to refine case definition for mechanical lowback pain in epidemiological studies: A systematic review. Spine 36,160–169.
Hancock, M., Maher, C., Macaskill, P., Latimer, J., Kos, W., Pik, J. (2012).MRI findings are more common in selected patients with acute lowback pain than controls? Eur Spine J 21, 240–246.
Hellum, C., Johnsen, L.G., Gjertsen, O., Berg, L., Necklmann, G.,Grundnes, O., Rossvoll, I., Skouen, J.S., Brox, J.I., Storheim, K. (2012).Predictors of outcome after surgery with disc prothesis and rehabilita-tion in patients with chronic low back pain and degenerative disc:2-year follow-up. Eur Spine J 21, 681–690.
Jarvik, J.G., Hollingworth, W., Heagerty, P.J., Haynor, D.R., Boyko, E.J.,Deyo, R.A. (2005). Three-year incidence of low back pain in an initially
MRI predicting future LBP D. Steffens et al.
© 2013 European Pain Federation - EFIC®10 Eur J Pain •• (2013) ••–••
131
asymptomatic cohort: Clinical and imaging risk factors. Spine 30, 1541–1548.
Jarvik, J.J., Hollingworth, W., Heagerty, P., Haynor, D.R., Deyo, R.A.(2001). The longitudinal assessment of imaging and disability of theback (LAIDBack) study. Spine 26, 1158–1166.
Jensen, R.K., Leboeuf-Yde, C., Wedderkopp, N., Sorensen, J.S., Jensen,T.S., Manniche, C. (2012). Is the development of Modic changes asso-ciated with clinical symptoms? A 14-month cohort study with MRI. EurSpine J 21, 2271–2279.
Jensen, T.S., Karppinen, J., Sorensen, J.S., Niinimaki, J., Leboeuf-Yde, C.(2008). Vertebral endplate signal changes (Modic change): A systematicliterature review of prevalence and association with non-specific lowback pain. Eur Spine J 17, 1407–1422.
Keller, A., Boyle, E., Skog, T.A., Cassidy, J.D., Bautz-Holter, E.(2012). Are Modic changes prognostic for recovery in a cohortof patients with non-specific low back pain? Eur Spine J 21, 418–424.
Keller, A., Hayden, J., Bombardier, C., van Tulder, M. (2007). Effect sizesof non-surgical treatments of non-specific low-back pain. Eur Spine J 16,1776–1788.
Kleinstuck, F., Dvorak, J., Mannion, A.F. (2006). Are ‘structural abnor-malities’ on magnetic resonance imaging a contraindication to the suc-cessful conservative treatment of chronic nonspecific low back pain?Spine 31, 2250–2257.
McNee, P., Shambrook, J., Harris, E.C., Kim, M., Sampson, M., Palmer,K.T., Coggon, D. (2011). Predictors of long-term pain and disability inpatients with low back pain investigated by magnetic resonanceimaging: A longitudinal study. BMC Musculoskelet Disord 12, 234.
Modic, M.T., Obuchowski, N.A., Ross, J.S., Brant-Zawadzki, M.N., Grooff,P.N., Mazanec, D.J., Benzel, E.C. (2005). Acute low back pain andradiculopathy: MR imaging findings and their prognostic role and effecton outcome. Radiology 237, 597–604.
Modic, M.T., Ross, J.S. (2007). Lumbar degenerative disk disease. Radiol-ogy 245, 43–61.
Pengel, L.H.M., Herbert, R.D., Maher, C.G., Refshauge, K.M. (2003).Acute low back pain: Systematic review of its prognosis. BMJ 327,323.
Schwarzer, A.C., Aprill, C.N., Derby, R., Fortin, J., Kine, G., Bogduk, N.(1995). The prevalence and clinical features of internal disc disruptionin patients with chronic low back pain. Spine 20, 1878–1883.
van Tulder, M., Becker, A., Bekkering, T., Breen, A., Del Real, M.T.G.,Hutchinson, A., Koes, B., Laerum, E., Malmivaara, A. (2006). Chapter3. European guidelines for the management of chronic nonspecific lowback pain. Eur Spine J 15, S169–S191.
Supporting Information
Additional Supporting Information may be found in theonline version of this article at the publisher’s web-site:
Appendix S1. Search strategy.Appendix S2. List of excluded full-text articles and theprimary reason for exclusion.
D. Steffens et al. MRI predicting future LBP
© 2013 European Pain Federation - EFIC® Eur J Pain •• (2013) ••–•• 11
132
Appendix S1. Search strategy
MEDLINE1 exp cohort studies/2 incidence/3 follow-up studies.mp.4 prognos$.mp.5 predict$.mp.6 course.mp.7 inception.mp.8 survival.mp.9 logistic.mp.
10 Cox.mp.11 life tables.mp.12 log rank.mp.13 or/1–1214 low back pain.mp.15 back pain.mp.16 Lumbago.mp.17 Back injuries.mp.18 Backache.mp.19 or/14–1820 Magnetic resonance Imaging/21 MRI.mp.22 Magnetic adj5 resonance.mp.23 NMR.mp.24 Nuclear magnetic resonance.mp.25 Disc degeneration.mp.26 Desiccation.mp.27 Loss of disc height.mp.28 Bulge.mp.29 Protrusion.mp.30 Extrusion.mp.31 Nerve root compromise.mp.32 Annular tear.mp.33 Endplate changes.mp.34 Stenosis.mp.35 Facet degeneration.mp.36 High intensity zone.mp.37 Modic changes.mp.38 Degenerative disc disease.mp.39 Spondylolisthesis.mp.40 or/20–3941 13 AND 19 AND 40EMBASE
1 (‘cohort analysis’/exp AND [embase]/lim)2 (‘incidence’/exp AND [embase]/lim)3 (‘follow up’/exp OR ‘follow up’ AND [embase]/lim)4 (‘prognosis’/exp OR prognos* AND [embase]/lim)5 (‘prediction’/exp OR predict* AND [embase]/lim)6 (‘disease course’/exp OR ‘course’ AND [embase]/lim)7 (‘inception’/exp AND [embase]/lim)8 (‘survival’/exp OR ‘survival’ AND [embase]/lim)9 (‘logistic regression analysis’/exp OR ‘logistic’ AND
[embase]/lim)10 (‘proportional hazards model’/exp OR ‘cox’ AND [embase]/lim)11 (‘life table’/exp OR ‘life table’ OR ‘life tables’/exp OR ‘life tables’ AND
[embase]/lim)12 (‘log rank test’/exp OR ‘log rank’ AND [embase]/lim)13 1 or 2 or 3 or 4 or 5 or 6 or 7 or 8 or 9 or 10 or 11 or 1214 (‘low back pain’/exp OR ‘low back pain’ AND [embase]/lim)15 (‘backache’/exp OR ‘low back pain’/exp AND [embase]/lim)16 (‘Lumbago’/exp AND [embase]/lim)17 (‘Back injuries’/exp AND [embase]/lim)18 14 or 15 or 16 or 17
19 13 AND 1820 (‘Magnetic resonance Imaging’/exp AND [embase]/lim)21 (‘MRI’/exp AND [embase]/lim)22 (‘Magnetic resonance’/exp AND [embase]/lim)23 (‘NMR’/exp AND [embase]/lim)24 (‘Nuclear magnetic resonance’/exp AND [embase]/lim)25 (‘Disc degeneration’/exp AND [embase]/lim)26 (‘Desiccation’/exp AND [embase]/lim)27 (‘Loss of disc height’/exp AND [embase]/lim)28 (‘Bulge’/exp AND [embase]/lim)29 (‘Protrusion’/exp AND [embase]/lim)30 (‘Extrusion’/exp AND [embase]/lim)31 (‘Nerve root compromise’/exp AND [embase]/lim)32 (‘Annular tear’/exp AND [embase]/lim)33 (‘Endplate changes’/exp AND [embase]/lim)34 (‘Stenosis’/exp AND [embase]/lim)35 (‘Facet degeneration’/exp AND [embase]/lim)36 (‘High intensity zone’/exp AND [embase]/lim)37 (‘Modic changes’/exp AND [embase]/lim)38 (‘Degenerative disc disease’/exp AND [embase]/lim)39 (‘Spondylolisthesis’/exp AND [embase]/lim)40 20 or 21 or 22 or 23 or 24 or 25 or 26 or 27 or 28 or 29 or 30 or 31
or 31 or 33 or 34 or 35 or 36 or 37 or 38 or 39 or 4019 AND 40
CINAHL1 (MH ‘Prospective Studies+’)2 (MH ‘incidence+’)3 ‘predic*’4 (MH ‘prognosis+’)5 ‘course’6 ‘Inception’7 (MH ‘Survival Analisis+’) or (MH ‘Cox Proportional Hazards Model’)8 (MH ‘Logistic Regression+’)9 (MH ‘Life Table Methods’)
10 (MH ‘Log-Rank Test’)11 1 or 2 or 3 or 4 or 5 or 6 or 7 or 8 or 9 or 1012 (MH ‘Low Back Pain’) or (MH ‘Back Pain+’)13 (MH ‘Lumbago+’)14 (‘Back injuries+’)15 (‘Backache+’)16 12 or 13 or 14 or 1517 11 AND 1618 (MH ‘MRI’) or (MH ‘Magnetic Resonance’)19 (MH ‘NRI’) or (MH ‘Nuclear Magnetic Resonance’)20 (MH ‘Disc degeneration+’)21 (MH ‘Desiccation+’)22 (MH ‘Loss of disc heigh+’)23 (MH ‘Bulge+’)24 (MH ‘Protrusion+’)25 (MH ‘Extrusion+’)26 (MH ‘Nerve root compromise+’)27 (MH ‘Annular tear+’)28 (MH ‘Endplate changes+’)29 (MH ‘Stenosis+’)30 (MH ‘Facet degeneration+’)31 (MH ‘High intensity zone+’)32 (MH ‘Modic changes+’)33 (MH ‘Degenerative disc disease+’)34 (MH ‘Spondylolisthesis+’)35 18 or 19 or 20 or 21 or 22 or 23 or 24 or 25 or 26 or 27 or 28 or 29
or 30 or 31 or 32 or 33 or 3436 17 AND 35
133
Appendix S2. List of excluded full-text articles and the primary reason forexclusion
# Study Title First reason for excluding
#1 Albert, H. B. et al. 2007 Modic changes following lumbar disc herniation No association
#2 Ash, L. M. et al. 2008 Effects of diagnostic information, per se, on patient outcomes in acute radiculopathy
and low back pain
No LBP outcome at
follow-up
#3 Baranto, A. et al. 2006 Back pain and degenerative abnormalities in the spine of young elite divers: A 5-year
follow-up magnetic resonance imaging study
No LBP outcome at
follow-up
#4 Baranto, A., M. et al. 2009 Back pain and MRI changes in the thoraco-lumbar spine of top athletes in four different
sports: A 15-year follow-up study
No LBP outcome at
follow-up
#5 Bartolozzi, C. et al. 1991 The incidence of disk changes in volleyball players. The magnetic resonance findings Not a prospective study
#6 Beattie, P. F. et al. 2000 Associations between patient report of symptoms and anatomic impairment visible on
lumbar magnetic resonance imaging
Not a prospective study
#7 Bennett, A. N. et al. 2008 Severity of baseline magnetic resonance imaging-evident sacroiliitis and HLA-B27
status in early inflammatory back pain predict radiographically evident ankylosing
spondylitis at eight years
No association
#8 Bennett, D. L. et al. 2006 Lumbar spine MRI in the elite-level female gymnast with low back pain No LBP outcome at
follow-up
#9 Boden, S. D. et al. 1990 Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects. A
prospective investigation
No LBP outcome at
follow-up
#10 Borthakur, A. et al. 2011 T1(rho) magnetic resonance imaging and discography pressure as novel biomarkers for
disc degeneration and low back pain
Not a prospective study
#11 Braithwaite, I. et al. 1998 Vertebral endplate (Modic) changes on lumbar spine MRI: correlation with pain
reproduction at lumbar discography
Not a prospective study
#12 Buirski, G. 1992 Magnetic resonance signal patterns of lumbar discs in patients with low back pain. A
prospective study with discographic correlation
Not a prospective study
#13 Buirski, G. and M.
Silberstein 1993
The symptomatic lumbar disc in patients with low-back pain. Magnetic resonance
imaging appearances in both a symptomatic and control population
Not a prospective study
#14 Buttermann, G. R. et al.
2008
Pain and disability correlated with disc degeneration via magnetic resonance imaging
in scoliosis patients
Not a prospective study
#15 Buttermann, G.R. 2004 The effect of spinal steroid injections for degenerative disc disease No association
#16 Carragee, E. J. et al. 2000 2000 Volvo Award winner in clinical studies: Lumbar high-intensity zone and
discography in subjects without low back problem.
Not a prospective study
#17 Carragee, E. J. et al. 2004 Prospective controlled study of the development of lower back pain in previously
asymptomatic subjects undergoing experimental discography
No association
#18 Chen, B., et al. 2001 The magnetic resonance imaging of the lumbar spine in out-patients with low back
pain
Not a prospective study
#19 Cheung, K. M. et al. 2009 Prevalence and pattern of lumbar magnetic resonance imaging changes in a
population study of one thousand forty-three individuals
Not a prospective study
#20 de Schepper, E. I. et al.
2010
The association between lumbar disc degeneration and low back pain: the influence of
age, gender, and individual radiographic features
Not a prospective study
#21 Erkintalo, M. O. et al. 1995 Development of degenerative changes in the lumbar intervertebral disk: Results of a
prospective MR imaging study in adolescents with and without low-back pain
No association
#22 Esposito, P. et al 2006 Predictive value of MRI vertebral end-plate signal changes (Modic) on outcome of
surgically treated degenerative disc disease. Results of a cohort study including 60
patients
No LBP outcome at
follow-up
#23 Fayad, F. et al. 2007 Relation of inflammatory modic changes to intradiscal steroid injection outcome in
chronic low back pain
Not a prospective study
#24 Fayad, F. et al. 2009 Reliability of a modified Modic classification of bone marrow changes in lumbar spine
MRI.
Not a prospective study
#25 Grable, H. R. 1993 Abnormal findings on magnetic resonance imaging in a group of motor vehicle
accident patients with low back pain
Not a prospective study
#26 Graves, J. M. et al. 2012 Early imaging for acute low back pain: One-year health and disability outcomes among
Washington state workers
No MRI at baseline
#27 Haig, A. J. et al. 2006 Predictors of pain and function in persons with spinal stenosis, low back pain, and no
back pain
Not a prospective study
#28 Hollingworth, W. et al.
1998
Self reported health status and magnetic resonance imaging findings in patients with
low back pain
No association
134
Appendix S2. (continued)
# Study Title First reason for excluding
#29 Iwamoto, J. et al. 2005 Relationship between radiographic abnormalities of lumbar spine and incidence of low
back pain in high school rugby players: A prospective study
No MRI at Baseline
#30 Jensen, O. K. et al. 2010 One-year prognosis in sick-listed low back pain patients with and without radiculopathy.
Prognostic factors influencing pain and disability
No MRI at Baseline
#31 Jensen, R.K. et al 2011 Is the presence of Modic changes associated with the outcomes of different
treatments? A systematic critical review
Not a prospective study
#32 Jensen, T. S. et al. 2009 Characteristics and natural course of vertebral endplate signal (Modic) changes in the
Danish general population
No LBP outcome at
follow-up
#33 Jensen, T. S. et al. 2010 Predictors of new vertebral endplate signal (Modic) changes in the general population No LBP outcome at
follow-up
#34 Jensen, T.S. et al 2007 Magnetic resonance imaging findings as predictors of clinical outcome in patients with
sciatica receiving active conservative treatment
No LBP outcome at
follow-up
#35 Kanayama, M. et al. 2009 Cross-sectional magnetic resonance imaging study of lumbar disc degeneration in 200
healthy individuals: Clinical article
Not a prospective study
#36 Kerttula, L. et al. 2012 Modic type I change may predict rapid progressive, deforming disc degeneration: a
prospective 1-year follow-up study
No LBP outcome at
follow-up
#37 Kuisma, M. et al 2006 A three-year follow-up of lumbar spine endplate (Modic) changes No LBP outcome at
follow-up
#38 Kujala, U. M. et al. 1996 Low-back pain in adolescent athletes No LBP outcome at
follow-up
#39 Kujala, U. M. et al. 1999 Prolonged low-back pain in young athletes: a prospective case series study of findings
and prognosis
No association
#40 Luoma, K. et al. 2008 MRI follow-up of subchondral signal abnormalities in a selected group of chronic low
back pain patients
Not a prospective study
#41 Luoma, K. et al. 2009 Relationship of Modic type 1 change with disc degeneration: A prospective MRI study No LBP outcome at
follow-up
#42 Marzo-Ortega, H. et al.
2009
Baseline and 1-year magnetic resonance imaging of the sacroiliac joint and lumbar
spine in very early inflammatory back pain. Relationship between symptoms,
HLA-B27 and disease extent and persistence
No LBP outcome at
follow-up
#43 Matsui, H. et al. 1998 Familial predisposition for lumbar degenerative disc disease Not a prospective study
#44 Mitra, D. et al. 2004 Longitudinal study of vertebral type-1 end-plate changes on MR of the lumbar spine Not a prospective study
#45 Siepe, C.J. et al 2006 Clinical results of total lumbar disc replacement with prodisc II No association
#46 Symmons, D. P. et al.
1991
A longitudinal study of back pain and radiological changes in the lumbar spines of
middle aged women. II. Radiographic findings
No MRI at Baseline
#47 Takatalo, J. et al. 2011 Does lumbar disc degeneration on magnetic resonance imaging associate with low
back symptom severity in young Finnish adults?
Not a prospective study
#48 Tung, G. A. et al. 1999 Spinal epidural abscess: Correlation between MRI findings and outcome Not a prospective study
#49 Videman, T. et al. 2003 Associations between back pain history and lumbar MRI findings Not a prospective study
#50 Waris, E. et al. 2007 Disc degeneration in low back pain: a 17-year follow-up study using magnetic
resonance imaging
No LBP outcome at
follow-up
#51 Williams, F. M. K. et al.
2011
Progression of lumbar disc degeneration over a decade: A heritability study No LBP outcome at
follow-up
135
Chapter Seven
Prognosis of chronic low back pain in patients presenting to a private community-
based group exercise program
Chapter Seven is published as:
Steffens D, Hancock MJ, Maher CG, Latimer J, Satchell R, Ferreira ML, Ferreira PH,
Partington M, Bouvier AL. Prognosis of chronic low back pain in patients presenting to a
private community-based group exercise program. European Spine Journal. 2014; 23: 113-
119.
136
Statement from co-authors confirming authorship contribution of the PhD candidate
As co-authors of the paper “Prognosis of chronic low back pain in patients presenting to a
private community-based group exercise program”, we confirm that Daniel Steffens has
made the following contributions:
Conception and design of the research
Data collection
Analysis and interpretation of the findings
Writing of the manuscript and critical appraisal of the content
Mark J Hancock Date: 01.01.2015
Christopher G Maher Date: 01.01.2015
Jane Latimer Date: 01.01.2015
Rob Satchell Date: 01.01.2015
Manuela L Ferreira Date: 01.01.2015
Paulo H Ferreira Date: 01.01.2015
Melissa Partington Date: 01.01.2015
Anna L Bouvier Date: 01.01.2015
137
ORIGINAL ARTICLE
Prognosis of chronic low back pain in patients presentingto a private community-based group exercise program
Daniel Steffens • Mark J. Hancock • Chris G. Maher • Jane Latimer •
Robert Satchell • Manuela Ferreira • Paulo H. Ferreira • Melissa Partington •
Anna-Louise Bouvier
Received: 10 October 2012 / Revised: 8 May 2013 / Accepted: 1 June 2013 / Published online: 23 June 2013
� Springer-Verlag Berlin Heidelberg 2013
Abstract
Purpose To examine the prognosis and prognostic factors
for patients with chronic low back pain presenting to a
private, community-based, group exercise program.
Methods A total of 118 consecutive patients with chronic
LBP were recruited. Baseline assessments included socio-
demographic characteristics, back pain history and clinical
examination findings. Primary outcome measures were pain
intensity and disability at 3, 6 and 12 months. Potential
prognostic factors to predict pain intensity and disability at
12 months were assessed using a multivariate regression
model.
Results 112 (95 %) participants were followed up at
12 months. The majority of participants were female
(73 %), had high educational levels (82 %) and resided in
suburbs with a high socio-economic status (99 %). Pain
intensity improved markedly during the first 6 months
(35 %) with further minimal reductions up to 12 months
(39 %). Interestingly, disability improved to a greater
degree than pain (48 % improvement at 6 months) and
continued to improve throughout the 12 months (60 %).
Baseline pain intensity accounted for 10 % of the variance
in the 1 year pain outcomes. Duration of current episode,
baseline disability and educational level accounted for
15 % of the variation in disability at 12 months.
Conclusions During a period of 12 months, patients with
chronic LBP presenting to a private, community-based,
group exercise program improved markedly, with greater
improvements in disability than pain. The predictors
investigated accounted for only 10 and 15 % of pain and
disability outcomes, respectively.
Keywords Chronic low back pain � Prognosis �Disability �Outcomes
Introduction
Clinical guidelines report the prognosis of chronic back
pain to be poor [1]. A recent systematic review of the
course of acute and chronic LBP [2] found moderate
within-study and between-study variability in both pain
and disability outcomes. This strongly suggests that while
the average prognosis may be poor this is not the case for a
substantial proportion of people. The moderate levels of
between-study variability suggest that factors related to
study design, setting and participants may significantly
impact on the reported prognoses.
Previous studies have identified factors associated with
prognosis in chronic LBP [3–6]; however, the lack of
quality studies means prognostic factors for chronic LBP
D. Steffens (&) � C. G. Maher � J. Latimer � M. Ferreira
Musculoskeletal Division, The George Institute for Global
Health, University of Sydney, Level 13, 321 Kent Street,
Sydney, NSW 2000, Australia
e-mail: [email protected]
M. J. Hancock
Discipline of Physiotherapy, Faculty of Human Sciences,
Macquarie University, 2 Technology Place, Macquarie Park,
Sydney, NSW 2113, Australia
R. Satchell
Coast Allied Health, 2/171 Prince Edward Ave,
Culburra Beach, NSW 2540, Australia
P. H. Ferreira
Discipline of Physiotherapy, Faculty of Health Sciences,
The University of Sydney, Lidcombe,
Sydney, NSW 2141, Australia
M. Partington � A.-L. Bouvier
Physiocise, Movement for Life, Suite 14, 77 Penshurst Street,
Willoughby, Sydney, NSW 2068, Australia
123
Eur Spine J (2014) 23:113–119
DOI 10.1007/s00586-013-2846-x
138
remain unclear [7]. A large Australian cohort study [8]
found previous sick leave due to LBP, high disability levels
or high pain intensity at onset of chronicity, low levels of
education, greater perceived risk of persistent pain, and
being born outside Australia (immigrants) were associated
with delayed recovery. Patients presenting for care in set-
tings where these adverse prognostic factors are uncommon
may have a more favorable prognosis than widely reported.
Until now no study has investigated the prognosis of
people with chronic low back pain attending a private,
community-based, group exercise program.
It is reasonable to expect that evidence-based treatments
which are endorsed in clinical guidelines will impact on the
prognosis reported and may be an important source of the
between-study variability [2]. The European guideline for
the management of chronic non-specific LBP recommends
supervised exercise therapy as a first-line treatment in the
management of chronic LBP. Furthermore, group exercise
and the use of cognitive behavioral therapy are also rec-
ommended [1]. Community-based group exercise programs
based on guideline recommendations for chronic LBP have
become increasingly common in the management of
chronic LBP. Many of these programs are private, and
given the requirement that patients must pay for the ser-
vice, attract patients without work related injuries with
higher average socioeconomic status and level of educa-
tion. However, the prognosis of this particular group of
private paying patients presenting to individualized group
exercise classes is not well reported in the literature.
In assessing the prognosis of chronic LBP it is important
to consider at a minimum both pain and disability out-
comes. A recent review found greater changes in pain than
disability but lower absolute scores for disability than pain
at 1 year, as the baseline pain levels were higher than
disability [2]. A better understanding of the relative prog-
nosis in terms of pain and disability for people paying for
and receiving high quality group exercise programs is
important. Therefore, the aim of the present study was to
examine the prognosis and prognostic factors for private
paying patients with chronic LBP who presented to a pri-
vate, community-based, group exercise program.
Materials and methods
We conducted a prospective study of participants with
chronic LBP presenting to a private, community-based,
group exercise program.
Setting and participants
Consecutive patients with LBP who presented to a private,
community-based, group exercise program were invited to
participate if they met all the following inclusion criteria;
(1) chronic non-specific LBP (symptoms greater than
3 months duration, according to the classification proposed
by de Vet et al. [4]) with or without leg pain (2) pain on a
numerical pain rating scale equal or greater than two out of
ten (3) adequate English communication for all data to be
recorded and (4) baseline assessment performed less than
4 weeks prior to exercise classes starting. Exclusion cri-
teria were (1) LBP that was not attributable to a recog-
nizable, known specific pathology (e.g., infection, tumor,
fracture, inflammatory disorder, cauda equina, radicular
syndrome) [1], or (2) nerve root compromise (with at least
two of the following signs: myotomal weakness, derma-
tomal sensory loss or hyporeflexia of the lower limb) or (3)
currently pregnant. The University of Sydney’s Human
Research Ethics Committee approved the study.
Baseline data collection
Baseline data were collected by a physiotherapist as part of
the standard 90-min assessment for all patients prior to
starting the group exercise program. Data collected inclu-
ded demographic information, baseline measures of out-
comes and potential prognostic factors.
Group exercise program
All participants were enrolled in a group exercise program,
at one of two private clinics in Sydney. The program
involved a strong educational component combined with
physical retraining. Patients paid up front for a 10 week
foundation program. Patients with private health insurance
(87 %) were able to claim up to 50 % of the total cost of
the classes from their insurer. The foundation program
focuses on movement and posture re-education, combined
with very specific pain behavior education, Acceptance and
Commitment Therapy principles (focusing on awareness,
acceptance, defusing of negative thoughts) [9] and CBT
specifically in the area of decreasing catastrophizing.
Educational and physical elements of the program focused
on practicing activities of daily living, in particular sitting,
standing, walking and bending. These were performed in
front of large mirrors which gave patients maximum visual
feedback about their physical movement patterns compared
to an idealized goal (e.g., using neutral spine and hip and
knee flexion for bending). The environment was light, non-
threatening, interactive and involved music as well as
education. Participants were also given a book of exercises
and educational materials related to back pain and posture
[10, 11]. At the end of the 10-week program, some par-
ticipants enrolled in more advanced classes while other
participants ceased participation in the group exercise
classes. Advanced classes focused on physical aspects such
114 Eur Spine J (2014) 23:113–119
123
139
as developing lumbo-pelvic stability, endurance with glu-
teal strength, and incorporating upper body strengthening
in functional positions. Whether participants continued in
classes was recorded, but did not impact on their
involvement in the study.
Outcome variables
Outcome measures were assessed at baseline, 3, 6 and
12 months. Follow-up measures were collected when
patients attended the exercise classes. Participants who did
not attend the classes during the week their follow-up
assessment was due, were contacted by telephone and a
telephone interview was conducted by a trained researcher.
Primary outcomes
The primary outcomes were average pain over the past
week measured using the numerical pain rating scale [12]
scored from 0 (no pain) to 10 (worst pain possible) and
disability, measured using the Roland Morris Disability
Questionnaire [13], scored from 0 to 24, with higher scores
indicating worse disability status. Pain was assessed as
both change in pain and also the proportion of patients who
fully recovered from pain (score 0 or 1 for 1 month at time
of assessment).
Secondary outcomes
Secondary outcomes were global impression of recovery
(Global Perceived Effect Scale) [12, 14], bothersomeness
of pain (Bothersome of Pain Scale) [15], function (Patient-
specific Functional Scale) [16] and kinesiophobia (TAMPA
Scale for Kinesiophobia) [17].
Prognostic factors
A limited number of baseline prognostic factors were
investigated. We limited the number of prognostic factors
to one per ten patients [18]. The prognostic factors were
measures of pain intensity, previous episodes of LBP,
duration of current episode, disability, global perceived
effect of improvement, function, kinesiophobia, educa-
tional level, location of pain (absence of pain below the
knee), catastrophizing, patients enrolled to the second term
(scored as 0 = patients that only attended the first term of
the classes or 1 = patients that attended two or more
terms) and an 11-point prognosis scale. The Physiocise
prognosis scale consists of ten items and is scored by
adding up the number of positive items. The score can
therefore vary from 0 to 10 with higher values indicating
worse prognosis. The items are (1) greater than 5 years
since first acute episode; (2) other painful areas, for
instance neck/shoulders; (3) CT/MRI/disc bulges/degener-
ative changes on X-Ray; (4) high kinesiophobia (defined as
scores [40 on the TAMPA Scale for Kinesiophobia); (5)
poor response to hands-on treatment in the last few years;
(6) degree of constant pain (scored as yes/no); (7) unable
to perform certain physical activities because of pain;
(8) difficulty standing for prolonged periods; (9) difficulty
sitting for prolonged periods; (10) trauma, such as
MVA/fall.
Statistical analysis
Analyses were performed using SPSS version 20 (SPSS,
Inc., Chicago, IL). Descriptive statistics (mean ± SD)
were used to summarize the baseline characteristics of the
patients and prognostic outcomes at baseline, 3, 6 and
12 months. Comparison between mean baseline and 3, 6 or
12 month outcomes were performed using Paired–samples
t test. P \ 0.05 was considered significant.
To evaluate prognostic factors, univariate associations
between each of the prognostic variables and pain scores
and disability (RMDQ) at 12 months were assessed using
linear regression. Variables with significant univariate
associations (p \ 0.2) were entered into a backwards
multivariate regression model.
For the regression analyses, the number of previous
episodes was dichotomized (0–1 episodes/2 or more epi-
sodes), duration of the current episode was recorded in
days and log transformed, and educational level was
dichotomized (0 = school, high school certificate and
trade/diploma and 1 = advanced diploma, bachelor degree
and postgraduate degree).
Results
From January 2010 to January 2011 consecutive patients
from two private physiotherapy clinics in Sydney, Aus-
tralia were screened. One hundred and eighteen met the
inclusion criteria and all consented to enter the study.
Follow-up rates were high, with 116 (98 %), 114 (97 %)
and 112 (95 %) participants being followed up at 3, 6
and 12 months, respectively. Baseline characteristics of
the 118 participants are shown in Table 1. The majority
of participants were female (73 %), had high educational
levels (82 %), did not smoke (96 %) and resided in
suburbs with a high socioeconomic status (99 %). All
participants were private paying and not covered by
workers compensation.
Participants’ outcome data at baseline, 3, 6 and
12 months are presented in Table 2 and Fig. 1. Pain
intensity, bothersomeness, disability and function reduced
during the follow-up period, with mean pain intensity,
Eur Spine J (2014) 23:113–119 115
123
140
bothersomeness, disability and function improving by 39,
41, 60 and 72 % of the initial levels, respectively. Pain
intensity and bothersomeness improved markedly during
the first 6 months (35 and 37 %, respectively) with mini-
mal further reductions up to 12 months (39 and 41 %,
respectively). Conversely, disability and function contin-
ued to improve considerably throughout the 12 months.
After 3, 6 and 12 months, 19 (16 %), 30 (25.5 %) and
29 (25 %) participants had completely recovered (pain
score 0 or 1 for 1 month at time of assessment) from their
LBP, respectively.
The results of the univariate analysis are presented in
Table 3. Table 4 presents the results of the multivariate
backward regression analysis. Baseline pain intensity was
the only independent predictor of 12-month pain scores and
accounted for only 10 % (R2 = 0.102) of the outcome
variance (Table 4). Duration of current episode, disability
and educational level were independent predictors of dis-
ability accounting for 15 % of the variation on disability at
12 months (Table 4).
Discussion
Summary of main findings
The primary finding of this study is that patients with
chronic LBP who presented to a private, community-based,
group exercise program incorporating cognitive behavior
therapy improved substantially over the course of 1 year.
During the first 6 months disability, function and pain
intensity improved similarly; however between 6 and
12 months disability and function continued to improve
while only small further improvements in pain occurred. At
12 months pain intensity had reduced on average by 39 %
while disability and function had improved by 60 and
72 %, respectively.
The predictors investigated did not explain a substantial
amount of the variation in outcome for either pain or dis-
ability. The only independent predictor of 12-month pain
outcomes was baseline pain intensity, but this accounted
for only 10 % of the variation. The independent predictors
of 12-month disability were duration of current episode,
baseline disability and educational level, accounting for
15 % of the variation at 12 months.
Strengths and limitations of the study
A strength of this study is the inclusion of a clearly defined
cohort of consecutive patients with chronic LBP
([3 months) that enrolled in a private paying group exer-
cise program. The high 1-year follow-up rate (95 %) and
the use of validated outcome measures are further
strengths. Nevertheless, we understand that an even longer
follow-up period with more regular sampling may give a
more comprehensive assessment of the course of chronic
LBP.
We limited the number of baseline prognostic factors
investigated to one per ten patients, which could have ruled
out some important prognostic factors already investigated
by others studies, although inclusion of too many variables
Table 1 Baseline characteristics of study population
Characteristics No (%) or mean
(±SD)
Gender (female) 86 (73)
Age (years) 46.5 ± 12.5
Weight (kg) 72.5 ± 15.5
Height (cm) 171 ± 8.5
Smoker 5 (4)
Socioeconomic status (n = 118)
Resides in suburb with mean household income
above Australian mean
117 (99)
Previous episodes of LBP (n = 113)
Never 9 (7.5)
1–5 26 (22.5)
6–10 11 (9.5)
11 or over 71 (60.5)
Previous sick leave due to LBP (n = 116) 65 (55)
Previous treatment for LBP (n = 118) 114 (96.5)
Duration of current episode of LBPa, median
(IQR) (n = 113)
365 (172-730)
Leg painb (n = 112) 23 (19.5)
Highest level of education diploma or higherc
(n = 109)
97 (82)
Employment status before episode of LBP (n = 113)
Full time/full duties 82 (69.5)
Part time/full duties 14 (12)
Not seeking employment (retired/child care) 12 (10)
Work status changed as result of LBP (n = 113) 10 (8.5)
Current employment status (n = 113)
Full time/full duties 62 (52.5)
Full time/selected duties 6 (5)
Part time/full duties 19 (16)
Part time/selected duties 2 (1.7)
Not seeking employment (retired/child care) 24 (20)
Private health insurance 103 (87)
Pain catastrophizing scale (n = 112) 16 ± 10
IQR interquartile rangea Measured in daysb Defined as back pain extending below the kneec University study based
116 Eur Spine J (2014) 23:113–119
123
141
into the model makes it less stable and less generalizable
[18].
Comparison with existing literature
Our study found a more favorable prognosis for people
with chronic LBP than widely reported in the literature.
Van Tulder et al. [19] reported only small improvements in
pain intensity and disability after 12 months (14.2 and
14.7 %, respectively). Grotle and colleagues [5], found
only moderate changes in disability after 1 year (25 %
reduction) for people with chronic LBP. When comparing
the prognosis of our study participants to previous
literature, it is important to realize we aimed to recruit a
cohort lacking many of the previously reported adverse
prognostic factors and who were receiving recommended
care. As such we hypothesized that patients presenting with
a high educational and socioeconomic status and drawn
from a private paying, community-based, group exercise
program incorporating cognitive behavioral therapy, would
have a more favorable prognosis than widely reported for
chronic LBP. The results of the study support our
hypothesis. The prognosis found in this study may not
generalize well to patients in other settings where these
favorable prognostic factors are not present.
An interesting finding in our study was that disability
and function improved more than pain, especially between
6 and 12 months. These findings are consistent with results
from a previous trial [20] where patients receiving a pro-
gram based on cognitive behavioral principles, similar to
our cohort, improved by 49 % for disability but only 29 %
for pain after 12 months. Similar findings of greater
changes in disability than pain were also reported by a
systematic review of multidisciplinary rehabilitation for
chronic LBP [21]. Conversely a recent systematic review
of the prognosis of persistent LBP [2] found greater
changes in pain than disability over 12 months. The studies
included in this review did not typically include exercise
programs with cognitive behavioral principles and may
explain these differences in findings.
Our study found few important predictors of 12 month
pain or disability. Multivariate models predicted only 10
Table 2 Primary and secondary outcomes
Outcomes Baseline
mean ± SD
3 months
mean ± SD
3 months
percentage of
change
6 months
mean ± SD
6 months
percentage of
change
12 months
mean ± SD
12 months
absolute change
scoresg ± SD
12 months
percentage
of change
Bothersomenessa 5.4 ± 2.5 4.1 ± 2.2* 24 3.4 ± 2.3* 37 3.2 ± 2.4* 2.2 ± 3.2 41
Global
impression of
recoveryb
0.25 ± 2.4 1.5 ± 1.9* – 2.1 ± 1.7* – 2.5 ± 2* – –
Painc 4.4 ± 2.1 3.7 ± 2.1* 16 2.9 ± 2* 35 2.7 ± 2.2* 1.7 ± 2.6 39
Functiond 12.3 ± 5.3 15.5 ± 6.1* 26 18 ± 6* 46 21.1 ± 6* 8.8 ± 9.4 72
Disabilitye 7.8 ± 4.2 5.2 ± 4.2* 34 4.1 ± 4* 48 3.1 ± 3.2* 4.7 ± 4.5 60
Kinesiophobiaf 36 ± 7.5 34.8 ± 7.3 4 32.8 ± 7* 9 31 ± 7* 5 ± 10.7 14
* Significant mean difference between baseline data and 3, 6 or 12 months (p \ 0.05)a Rated on scale from 0 = not at all bothersome to 10 = extremely bothersomeb Rated on scale from -5 = vastly worse, 0 = unchanged to 5 = completely recoveredc Rated on scale from 0 = no pain to 10 = worst pain possibled Sum of the activities scores on a scale from 0 = unable to perform activity to 10 = able to perform activity at pre-injury level, divided by the
number of activitiese Rated from 0 to 24, with higher scores indicating a higher level of disabilityf A total score was calculated after inversion of the individual scores of items 4, 8, 12 and 16. Rated from 17 to 68, with higher scores indicating
a high degree of kinesiophobiag 12 months absolute scores are based on the difference between baseline scores and 12 months follow-up
Fig. 1 Percentage improvement in function, disability, pain intensity
and bothersomeness
Eur Spine J (2014) 23:113–119 117
123
142
and 15 % of pain and disability outcomes, respectively.
These findings are somewhat lower than previous studies
although most previous studies have failed to identify
strong predictors of outcome in chronic LBP. Bekkering
et al. [22] followed a mixed group (acute/chronic LBP) of
500 patients with non-specific LBP for 12 months. This
study evaluated prognostic factors associated with pain and
disability at 12 months follow-up. The final model con-
sisted of two factors for pain (duration of the current epi-
sode and pain intensity at baseline) and three for disability
(paid job, episode duration and disability), these factors
explained 10 and 28 %, respectively, of the variance.
Grotle et al. [5], found five prognostic factors associated
with 12-month disability in people with chronic LBP
(being not employed widespread pain, chronic pain grade,
fear of pain and catastrophizing), representing 52.7 % of
variance. However, they note that beyond baseline
disability the effect size for most predictors is relatively
low. A possible reason predictors in our study failed to
explain much of the variance may be that we deliberately
included a cohort lacking most of the previously described
prognostic factors. In this population, predicting outcome
may be more difficult or other predictors may be more
important.
Conclusions
Over the course of 1 year, patients with chronic LBP who
presented to a private paying, community-based, group
exercise program incorporating cognitive behavioral ther-
apy, improved markedly. During the first 6 months, pain
intensity, bothersomeness, disability and function improved
similarly, but from 6 to 12 months, disability and function
Table 3 Univariate regression analysis with pain intensity and disability at 12 months follow-up as the dependent variable
Prognostic factors Pain intensity Disability
N R2 Unstandardized coefficient
(95 % CI)
p value R2 Unstandardized coefficient
(95 % CI)
p value
Number of previous episodesa 113 0.010 -0.650 (-1.889 to 0.589) 0.589 0.011 -0.016 (-2.798 to 0.766) 0.261
Pain intensityb 113 0.101 0.342 (0.150 to 0.534) 0.001 0.039 0.307 (0.021 to 0.592) 0.035
Duration of current episodec 113 0.006 0.148 (-0.211 to 0.508) 0.416 0.047 0.601 (0.094 to 1.108) 0.021
Disabilityd 113 0.013 0.061 (-0.039 to 0.160) 0.231 0.106 0.249 (0.113 to 0.386) \0.001
Functione 107 0.001 -0.013 (-0.095 to 0.069) 0.753 0.003 -0.035 (-0.154 to 0.083) 0.556
Global impression of recoveryf 113 0.054 -0.218 (-0.390 to -0.046) 0.014 0.007 -0.116 (-0.369 to 0.138) 0.369
Kinesiophobiag 113 0.034 0.055 (0.001 to 0.110) 0.049 0.040 0.085 (0.006 to 0.164) 0.034
Educational Levelh 109 0.006 0.485 (-0.743 to 1.714) 0.435 0.028 1.536 (-0.210 to 3.281) 0.084
Leg Paini 112 0.008 0.500 (-0.551 to 1.550) 0.348 0.006 0.617 (-0.894 to 2.128) 0.420
Catastrophizingj 112 0.044 0.047 (0.006 to 0.089) 0.027 0.031 0.057 (-0.003 to 0.118) 0.063
Patients enrolled for the 2nd termk 113 0.014 0.553 (-0.320 to 1.425) 0.212 0.001 -0.253 (-1.517 to 1.010) 0.692
11 point prognosis scalel 113 0.001 -0.040 (-0.278 to 0.198) 0.739 0.017 0.234 (-0.105 to 0.574) 0.174
a An episode of LBP was classified as pain lasting for more than 24 h. Scored as 0 (from 0 to 1 episode) or 1 (from two or more episodes)b Rated on a scale from 0 = no pain to 10 = worst pain possiblec Duration of the current episode was recorded in days and log transformed for the analysesd Rated from 0 to 24, with higher scores indicating a higher level of disabilitye Sum of the activities scores on a scale from 0 = unable to perform activity to 10 = able to perform activity at pre-injury level divided by the
number of activitiesf Rated on scale from -5 = vastly worse, 0 = unchanged to 5 = completely recoveredg A total score was calculated after inversion of the individual scores of items 4, 8, 12 and 16. Rated from 17 to 78, with higher scores indicating
a high degree of kinesiophobiah Educational level was score from 0 = school and technical college (school, high school certificate and trade) to 1 = University study based
(diploma, advanced diploma, bachelor degree and postgraduate degree)i Defined as back pain extended below the knee. Scored as 0 = no or 1 = yesj The Pain Catastrophizing Scale sum score was calculated from all items (range, 13–65), with a higher scores indicating a higher level of pain
catastrophizingk Patients who continues classes after the first term. Scored as 0 = patients enrolled for one term only or 1 = patients enrolled for two or more
termsl Rated from 0 to 10, with higher values indicating worse prognosis
118 Eur Spine J (2014) 23:113–119
123
143
continued to improve while only small further changes in
bothersomeness and pain intensity occurred.
Pain intensity at baseline was the only independent
predictor of 12-month pain scores, accounting for 10 % of
the variation. There were three independent predictors of
12 months disability; duration of current episode, baseline
disability and educational level, accounting for 15 % of the
variation. Most of the variance in outcome was not
explained by any of the predictors we investigated in this
study.
Acknowledgments We thank all staff at the Willoughby and Sta-
dium Physiocise clinics for their valuable assistance and support of
this study.
Conflict of interest None.
References
1. Airaksinen O, Brox JI, Cedraschi C, Hildebrandt J, Klaber-
Moffett J, Kovacs F, Mannion AF, Reis S, Staal JB, Ursin H,
Zanoli G (2006) European guidelines for the management of
chronic nonspecific low back pain. Eur Spine J 15:192–300
2. LdCM Costa, Maher CG, Hancock MJ, McAuley JH, Hebert RD,
Costa LOP (2012) The prognosis of acute and persistent low-back
pain: a meta-analysis. CMAJ 184(11):E613–E624
3. Burton AK, McClune TD, Clarke RD, Main CJ (2004) Long-term
follow-up of patients with low back pain attending for manipu-
lative care: outcomes and predictors. Man Ther 9(1):30–35
4. de Vet HCW, Heymans MW, Dunn KM, Pope DP, van der Beek
AJ, Macfarlane GJ, Bouter LM, Croft OR (2002) Episodes of low
back pain: a proposal for uniform definitions to be used in
research. Spine 27:2409–2416
5. Grotle M, Foster NE, Dunn KM, Croft P (2010) Are prognostic
indicators for poor outcome different for acute and chronic low
back pain consulters in primary care? Pain 151:790–797
6. Hayden JA, Dunn KM, van der Windt DA, Shaw WS (2010)
What is the prognosis of back pain? Best Pract Res Clin Rheu-
matol 24(2):167–179
7. Hayden JA, Chou R, Hogg-Johnson S, Bombardier C (2009)
Systematic reviews of low back pain prognosis had variable
methods and results: guidance for future prognosis reviews.
J Clin Epidemiol 62:781–796
8. Costa Lda C, Maher CG, McAuley JH, Hancock MJ, Herbert RD,
Refshauge KM, Henschke N (2009) Prognosis for patients with
chronic low back pain: inception cohort study. BMJ 339:b3829
9. Melzack R (2001) Pain and the Neuromatrix in the Brain. J Dent
Educ 65(12):1378–1382
10. Bouvier AL (2008) Physiocise moviment for life: Backs, brains,
breathing. Physiocise, Australia
11. Bouvier AL, Fleming J (2010) The feel good body: 7 steps to
easing aches and looking great. Harper Collins, Australia
12. Pengel LHM, Refshauge KM, Maher CG (2004) Responsiveness
of pain, disability, and physical impairment outcomes in patients
with low back pain. Spine 29(8):879–883
13. Roland M, Morris R (1983) A study of the natural history of back
pain. Part I: development of a reliable and sensitive measure of
disability in low-back pain. Spine 8(2):141–144
14. Scrimshaw SV, Maher CG (2001) Responsiveness of Visual
Analogue and McGill Pain Scale Measures. J Manipulative
Physiol Ther 24(8):501–504
15. Deyo RA, Battie M, Beurskens AJ, Bombardier C, Croft P, Koes
B, Malmivaara A, Roland M, Von Korff M, Waddell G (1998)
Outcome measures for low back pain research. A proposal for
standardized use. Spine 23(18):2003–2012
16. Westaway MD, Stratford PW, Binkley JM (1998) The patient-
specific functional scale: validation of lts use in persons with
neck dysfunction. J Orthop Sports Phys Ther 27(5):331–338
17. Miller RP, Kori S, Todd D (1991) The Tampa Scale: a measure of
kinesiophobia. Clin J Pain 7(1):51–52
18. Harrell FE, Lee KL (1984) Regression modelling strategies for
improved prognostic prediction. Stat Med 3:143–152
19. van Tulder MW, Koes BW, Metsemakers JFM, Bouter LM
(1998) Chronic low back pain in primary care: a prospective
study on the management and course. Fam Pract 15:126–132
20. Lambeek LC, van Mechelen W, Knol DL, Loisel P, Anema JR
(2010) Randomised controlled trial of integrated care to reduce
disability from chronic low back pain in working and private life.
BMJ 340:c1035
21. Guzman J, Esmail R, Karjalainen K, Malmivaara A, Irvin E,
Bombardier C (2001) Multidisciplinary rehabilitation for chronic
low back pain: systematic review. BMJ 322:1511–1516
22. Bekkering GE, Hendriks HJM, van Tulder MW, Knol LD,
Simmonds MJ, Oostendorp RAB, Bouter LM (2005) Prognostic
factors for low back pain in patients referred for physiotherapy:
comparing outcomes and varying modeling techniques. Spine
30:1881–1886
Table 4 Backward regression analyses with pain intensity (n = 112)
and disability (n = 108) at 12 months follow up as dependent
variable
Predictors R2 Regression coefficient
(95 % CI)
Pain intensity at 12 months
(n = 112)
0.102
Pain intensity at baselinea 0.344 (0.050 to 0.534)
Constant 1.244 (0.323 to 2.195)
Disability at 12 months
(n = 109)
0.154
Duration of current episodeb 0.457 (-0.048 to 0.961)
Disabilityc 0.234 (0.095 to 0.372)
Educational leveld 1.408 (-0.260 to 3.075)
Constant -2.505 (-5.825 to 0.815)
a Rated on a scale from 0 = no pain to 10 = worst pain possibleb Duration of the current episode was recorded in days and log
transformed for the analysesc Rated from 0 to 24, with higher scores indicating a higher level of
disabilityd Educational level was scored from 0 = school and technical col-
lege (school, high school certificate and trade) to 1 = University
study based (diploma, advanced diploma, bachelor degree and post-
graduate degree)
Eur Spine J (2014) 23:113–119 119
123
144
Chapter Eight
Do magnetic resonance imaging findings identify patients with low back pain who
respond better to particular interventions? A systematic review
Chapter Eight published as:
Steffens D, Hancock MJ, Pereira LSM, Kent PM, Latimer J, Maher CG. Do magnetic
resonance imaging findings identify patients with low back pain who respond better to
particular interventions? A systematic review. Submitted for publication to European
Journal of Pain on 28th
October 2014.
145
Statement from co-authors confirming authorship contribution of the PhD candidate
As co-authors of the paper “Do magnetic resonance imaging findings identify patients with
low back pain who respond better to particular interventions? A systematic review”, we
confirm that Daniel Steffens has made the following contributions:
Data extraction, analysis and interpretation of the findings
Writing of the manuscript and critical appraisal of the content
Mark J Hancock Date: 01.01.2015
Leani SM Pereira Date: 01.01.2015
Peter M Kent Date: 01.01.2015
Jane Latimer Date: 01.01.2015
Christopher G Maher Date: 01.01.2015
146
Title page
Title: Do magnetic resonance imaging findings identify patients with low back pain who
respond better to particular interventions? A systematic review.
Running head: MRI findings as effect modifiers for specific interventions.
Authors: D. Steffens1,3
, M.J. Hancock2, L.S.M. Pereira
3, P.M. Kent
4,5, J. Latimer
1, C.G.
Maher1
1 Musculoskeletal division, The George Institute for Global Health, Sydney Medical School,
The University of Sydney, Australia.
2 Discipline of Physiotherapy, Faculty of Human Sciences, Macquarie University, Sydney,
Australia.
3 Department of Physiotherapy, Federal University of Minas Gerais, Minas Gerais, Brazil.
4 Department of Sports Science and Clinical Biomechanics, University of Southern Denmark,
Odense, Denmark.
5 Research Department, The Spine Centre of Southern Denmark, Institute of Regional Health
Services Research, University of Southern Denmark, Middelfart, Denmark.
Correspondence: Daniel Steffens, The George Institute for Global Health, Sydney Medical
School, The University of Sydney, P.O. Box M201 Missenden Rd, Sydney, 2050, New South
Wales, Australia, phone 61 2 8238-24 34, fax 61 2 9657-0301, email address
Article category: Review article.
Funding sources: None declared.
Conflict of interest: None declared.
147
Databases:
This systematic review identified relevant studies by electronic searches of MEDLINE,
EMBASE, The Cochrane Central Register of Controlled Trials and by examination of
the reference lists of identified papers.
What does this review add?
The included studies investigated 38 interactions for combinations of different MRI
findings, interventions and outcomes.
Individual trials suggested some MRI findings might be effect modifiers for specific
interventions.
The limited number of suitable studies and the heterogeneity between them did not
permit definitive conclusions about effect modification.
Abstract
Background and Objective: Magnetic resonance imaging (MRI) can reveal a range of
degenerative findings and anatomical abnormalities; however, the clinical importance of
these remains uncertain and controversial. We aimed to investigate if the presence of MRI
findings identifies patients with LBP who respond better to particular interventions.
Databases and data treatment: MEDLINE, EMBASE and CENTRAL databases were
searched. We included RCTs investigating MRI findings as treatment effect modifiers for
patients with LBP or sciatica. We excluded studies with specific diseases as the cause of
LBP. Risk of bias was assessed using the criteria of the Cochrane Back Review Group.
Each MRI finding was examined for its individual capacity for effect modification.
148
Results: Eight published trials met the inclusion criteria. The methodological quality of trials
was inconsistent. Substantial variability in MRI findings, treatments and outcomes across
the eight trials prevented pooling of data. Patients with Modic Changes type 1 when
compared with patients with Modic Changes type 2 had greater improvements in function
when treated by Diprospan (steroid) injection, compared with saline. Patients with central
disc herniation when compared with patients without disc herniation had greater
improvements in pain when treated by surgery, compared with rehabilitation.
Conclusions: Although individual trials suggested some MRI findings might be effect
modifiers for specific interventions, none of these interactions were investigated in more
than a single trial. High quality, adequately powered trials investigating MRI findings as
effect modifiers are essential to determine the clinical importance of MRI findings in LBP
and sciatica (PROSPERO: CRD42013006571).
Systematic Review Registration Number: PROSPERO: CRD42013006571.
1. Introduction
Low back pain (LBP) is an extremely common health problem (Hoy et al., 2010), with an
enormous global burden (Buchbinder et al., 2013). Limited progress has been made in the
management of LBP with most treatments showing little or no effect (Keller et al., 2007; van
Tulder et al., 2006). One explanation for this lack of progress might be the current inability to
identify a specific cause for LBP in most people (van Tulder et al., 2006). As a result, a single
intervention is usually provided to heterogeneous groups of patients with potentially different
causes of their pain. Identifying more homogenous subgroups of LBP patients has been
identified as a key research priority in the field (Costa Lda et al., 2013). Most previous
149
research in this area has focussed on identifying clinical and psychosocial variables
associated with patients who respond better to different interventions (Kent and Kjaer, 2012;
Kent et al., 2010b). However, very little attention has focussed on identifying subgroups
based on biological mechanisms or anatomical structures. Some early work has investigated
subgroups based on different pain mechanisms (Smart et al., 2012; Rabey et al., 2014; Vibe
Fersum et al., 2013) due to increasing evidence for the role of central mechanisms in the
development of chronic LBP (O’Sullivan 2005). Subgrouping based on possible peripheral
patho-anatomical causes of LBP has received little attention and its value is unknown.
The importance of magnetic resonance imaging (MRI) findings such as disc herniation, facet
joint arthropathy and modic changes (bone marrow and endplate lesions visible on MRI) in
identifying the source of an individual patient’s LBP remains unclear and controversial.
Many MRI findings are common in people without LBP, yet these findings are typically
more common in people with LBP than those without (Cheung et al., 2009; Hancock et al.,
2012; Steffens et al., 2013). Research into the importance or otherwise of MRI findings has
been frustrated by the lack of a widely accepted gold standard (Hancock et al., 2012). An
alternative approach in such cases is to investigate if the presence of MRI findings predicts
different response to interventions (Rutjes et al., 2007). If this were the case, it would provide
evidence for the importance of such findings and a logical rationale for selecting specific
interventions for individual patients.
To our knowledge, there has been no review of diverse MRI findings as effect modifiers for
LBP interventions. Therefore, the aim of this systematic review was to investigate if the
presence of MRI findings at baseline identifies patients with LBP who respond better to
particular interventions.
150
2. Methods
The review protocol was specified in advance and registered on PROSPERO: International
prospective register of systematic reviews (refer to this link for full access of the protocol,
http://www.crd.york.ac.uk/PROSPERO/display_record.asp?ID=CRD42013006571). The
PRISMA statement was used to guide the conduct and reporting of the study (Moher et al.,
2009).
2.1 Search strategy
A sensitive search was performed of MEDLINE, EMBASE and The Cochrane Central
Register of Controlled Trials to identify potential studies from the earliest records up to 1st of
December, 2013. We used a search strategy based on the recommendations of the Cochrane
Back Review Group (Furlan et al., 2009) for randomised controlled trials (RCTs) and LBP,
combined with Medical Subject Headings and keywords related to ‘MRI’ and ‘effect
modification/ subgroups’. After piloting the search strategy we decided to use two different
searches and then combine the results.
Search 1 included terms from each of the following domains (i) RCTs, (ii) LBP and (iii)
MRI. Search 2 included terms from each of the following domains (i) RCTs, (ii) LBP and
(iii) effect modification/ subgroup. Searches 1 and 2 were merged to generate the final search
strategy (Refer to Appendix S1 and S2 for the full search strategy). Reference and citation
tracking of relevant articles were performed. A final list of the included studies was sent to
two experts in the field who reviewed the list for possible omissions.
2.2 Study selection
To be included, studies were required to meet all of the following criteria:
151
(i) Participants: Recruited samples of populations with current LBP or sciatica, who were not
diagnosed with serious disease (e.g. cancer, spinal infection, spinal fracture, inflammatory
arthritis or cauda equina syndrome) as the source of LBP.
(ii) Interventions: Investigated any type of intervention for LBP, including conservative,
surgical, or placebo. Included studies needed to have compared any intervention for LBP or
sciatica, with any type of intervention, placebo or no treatment control.
(iii) Outcome: Reported for either pain (e.g. measured by the Visual Analogue Scale,
Numerical Rating Scale) or disability (e.g. measured by the Roland Morris Disability Scale,
Oswestry Disability Scale). In studies that included participants with a primary complaint of
LBP, self-reported LBP was considered the primary outcome while in trials of sciatica self-
reported leg pain was considered the primary outcome.
(iv) Study design: Included studies needed to be an RCT which had used methods capable of
identifying whether patients with a specific MRI finding had a different treatment effect than
those without the MRI finding or with a different MRI finding. Studies were required to have
included and reported a patient’s results separately for either (a) sample with and without a
particular MRI finding (i.e. disc herniation) or (b) people with a different type or severity of
MRI finding (i.e. mild vs. severe disc degeneration).
One reviewer screened titles and abstracts of each citation and excluded clearly irrelevant
studies. For each potentially eligible study the full text was retrieved and two reviewers
independently assessed whether the study fulfilled the inclusion criteria. In cases of
disagreement, a third reviewer was consulted and a decision made by consensus. The search
had no language restrictions.
152
2.3 Data extraction
Relevant data were independently extracted by two reviewers using a standardised form. In
cases of disagreement, a joint review of the original article was performed until consensus
was reached. The extraction form included the following criteria: clinical settings, sample,
age, treatment groups, MRI findings and point estimates and measures of variability for
outcomes. Outcome data were extracted for short-term outcomes (0 to ≤ 6 months) and long-
term outcomes (>6 months). When multiple time points fell within the same category, we
used the one closest to 3 months for short-term and closest to 12 months for long-term.
2.4 Risk of bias
Risk of bias was assessed using criteria recommended by the Cochrane Back Review Group
(Furlan et al., 2009). Two reviewers independently assessed the criteria of all included
studies. In cases of disagreement, a third reviewer was consulted and a decision made by
consensus (refer to Appendix S3 for further details on the criteria list for the methodological
quality assessment). Data pooling was appropriate only if the studies were considered
homogeneous with regard to population sample, MRI measure, clinical outcomes and
treatment.
2.5 Analysis
It eventuated that we were unable to undertake the pre-specified meta-analysis due to the
small number of included trials and the heterogeneity between them in terms of MRI
findings, treatment and clinical outcomes. Therefore, each MRI finding of the lumbar spine
was examined for its individual capacity for effect modification and interaction. The results
are presented descriptively for LBP and sciatica populations.
153
We extracted (i) mean difference and 95% confidence intervals (95% CI) from studies that
reported continuous outcomes, (ii) hazard ratios (HR) and 95% CI from studies that reported
time-to-event categorical outcomes, and (iii) contingency table data to calculate Odds Ratios
(OR) for categorical outcomes. If not reported or provided, the effect modification and
subgroup interaction was calculated using the method suggested by Kent et al (Kent et al.,
2010b) for continuous outcomes and the method suggested by Hancock et al (Hancock et al.,
2013) for categorical outcomes.
Four studies had key information not available from published manuscripts and additional
information was requested (Arts et al., 2010; Pearson et al., 2012; Pearson et al., 2008; Peul
et al., 2009). Two studies reported combined RCT and observational cohort data (Pearson et
al., 2012; Pearson et al., 2008). The separated RCT data for the intention-to-treat analysis was
requested. The effect modification and/or the subgroup interaction were calculated by the
current review authors, for six studies (Buttermann, 2004; Cao et al., 2011; Hellum et al.,
2012; Pearson et al., 2012; Pearson et al., 2008; Tafazal et al., 2009).
In this review, the term subgroup interaction refers to how much more effective (compared
with the control intervention) the intervention is in the subgroup (MRI positive) than for
those not in the subgroup (MRI negative).
3. Results
3.1 Study Selection
The search identified 6239 papers. After review of titles and abstracts, we excluded 6186
(Figure 1). Based on full-text review of 53 papers, we excluded a further 45 and included
eight trials in the review (Arts et al., 2010; Buttermann, 2004; Cao et al., 2011; Hellum et al.,
2012; Pearson et al., 2012; Pearson et al., 2008; Peul et al., 2009; Tafazal et al., 2009). The
154
primary reasons for the exclusion of trials retrieved in full-text are noted in Appendix S4. No
additional studies were identified after contacting two experts in the field of MRI and LBP.
3.2 Risk of bias
The risk of bias assessments for the included studies are shown in Table 1. Randomisation,
drop-out rate, co-interventions and outcome timing were the only criteria scored ‘yes’ in all
trials. Participant blinding, outcome assessor blinding and absence of selective outcome
reporting were the criteria most commonly scored ‘no’.
3.3 Study Characteristics
The characteristics of the included studies are shown in Table 2. Three trials studied patients
with LBP (Buttermann, 2004; Cao et al., 2011; Hellum et al., 2012) and five studied patients
with sciatica (Arts et al., 2010; Pearson et al., 2012; Pearson et al., 2008; Peul et al., 2009;
Tafazal et al., 2009). The samples were recruited from secondary health care (Arts et al.,
2010; Buttermann, 2004; Pearson et al., 2012; Pearson et al., 2008; Tafazal et al., 2009), and
tertiary health care (Cao et al., 2011; Hellum et al., 2012; Peul et al., 2009) settings. The
number of participants varied from 120 to 472 and most studies sampled predominantly
adults in their middle age. The treatments evaluated in the trials included surgery, injections
and rehabilitation. No study had the primary aim of investigating MRI effect modifiers. LBP
duration was categorised as acute (less than 6 weeks), sub-acute (6-12 weeks) and chronic
(greater than 12 weeks) (Furlan et al., 2009).
3.4 Results of the review
Due to the heterogeneity of samples, MRI findings, clinical outcomes and treatment, it was
not possible to perform meta-analysis of the results for any of the included studies. For ease
of interpretation, the studies were grouped into LBP population (Buttermann, 2004; Cao et
155
al., 2011; Hellum et al., 2012) or sciatica population (Arts et al., 2010; Pearson et al., 2012;
Pearson et al., 2008; Peul et al., 2009; Tafazal et al., 2009) as the importance of MRI findings
might be quite different in these two populations. Detailed findings of all included studies are
presented in Table 3.
3.4.1 Low back pain population samples
One study reported on a population with sub-acute LBP (symptoms ≥ 6 weeks) (Cao et al.,
2011) and two reported on populations with chronic LBP (symptoms ≥ 1 year) (Buttermann,
2004; Hellum et al., 2012). All three studies investigated Modic changes (Modic changes type
1 corresponding to vertebral body edema and hyper-vascularity; Modic changes type 2
reflecting fatty replacements of the red bone marrow; and Modic changes type 3 consisting of
subchondral bone sclerosis (Modic et al., 1988a; Modic et al., 1988b)) as effect modifiers
(Buttermann, 2004; Cao et al., 2011; Hellum et al., 2012), while one study investigated disc
herniation and facet joint arthritis (Hellum et al., 2012).
Cao et al (Cao et al., 2011) investigated various intradiscal injection regimens for patients
with Modic changes (n=120). Patients with Modic changes type 1, when compared with
patients with Modic changes type 2, had greater improvements in disability in the short-term
(3 months) when treated by Diprospan (steroid) injection, compared with saline (mean
difference 8.30; 95% CI, 1.01 to 15.59, on a 0 to 100 disability scale). Other subgroup
interactions for pain and disability with Modic changes were not significant.
Hellum et al (Hellum et al., 2012) investigated whether features of degenerative disc were
effect modifiers for disc prosthesis compared with multidisciplinary rehabilitation at two-year
follow up (n=154). The presence of Modic changes type 1 and/or 2 was not a significant
effect modifier for improvements in disability (percentage of patients improved ≥15 points on
a 0 to 100 scale, categorized by yes/no), OR ranging from 0.63 (95% CI, 0.15 to 2.65) to 2.96
156
(95% CI, 0.65 to 13.52). Similarly, disc herniation, facet joint arthropathy and high intensity
zone were not significant effect modifiers for improvement in disability when treated with
surgery, compared with rehabilitation (Hellum et al., 2012).
Buttermann (Buttermann, 2004) investigated whether Modic changes type 1 was an effect
modifier for spinal injection and steroid, compared with discography alone at 1-3 and 12-24
months (n=171). Presence of Modic changes type 1 was not a significant effect modifier for
injection success (coded as ‘yes’ if the overall opinion about their injection was considered
successful) at short (OR, 7.94; 95% CI, 0.40 to 156.46) or long-term follow up (OR, 2.20;
95% CI, 0.11 to 45.98).
3.4.2 Sciatica population samples
Three studies reported potential MRI effect modifiers in one population sample with sub-
acute sciatica (symptoms ≥6 weeks) (Arts et al., 2010; Peul et al., 2009; Tafazal et al., 2009)
and two with chronic sciatica (symptom ≥12 weeks) (Pearson et al., 2012; Pearson et al.,
2008). Three studies investigated disc herniation (Arts et al., 2010; Pearson et al., 2008; Peul
et al., 2009), two investigated spinal stenosis (Arts et al., 2010; Pearson et al., 2012), one
investigated disc height (Arts et al., 2010) and one investigated different types of MRI
findings (disc prolapse vs. spinal stenosis) (Tafazal et al., 2009) as effect modifiers.
Pearson et al (Pearson et al., 2008) studied whether features of disc herniation were effect
modifiers for discectomy, compared with conservative rehabilitation at three and 12 months
follow up (n=472). Patients with central disc herniation, when compared with patients
without central disc herniation, had better response to surgery at long-term follow up (24
months), mean difference 1.60; 95% CI, 0.17 to 3.03 (0 to 6 point Likert scale). In patients
with central herniation, one-year pain outcomes were better (mean difference 1.60; 95% CI,
0.10 to 3.10; 0 to 6 point Likert scale) for those receiving surgery compared with
157
rehabilitation. In those without central herniation, surgery was no better than rehabilitation
(mean difference 0.00; 95% CI, -0.40 to 0.40; 0 to 6 point Likert scale). Other disc herniation
characteristics (e.g. posterolateral and protrusion) were not associated with significant
treatment interactions.
Peul et al (Peul et al., 2009) investigated if disc herniation was an effect modifier for
response to early surgery compared with prolonged conservative care (n=283). Sequestrated
disc herniation (Hazard ratio, 0.94; 95% CI, 0.56 to 1.57) and disc herniation enhancement
(Hazard ratio, 0.85; 95% CI, 0.47 to 1.54) did not have any significant interaction with
treatment at 12 months (very much improved and much improved were coded as recovered).
Arts et al (Arts et al., 2010) investigated if disc herniation, spinal stenosis and disc height
were effect modifiers for response to tubular discectomy, compared with conventional
microdiscectomy, at one-year follow up (n=325). None of the MRI findings produced
significant interactions with treatment for long-term recovery outcomes.
Pearson et al (Pearson et al., 2012) investigated whether features of spinal stenosis were
effect modifiers for response to surgery, compared with rehabilitation, in 278 patients at three
and 24 months follow up. Spinal stenosis did not produce any significant interactions with
treatment for short- and long-term disability outcomes.
Tafazal et al (Tafazal et al., 2009) investigated whether features of disc herniation (disc
prolapse) or lumbar spinal stenosis were effect modifiers for the efficacy of corticosteroids
injection in 150 patients. Neither MRI features produced significant interactions with
bupivacaine (a local anaesthetic) and steroid or bupivacaine alone at short-term follow up.
158
4. Discussion
4.1 Statement of principal findings
This review could only identify eight studies, which provided adequate data to assess if MRI
findings were treatment effect modifiers. The included studies investigated 38 interactions for
combinations of different MRI findings, interventions and outcomes. No effect modifiers
were consistently identified across more than one study. Individual trials suggested some
MRI findings might be effect modifiers for specific interventions. However, these are single
study results and caution should be taken when interpreting the findings. Some other
subgroup interactions presented trends and confidence intervals that included potentially
important interactions; however, these trials were underpowered due to their small sample
sizes.
4.2 Strengths and weaknesses of the study
We believe this is the first systematic review of RCTs to investigate if diverse MRI findings
are effect modifiers for interventions in people with LBP and/or sciatica. The strength of this
review is the use of a pre-specified protocol and the comprehensive approach to identifying
all suitable RCTs. We also provide data for all included trials on the interaction effect as well
as the subgroup effects for those with and without the MRI finding of interest. We used a
sensitive search strategy and contacted experts in the field, reducing the risk of missing any
important trial. Despite this, we could have missed important studies because of human error
or because they were contained in databases that were not searched. A limitation of our
review is that the inconsistency of MRI findings, interventions and outcomes investigated
across the studies, inhibited our ability to perform meta-analysis. Furthermore, most trials
were not powered for subgroup interaction analysis, as it was not the primary aim of the
study. As a result, some non-significant findings may include a potentially important
159
interaction (e.g. OR, 7.94; 95% CI, 0.40 to 156.46) (Buttermann, 2004). Another limitation of
our review is the possibility of publication bias as, beyond contacting two content experts, we
did not attempt to identify unpublished trials that might have been found in other clinical
trials registries and in conference proceedings.
4.3 Comparison with other studies
Three previous reviews have investigated effect modifiers for LBP treatments. Two of these
reviews investigated effect modifiers for specific interventions (manual therapy/exercise and
psychosocial intervention) (Kent and Kjaer, 2012; Kent et al., 2010b). These reviews did not
include MRI findings as potential effect modifiers. One review specifically investigated
Modic changes as effect modifiers (Jensen and Leboeuf-Yde, 2011). Interestingly, all reviews
found a limited number of suitable studies, which had inconsistent findings, had small sample
sizes, and provided limited evidence for strong effect modifiers. These results corroborate our
findings. The review investigating Modic changes as an effect modifier for different LBP
treatments had several method limitations (Jensen and Leboeuf-Yde, 2011); for example, the
inclusion of single subgroup designs ( i.e. studies including all people with Modic changes
and no people without Modic changes) as these types of studies cannot robustly test if effect
modification occurred (Kent et al., 2010a).
4.4 Meaning of the study
From 38 subgroup interactions investigated, one presented a significant effect modifier for
LBP and one for sciatica populations. These positive findings could represent spurious
findings. However, the lack of statistically significant interactions may also be partly due to
most studies being underpowered for this type of analysis. Consequently, it remains unclear
whether MRI findings are important effect modifiers for interventions for LBP and sciatica
populations. What is clear is that there are very few trials and most of these are
160
underpowered, reinforcing the need for more and larger trials in this potentially important and
evolving area.
4.5 Recommendations for future research
Studies on subgroup interaction are a research priority in LBP (Costa Lda et al., 2013) and
well conducted trials provide the possibility to answer the important and controversial
question about the importance or otherwise of MRI findings. The need for larger, high-
quality trials is evident. Due to the nature of subgroup and interaction analyses, such trials
need a larger sample size than if their only interest was the main effect of treatment. Perhaps
one way to gain statistical power would be to combine several sets of individual patient data,
to acquire an adequate number of individuals with and/or without an MRI finding of interest.
Furthermore, future trials should adopt comprehensive and standardised methods for
measuring pain (i.e. pain rating scale).
A key finding from our review was that only trials including surgery or injections had
investigated MRI findings as effect modifiers for LBP interventions. We could find no
evidence for the importance or otherwise of MRI findings for conservative interventions.
While we recommend the need for larger, high-quality trials, it is important to note that
limited evidence exists for the use of surgery in most patients with LBP (Chou et al., 2009).
Therefore future trials investigating the importance of pathoanatomic findings in improving
outcomes from surgery should be limited to patient groups with indications for surgery, such
as those with sciatica or degenerative spondylolisthesis. The role of central pain processing is
known to be important in many people with chronic LBP (O’Sullivan 2005) and where this
predominates rather than peripheral nociceptive mechanisms it is unlikely that surgical
interventions will be effective regardless of pathoanatomic changes identified on MRI.
161
5. Conclusions
This review identified eight studies that investigated if MRI findings identify patients with
LBP and/ or sciatica who respond better to a variety of interventions. While two statistically
significant interactions were found between specific MRI findings and response to treatment,
the limited number of suitable studies and the heterogeneity between them did not permit
definitive conclusions about effect modification. Further well-designed, adequately powered
studies are required.
Acknowledgements
We thank Professor Michele Crites-Battie and Professor Jeffrey G. Jarvik for reviewing
included studies and suggesting possible additional studies. We also thank authors from the
included studies for providing additional information.
Author’s contributions
D.S., M.J.H. and C.G.M. contributed to the conception and design. All authors participated in
data acquisition, analysis and interpretation. D.S. drafted the article and all authors revised it
critically and gave the final approval of the version to be published.
162
References
Arts, M.P., Brand, R., Koes, B.W., and Peul, W.C. (2010). Effect modifiers of outcome of
surgery in patients with herniated disc related sciatica? A subgroup analysis of a
randomised clinical trial. J Neurol Neurosurg Psychiatry 81, 1265-1274.
Buchbinder, R., Blyth, F.M., March, L.M., Brooks, P., Woolf, A.D., and Hoy, D.G. (2013).
Placing the global burden of low back pain in context. Best Pract Res Clin Rheumatol 27,
575-589.
Buttermann, G.R. (2004). The effect of spinal steroid injections for degenerative disc disease.
Spine J 4, 495-505.
Cao, P., Jiang, L., Zhuang, C., Yang, Y., Zhang, Z., Chen, W., and Zheng, T. (2011).
Intradiscal injection therapy for degenerative chronic discogenic low back pain with end
plate Modic changes. Spine J 11, 100-106.
Cheung, K.M., Karppinen, J., Chan, D., Ho, D.W., Song, Y.Q., Sham, P., Cheah, K.S.,
Leong, J.C., and Luk, K.D. (2009). Prevalence and pattern of lumbar magnetic resonance
imaging changes in a population study of one thousand forty-three individuals. Spine
(Phila Pa 1976) 34, 934-940.
Chou R., Baisden J., Carragee E.J., Resnick D.K., Shaffer W.O., Loeser J.D. (2009). Surgery
for low back pain: a review of the evidence for an American Pain Society Clinical Practice
Guideline. Spine (Phila Pa 1976) 34, 1094-1109.
Costa Lda, C., Koes, B.W., Pransky, G., Borkan, J., Maher, C.G., and Smeets, R.J. (2013).
Primary care research priorities in low back pain: an update. Spine (Phila Pa 1976) 38,
148-156.
Furlan, A.D., Pennick, V., Bombardier, C., and van Tulder, M. (2009). 2009 updated method
guidelines for systematic reviews in the Cochrane Back Review Group. Spine (Phila Pa
1976) 34, 1929-1941.
163
Hancock, M., Maher, C., Macaskill, P., Latimer, J., Kos, W., and Pik, J. (2012). MRI findings
are more common in selected patients with acute low back pain than controls? Eur Spine J
21, 240-246.
Hancock, M.J., Kjaer, P., Korsholm, L., and Kent, P. (2013). Interpretation of subgroup
effects in published trials. Phys Ther 93, 852-859.
Hellum, C., Johnsen, L.G., Gjertsen, O., Berg, L., Neckelmann, G., Grundnes, O., Rossvoll,
I., Skouen, J.S., Brox, J.I., and Storheim, K. (2012). Predictors of outcome after surgery
with disc prosthesis and rehabilitation in patients with chronic low back pain and
degenerative disc: 2-year follow-up. Eur Spine J 21, 681-690.
Hoy, D., Brooks, P., Blyth, F., and Buchbinder, R. (2010). The Epidemiology of low back
pain. Best Pract Res Clin Rheumatol 24, 769-781.
Jensen, R.K., and Leboeuf-Yde, C. (2011). Is the presence of modic changes associated with
the outcomes of different treatments? A systematic critical review. BMC Musculoskelet
Disord 12, 183.
Keller, A., Hayden, J., Bombardier, C., and van Tulder, M. (2007). Effect sizes of non-
surgical treatments of non-specific low-back pain. Eur Spine J 16, 1776-1788.
Kent, P., Hancock, M., Petersen, D.H., and Mjosund, H.L. (2010a). Clinimetrics corner:
choosing appropriate study designs for particular questions about treatment subgroups. J
Man Manip Ther 18, 147-152.
Kent, P., and Kjaer, P. (2012). The efficacy of targeted interventions for modifiable
psychosocial risk factors of persistent nonspecific low back pain - a systematic review.
Man Ther 17, 385-401.
Kent, P., Mjosund, H.L., and Petersen, D.H. (2010b). Does targeting manual therapy and/or
exercise improve patient outcomes in nonspecific low back pain? A systematic review.
BMC Med 8, 22.
164
Modic M.T., Masaryk T.J., Ross J.S., Carter J.R. (1988a). Imaging of degenerative disk
disease. Radiol 168, 177–186.
Modic M.T., Steinberg P.M., Ross J.S., Masaryk T.J., Carter J.R. (1988b). Degenerative disk
disease: assessment of changes in vertebral body marrow with MR imaging. Radiol 166,
193–199.
Moher, D., Liberati, A., Tetzlaff, J., and Altman, D.G. (2009). Preferred reporting items for
systematic reviews and meta-analyses: the PRISMA statement. Ann Intern Med 151, 264-
269, W264.
O'Sullivan P. (2005). Diagnosis and classification of chronic low back pain disorders:
maladaptive movement and motor control impairments as underlying mechanism. Man
Ther 10, 242-255.
Pearson, A., Lurie, J., Tosteson, T., Zhao, W., Abdu, W., and Weinstein, J.N. (2012). Who
should have surgery for spinal stenosis? Treatment effect predictors in SPORT. Spine
(Phila Pa 1976) 37, 1791-1802.
Pearson, A.M., Blood, E.A., Frymoyer, J.W., Herkowitz, H., Abdu, W.A., Woodward, R.,
Longley, M., Emery, S.E., Lurie, J.D., Tosteson, T.D., and Weinstein, J.N. (2008). SPORT
lumbar intervertebral disk herniation and back pain: does treatment, location, or
morphology matter? Spine (Phila Pa 1976) 33, 428-435.
Peul, W.C., Arts, M.P., Brand, R., and Koes, B.W. (2009). Timing of surgery for sciatica:
subgroup analysis alongside a randomized trial. Eur Spine J 18, 538-545.
Rabey M., Beales D., Slater H., O'Sullivan P. (2014). Multidimensional pain profiles in four
cases of chronic non-specific axial low back pain: An examination of the limitations of
contemporary classification systems. Man Ther 14, S1356-689x.
165
Rutjes, A.W., Reitsma, J.B., Coomarasamy, A., Khan, K.S., and Bossuyt, P.M. (2007).
Evaluation of diagnostic tests when there is no gold standard. A review of methods. Health
Technol Assess 11, iii, ix-51.
Smart K.M., Blake C., Staines A., Thacker M., Doody C. (2012). Mechanisms-based
classifications of musculoskeletal pain: part 1 of 3: symptoms and signs of central
sensitisation in patients with low back (± leg) pain. Man Ther 17, 336-344.
Steffens, D., Hancock, M.J., Maher, C.G., Williams, C., Jensen, T.S., and Latimer, J. (2013).
Does magnetic resonance imaging predict future low back pain? A systematic review. Eur
J Pain.
Tafazal, S., Ng, L., Chaudhary, N., and Sell, P. (2009). Corticosteroids in peri-radicular
infiltration for radicular pain: a randomised double blind controlled trial. One year results
and subgroup analysis. Eur Spine J 18, 1220-1225.
van Tulder, M.W., Koes, B., and Malmivaara, A. (2006). Outcome of non-invasive treatment
modalities on back pain: an evidence-based review. Eur Spine J 15 Suppl 1, S64-81.
Vibe Fersum K., O'Sullivan P., Skouen J.S., Smith A., Kvåle A. (2013). Efficacy of
classification-based cognitive functional therapy in patients with non-specific chronic low
back pain: a randomized controlled trial. Eur J Pain 17, 916-928.
166
Figure and Tables’ legends
Figure 1. Flow chart diagram of review process.
Table 1. Assessment of risk of bias of the included studies.
Table 2. Individual characteristics of the included studies.
Table 3. Subgroup treatment effect and interaction for low back pain and sciatica population.
Appendix S1. Search strategy 1 (MEDLINE, EMBASE AND CENTRAL).
Appendix S2. Search strategy 2 (MEDLINE, EMBASE AND CENTRAL).
Appendix S3. Criteria list for the risk of bias assessment.
Appendix S4. List of excluded full-text articles and the primary reason for exclusion.
167
Records identified through database searching
MEDLINE = 2118 EMBASE = 5228
Cochrane Central = 438
Full-text articles assessed for eligibility (n=53)
RCTs included in review (n=8)
Full-text articles excluded
- Not an RCT (n=10) - No evaluation of MRI
findings (n=9) - Not possible to
elucidate association between MRI and outcome (n=26)
Ide
nti
fica
tio
n
Scre
en
ing
Incl
ud
ed
Additional records identified
through other sources (n=1)
Figure 1. Flow diagram of review process
Records excluded (n=6186)
Elig
ibili
ty
Records after duplicates removed (n=6239)
168
Ta
ble
1.
Ris
k o
f b
ias
of
the
incl
ud
ed s
tud
iesa
M
etho
d c
rite
riab
Stu
dy
R
an
do
mis
ati
on
C
on
cea
led
all
oca
tio
n
Pa
rtic
ipa
n
t b
lin
din
g
Cli
nic
ian
s
bli
nd
ing
Ou
tco
me
ass
esso
r
bli
nd
ing
Acc
epta
ble
dro
p-o
ut
rate
An
aly
sed
acc
ord
ing
to
trea
tmen
t
all
oca
tio
n
Fre
e o
f
sele
cti
ve
ou
tco
mes
Ba
seli
ne
sim
ila
rit
y
Co
-in
terv
enti
on
s C
om
pli
an
ce
Ou
tco
me
tim
ing
Art
s et
al.
20
10
Y
es
Yes
Y
es
Yes
Y
es
Yes
Y
es
Yes
Y
es
Yes
N
A
Yes
Butt
erm
ann 2
00
4
Yes
Y
es
No
N
o
No
Y
es
Yes
N
o
Yes
Y
es
NA
Y
es
Cao
et
al.
20
11
Y
es
? Y
es
Yes
Y
es
Yes
Y
es
No
Y
es
Yes
N
A
Yes
Hel
lum
et
al.
20
12
Y
es
Yes
N
o
Yes
N
o
Yes
Y
es
No
Y
es
Yes
Y
es
Yes
Pea
rso
n e
t al
. 2
01
2
Yes
Y
es
No
N
o
No
Y
es
yes
N
o
No
Y
es
Yes
Y
es
Pea
rso
n e
t al
. 2
00
8
Yes
Y
es
No
N
o
No
Y
es
yes
N
o
Yes
Y
es
Yes
Y
es
Peu
l et
al.
20
09
Yes
Y
es
No
N
o
No
Y
es
? Y
es
Yes
Y
es
Yes
Y
es
Taf
azal
et
al.
200
9
Yes
Y
es
Yes
Y
es
Yes
Y
es
Yes
N
o
Yes
Y
es
NA
Y
es
a E
ach c
rite
rio
n w
as
sco
red
as
yes
, u
ncl
ear
(?),
no
t ap
pli
cab
le (
NA
) o
r no
, w
her
e yes
ind
icat
es t
he
crit
erio
n h
as b
een m
et.
b Q
ual
ity o
f in
clud
ed s
tud
ies
bas
ed o
n t
he
Co
chra
ne
Bac
k R
evie
w G
roup
meth
od
(F
url
an e
t al
. 2
009
).
169
Ta
ble
2.
Ind
ivid
ual
stu
dy c
har
acte
rist
ics
Stu
dy
C
lin
ica
l se
ttin
g
Sa
mp
le
Ag
e, m
ean
(S
D)
Ou
tco
mes
(th
resh
old
) T
rea
tmen
t g
rou
ps
Fo
llo
w-u
p,
du
rati
on
(%
)a
Art
s et
al.
20
10
Sec
ond
ary c
are
(neu
rosu
rgic
al
outp
atie
nt
clin
ic).
32
5 p
atie
nts
wit
h
sub
-acu
te s
ciat
ica
(>6
to
8 w
eek
s).
41
.45 (
10
.75)
- R
eco
ver
y (
„co
mp
lete
rec
over
y‟
and
„alm
ost
co
mp
lete
rec
over
y w
ere
co
ded
as r
eco
ver
ed).
1)
Surg
ery:
con
venti
onal
mic
ro-
dis
cect
om
y;
2)
Surg
ery:
Tub
ula
r d
isce
cto
my.
12
mo
nth
s
(10
0%
)
Butt
erm
ann
et a
l. 2
004
Sec
ond
ary c
are
(sp
ine
inst
itu
te).
17
1 p
atie
nts
wit
h
chro
nic
LB
P (
>1
yea
r).
42
.83 (
8.6
6)
- S
ucc
ess
(was
cod
ed „
yes
‟ o
r „n
o‟
bas
ed o
n o
ver
all
op
inio
n a
s to
wh
ether
pat
ients
tho
ug
ht
their
inje
ctio
n w
as
succ
ess
ful
in t
he
trea
tmen
t o
f th
eir
sym
pto
ms)
.
1)
Inje
ctio
n:
dis
cogra
ph
y a
nd
ste
roid
;
2)
Inje
ctio
n:
dis
cogra
ph
y o
nly
.
1-3
(1
00
%)
and
12
-24
mo
nth
s
(10
0%
)
Cao
et
al.
20
11
Ter
tiar
y c
are
(ho
spit
al).
12
0 p
atie
nts
wit
h
sub
-acu
te L
BP
(≥
6
wee
ks)
.
42
.30 (
8.7
2)
- P
ain (
VA
S,
ran
ges
fro
m 0
to
10
, w
ith
0 c
orr
espo
nd
ing t
o n
o p
ain);
- D
isab
ilit
y (
OD
I ra
nges
fro
m 0
% t
o
10
0%
, w
ith 0
% c
orr
esp
ond
ing
to
no
dis
abil
ity).
1)
Inje
ctio
n:
3m
L D
ipro
span
;
2)
Inje
ctio
n:
1m
L D
ipro
span
and
2m
L
So
ng
mei
le;
3)
Inje
ctio
n:
3m
L n
orm
al s
alin
e.
3 m
onth
s (1
00
%)
Hel
lum
et
al.
20
12
Ter
tiar
y c
are
(fiv
e
No
rweg
ian u
niv
ersi
ty
ho
spit
als)
.
15
4 p
atie
nts
wit
h
chro
nic
LB
P (
≥1
yea
r).
41
.20 (
7.0
0)
- D
isab
ilit
y (
OD
I, r
anges
fro
m 0
% t
o
10
0%
, w
ith 0
% c
orr
esp
ond
ing
to
no
dis
abil
ity.
Per
centa
ge
of
pat
ients
imp
roved
≥1
5 O
DI
po
ints
cat
ego
rize
d
by y
es/n
o).
1)
Surg
ery:
rep
lace
ment
of
the
deg
ener
ativ
e lu
mb
ar d
isc
wit
h a
n a
rtif
icia
l
lum
bar
dis
c;
2)
Reh
abil
itat
ion
: m
ult
idis
cip
linar
y
trea
tment
consi
sted
of
a co
gnit
ive
app
roac
h a
nd
sup
ervis
ed p
hysi
cal
acti
vit
y.
24
mo
nth
s
(10
0%
)
Pea
rso
n e
t
al.
20
12
Sec
ond
ary c
are
(11
mu
ltid
isci
pli
nar
y s
pin
e
pra
ctic
es).
27
8 p
atie
nts
wit
h
chro
nic
sci
atic
a
(≥1
2 w
eeks)
.
? (
?)
- D
isab
ilit
y (
OD
I, r
anges
fro
m 0
% t
o
10
0%
, w
ith 0
% c
orr
esp
ond
ing
to
no
dis
abil
ity).
1)
Surg
ery:
stan
dar
d o
pen
dec
om
pre
ssiv
e
lam
inec
tom
y;
2)
Reh
abil
itat
ion
: u
sual
car
e –
at
leas
t
ph
ysi
cal
ther
apy,
educa
tio
n a
nd
counse
llin
g w
ith h
om
e exer
cise
s, a
nd
no
n-
ster
oid
al a
nti
-in
flam
mat
ory
dru
gs.
3 (
88.4
9%
) an
d
12
mo
nth
s
(87
.41
%)
Pea
rso
n e
t
al.
20
08
Sec
ond
ary c
are
(11
mu
ltid
isci
pli
nar
y s
pin
e
pra
ctic
es).
47
2 p
atie
nts
wit
h
chro
nic
sci
atic
a
(≥1
2 w
eeks)
.
? (
?)
- P
ain (
Pai
n b
oth
erso
menes
s, r
anges
fro
m 0
to
6,
wit
h 0
co
rres
po
ndin
g t
o
no
t b
oth
erso
me)
.
1)
Surg
ery:
stan
dar
d o
pen
dis
cect
om
y w
ith
exam
inat
ion a
nd
dec
om
pre
ssio
n o
f ner
ve
roo
t;
2)
Reh
abil
itat
ion
: u
sual
car
e –
at
leas
t
ph
ysi
cal
ther
apy,
educa
tio
n a
nd
counse
llin
g w
ith h
om
e exer
cise
s, a
nd
no
n-
ster
oid
al a
nti
-in
flam
mat
ory
dru
gs.
3 (
86.0
2%
) an
d
12
mo
nth
s
(87
.5%
)
Peu
l et
al.
20
09
Ter
tiar
y c
are
(9
ho
spit
als)
.
28
3 p
atie
nts
wit
h
sub
-acu
te s
ciat
ica
(>6
to
8 w
eek
s).
42
.55 (
9.3
0)
- R
eco
ver
y (
„ver
y m
uch
im
pro
ved
‟ and
„much i
mp
roved
‟ w
ere
cod
ed a
s
reco
ver
ed).
1)
Surg
ery:
dis
cect
om
y;
2)
Reh
abil
itat
ion
: E
duca
tio
n,
pai
n
med
icat
ion,
ph
ysi
oth
erap
y i
f n
eces
sary
.
12
mo
nth
s
(10
0%
)
170
Taf
azal
et
al.
20
09
Sec
ond
ary c
are
(sp
ecia
list
sp
ine
clin
ic).
15
0 p
atie
nts
wit
h
sub
-acu
te s
ciat
ica
(≥6
wee
ks)
.
51
.90 (
?)
- P
ain (
VA
S,
ran
ges
fro
m 0
to
10
0,
wit
h 0
co
rres
po
nd
ing t
o n
o p
ain);
- D
isab
ilit
y (
OD
I, r
anges
fro
m 0
% t
o
10
0%
, w
ith 0
% c
orr
esp
ond
ing
to
no
dis
abil
ity).
1)
Inje
ctio
n:
2m
L o
f 0
.25
% b
up
ivac
aine
and
40
mg o
f m
eth
ylp
red
nis
olo
ne
(Dep
om
edro
ne)
;
2)
Inje
ctio
n:
2m
L o
f 0
.25
% b
up
ivac
aine
alo
ne.
3 m
onth
s
(82
.66
%)
?=
dat
a no
t av
aila
ble
; V
AS
=V
isual
anal
og
ue
scal
e;
OD
I=O
swest
ry d
isab
ilit
y i
nd
ex;
a Per
centa
ge
bas
ed o
n t
he
sam
ple
avai
lab
le f
or
the
sub
gro
up
inte
ract
ion.
171
Ta
ble
3.
Sub
gro
up
tre
atm
ent
effe
ct
and
in
tera
ctio
n f
or
low
bac
k p
ain a
nd
sci
atic
a p
op
ula
tio
n
MR
I fe
atu
re
MR
I th
resh
old
Stu
dy
Tre
atm
en
t
Tre
atm
en
t ef
fect
for
MR
I +
Tre
atm
en
t ef
fect
for
MR
I -
Cli
nic
al
ou
tco
me
(tim
e),
thre
sho
ld
Su
bg
rou
p
Inte
ract
ion
, m
ean
dif
feren
ce (
95
%
CI)
, u
nle
ss
oth
erw
ise
ind
ica
ted
Po
siti
ve
(+)
Neg
ati
ve
(-)
Tre
atm
en
t 1
T
rea
tmen
t 2
Lo
w b
ack
pa
in p
op
ula
tio
ns
Mo
dic
typ
e
Typ
e 1
T
yp
e 2
C
ao e
t al
. 2
01
1
Dip
rosp
an
Sal
ine
5.2
0 (
4.4
4 t
o 5
.96)
5.2
0 (
4.6
0 t
o 5
.80)
Pai
n (
ST
), 0
to
10
0.0
0 (
-0.9
8 t
o 0
.98
)
Mo
dic
typ
e
Typ
e 1
T
yp
e 2
C
ao e
t al
. 2
01
1
Dip
rosp
an +
song
mei
le
Sal
ine
5.0
0 (
4.2
9 t
o 5
.71)
5.2
0 (
4.6
0 t
o 5
.80)
Pai
n (
ST
), 0
to
10
-0.2
0 (
-0.7
4 t
o 1
.14
)
Mo
dic
typ
e
Typ
e 1
T
yp
e 2
C
ao e
t al
. 2
01
1
Dip
rosp
an+
song
mei
le
Dip
rosp
an
0.2
0 (
-0.4
0 t
o 0
.80
) 0
.00
(-0
.54
to
0.5
4)
Pai
n (
ST
), 0
to
10
0.2
0 (
-0.6
2 t
o 1
.02
)
Mo
dic
typ
e
Typ
e 1
T
yp
e 2
C
ao e
t al
. 2
01
1
Dip
rosp
an
Sal
ine
28
.90 (
22
.52 t
o
35
.28)
20
.60 (
15
.69 t
o
25
.51)
Dis
abil
ity
(ST
), 0
to
10
0
8.3
0 (
1.0
1 t
o 1
5.5
9)a
Mo
dic
typ
e
Typ
e 1
T
yp
e 2
C
ao e
t al
. 2
01
1
Dip
rosp
an +
song
mei
le
Sal
ine
28
.40 (
21
.95 t
o
34
.85)
20
.20 (
15
.17 t
o
25
.23)
Dis
abil
ity
(ST
), 0
to
10
0
8.2
0 (
-0.1
1 t
o 1
6.5
1)
Mo
dic
typ
e
Typ
e 1
T
yp
e 2
C
ao e
t al
. 2
01
1
Dip
rosp
an +
song
mei
le
Dip
rosp
an
0.5
0 (
-1.2
1 t
o 2
.21
) 0
.40
(-1
.35
to
2.1
5)
Dis
abil
ity
(ST
), 0
to
10
0
0.1
0 (
-2.3
9 t
o 2
.59
)
Mo
dic
typ
e 1
P
rese
nt
Ab
sent
Hel
lum
et
al.
20
12
Surg
ery
R
ehab
ilit
atio
n
6.0
7 (
1.6
6 t
o 2
2.1
2)b
2
.05
(0
.92
to
4.5
5)b
D
isab
ilit
y
(LT
), 0
to
10
0,
≥1
5po
ints
2.9
6 (
0.6
5 t
o 1
3.5
2)b
Mo
dic
typ
e 1
and
2
Pre
sent
A
bse
nt
Hel
lum
et
al.
20
12
Surg
ery
R
ehab
ilit
atio
n
3.2
1 (
0.6
6 t
o 1
5.5
9)b
2
.94
(1
.40
to
6.1
6)b
D
isab
ilit
y
(LT
), O
DI
0 t
o
10
0, ≥
15p
oin
ts
1.1
0 (
0.1
9 t
o 6
.27)b
Mo
dic
typ
e 2
P
rese
nt
A
bse
nt
Hel
lum
et
al.
20
12
Surg
ery
R
ehab
ilit
atio
n
2.1
6 (
0.6
7 t
o 6
.93)b
3
.43
(1
.48
to
7.9
3)b
D
isab
ilit
y
(LT
), 0
to
10
0,
≥1
5po
ints
0.6
3 (
0.1
5 t
o 2
.65)b
Mo
dic
typ
e 1
P
rese
nt
Ab
sent
Butt
erm
ann
20
04
Dis
cogra
ph
y +
ster
oid
D
isco
gra
ph
y
76
.85 (
9.4
7 t
o
62
3.5
2)b
9
.68
(1
.15
to
80
.91
)b
Succ
ess
(ST
),
yes
7
.94
(0
.40
to
15
6.4
6)b
Mo
dic
typ
e 1
P
rese
nt
Ab
sent
Butt
erm
ann
20
04
Dis
cogra
ph
y +
ster
oid
D
isco
gra
ph
y
12
.33 (
1.4
9 t
o
10
1.8
6)b
5
.61
(0
.63
to
50
.02
)b
Succ
ess
(LT
),
yes
2
.20
(0
.11
to
45
.98
)b
Dis
c
her
nia
tio
n
Hei
ght
red
uct
ion
No
hei
ght
red
uct
ion
Hel
lum
et
al.
20
12
Surg
ery
R
ehab
ilit
atio
n
2.6
1 (
1.1
7 t
o 5
.82)b
3
.64
(1
.04
to
12
.78
)b
Dis
abil
ity
(LT
), 0
to
10
0,
≥1
5po
ints
0.7
2 (
0.1
6 t
o 3
.18)b
Dis
c
her
nia
tio
n
Sig
nal
inte
nsi
ty
No
sig
nal
inte
nsi
ty
Hel
lum
et
al.
20
12
Surg
ery
R
ehab
ilit
atio
n
2.5
1 (
1.2
3 t
o 5
.13)b
1
2.0
0 (
1.0
5 t
o
13
6.7
9)b
Dis
abil
ity
(LT
), 0
to
10
0,
≥1
5po
ints
0.2
1 (
0.0
2 t
o 2
.64)b
172
Fac
et j
oin
t
arth
rop
aty
≥m
od
erat
e <
mo
der
ate
Hel
lum
et
al.
20
12
Surg
ery
R
ehab
ilit
atio
n
0.7
8 (
0.0
6 t
o 1
0.8
6)b
3
.15
(1
.55
to
6.3
8)b
D
isab
ilit
y
(LT
), 0
to
10
0,
≥1
5po
ints
0.2
5 (
0.2
0 t
o 3
.79)b
Hig
h i
nte
nsi
ty
zone
Pre
sent
Ab
sent
Hel
lum
et
al.
20
12
Surg
ery
R
ehab
ilit
atio
n
3.3
5 (
1.1
6 t
o 9
.72)b
2
.83
(1
.16
to
6.9
3)b
D
isab
ilit
y
(LT
), 0
to
10
0,
≥1
5po
ints
1.1
8 (
0.2
9 t
o 4
.75)b
Sci
ati
ca p
op
ula
tio
ns
Dis
c
her
nia
tio
n
Cen
tral
N
o C
entr
al
Pea
rso
n e
t al
.
20
08
Surg
ery
R
ehab
ilit
atio
n
1.8
0 (
0.3
0 t
o 3
.30)
0.1
0 (
-0.4
0 t
o 0
.60
) P
ain (
ST
), 0
to
6
1.7
0 (
-0.0
7 t
o 3
.47
)
Dis
c
her
nia
tio
n
Cen
tral
N
o C
entr
al
Pea
rso
n e
t al
.
20
08
Surg
ery
R
ehab
ilit
atio
n
1.6
0 (
0.1
0 t
o 3
.10)
0.0
0 (
-0.4
0 t
o 0
.40
) P
ain (
LT
), 0
to
6
1.6
0 (
0.1
7 t
o 3
.03)a
Dis
c
her
nia
tio
n
Po
ster
ola
tera
l N
o
po
ster
ola
tera
l
Pea
rso
n e
t al
.
20
08
Surg
ery
R
ehab
ilit
atio
n
0.2
0 (
-0.3
0 t
o 0
.70
) 0
.50
(-0
.50
to
1.5
0)
Pai
n (
ST
), 0
to
6
-0.3
0 (
-1.4
5 t
o 0
.85
)
Dis
c
her
nia
tio
n
Po
ster
ola
tera
l N
o
po
ster
ola
tera
l
Pea
rso
n e
t al
.
20
08
Surg
ery
R
ehab
ilit
atio
n
0.0
0 (
-0.5
0 t
o 0
.50
) 0
.60
(-0
.40
to
1.6
0)
Pai
n (
LT
), 0
to
6
-0.6
0 (
-1.7
8 t
o 0
.58
)
Dis
c
her
nia
tio
n
Pro
trusi
on
N
o p
rotr
usi
on
P
ears
on e
t al
.
20
08
Surg
ery
R
ehab
ilit
atio
n
0.6
0 (
-02
0 t
o 1
.40)
0.1
0 (
-0.4
0 t
o 0
.60
) P
ain (
ST
), 0
to
6
0.5
0 (
-0.4
5 t
o 1
.45
)
Dis
c
her
nia
tio
n
Pro
trusi
on
N
o p
rotr
usi
on
P
ears
on e
t al
.
20
08
Surg
ery
R
ehab
ilit
atio
n
0.3
0 (
-0.5
0 t
o 1
.10
) 0
.10
(-0
.40
to
0.6
0)
Pai
n (
LT
), 0
to
6
0.2
0 (
-0.7
6 t
o 1
.16
)
Dis
c
her
nia
tio
n
Seq
ues
trat
ed
Co
nta
ined
P
eul
et a
l. 2
009
S
urg
ery
R
ehab
ilit
atio
n
1.8
4 (
1.2
3 t
o 2
.75)c
1.9
6 (
1.4
0 t
o 2
.74)c
Rec
over
y
(LT
), ≥
much
imp
roved
0.9
4 (
0.5
6 t
o 1
.57)c
Dis
c
her
nia
tio
n
Seq
ues
trat
ed
Co
nta
ined
A
rts
et a
l. 2
01
0
Tub
ula
r
dis
cect
om
y
Co
nven
tio
nal
mic
rod
isce
cto
my
1
.10
(0
.82
to
1.4
6)c
0.7
3 (
0.4
9 t
o 1
.09)c
Rec
over
y
(LT
), ≥
alm
ost
com
ple
te
reco
ver
y
0.6
6 (
0.4
1 t
o 1
.09)c
Dis
c
her
nia
tio
n
Enhance
men
t N
o
enhance
men
t P
eul
et a
l. 2
009
S
urg
ery
R
ehab
ilit
atio
n
2.3
2 (
1.4
3 t
o 3
.77)c
1.9
7 (
1.3
8 t
o 2
.83)c
Rec
over
y
(LT
), ≥
much
imp
roved
0.8
5 (
0.4
7 t
o 1
.54)c
Dis
c
her
nia
tio
n
>1
/3 o
f sp
inal
canal
≤1
/3 o
f sp
inal
canal
A
rts
et a
l. 2
01
0
Tub
ula
r
dis
cect
om
y
Co
nven
tio
nal
mic
rod
isce
cto
my
0
.93
(0
.70
to
1.2
4)c
1.0
0 (
0.6
6 t
o 1
.49)c
Rec
over
y
(LT
), ≥
alm
ost
com
ple
te
reco
ver
y
0.9
4 (
0.5
7 t
o 1
.53)c
Dis
c
her
nia
tio
n
Med
iola
tera
l
and
lat
eral
M
edia
n
Art
s et
al.
20
10
T
ub
ula
r
dis
cect
om
y
Co
nven
tio
nal
mic
rod
isce
cto
my
0
.91
(0
.67
to
1.2
4)c
0.9
8 (
0.6
8 t
o 1
.40)c
Rec
over
y
(LT
), ≥
alm
ost
com
ple
te
reco
ver
y
1.0
7 (
0.6
7 t
o 1
.72)c
Sp
inal
C
entr
al
No
cen
tral
P
ears
on e
t al
. S
urg
ery
R
ehab
ilit
atio
n
0.6
0 (
-5.4
0 t
o 6
.60
) -1
1.0
0 (
-25
.70
to
D
isab
ilit
y
11
.60 (
-4.7
9 t
o 2
7.9
9)
173
sten
osi
s 2
00
12
3.7
0)
(ST
), 0
to
10
0
Sp
inal
sten
osi
s C
entr
al
No
cen
tral
P
ears
on e
t al
.
20
012
Surg
ery
R
ehab
ilit
atio
n
2.3
0 (
-3.4
0 t
o 7
.90
) -2
.40
(-1
6.9
0 t
o
12
.10)
Dis
abil
ity
(LT
), 0
to
10
0
4.7
0 (
-10
.55
to
19.9
5)
Sp
inal
sten
osi
s L
ater
al r
eces
s N
o l
ater
al r
eces
s P
ears
on e
t al
.
20
012
Surg
ery
R
ehab
ilit
atio
n
-1.8
0 (
-7.8
0 t
o 4
.20
) 2
.80
(-1
1.5
0 t
o
17
.10)
Dis
abil
ity
(ST
), 0
to
10
0
-4.6
0 (
-20
.33
to
11
.13)
Sp
inal
sten
osi
s L
ater
al r
eces
s N
o l
ater
al r
eces
s P
ears
on e
t al
.
20
012
Surg
ery
R
ehab
ilit
atio
n
2.5
0 (
-3.2
0 t
o 8
.20
) -3
.80
(-1
7.6
0 t
o
9.9
0)
Dis
abil
ity
(LT
), 0
to
10
0
6.3
0 (
-8.1
3 t
o 2
0.7
3)
Sp
inal
sten
osi
s
Neu
rofo
ram
in
al
No
neu
rofo
ram
inal
Pea
rso
n e
t al
.
20
012
Surg
ery
R
ehab
ilit
atio
n
-3.2
0 (
-12
.80
to
6.3
0)
-0.4
0 (
-6.9
0 t
o 6
.10
) D
isab
ilit
y
(ST
), 0
to
10
0
-2.8
0 (
-14
.33
to
8.7
3)
Sp
inal
sten
osi
s
Neu
rofo
ram
in
al
No
neu
rofo
ram
inal
Pea
rso
n e
t al
.
20
012
Surg
ery
R
ehab
ilit
atio
n
0.5
0 (
-8.8
0 t
o 9
.90
) 2
.00
(-4
.30
to
8.2
0)
Dis
abil
ity
(LT
), 0
to
10
0
-1.5
0 (
-12
.85
to
9.8
5)
Sp
inal
sten
osi
s S
ever
e
Mil
d/
mo
der
ate
Pea
rso
n e
t al
.
20
012
Surg
ery
R
ehab
ilit
atio
n
3.4
0 (
-4.1
0 t
o 1
0.9
0)
-5.6
0 (
-13
.40
to
2.2
0)
Dis
abil
ity
(ST
), 0
to
10
0
9.0
0 (
-1.8
7 t
o 1
9.8
7)
Sp
inal
sten
osi
s S
ever
e
Mil
d/
mo
der
ate
Pea
rso
n e
t al
.
20
012
Surg
ery
R
ehab
ilit
atio
n
3.4
0 (
-3.8
0 t
o 1
0.7
0)
-0.3
0 (
-7.9
0 t
o 7
.30
) D
isab
ilit
y
(LT
), 0
to
10
0
3.7
0 (
-6.8
5 t
o 1
4.2
5)
Sp
inal
sten
osi
s L
ater
al r
eces
s N
o l
ater
al r
eces
s A
rts
et a
l. 2
01
0
Tub
ula
r
dis
cect
om
y
Co
nven
tio
nal
mic
rod
isce
cto
my
0
.63
(0
.34
to
1.1
5)2
1
.03
(0
.80
to
1.3
2)2
Rec
over
y
(LT
), ≥
alm
ost
com
ple
te
reco
ver
y
1.6
4 (
0.8
5 t
o 3
.15)2
Dis
c hei
ght
≥7
mm
<
7m
m
Art
s et
al.
20
10
T
ub
ula
r
dis
cect
om
y
Co
nven
tio
nal
mic
rod
isce
cto
my
0
.92
(0
.71
to
1.1
8)2
1
.24
(0
.70
to
2.2
0)2
Rec
over
y
(LT
), ≥
alm
ost
com
ple
te
reco
ver
y
1.3
5 (
0.7
3 t
o 2
.52)2
Her
nia
tio
n/
sten
osi
s D
isc
pro
lap
se
Sp
inal
ste
no
sis
Taf
azal
et
al.
20
09
Bup
ivac
aine
+
ster
oid
B
up
ivac
aine
3.1
0 (
-11
.23
to
17
.43)
-1.3
0 (
-15
.21
to
17
.81)
Pai
n (
ST
), 0
to
10
0
4.4
0 (
-18
.13
to
26.9
3)
Her
nia
tio
n/
sten
osi
s D
isc
pro
lap
se
Sp
inal
ste
no
sis
Taf
azal
et
al.
20
09
Bup
ivac
aine
+
ster
oid
B
up
ivac
aine
-0.2
0 (
-9.3
4 t
o 9
.47
) -5
.00
(-3
.73
to
13
.73)
Dis
abil
ity
(ST
), 0
to
10
0
4.8
0 (
-9.0
6 t
o 1
8.6
6)
ST
=sh
ort
-ter
m (
0 t
o ≤
6m
onth
s);
LT
=lo
ng
-ter
m (
>6
mo
nth
s).
Mea
n d
iffe
rence
and
95
% C
I, p
osi
tive
valu
es
favo
rs t
reat
ment
effe
ct f
or
MR
I p
osi
tive
(+).
a S
tati
stic
all
y s
ignif
icant.
b V
alues
are
rep
rese
nte
d a
s o
dd
s ra
tio
s an
d 9
5%
co
nfi
den
ce i
nte
rvals
. A
n o
dd
rat
io g
reat
er t
han
1 f
avo
rs t
reat
men
t ef
fect
fo
r M
RI
po
siti
ve
(+).
c V
alues
are
rep
rese
nte
d a
s haz
ard
rat
io a
nd
95
% c
onfi
den
ce i
nte
rvals
. A
haz
ard
rat
io g
reat
er t
han
1 f
avo
rs t
reat
ment
eff
ect
fo
r M
RI
po
siti
ve
(+).
174
Appendix S1. Search strategy 1
MEDLINE via Ovid and Cochrane Central of Controlled trials via The Cochrane Library
1. (randomized controlled trial or controlled clinical trial or comparative study or clinical
trial or clinical trials or randomized or placebo$ or random allocation or random$ or
double-blind method or single-blind method).mp.
[mp=title, abstract, original title, name of substance word, subject heading word, keyword
heading word, protocol supplementary concept, rare disease supplementary concept,
unique identifier]
2. animal/ not human/
3. 1 not 2
4. (low back pain or back pain or back strain or simple back pain or non-specific back pain
or low back syndrome or low back dysfunction or lumbar pain or backache or lumbago or
sciatica or radiculopathy).mp.
[mp=title, abstract, original title, name of substance word, subject heading word, keyword
heading word, protocol supplementary concept, rare disease supplementary concept,
unique identifier]
5. 3 and 4
6. (magnetic resonance imaging or mri or magnetic resonance or nmr or nuclear magnetic
resonance or disc degeneration or desiccation or loss of disc height or bulge or protrusion
or extrusion or nerve root compromise or annular tear or endplate changes or stenosis or
facet degeneration or high intensity zone or modic changes or degenerative disc disease or
spondylolisthesis).mp.
[mp=title, abstract, original title, name of substance word, subject heading word, keyword
heading word, protocol supplementary concept, rare disease supplementary concept,
unique identifier]
7. 5 and 6
EMBASE (www.embase.com)
1. ‘randomized controlled trial’/exp OR ‘randomized controlled trial’ OR ‘controlled
study’/exp OR ‘controlled study’ OR ‘double blind procedure’/exp OR ‘double blind
procedure’ OR ‘placebo’/exp OR ‘placebo’ OR ‘random allocation’/exp OR ‘random
allocation’ OR ‘clinical trial’/exp OR ‘clinical trial’ OR ‘clinical trials’/exp OR ‘clinical
trials’ OR ‘double blind’ OR ‘single blind’
2. ‘animal’/exp OR ‘animal’ OR ‘not human’
3. #1 NOT #2
4. ‘low back pain’/exp OR ‘low back pain’ OR ‘back pain’/exp OR ‘back pain’ OR ‘lumbar
pain’/exp OR ‘lumbar pain’ OR ‘backache’/exp OR ‘backache’ OR ‘lumbago’/exp OR
‘lumbago’ OR ‘radiculopathy’/exp OR ‘radiculopathy’ Or ‘sciatic$’
5. #3 AND #4
6. 'magnetic resonance imaging'/exp OR 'magnetic resonance imaging' OR 'mri'/exp OR 'mri'
OR 'nuclear magnetic resonance'/exp OR 'nuclear magnetic resonance' OR 'nmr'/exp OR
'nmr' OR 'disc degeneration'/exp OR 'disc degeneration' OR 'desiccation'/exp OR
'desiccation' OR 'loss of disc height' OR 'bulge' OR 'protrusion' OR 'extrusion' OR 'nerve
root compression'/exp OR 'nerve root compression' OR 'annular tear' OR 'endplate changes'
OR 'stenosis'/exp OR 'stenosis' OR 'facet degeneration' OR 'high intensity zone' OR 'modic
changes' OR 'degenerative disc disease' OR 'spondylolisthesis'/exp OR 'spondylolisthesis'
7. #5 AND #6
175
Appendix S2. Search strategy 2
MEDLINE via Ovid and Cochrane Central of Controlled trials via The Cochrane
Library
1. (randomized controlled trial or controlled clinical trial or comparative study or
clinical trial or clinical trials or randomized or placebo$ or random allocation or
random$ or double-blind method or single-blind method).mp.
[mp=title, abstract, original title, name of substance word, subject heading word,
keyword heading word, protocol supplementary concept, rare disease supplementary
concept, unique identifier]
2. animal/ not human/
3. 1 not 2
4. (low back pain or back pain or back strain or simple back pain or non-specific back
pain or low back syndrome or low back dysfunction or lumbar pain or backache or
lumbago or sciatica or radiculopathy).mp.
[mp=title, abstract, original title, name of substance word, subject heading word,
keyword heading word, protocol supplementary concept, rare disease supplementary
concept, unique identifier]
5. 3 and 4
6. (target intervent$ or targeted treatment$ or subgroup$ or treatment effect or effect
mod$ or effect med$ or subgroup anal$).mp.
[mp=title, abstract, original title, name of substance word, subject heading word,
keyword heading word, protocol supplementary concept, rare disease supplementary
concept, unique identifier]
7. 5 and 6
EMBASE (www.embase.com)
1. ‘randomized controlled trial’/exp OR ‘randomized controlled trial’ OR ‘controlled
study’/exp OR ‘controlled study’ OR ‘double blind procedure’/exp OR ‘double blind
procedure’ OR ‘placebo’/exp OR ‘placebo’ OR ‘random allocation’/exp OR ‘random
allocation’ OR ‘clinical trial’/exp OR ‘clinical trial’ OR ‘clinical trials’/exp OR
‘clinical trials’ OR ‘double blind’ OR ‘single blind’
2. ‘animal’/exp OR ‘animal’ OR ‘not human’
3. #1 NOT #2
4. ‘low back pain’/exp OR ‘low back pain’ OR ‘back pain’/exp OR ‘back pain’ OR
‘lumbar pain’/exp OR ‘lumbar pain’ OR ‘backache’/exp OR ‘backache’ OR
‘lumbago’/exp OR ‘lumbago’ OR ‘radiculopathy’/exp OR ‘radiculopathy’ Or
‘sciatic$’
5. #3 AND #4
6. 'target intervent$' OR 'targeted treatment$' OR 'subgroup$' OR 'treatment effect' OR
'effect mod$' OR 'effect med$' OR 'subgroup anal$'
7. #5 AND #6
176
Appendix S3. Criteria list for the risk of bias assessment
1) Randomization: A random (unpredictable) assignment sequence. Examples of adequate methods are
coin toss (for studies with 2 groups), rolling a dice (for studies with 2 or more groups), drawing of balls
of different colors, drawing of ballots with the study group labels from a dark bag, computer-generated
random sequence, pre-ordered sealed envelopes, sequentially-ordered vials, telephone call to a central
office, and pre-ordered list of treatment assignments Examples of inadequate methods are: alternation,
birth date, social insurance/ security number, date in which they are invited to participate in the study,
and hospital registration number.
2) Concealed allocation: Assignment generated by an independent person not responsible for
determining the eligibility of the patients. This person has no information about the persons included in
the trial and has no influence on the assignment sequence or on the decision about eligibility of the
patient.
3) Participant blinding: This item should be scored “yes” if the index and control groups are
indistinguishable for the patients or if the success of blinding was tested among the patients and it was
successful.
4) Clinicians blinding: This item should be scored “yes” if the index and control groups are
indistinguishable for the care providers or if the success of blinding was tested among the care providers
and it was successful.
5) Outcome assessor blinding: Adequacy of blinding should be assessed for the primary outcomes. This
item should be scored “yes” if the success of blinding was tested among the outcome assessors and it was
successful or:
–for patient-reported outcomes in which the patient is the outcome assessor (e.g., pain, disability): the
blinding procedure is adequate for outcome assessors if participant blinding is scored “yes”;
–for outcome criteria assessed during scheduled visit and that supposes a contact between participants
and outcome assessors (e.g., clinical examination): the blinding procedure is adequate if patients are
blinded, and the treatment or adverse effects of the treatment cannot be noticed during clinical
examination;
–for outcome criteria that do not suppose a contact with participants (e.g., radiography, magnetic
resonance imaging): the blinding procedure is adequate if the treatment or adverse effects of the
treatment cannot be noticed when assessing the main outcome;
–for outcome criteria that are clinical or therapeutic events that will be determined by the interaction
between patients and care providers (e.g., co-interventions, hospitalization length, treatment failure), in
which the care provider is the outcome assessor: the blinding procedure is adequate for outcome
assessors if item “4” (caregivers) is scored “yes”;
–for outcome criteria that are assessed from data of the medical forms: the blinding procedure is adequate
if the treatment or adverse effects of the treatment cannot be noticed on the extracted data.
6) Acceptable drop-out rate: The number of participants who were included in the study but did not
complete the observation period or were not included in the analysis must be described and reasons
given. If the percentage of withdrawals and drop outs does not exceed 20% for short-term follow up and
30% for long-term follow up and does not lead to substantial bias a “yes” is scored. (N.B. these
percentages are arbitrary, not supported by literature).
7) Analysed according to treatment allocation: All randomized patients are reported/analyzed in the
group they were allocated to by randomization for the most important moments of effect measurement
(minus missing values) irrespective of non-compliance and co-interventions.
8) Free of selective outcomes: In order to receive a “yes”, the review author determines if all the results
from all pre-specified outcomes have been adequately reported in the published report of the trial. This
information is either obtained by comparing the protocol and the report, or in the absence of the protocol,
assessing that the published report includes enough information to make this judgment.
9) Baseline similarity: In order to receive a “yes”, groups have to be similar at baseline regarding
demographic factors, duration and severity of complaints, percentage of patients with neurological
177
symptoms, and value of main outcome measure(s).
10) Co-interventions: This item should be scored “yes” if there were no co-interventions or they were
similar between the index and control groups.
11) Compliance: The reviewer determines if the compliance with the interventions is acceptable, based
on the reported intensity, duration, number and frequency of sessions for both the index intervention and
control intervention(s). For example, physiotherapy treatment is usually administered over several
sessions; therefore it is necessary to assess how many sessions each patient attended. For single session
interventions (e.g., surgery), this item is irrelevant.
12) Outcome timing: Timing of outcome assessment should be identical for all intervention groups and
for all important outcome assessments.
178
Ap
pen
dix
S4.
Lis
t of
excl
uded
full
-tex
t ar
ticl
es a
nd t
he
pri
mar
y r
easo
n f
or
excl
usi
on.
Stu
dy
Tit
le
Fir
st r
easo
n f
or
excl
ud
ing
Ack
erm
an, S
. J.
, et
al.
1997
Per
sist
ent
low
bac
k p
ain i
n p
atie
nts
susp
ecte
d o
f h
avin
g h
ernia
ted n
ucl
eus
pulp
osu
s:
Rad
iolo
gic
pre
dic
tors
of
funct
ional
outc
om
e -
Imp
lica
tions
for
trea
tmen
t se
lect
ion
N
ot
an R
CT
Ahn, S
. H
., e
t al
. 2002
C
om
par
ison o
f cl
inic
al o
utc
om
es a
nd n
atura
l m
orp
holo
gic
ch
anges
bet
wee
n
seques
tere
d a
nd l
arge
centr
al e
xtr
uded
dis
c her
nia
tions
Not
an R
CT
Alb
ert,
H. B
., e
t al
. 2013
Anti
bio
tic
trea
tmen
t in
pat
ients
wit
h c
hro
nic
low
bac
k p
ain a
nd v
erte
bra
l b
one
edem
a (M
odic
typ
e 1 c
han
ges
): a
double
-bli
nd r
andom
ized
cli
nic
al c
ontr
oll
ed t
rial
of
effi
cacy
Not
poss
ible
to e
luci
dat
e
asso
ciat
ion b
etw
een M
RI
and
outc
om
e
Art
s, M
. P
., e
t al
. 2011
Tubula
r dis
kec
tom
y v
s co
nven
tional
mic
rodis
kec
tom
y f
or
the
trea
tmen
t o
f lu
mbar
dis
k h
ernia
tion:
2-Y
ear
resu
lts
of
a double
-bli
nd r
andom
ized
contr
oll
ed t
rial
Not
poss
ible
to e
luci
dat
e
asso
ciat
ion b
etw
een M
RI
and
outc
om
e
Bro
uw
er, P
. A
., e
t al
.
2009
Eff
ecti
ven
ess
of
per
cuta
neo
us
lase
r dis
c d
ecom
pre
ssio
n v
ersu
s co
nven
tional
open
dis
cect
om
y i
n t
he
trea
tmen
t of
lum
bar
dis
c her
nia
tion;
des
ign o
f a
pro
spec
tive
random
ized
contr
oll
ed t
rial
Not
an R
CT
Bro
wd
er, D
. A
., e
t al
.
2007
Eff
ecti
ven
ess
of
an e
xte
nsi
on
-ori
ente
d t
reat
men
t ap
pro
ach i
n a
sub
gro
up o
f su
bje
cts
wit
h l
ow
bac
k p
ain:
a ra
ndom
ized
cli
nic
al t
rial
No e
val
uat
ion o
f M
RI
findin
gs
Bro
wn,
L.
L. 2012
A d
ouble
-bli
nd, ra
ndom
ized
, pro
spec
tive
stud
y o
f ep
idura
l st
eroid
inje
ctio
n v
s. t
he
mil
d p
roce
dure
in p
atie
nts
wit
h s
ym
pto
mat
ic l
um
bar
spin
al s
tenosi
s
Not
poss
ible
to e
luci
dat
e
asso
ciat
ion b
etw
een M
RI
and
outc
om
e
Bro
x, J.
I., e
t al
. 2010
Four-
yea
r fo
llow
up o
f su
rgic
al v
ersu
s non
-surg
ical
ther
apy f
or
chro
nic
low
bac
k
pai
n
Not
poss
ible
to e
luci
dat
e
asso
ciat
ion b
etw
een M
RI
and
outc
om
e
Bro
x, J.
I., e
t al
. 2003
Ran
dom
ized
cli
nic
al t
rial
of
lum
bar
inst
rum
ente
d f
usi
on
and c
ognit
ive
inte
rven
tion
and e
xer
cise
s in
pat
ients
wit
h c
hro
nic
low
bac
k p
ain a
nd d
isc
deg
ener
atio
n
Not
poss
ible
to e
luci
dat
e
asso
ciat
ion b
etw
een M
RI
and
outc
om
e
Chil
ds,
J. D
., e
t al
. 2004
A
cli
nic
al p
redic
tion r
ule
to i
den
tify
pat
ients
wit
h l
ow
bac
k p
ain m
ost
lik
ely t
o
ben
efit
fro
m s
pin
al m
anip
ula
tion:
a val
idat
ion s
tud
y
No e
val
uat
ion o
f M
RI
findin
gs
Erg
inou
sakis
, D
., e
t al
.
2011
Com
par
ativ
e pro
spec
tive
random
ized
stu
dy c
om
par
ing c
onse
rvat
ive
trea
tmen
t an
d
per
cuta
neo
us
dis
k d
ecom
pre
ssio
n f
or
trea
tmen
t of
inte
rver
tebra
l dis
k h
ernia
tion
Not
poss
ible
to e
luci
dat
e
asso
ciat
ion b
etw
een M
RI
and
outc
om
e
Fil
iz, M
., e
t al
. 2005
T
he
effe
ctiv
enes
s of
exer
cise
pro
gra
mm
es a
fter
lum
bar
dis
c su
rger
y:
a ra
nd
om
ized
N
ot
poss
ible
to e
luci
dat
e
179
contr
oll
ed s
tud
y
asso
ciat
ion b
etw
een M
RI
and
outc
om
e
Fre
bu
rger
, J.
K., e
t al
.
2006
Eff
ecti
ven
ess
of
ph
ysi
cal
ther
apy f
or
the
man
agem
ent
of
chro
nic
spin
e dis
ord
ers:
A
pro
pen
sity
sco
re a
ppro
ach
N
ot
an R
CT
Fri
tz, J.
M., e
t al
. 2007
Is t
her
e a
sub
gro
up o
f pat
ients
wit
h l
ow
bac
k p
ain l
ikel
y t
o b
enef
it f
rom
mec
han
ical
trac
tion? R
esult
s of
a ra
ndom
ized
cli
nic
al t
rial
and s
ubgro
upin
g a
nal
ysi
s
No e
val
uat
ion o
f M
RI
findin
gs
Fri
tzel
l, P
., e
t al
. 2001
Lum
bar
fu
sion
ver
sus
no
nsu
rgic
al t
reat
men
t fo
r ch
ronic
low
bac
k p
ain. A
mult
icen
ter
random
ized
contr
oll
ed t
rial
fro
m t
he
Sw
edis
h L
um
bar
Spin
e S
tud
y
Gro
up
Not
poss
ible
to e
luci
dat
e
asso
ciat
ion b
etw
een M
RI
and
outc
om
e
Fri
tzel
l, P
., e
t al
. 2002
Chro
nic
low
bac
k p
ain a
nd f
usi
on:
A c
om
par
ison o
f th
ree
surg
ical
tec
hniq
ues
: A
pro
spec
tive
mult
icen
ter
random
ized
stu
dy f
rom
th
e S
wed
ish L
um
bar
Spin
e S
tud
y
Gro
up
Not
poss
ible
to e
luci
dat
e
asso
ciat
ion b
etw
een M
RI
and
outc
om
e
Fro
hold
t, A
., e
t al
. 2011
No d
iffe
rence
in l
on
g-t
erm
tru
nk m
usc
le s
tren
gth
, cr
oss
-sec
tional
are
a, a
nd d
ensi
ty
in p
atie
nts
wit
h c
hro
nic
low
bac
k p
ain 7
to 1
1 y
ears
aft
er l
um
bar
fusi
on
ver
sus
cognit
ive
inte
rven
tion a
nd e
xer
cise
s
Not
poss
ible
to e
luci
dat
e
asso
ciat
ion b
etw
een M
RI
and
outc
om
e
Gore
n, A
., e
t al
. 2010
Eff
icac
y o
f ex
erci
se a
nd u
ltra
sound i
n p
atie
nts
wit
h l
um
bar
spin
al s
tenosi
s: a
pro
spec
tive
random
ized
contr
oll
ed t
rial
Not
poss
ible
to e
luci
dat
e
asso
ciat
ion b
etw
een M
RI
and
outc
om
e
Gudav
alli
, M
. R
., e
t al
.
2006
A r
andom
ized
cli
nic
al t
rial
and s
ub
gro
up a
nal
ysi
s to
com
par
e fl
exio
n-d
istr
acti
on
wit
h a
ctiv
e ex
erci
se f
or
chro
nic
low
bac
k p
ain
Not
poss
ible
to e
luci
dat
e
asso
ciat
ion b
etw
een M
RI
and
outc
om
e
Hel
lum
, C
., e
t al
. 2011
Surg
ery w
ith d
isc
pro
sth
esis
ver
sus
reh
abil
itat
ion i
n p
atie
nts
wit
h l
ow
bac
k p
ain a
nd
deg
ener
ativ
e dis
c: t
wo y
ear
foll
ow
-up o
f ra
ndom
ised
stu
dy
Not
poss
ible
to e
luci
dat
e
asso
ciat
ion b
etw
een M
RI
and
outc
om
e
Hem
mil
a, H
. M
., e
t al
.
2002
Lon
g-t
erm
eff
ecti
ven
ess
of
bone-
sett
ing, li
ght
exer
cise
ther
apy, an
d p
hysi
oth
erap
y
for
pro
lon
ged
bac
k p
ain:
a ra
ndom
ized
contr
oll
ed t
rial
Not
poss
ible
to e
luci
dat
e
asso
ciat
ion b
etw
een M
RI
and
outc
om
e
Huda,
N., e
t al
. 2010
The
effi
cacy o
f ep
idura
l dep
o-m
eth
ylp
rednis
olo
ne
and t
riam
cino
lone
acet
ate
in
reli
evin
g t
he
sym
pto
ms
of
lum
bar
can
al s
tenosi
s: A
com
par
ativ
e st
ud
y
Not
poss
ible
to e
luci
dat
e
asso
ciat
ion b
etw
een M
RI
and
outc
om
e
Hurr
i, H
., e
t al
. 1998
L
um
bar
spin
al s
tenosi
s: a
sses
smen
t of
long-t
erm
outc
om
e 12 y
ears
aft
er o
per
ativ
e
and c
onse
rvat
ive
trea
tmen
t N
ot
an R
CT
180
Jense
n, R
. K
., e
t al
. 2012
Res
t ver
sus
exer
cise
as
trea
tmen
t fo
r p
atie
nts
wit
h l
ow
bac
k p
ain a
nd M
odic
chan
ges
. A
ran
dom
ized
contr
oll
ed c
linic
al t
rial
Not
poss
ible
to e
luci
dat
e
asso
ciat
ion b
etw
een M
RI
and
outc
om
e
Kaa
pa,
E., e
t al
. 2012
Corr
elat
ion o
f si
ze a
nd t
ype
of
Modic
types
1 a
nd 2
les
ions
wit
h c
linic
al s
ym
pto
ms:
a des
crip
tiv
e st
ud
y i
n a
subgro
up o
f pat
ients
wit
h c
hro
nic
low
bac
k p
ain o
n t
he
bas
is
of
a univ
ersi
ty h
osp
ital
pat
ient
sam
ple
Not
an R
CT
Kaw
u, A
. A
., e
t al
. 2011
F
acet
join
ts i
nfi
ltra
tion:
A v
iable
alt
ern
ativ
e tr
eatm
ent
to p
hysi
oth
erap
y i
n p
atie
nts
wit
h l
ow
bac
k p
ain d
ue
to f
acet
join
t ar
thro
pat
hy
Not
an R
CT
Ken
ned
y, D
. J.
, et
al.
2013
Mult
icen
ter
random
ized
contr
oll
ed t
rial
com
par
ing p
arti
cula
te v
ersu
s nonp
arti
cula
te
cort
icost
eroid
s v
ia l
um
bar
tra
nsf
ora
min
al e
pid
ura
l in
ject
ion f
or
acute
unil
ater
al,
unil
evel
rad
icula
r pai
n d
ue
to h
ernia
ted n
ucl
eus
pulp
osu
s
Not
poss
ible
to e
luci
dat
e
asso
ciat
ion b
etw
een M
RI
and
outc
om
e
Koc,
Z., e
t al
. 2009
Eff
ecti
ven
ess
of
ph
ysi
cal
ther
apy a
nd e
pid
ura
l st
eroid
inje
ctio
ns
in l
um
bar
spin
al
sten
osi
s
Not
poss
ible
to e
luci
dat
e
asso
ciat
ion b
etw
een M
RI
and
outc
om
e
Koes
, B
. W
., e
t al
. 1993
A
ran
dom
ized
cli
nic
al t
rial
of
man
ual
ther
apy a
nd p
hysi
oth
erap
y f
or
per
sist
ent
bac
k
and n
eck c
om
pla
ints
: S
ubgro
up a
nal
ysi
s an
d r
elat
ionsh
ip b
etw
een o
utc
om
e m
easu
res
No e
val
uat
ion o
f M
RI
findin
gs
Lon
g, A
., e
t al
. 2004
D
oes
it
mat
ter
whic
h e
xer
cise
? A
ran
dom
ized
contr
ol
tria
l of
exer
cise
for
low
bac
k
pai
n
No e
val
uat
ion o
f M
RI
findin
gs
Mal
miv
aara
, A
., e
t al
.
2007
Surg
ical
or
nonoper
ativ
e tr
eatm
ent
for
lum
bar
spin
al s
tenosi
s? A
ran
dom
ized
contr
oll
ed t
rial
Not
poss
ible
to e
luci
dat
e
asso
ciat
ion b
etw
een M
RI
and
outc
om
e
Med
rik
-Gold
ber
g,
T., e
t
al. 1999
Intr
aven
ous
lidoca
ine,
am
anta
din
e, a
nd p
lace
bo i
n t
he
trea
tmen
t of
scia
tica
: A
double
-bli
nd, ra
ndom
ized
, co
ntr
oll
ed s
tud
y
Not
poss
ible
to e
luci
dat
e
asso
ciat
ion b
etw
een M
RI
and
outc
om
e
Ost
erm
an, H
., e
t al
. 2006
Eff
ecti
ven
ess
of
mic
rodis
cect
om
y f
or
lum
bar
dis
c her
nia
tion:
a ra
ndom
ized
contr
oll
ed t
rial
wit
h 2
year
s of
foll
ow
-up
Not
poss
ible
to e
luci
dat
e
asso
ciat
ion b
etw
een M
RI
and
outc
om
e
Pen
g,
B., e
t al
. 2009
D
iagnosi
s an
d s
urg
ical
tre
atm
ent
of
bac
k p
ain o
rigin
atin
g f
rom
endpla
te
Not
an R
CT
Rad
clif
f, K
., e
t al
. 2011
D
oes
opio
id p
ain m
edic
atio
n u
se a
ffec
t th
e outc
om
e of
pat
ients
wit
h l
um
bar
dis
c
her
nia
tion? A
subgro
up a
nal
ysi
s of
the
SP
OR
T s
tud
y
No e
val
uat
ion o
f M
RI
findin
gs
Raj
asek
aran
, S
., e
t al
.
2013
Lum
bar
spin
ous
pro
cess
spli
ttin
g d
ecom
pre
ssio
n p
rovid
es e
quiv
alen
t outc
om
es t
o
conven
tional
mid
line
dec
om
pre
ssio
n i
n d
egen
erat
ive
lum
bar
can
al s
tenosi
s: A
Not
poss
ible
to e
luci
dat
e
asso
ciat
ion b
etw
een M
RI
and
181
pro
spec
tive,
ran
dom
ised
contr
oll
ed s
tud
y o
f 51 p
atie
nts
outc
om
e
San
till
i, V
., e
t al
. 20
06
Chir
opra
ctic
man
ipula
tio
n i
n t
he
trea
tmen
t of
acute
bac
k p
ain a
nd s
ciat
ica
wit
h d
isc
pro
trusi
on:
a ra
ndom
ized
double
-bli
nd c
linic
al t
rial
of
acti
ve
and s
imula
ted s
pin
al
man
ipula
tions
Not
poss
ible
to e
luci
dat
e
asso
ciat
ion b
etw
een M
RI
and
outc
om
e
Sher
man
, K
. J.
, et
al.
2009
Char
acte
rist
ics
of
pat
ients
wit
h c
hro
nic
bac
k p
ain w
ho b
enef
it f
rom
acu
pun
cture
N
o e
val
uat
ion o
f M
RI
findin
gs
Sla
tis,
P., e
t al
. 2011
Lon
g-t
erm
res
ult
s of
surg
ery f
or
lum
bar
spin
al s
tenosi
s: a
ran
dom
ised
contr
oll
ed
tria
l
Not
poss
ible
to e
luci
dat
e
asso
ciat
ion b
etw
een M
RI
and
outc
om
e
Ste
enst
ra,
I. A
., e
t al
.
2009
What
work
s bes
t fo
r w
ho
m? A
n e
xplo
rato
ry, su
bgro
up a
nal
ysi
s in
a r
ando
miz
ed,
contr
oll
ed t
rial
on t
he
effe
ctiv
enes
s of
a w
ork
pla
ce i
nte
rven
tion i
n l
ow
bac
k p
ain
pat
ients
on
ret
urn
to w
ork
Not
poss
ible
to e
luci
dat
e
asso
ciat
ion b
etw
een M
RI
and
outc
om
e
Sty
czynsk
i, T
., e
t al
.
2007
The
effe
ct o
f th
e gra
de
of
deg
ener
ativ
e ch
anges
in t
he
spin
e on t
he
outc
om
es o
f
surg
ery f
or
lum
bar
dis
copat
hy w
ith a
rad
icula
r sy
ndro
me
Not
an R
CT
Under
wood, M
. R
., e
t al
.
2007
Do b
asel
ine
char
acte
rist
ics
pre
dic
t re
sponse
to t
reat
men
t fo
r lo
w b
ack p
ain
?
Sec
ondar
y a
nal
ysi
s of
the
UK
BE
AM
dat
aset
No e
val
uat
ion o
f M
RI
findin
gs
Voll
enbro
ek-H
utt
en, M
.
M., e
t al
. 2004
Dif
fere
nce
s in
outc
om
e o
f a
mult
idis
cipli
nar
y t
reat
men
t bet
wee
n s
ub
gro
ups
of
chro
nic
low
bac
k p
ain p
atie
nts
def
ined
usi
ng t
wo m
ult
iaxia
l as
sess
men
t in
stru
men
ts:
the
mult
idim
ensi
onal
pai
n i
nven
tory
and l
um
bar
dyn
amom
etry
No e
val
uat
ion o
f M
RI
findin
gs
Wil
ken
s, P
., e
t al
. 2012
No e
ffec
t of
6-m
onth
inta
ke
of
glu
cosa
min
e su
lfat
e on M
odic
chan
ges
or
hig
h
inte
nsi
ty z
ones
in t
he
lum
bar
spin
e: s
ub
-gro
up a
nal
ysi
s of
a ra
ndom
ized
co
ntr
oll
ed
tria
l
Not
poss
ible
to e
luci
dat
e
asso
ciat
ion b
etw
een M
RI
and
outc
om
e
Zhuo, X
., e
t al
. 2010
Eff
ecti
ven
ess
com
par
ison o
f tw
o s
urg
ical
pro
cedu
res
on l
um
bar
dis
c pro
tru
sion
N
ot
an R
CT
182
Chapter Nine
Influence of clinician characteristics and operational factors on recruitment of
participants with low back pain: an observational study
Chapter Nine published as:
Steffens D, Maher CG, Ferreira ML, Hancock MJ, Pereira LSM, Williams CM, Latimer J.
Influence of clinician characteristics and operational factors on recruitment of participants
with low back pain: an observational study. Journal of Manipulative Physiological
Therapeutics. 2014; 38:151-158.
183
Statement from co-authors confirming authorship contribution of the PhD candidate
As co-authors of the paper “Influence of clinician characteristics and operational factors
on recruitment of participants with low back pain: an observational study”, we confirm that
Daniel Steffens has made the following contributions:
Conception and design of the research
Data collection
Analysis and interpretation of the findings
Writing of the manuscript and critical appraisal of the content
Christopher G Maher Date: 01.01.2015
Manuela L Ferreira Date: 01.01.2015
Mark J Hancock Date: 01.01.2015
Leani SM Pereira Date: 01.01.2015
Christopher M Williams Date: 01.01.2015
Jane Latimer Date: 01.01.2015
184
185
INFLUENCE OF CLINICIAN CHARACTERISTICS AND
OPERATIONAL FACTORS ON RECRUITMENT OF
PARTICIPANTS WITH LOW BACK PAIN: AN
OBSERVATIONAL STUDY
Daniel Steffens, BPT (Hons), a, b Chris G. Maher, PhD, c Manuela L. Ferreira, PhD, d Mark J. Hancock, PhD, eLeani S.M. Pereira, PhD, f Christopher M. Williams, PhD, g and Jane Latimer, PhDc
ABSTRACT
a PhD Student,lobal Health, Syydney, Australiab PhD Student,
f Minas Gerais,c Professor, Mlobal Health, Syydney, Australiad Senior Reseastitute for Globaf Sydney, Sydnee Senior Lectuuman Sciencesf Professor, Deinas Gerais, Be
Objective: The purpose of this study was to identify factors that influence recruitment of patients to an observationalstudy of low back pain (LBP).Methods: From 1147 primary care (first health contact) clinicians initially contacted, 138 (physiotherapists andchiropractors) agreed to participate in a large observational study of LBP and were the focus of the current study. Datawere collected pertaining to clinicians' characteristics, operational factors, and the number of patients recruited. Theassociation of a variety of clinician characteristics and operational factors with recruitment rate was determined using amultivariate negative binomial regression analysis.Results: From October 2011 to November 2012, 1585 patients were screened by 138 study clinicians with 951 eligiblepatients entering the observational study. Clinicians who were members of their professional association had a recruitmentrate less than half that of those who were nonmembers (P b .0001). Clinicians who were trained by telephone had arecruitment rate 4.01 times higher than those trained face to face (P b .0001). Similarly, clinicians who referred a largernumber of ineligible participants had a slightly higher recruitment rate with an incident rate ratio of 1.04 per ineligiblepatient (P b .0001). Other clinicians' characteristics and operational factors were not associated with recruitment.Conclusion: This study provides evidence that it is feasible to recruit participants from primary care practices to asimple observational study of LBP. Factors identified as influencing recruitment were professional association(negative association), training by telephone, and referring a higher number of ineligible participants. (J ManipulativePhysiol Ther 2015;xx:1-8)
Key Indexing Terms: Patient Selection; Back Pain; Primary Health Care; Physical Therapy; ChiropracticParticipant recruitment is one of the most challengingphases of the research process and may cause studiesto become unfeasible.1,2 It is estimated that 85% of
Musculoskeletal Division, The George Institute fordney Medical School, The University of Sydney,.Department of Physiotherapy, Federal UniversityBelo Horizonte, Brazil.usculoskeletal Division, The George Institute fordney Medical School, The University of Sydney,.rch Fellow,Musculoskeletal Division, The Georgel Health, Sydney Medical School, The Universityy, Australia.rer, Discipline of Physiotherapy, Faculty of, Macquarie University, Sydney, Australia.partment of Physiotherapy, Federal University oflo Horizonte, Brazil.
g Research Fellow, Hunter Medical Research Institute, Schoolof Medicine and Public Health, University of Newcastle,Newcastle, Australia.
Submit requests for reprints to: Daniel Steffens, BPT(Hons), PhD Student, Musculoskeletal Division, The GeorgeInstitute for Global Health, Sydney Medical School, TheUniversity of Sydney, PO Box M201, Missenden Road, Sydney,New South Wales, 2050, Australia. (e-mail: [email protected]).
Paper submitted April 11, 2014; in revised form October 1,2014; accepted October 10, 2014.
0161-4754Copyright © 2014 by National University of Health
Sciences.http://dx.doi.org/10.1016/j.jmpt.2014.10.016
GS
o
GS
Ino
H
M
studies do not conclude on schedule due to low participation,60% to 80% of studies do not meet their chronologicalendpoint because of challenges in recruitment, and 30% of
2 Journal of Manipulative and Physiological TherapeuticsSteffens et alMonth 2015Factors Predicting Recruitment of Participants
186
study sites fail to recruit even a single participant.1,3,4
Unsatisfactory and/or untimely participant recruitment hasserious consequences, leading to an underpowered study,increased resource use and higher costs.5-7 Importantly, theintegrity and validity of the study also rely on obtaining anadequate sample size, and failure to achieve this may cause astudy with inconclusive findings.8
Most previous studies have focused on investigating factorsthat increase recruitment to randomized controlled trials(RCTs).3-5,7,9-12 Although RCTs are considered the “goldstandard” of study design,13 not all scientific questions can beanswered with this design. Researchers are often interested inquestions regarding etiology and prognosis, which may bebetter answered using an observational study design. Many ofthe barriers encountered when recruiting participants to RCTsmay be similar to those encountered when conductingobservational studies; however, factors affecting recruitmentto observational studies have not been carefully evaluated.14
Previous studies have identified reasons clinicians do notenroll eligible patients into clinical trials.15,16 Although thesereasons have been identified predominantly from studiesevaluating general practitioners, it is likely that many alsoapply to allied health practitioners (physiotherapists andchiropractors) who are operating as first contact practitionerfor patients presenting with back pain. These reasons includedifficulty for practitioners in following the study protocol andcompleting the recruitment process and patient preference fora certain therapy and difficulties obtaining informed consentfrom patients. In primary care, these recruitment barriers areoften heightened by the clinician's lack of time, whichsignificantly affects their ability to recruit participants.17
Other factors reported to influence recruitment of patientsinclude the importance of the research question, the simplicityof the research design, and ease of access to treatment.Financial reimbursement has been suggested as a possiblefactor10,18,19; however, a recent systematic review found that,in randomized controlled trials, reimbursement for time spenton recruitment is not associated with better recruitment.20 Inaddition, it is possible that recruiting fromhealth professionalsother than general practitioners such as physiotherapists andchiropractors may produce a different outcome. Regardless,recruitment of patients in primary care remains a significantissue.5,7 Therefore, studies that use simple recruitmentstrategies, minimal clinical involvement, and health profes-sionals other than general practitioners may have anadvantage in recruiting patients in primary care settings.
The reasons certain studies recruit successfully whileothers do not remain unclear.21 A better understanding ofclinicians' characteristics and the study operational charac-teristics (eg, method of training and type and number ofcontacts) may lead researchers to identify study strategiesassociated with recruitment of a larger number ofparticipants. Therefore, the aim of this study was to identifyfactors that influence recruitment to an observational studyof triggers for low back pain (LBP).
METHODS
DesignThis observational study investigated primary care
clinicians enrolling patients with acute LBP to a case-cross-over study (TRIGGERS). Participants were recruited fromOctober 2011 to November 2012. The methods andprocedures for recruitment of patients to the TRIGGERSstudy have been published elsewhere.22 Participants in theTRIGGERS study (n = 999)were also eligible to enroll in thePACE clinical trial. 23 The PACE clinical trial is adouble-blind placebo-controlled trial assessing the effectthat paracetamol has on recovery from acute nonspecific LBP.The inclusion criteria for the TRIGGERS and PACE studieswere similar; therefore, patients recruited for the PACEclinical trial could also be enrolled in the TRIGGERS study.However, data collected from recruiting clinicians (eg,personal information) and the study operational procedureswere different for both studies. Therefore, we reported thedata collected from participants who enrolled in theTRIGGERS study only (n = 951). Ethical approval for thestudy was granted by the University of Sydney HumanResearch Ethics Committee (protocol no. 05-2011/13742).
ParticipantsTRIGGERS recruited patients seeking care for LBP in
primary care clinics across Sydney, Australia. Eligibleparticipants met the following inclusion criteria: (1) compre-hends spoken English, (2) main complaint of LBP with orwithout leg pain (pain between 12th rib and buttock crease),(3) current episode of back pain less than or equal to 7 daysduration, (4) new episode (preceded by at least 1 monthwithout LBP), (5) pain of at leastmoderate intensity during thefirst 24 hours of this episode (scored on a 6-point scale fromnone to very severe). The exclusion criterion was confirmedor suspected serious spinal pathology (ie, cancer, fracture,and infection).
Clinician RecruitmentPrimary care clinicians were recruited for this study. In
Australia, primary care clinicians are those registered toprovide the first health contact for patients presenting fromthe community and include general practitioners, practicenurses, psychologists, physiotherapists, chiropractors, andpharmacists.24 According to the original protocol, generalpractitioners and pharmacists would be contacted to aidrecruitment. However, no attempts were made to recruitgeneral practitioners or pharmacists as adequate numbers ofpatients were recruited through physiotherapists and chiro-practors. In this study, the recruiting primary care clinicianswere physiotherapists and chiropractors.
Lists of physiotherapistsworking in Sydneywere acquiredfrom their association's Web site. All physiotherapists drawnfrom theAustralian PhysiotherapyAssociation databasewere
3Steffens et alJournal of Manipulative and Physiological TherapeuticsFactors Predicting Recruitment of ParticipantsVolume xx, Number x
187
members of the association. Thirty-five physiotherapists whoparticipated in the study were not members of the AustralianPhysiotherapy Association and were identified by theircolleagues (who were members and received our invitation).The chiropractors were selected from aGoogle search. A totalof 1147 clinicians (39 chiropractors and 1108 physiothera-pists) were invited to participate by letter. The letter outlinedthe study aims, sample size, inclusion/exclusion criteria, andthe benefits to the clinician and patient of participation.Interested clinicianswere invited to contact the study researchteam to obtain further information.A study researcher phonedthose who responded to further explain the study procedures.Additional training was provided for clinicians interested inrecruiting to the study. A total of 138 clinicians (135physiotherapists and 3 chiropractors) agreed to participate inthe study.
Training MethodsAfter confirming their interest in recruiting, clinicians
were offered 2methods of training: (1) face-to-face training attheir clinics or (2) training by a telephone call. The method oftraining was selected by the clinician.
Face-to-Face TrainingClinicians who chose face-to-face training were visited
and trained by an experienced research assistant at their ownpractice. Face-to-face training was supplemented withdistribution of a paper copy of the study protocol. Trainingtook around 30 minutes and was done in a group of up to 5clinicians working at the same practice.
Training by Telephone CallClinicianswho chose telephone training received their hard
copy of the study protocol by post approximately 1 weekbefore their telephone training call was scheduled. The callswere made by a research assistant and covered all the topics inthe face-to-face training. This training took around 30 minutesand was done individually.
Features Covered in Both Training MethodsIrrespective of whether the clinician chose face-to-face or
telephone training, the following topics were covered duringtraining: study background, aims, screening form (inclusion/exclusion criteria—refer to supplementary material forfurther details), informed consent form, referring patients(providing patient contact information to the research team),terms and conditions, human ethics, and study benefits.Clinicians could opt out at any time during the study period.
Screening PatientsClinicians were asked to screen for eligibility all (ie,
consecutive) patients who presented with LBP. Clinicians
were instructed to fax screening forms for both eligible andineligible patients to the study researchers as soon as theforms were completed. For those participants agreeing to beinvolved, consent forms were signed by the participants andclinicians at the participating sites.
ReimbursementClinicians were reimbursed AU $99 per eligible patient
referred to the study. This sum was used to cover theclinician's time spent in recruiting participants, explaining thestudy to them, and liaising with the study staff. Clinicianswere also reimbursed AU $10 per ineligible patient screened,to cover clerical and administration costs. Participants werereimbursed with AU $50 gift card for the time spentanswering the questions and to cover the cost of the mobiletelephone calls to the researcher. The typical duration of theinterview was approximately 30 minutes.
Clinician's Characteristics and Data CollectionPersonal information from the recruiting clinicians was
collected, including sex, date of birth, practice details(location/postcode), profession, current position, years ofpractice, years managing LBP, and whether the clinician wasa member of their professional association. All contacts madebetween the study researchers and the clinicians were enteredinto a database. Contacts were classified as phone call, letter,or e-mails.
Recruitment Outcome and Recruitment Predictor VariablesThe recruitment outcome was the total number of eligible
patients recruited by each individual clinician by the end ofthe study. Eligible patients were patients referred by theclinician successfully enrolled in the TRIGGERS study.
Although the prediction of recruitment study wasconceived after the main TRIGGERS study commenced,the recruitment predictor variables and analysis were defineda priori as presented in the manuscript. Clinicians' characte-ristics included (1) sex (male/female), (2) age (years), (3)suburb socioeconomic status (determined by comparing theclinic postcode to Australia Bureau of Statistics data oneconomic advantage and disadvantage by postcode anddichotomized into high ≥AU $577 or low socioeconomicstatus bAU $577, based on the average individual weeklyincome), (4) profession (physiotherapist or chiropractor), (5)clinical experience as practicing clinician (years), (6) clinicalexperience managing LBP (years), (7) current position(employee or business owner), and (8) professional associa-tionmembership status (member or not member). Operationalfactors included (1) trainingmethod (face-to-face or telephonecall), (2) number of letters (total number of letters sent to theclinician by end of the study), (3) number of telephone calls(total number of phone calls made to the clinician by end ofthe study), (4) total number of e-mails (total number of e-mails
Table 1. Characteristics of Recruiting Clinicians Stratified byRecruitment Rate
RecruitmentRate perMonth a
No. ofClinicians(%)
No. of EligibleParticipants perStrata (%)
No. of IneligibleParticipants perStrata (%)
0 32 (23.2) 0 (0) 8 (1.3)N0-0.5 44 (31.9) 112 (11.6) 69 (10.9)N0.5-1 27 (19.6) 162 (17.1) 235 (37.0)N1-2 20 (14.5) 197 (20.7) 158 (24.9)N2 15 (10.9) 480 (50.6) 164 (25.9)Total 138 (100) 951 (100) 634 (100)
a Recruitment rate: total number of participants recruited divided bythe number of months in the study.
Table 2. Clinician's Descriptive Data (n = 138)
VariablesMean ± SD orn (%)
Sex, male 73 (53)Age 42 ± 10Profession, physiotherapist 135 (98)Current position
Employee 67 (48.5)Business owner 71 (51.5)
Clinical experience (y) 19.5 ± 10Clinical experience managing LBP (y) 18.5 ± 9.5SES of suburb of clinician clinic (high) a 104 (75.5)Member of their respective association 103 (74.5)Training method (telephone) 79 (57.2)No. of letters b 1.1 ± 0.3No. of telephone call b 0.4 ± 0.3No. of e-mails b 0.3 ± 0.2
4 Journal of Manipulative and Physiological TherapeuticsSteffens et alMonth 2015Factors Predicting Recruitment of Participants
188
Total no. of contacts (letter/e-mail/telephone call) b 1.8 ± 0.6No. of ineligible patients b 4.6 ± 13.9
LBP, low back pain; SES, socioeconomic status.a Suburb socioeconomic status—determined by comparing the clinic
postcode to Australia Bureau of Statistics data on economic advantage anddisadvantage.
b Number of contacts divided by the total time (months) participating
sent to the clinician by end of the study), (5) total number ofcontacts (total number of phone calls, letters, or e-mails madeand/or sent to the clinician by end of the study), and (6)number of ineligible patients referred (ineligible patients weredefined as patients not willing to participate or not fulfillingstudy inclusion criterion).
in the study.
Data AnalysisAnalyses were performed using STATA version 12
(College Station, TX).25 Descriptive statistics were per-formed to describe the clinician's characteristics and therecruitment rate for the study (defined as the number ofpatients per month). To evaluate factors that influencedclinicians' recruitment rate, a negative binomial regressionanalysis was conducted where recruitment rate was thedependent variable and the predictors described above(clinicians and operational characteristics) were independentvariables. We used the negative binomial regression analysisbecause the outcome data were overdispersed (tested bycomparing the variance of the data to the mean patient countrecruited by clinicianswith the likelihood ratio test). Variableswith significant univariate associations (P b .2) were enteredinto a backward stepwise multivariate regression model.Statistical significance was defined as P b .05. As cliniciansstarted the study on different dates, this was accounted for inthe analysis by including the number of days in the study as anoffset variable in the model. For continuous variables, theincident rate ratio (IRR) can be interpreted as the rate ratio inwhich the total number of participants is expected to changewith a 1-unit increase in the exposure variable. For binaryvariables, the IRR indicates the expected change in rate ofpatient recruitment when the variable is positive.
RESULTS
From 1147 clinicians initially contacted, 135 physiothera-pists (12.2%) and 3 chiropractors (7.7%) agreed toparticipate. Between October 2011 and November 2012,study clinicians screened 1585 patients. There were 951
eligible patients who entered the study (943 referred byphysiotherapists and 8 referred by chiropractors). Table 1shows participant recruitment rate per month. The overallrecruitment rate per clinician was 0.99 patients per month ofparticipation. A minority of study clinicians (n = 15 and allphysiotherapists) recruited more than 50% of the participants(n = 480). Thirty-two clinicians (23.2%) did not recruit asingle participant during the study period. The top 15clinicians (clinicians with recruitment rate N2 patients permonth) recruited a median of 24 participants to the study anddetermined that 164 patients were ineligible. For the lowrecruiters (clinicians with recruitment rate ≤2 patients permonth), the median was 3 and determined that 472 patientswere ineligible.
Clinician's descriptive data are presented in Table 2. Mostof the study clinicians were physiotherapists (98%) and had amean clinical experience managing LBP of 18.5 years. Morethan half of the clinicians preferred the training to be performedby telephone (57.2%) rather than face to face (42.8%).
Factors That Influenced Recruitment Rate: Univariate and MultivariateAnalyses
Five clinician factors (sex, age, clinical experience aspracticing clinician, clinical experience managing LBP, andwhether clinicians were members of their respective associa-tions) and 5 operational factors (training method, number ofletters, number of telephone calls, number of contacts—letter/e-mail/telephone call, and number of ineligible patientsreferred) revealed a significant association (P b .2) with
Table 3. Characteristics Associated With Recruitment oParticipants, Univariate and Multivariate Analysis (n = 138)
Factors
UnivariateAnalysis
MultivariateAnalysis
IRR (95% CI) IRR (95% CI)
Clinicians factorsSex, male 2.02 (1.23-3.31) a –Age 1.04 (1.01-1.06) a –Profession,physiotherapist
1.32 (0.80-2.18) –
Current position,employee c
0.49 (0.08-2.95) –
Clinical experience, y 1.03 (1.00-1.05) a –Clinical experiencemanaging LBP, y
1.03 (1.01-1.06) a –
SES of suburb ofclinician clinic, high d
1.13 (0.63-2.03) –
Member of theirrespective association
0.41 (0.24-0.72) a 0.42 (0.25-0.71) b
Operational factorsTraining method,telephone
2.98 (1.84-4.81) a 4.01 (2.38-6.79) b
No. of letters 0.95 (0.89-1.01) a –No. of telephone call 0.92 (0.82-1.03) a –No. of e-mails 0.94 (0.79-1.12) –Total no. of contacts,letter/e-mail/telephone call
0.97 (0.93-1.01) a –
No. of ineligible patients 1.04 (1.01-1.08) a 1.03 (1.02-1.06) b
With continuous variables, the IRR can be interpreted as the rate ratio in whichthe total number of participants is expected to change with a 1-unit increase inthe exposure variable. With binary variables, the IRR indicates the expectedchange in rate of patient recruitment when the variable is positive.CI, confidence interval; IRR, Incident rate ratio; LBP, low back pain.
a Candidate variables with significant univariate association (P b .2)that entered the multivariate analysis.
b P b .0001.c Employee compared with business owner.d Suburb socioeconomic status—determined by comparing the clinic
postcode to Australia Bureau of Statistics data on economic advantage anddisadvantage, defined as high, greater than or equal to AU $577, or lowless than AU $577.
5Steffens et alJournal of Manipulative and Physiological TherapeuticsFactors Predicting Recruitment of ParticipantsVolume xx, Number x
189
f
,
patient recruitment in the univariate analyses (Table 3) andwere candidates for the multivariate analysis.
After the backward stepwise regression, 3 variables wereremaining in the model. These variables are presented inTable 3 with incident rate ratios. From the clinician'scharacteristics, only whether clinicians were members oftheir respective associations was associated (inversely) withrecruitment. Clinicians that were members of theirrespective associations had a recruitment rate less thanhalf that of nonmembers (P b .001). The other 2 variablesassociated with recruitment were operational factors(training method and number of ineligible patientsreferred). Clinicians that were trained over the telephonehad a recruitment rate 4.01 times greater than those trainedface to face. Similarly, clinicians that referred a highernumber of ineligible participants had a greater recruitmentrate, with incident rate ratio of 1.03 (P b .0001).
DISCUSSION
Main FindingsAlthough 41.3% of the clinicians referred 2 or less eligible
participants during the study period, we successfully recruitedour target sample (n = 951) in a reasonable period of time(13.8 months). The overall recruitment rate was 0.99 patients,per clinician, per month of participation. This providesevidence that, in relatively simple observational studies forLBP, where clinicians are reimbursed for their time, it shouldbe relatively easy to recruit large numbers of participants fromprimary care. The recruitment success of this study wasachieved mainly because 15 primary care clinicians recruited50.6% of the sample.
Among the clinician and operational characteristicsinvestigated, 3 of 14 factors increased recruitment. However,these factors must be considered carefully as they areunsurprising or uninterpretable and the practical implicationsseem limited. Clinicians that were members of theirrespective associations had a recruitment rate less thannonmembers conflicts with the view that members whoengage in continuing education are more likely to beinterested in research. Even in studies that recruit the requiredsample size in a reasonable time frame, identifying factorsthat increase recruitment seems challenging, providing astrong case for the urgent need for more studies.
This study investigated clinician and operational charac-teristics and did not assess the characteristics of patients;investigation would require a different study design, that is,one where the characteristics of patients not recruited to thetrial are also determined. Patients may decline participationfor a variety of reasons including lack of time, lack ofunderstanding of relevance of research question, alreadyanxious about their disease, and others. Understanding betterthe patient characteristics that predict participation in clinicaltrials of back pain is an important area for future research.
Comparison With Other StudiesAlmost universally, recruitment is a challenge.26 To date,
most of the studies investigating factors that influencerecruitment of patients in primary care have focused onRCTs.27 Although many of the challenges encountered withpatient recruitment to RCTs are also applicable to observationalstudies, there may be important differences.28 There is asignificant lack of research on observational study designs. Weidentified no previous observational studies that reportedrecruitment rates in primary care and, therefore, could notcompare our research findingswith previous studies in the field.
Findings fromour observational study show that clinicianstrained by telephone and those who refer ineligible patientsthroughout the study are likely to have higher recruitmentrates. Clinicians who are a member of their professionalassociation are less likely to recruit. These factors have notpreviously been identified in earlier studies as important to
6 Journal of Manipulative and Physiological TherapeuticsSteffens et alMonth 2015Factors Predicting Recruitment of Participants
190
recruitment. The latest Cochrane review on strategies toinfluence recruitment for RCTs found that using telephonereminders, opt-out procedures requiring potential partici-pants to contact the trial team if they did not want to becontacted about a trial, making the trial open rather thanblinded, and mailing a questionnaire about home safety topotential participants to an injury prevention trial arefactors that improved recruitment in high-quality studies.5,7
A systematic review reported on a variety of strategies toimprove recruitment, the most common being the use ofletters, e-mails, and telephone calls to clinicians3,4; however,similar to our findings, these factors did not significantlyincrease recruitment.
Limitations and StrengthsSome of the strengths of this study are the large number
of clinicians that participated in this LBP study and thelarge number of patients recruited in a short period. Theselarge numbers have enabled us to robustly assess clinicianand operational features that, in combination, could leadto successful recruitment of patients to LBP studies inprimary care.
Oneweakness of this studywas that the factors investigatedmay apply predominantly to simple observational studies. Thesimplified design, minimal role required by the studyclinicians, and the reimbursement for the time and inconve-nience may have contributed to the rapid patient recruitment.The factors associated with recruitment were relativelyunexpected. Other clinician characteristics not investigated inthis study may be important in influencing recruitment.
Although previous studies have described financialreimbursement as important for recruiting clinicians andpatients,9,29 one of the few systematic reviews does notsupport this. Clinicians who identify reimbursement as a keyreason for participating in anRCT are nomore likely to recruitpatients than those who do not.20 In the current observationalstudy, financial reimbursement for both clinicians andparticipants may have influenced recruitment; however, wecould not assess this using our current methods. In addition,we could not assess if practice-level characteristics of theproviders affected recruitment. Factors such as full-time vspart-time employment status, ownership ofmultiple practices,employment of other therapists, specialty practices, number ofpatients treated per week, average duration of consultationsession, referral patterns, university affiliation, or otherorganizational factors were not measured in the currentstudy, and therefore, their effect on patient recruitmentremains unclear. Future research might explore the influenceof practice characteristics on research recruitment rates. Inaddition, we did not attend the clinics to observe if theproviders were completing participant recruitment as perprotocol, and this is a limitation of the study.
In this study, the money reimbursed for eligible and/orineligible patients was to cover clinicians' time spent in
recruiting participants, explaining the study to them, andliaising with the study staff and clerical and administrationcosts. The time involved in this process took from 30 to 45minutes, and the reimbursement valued the clinician's timeaccording to prevailing physiotherapy consultation fees. Thisstrategy was used to ensure that financial reimbursement wasnot considered an inducement to participate. To minimizeerrors, eligibility criteria were double checked by a studyresearcher at the time of the interview.
We advised at the initial training and re-enforcedthroughout the whole study period that all study cliniciansshould invite all consecutive patients presenting with LBP tothe study. If clinicians did not enroll consecutive patients, itwould have the potential to include sampling bias in the parentTRIGGERS study. However, we do not believe that thiswouldintroduce bias into this study of factors influencing recruitment.
In this study, clinicians were not randomly allocated toeither training by telephone or by face-to-face visit. Thetraining method was determined by the clinician, and thischoice may reflect other confounders in the practice.30
Clinicians that opted to be trained by telephone may havechosen this due to their busier clinic schedule suggestingcontact with a larger number of patients per day than otherclinicians and, hence, an increased opportunity to recruit.Regardless, the finding that, in a simple observational study,training of clinicians by telephone appears to be at least aseffective as face-to-face training for recruitment has impor-tant implications. The training administered by telephonewasdelivered one to one, as opposed to face-to-face trainingwhere 1 or more clinicians (up to 5) were trained at a giventime. The individualized training and feedback are effectivein improving recruitment.31 The results that better recruit-ment is associatedwith referral of more ineligible participantscould be due to a higher overall number of invitations. Therelationwith professionalmembership is a complete mystery.
The recruitment of primary care clinicians in this studywas based on an invitation letter sent bymail, and despite thisrelatively passive method of recruitment, we could interest asuitable number of clinicians in participating in our study in arelatively short while. Had we used more active methods ofencouraging clinicians to participate, such as providingeducational seminars and distributing advertisements andnewsletters to association databases, we may have had morerapid recruitment of clinicians. Chiropractors were identifiedby a Google search using the words “Chiropractor Sydney.”The order of appearance in the search may be affected by thesearch engine optimization, hence, favoring chiropractorswho have greater knowledge. However, it remains unclearwhether these clinicians would have recruited more subjectsto the study.
In this study, we contacted the Australian PhysiotherapyAssociation as our primary means of identifying physiothera-pists but used a Google search to identify chiropractors. Itwould have been better to use similar methods to identifyboth professions. Future studies should use similar methods
7Steffens et alJournal of Manipulative and Physiological TherapeuticsFactors Predicting Recruitment of ParticipantsVolume xx, Number x
191
to recruit primary care clinicians. Either, physiotherapy andchiropractic associations should be contacted and using theGoogle engine to identify nonmember clinicians.
Practical Applications• This study provides evidence that, in relativelysimple observational studies for LBP, it should berelatively easy to recruit large numbers ofparticipants from primary care.
• However, even in studies that recruit the requiredsample size in a reasonable time frame, identifyingfactors that increase recruitment seems challeng-
Future ResearchThere is a small but emerging body of literature on factors
influencing recruitment. The operational factor (trained bytelephone) identified as influencing recruitment in this studymay only be appropriate in simple study designs but should beinvestigated further due to the potential to make clinicianrecruitment easier and cheaper. To date, there are no studiesinvestigating if primary care clinicians that are members oftheir respective associations are more or less likely toparticipate and recruit patients for research. This informationwould be of value, as clinicians that aremembersmay be easierto contact through their professional association. Future studiesshould also investigate if practice-level characteristics couldinfluence patient recruitment.
In addition, other potentially important factors that couldinfluence recruitment and/or clinicians' behavior, such asnumber of contacts madewith the clinician and reimbursementfor time involved for the clinician and administrative staff, needto be considered in future studies. A better understanding of thepatient characteristics associated with successful recruitment isalso urgently needed. Further research on factors that couldmaximize recruitment rate must be conducted. Factors thatinfluence patient recruitment in primary care are complex andremain unclear.
ing, providing a strong case for the urgent need formore studies in this area.
CONCLUSIONS
Although patient recruitment is a challenge, this study ofrecruiting participants from primary care clinicians for a largeobservational study of LBP has been positive. Factorsidentified as influencing recruitment were professionalassociation (negative association), training by telephone, andreferring a higher number of ineligible participants.
This study has revealed factors associated with recruit-ment rate, although the ability to predict which clinician willrecruit based on operational and clinicians characteristicsseems restricted.
FUNDING SOURCES AND POTENTIAL CONFLICTS OF INTEREST
No funding sources or conflicts of interest were reportedfor this study.
CONTRIBUTORSHIP INFORMATION
Concept development (provided idea for the research):D.S., CM., M.F., M.H., L.P., C.W., J.L.Design (planned the methods to generate the results): DS.,C.M., M.F., M.H., L.P., C.W., J.L.
Supervision (provided oversight, responsible for orga-nization and implementation, writing of the manu-script): D.S., C.M., M.F, M.H, L.P, C.W, J.L.Data collection/processing (responsible for experi-ments, patient management, organization, or reportingdata): D.S., C.M., M.F., M.H., L.P., C.W., J.L.Analysis/interpretation (responsible for statistical anal-ysis, evaluation, and presentation of the results): D.S.,C.M., M.F., M.H., L.P., C.W., J.L.Literature search (performed the literature search): N.A.Writing (responsible for writing a substantive part of themanuscript): D.S., C.M., M.F., M.H., L.P., C.W., J.L.Critical review (revised manuscript for intellectual content,this does not relate to spelling and grammar checking):D.S.,C.M., M.F., M.H., L.P., C.W., J.L.
REFERENCES
1. Blanton S, Morris D, Prettyman M, et al. Lessons learned inparticipant recruitment and retention: the EXCITE trial. PhysTher 2006;86:1520-33.
2. Bowen J, Hirsch S. Recruitment rates and factors affectingrecruitment for a clinical trial of a putative anti-psychotic agentin the treatment of acute schizophrenia. Hum Psychopharmacol1992;7:337-41.
3. McDonald A, Knight R, Campbell M, et al. What influencesrecruitment to randomised controlled trials? A review of trialsfunded by two UK funding agencies. Trials 2006;7:1-8.
4. Sully BG, Julious SA, Nicholl J. A reinvestigation of recruitmentto randomised, controlled, multicenter trials: a review of trialsfunded by two UK funding agencies. Trials 2013;14:166.
5. Treweek S, Pitkethly M, Cook J, et al. Strategies to improverecruitment to randomised controlled trials. Cochrane DatabaseSyst Rev 2010;(4):MR000013.
6. Mapstone J, Elbourne D, Roberts I. Strategies to improverecruitment to research studies. Cochrane Database Syst Rev2007;(2):MR000013.
7. Treweek S, Lockhart P, Pitkethly M, et al. Methods to improverecruitment to randomised controlled trials: Cochrane systematicreview and meta-analysis. BMJ Open 2013;3:e002360.
8 Journal of Manipulative and Physiological TherapeuticsSteffens et alMonth 2015Factors Predicting Recruitment of Participants
192
8. Thoma A, Farrokhyar F, McKnight L, Bhandari M. How tooptimize patient recruitment. Can J Surg 2010;53:205-10.
9. Rosemann T, Szecsenyi J. General practitioners' attitudestowards research in primary care: qualitative results of a crosssectional study. BMC Family Pract 2004;5:1-5.
10. Foy R, Parry J, Duggan A, et al. How evidence based arerecruitment strategies to randomized controlled trials in primarycare? Experience from seven studies. Fam Pract 2003;20:83-92.
11. Lannin N, Cusick A. Factors affecting patient recruitment in anacute rehabilitation randomized controlled trial. Am J OccupTher 2006;60:177-81.
12. Page MJ, French SD, McKenzie JE, O'Connor DA, Green SE.Recruitment difficulties in a primary care cluster randomisedtrial: investigating factors contributing to general practitioners'recruitment of patients. BMC Med Res Methodol 2011;11:35.
13. Chalmers I, Rounding C, Lock K. Descriptive survey of non-commercial randomised controlled trials in the UnitedKingdom, 1980-2002. BMJ 2003;327:1-4.
14. Bower P, Wilson S, Mathers N. Short report: how often do UKprimary care trials face recruitment delays? Family Pract 2007;24:601-3.
15. Abraham N, Young J, Solomon M. A systematic review ofreasons for nonentry of eligible patients into surgicalrandomized controlled trials. Surgery 2006;139:469-83.
16. Jenkinson CE, Winder RE, Sugg HV, et al. Why do GPsexclude patients from participating in research? An explorationof adherence to and divergence from trial criteria. Fam Pract2014;31:364-70.
17. Spaar A, Frey M, Turk A, Karrer W, Puhan MA. Recruitmentbarriers in a randomized controlled trial from the physicians'perspective: a postal survey. BMCMedResMethodol 2009;9:14.
18. Murray CJ, Vos T, Lozano R, et al. Disability-adjusted lifeyears (DALYs) for 291 diseases and injuries in 21 regions,1990-2010: a systematic analysis for the Global Burden ofDisease Study 2010. Lancet 2012;380:2197-223.
19. Williams C, Latimer J, Maher C, et al. PACE—the first placebocontrolled trial of paracetamol for acute low back pain: design
of a randomised controlled trial. BMC Musculoskelet Disord2010;11:1-6.
20. Rendell JM, Merritt RD, Geddes JR. Incentives and disincen-tives to participation by clinicians in randomised controlledtrials. Cochrane Database Syst Rev 2007:MR000021.
21. Prescott R, Counsell C, Gillespie W, et al. Factors that limit thequality, number and progress of randomised controlled trials.Health Technol Assess 1999;3:1-143.
22. Steffens D, Ferreira ML, Maher CG, et al. Triggers for anepisode of sudden onset low back pain: study protocol. BMCMusculoskelet Disord 2012;13:7.
23. Williams CM, Maher CG, Latimer J, et al. Efficacy ofparacetamol for acute low-back pain: a double-blind, rando-mised controlled trial. Lancet 2014;384:1586-96.
24. Improving primary health care for all Australians. AgeingDoHa. Canberra: Commonwealth of Australia; 2011.
25. Stata Statistical Software: Release 12 [computer program].Version 12. College Station, TX: StataCorp LP; 2011.
26. Ewing G, Rogers M, Barclay S, et al. Recruiting patients into aprimary care based study of palliative care: why is it sodifficult? Palliat Med 2004;18:452-9.
27. Rollman B, Fischer G, Zhu F, Belnap B. Comparison ofelectronic physician prompts versus waitroom case-finding onclinical trial enrollment. J Gen Intern Med 2008;23:447-50.
28. Hayward R, Porcheret M, Mallen C, Thomas E. Recruitingpatients and collecting data for an observational study usingcomputerised record pop-up prompts: the PROG-RES study.Prim Health Care Res Dev 2013;14:21-8.
29. Langley C, Gray S, Selley S, Bowie C, Price C. Clinicians'attitudes to recruitment to randomised trials in cancer care: aqualitative study. J Health Serv Res Policy 2000;5:164-9.
30. Mann B, Wood E. Confounding in observational studiesexplained. Open Epidemiol J 2012;5:18-20.
31. Donovan JL, Lane JA, Peters TJ, et al. Development of acomplex intervention improved randomization and informedconsent in a randomized controlled trial. J Clin Epidemiol 2009;62:29-36.
Chapter Ten
Conclusions
193
10.1. Aim
The primary aim of this thesis was to contribute to a better understanding of the
mechanisms for low back pain. New knowledge was acquired in a number of ways that
included interviewing primary care clinicians, conducting relevant systematic reviews,
measuring exposure to back pain risk factors, and exploring prognosis for patients with
chronic low back pain.
The first study contributed knowledge on the mechanisms of onset of back pain, identifying
the short and long-term risk factors that primary care clinicians consider important in
triggering an episode of low back pain (Chapter Two). The studies described in Chapter
Four and Chapter Five continued this theme investigating a range of physical, psychosocial
(Chapter Four) and environmental factors (Chapter Five) that increase risk for an episode
of sudden onset, acute low back pain. The study presented in Chapter Six aimed to
systematically review whether magnetic resonance imaging findings of the lumbar spine
predict future low back pain. In terms of back pain management, the study presented in
Chapter Seven aimed to examine the prognosis and prognostic factors for patients with
chronic low back pain. The systematic review presented in Chapter Eight aimed to
investigate if the presence of magnetic resonance imaging findings identifies patients with
low back pain who respond better to particular interventions. Finally, the study presented in
Chapter Nine aimed to identify factors that influence recruitment of participants to a large
observational study.
10.2. Overview of principal findings
The observational study described in Chapter Two revealed that Australian primary
care clinicians believe that biomechanical risk factors (89.3%), such as lifting (17.5%),
prolonged sitting (9.1%) and physical trauma (8.9%), are the most likely short-term risk
factors for low back pain. Biomechanical risk factors (54.2%), such as prolonged sitting
(13.4%) and lifting (10.9%), and individual risk factors (39%), such as physical inactivity
(9.1%) and other individual risk factors (5.8%) are the most endorsed long-term risk factors.
Surprisingly, commonly reported risk factors, such as psychological or psychosocial factors
(0.6% and 3.1% for short and long-term respectively), and genetic risk factors (0.0% and
0.2% for short and long-term respectively) were considered unimportant by clinicians.
194
Prior to this thesis there had been no high quality study that used a case-crossover
design to determine the effects of physical, psychosocial and meteorological factors on the
risk of an episode of sudden onset, acute back pain. The case-crossover study described in
Chapter Four demonstrated for the first time that brief exposure to a range of physical
factors (e.g. manual tasks involving awkward postures, or manual tasks involving an object
that could not be positioned close to the body) and psychosocial factors (being distracted
during a task or being fatigued) can considerably increase the risk of an episode of low back
pain. However, these associations were not moderated by habitual physical activity, BMI,
previous episodes of low back pain, depression or anxiety. Age moderated the risk associated
with exposure to heavy loads and sexual activity. Chapter Five presents a case-crossover
study investigating the influence of weather conditions on risk of low back pain. The findings
demonstrated that there was no association between temperature, relative humidity, air
pressure, wind direction and precipitation and risk of back pain. Higher wind speeds slightly
increased the odds of back pain onset, although the effect was not considered clinically
important.
The systematic review investigating magnetic resonance imaging (MRI) findings as a
predictor of future low back pain (Chapter Six) identified twelve longitudinal studies. Of
these, most enrolled small samples, investigated different MRI findings and presented varied
clinical outcomes. Across the 46 MRI findings investigated, no consistent associations with
clinical outcomes were identified. Three different studies reported associations for Modic
changes with pain, disc degeneration with disability in samples with current low back pain
and disc degeneration with pain in a mixed sample of patients with and without current low
back pain.
The prognosis study described in Chapter Seven revealed that patients with chronic
low back pain presenting to a private, community-based group exercise program improved
clinical outcomes significantly, with greater improvements in disability compared to pain at
12 months. The predictors investigated accounted for only 10% and 15% of pain and
disability outcomes, respectively, suggesting that there is much to learn about the factors
influencing recovery in this group of patients.
Chapter Eight reports the findings from a systematic review investigating if the
presence of magnetic resonance imaging findings identifies patients with low back pain who
respond better to particular interventions. Although this review identified eight clinical trials,
195
investigating 38 interactions for low back pain and sciatica, only two individual trials
suggested some magnetic resonance imaging findings that might be effect modifiers for
specific interventions. It is unknown if these subgroup interactions accurately represent the
association, given the limited number of suitable trials and the heterogeneity across them.
The observational study described in Chapter Nine found three variables (clinicians
not members of their professional association, clinicians trained by phone and clinicians who
referred a larger number of ineligible patients) associated with the rate at which primary care
clinicians recruited patients to the study. However, the applicability and understanding of
some of these factors seems counterintuitive; indicating that identifying primary care
clinicians likely to recruit at faster rates is complex.
The findings of these studies have advanced the understanding of mechanism of low
back pain in relation to risk, prognosis and response to treatment. There are several important
implications and directions for future research that arise from these studies.
10.3. Implications and suggestions for future research
10.3.1. Mechanism: Risk factors for low back pain
Currently, there are a number of recognised risk factors for low back pain
(HOOGENDOORN et al., 2000; LINTON, 2001; HAMBERG-VAN REENEN et al., 2007;
HENEWEER et al., 2011; LANG et al., 2012), however, most of these risk factors are based
on long term exposure (e.g. smoking), and many are not modifiable (e.g. age). The
identification of risk factors in primary care is crucial to help the development of new
research, which may lead to future prevention programs (RUBIN, 2007). The study presented
in Chapter Two, based on primary care clinicians views, identified important short
(biomechanical) and long-term (biomechanical and individual) risk factors for low back pain.
While primary care clinicians beliefs on biomechanical and individual risk factors are aligned
with past research (TAYLOR et al., 2014), the lack of consideration towards psychosocial
and genetic risk factors is quiet surprising. Thus, the reasons why primary care clinicians
consider psychosocial and genetic risk factors unimportant need to be further investigated to
aid management and prevention of this condition. Previous studies suggest that psychosocial
risk factors (e.g. low job control) are often correlated with biomechanical risk factors (e.g.
intensive load) (MACDONALD et al., 2001). One reason why experienced clinicians think
196
these factors are not important, may be that they have limited expertise in assessing these
factors as triggers for low back pain. Another reason may be that this population represents a
general sample of the population, while previous studies have focused on occupational
settings (HOOGENDOORN, VAN POPPEL et al., 2000; KERR et al., 2001; HOY et al.,
2010). Although low back pain is commonly reported as multifactorial (TAYLOR, GOODE
et al., 2014), future studies are needed to investigate if two or more factors present higher risk
of back pain development.
The large case-crossover study presented in Chapter Four provides clear evidence
that brief exposure to a range of physical and psychosocial triggers substantially increased
risk for a new episode of back pain. One of the advantages of this study is the novel design
used and that the risk factors found to increase the risk of a low back pain episode are readily
modifiable. In this robust design, participants act as their own controls, and therefore the
perfect matching of cases and controls eliminates potential effects of unmeasured
confounders, such as genetic and lifestyle influences, on back pain development
(HOOGENDOORN, VAN POPPEL et al., 2000; HENEWEER, STAES et al., 2011). The
fact that the risk factors found in this study are modifiable (e.g. lifting) will support the
development of new prevention approaches for back pain. Previous research has focused on
factors that are not modifiable (e.g. age and height) or involve long-term exposure (e.g.
smoking) (KOPEC, SAYRE and ESDAILE, 2004; SHIRI et al., 2010). While we found a
strong association with most of factors investigated, future studies are needed to validate
these factors in other populations. Additionally, there may be other potential risk factors we
failed to measure that may be modifiable.
Well-designed studies controlling exposure to these risk factors, either at home or in
the workplace, should be a priority as secondary prevention of low back pain could reduce
individuals’ suffering and reduce heath expenditure. Also, future studies could evaluate the
effect of educating patients with previous history of back pain, providing accurate
information about the natural history of the condition to help reduce patient’s concerns and to
promote compliance with prevention strategies. The results of this study will also have
significant implications for clinicians and policy makers for the control of low back pain
episode.
The results of the case-crossover study presented in Chapter Five showed no
association between temperature, relative humidity, air pressure, wind direction, precipitation
197
and sudden onset, acute low back pain. Higher wind speed and wind gust speed, only slightly
increase the risk of back pain and, while this reached statistical significance, the magnitude of
the increase was not considered clinically important. Interestingly, this is the first study to use
a robust case-crossover design to investigate the influence of the weather on back pain.
Future research could focus on a wide range of patients’ characteristics (e.g. beliefs, mood,
memory) to explain individual differences in weather sensitivity. Future research should
determine if this insignificant association of weather parameters with back pain found in
Sydney, Australia, holds in more extreme climate conditions and in different clinical settings.
At the present, it seems that other risk factors are more important for the development of
acute back pain, such the factors investigated in Chapter Four (physical and psychosocial).
Lumbar imaging is routinely prescribed for the diagnosis of patients with low back
pain (JENSEN et al., 2008), however, the importance of the findings remains controversial
(MODIC and ROSS, 2007). Previous studies revealed high rates of abnormalities on MRI in
people without low back pain (JARVIK et al., 2001), though, this may represent markers of
early pre-symptomatic disease that is later characterized by episodes of back pain. Chapter
Six reported the results from a systematic review on the association of magnetic resonance
imaging and future low back pain. Although this review found that three single studies
presented significant associations (Modic changes with pain and disc degeneration with
disability, in samples with current low back pain; and disc degeneration with pain in a mixed
sample), it is uncertain if these estimates accurately represent the association given the
quality, sample size and heterogeneity among the included studies. Thus, further large, high-
quality studies that address the aforementioned problems are clearly needed to help determine
the clinical meaningfulness of lumbar imaging in relation to low back pain.
Investigations into the association between lumbar MRI findings and low back pain
are complicated as multiple findings are present at the same time. Findings such as lumbar
intervertebral disc protrusions or endplate changes, almost always co-exist with other
degenerative disc findings, such as disc height reduction and signal intensity (WANG,
VIDEMAN and BATTIE, 2012). An initial strategy to advance this area of investigation
would be to recognise which MRI findings typically occur together and whether clusters of
findings are more predictive of outcome than single findings.
198
10.3.2. Management: Prognosis and subgroups for low back pain
Understanding prognostic factors that are associated with better or worse disease
outcome can help identify possible determinants and causal pathways for low back pain,
which may lead to more effective management strategies (HAYDEN et al., 2010). The
findings of the prognosis study reported in Chapter Seven showed that patients with chronic
low back pain who presented to an exercise program incorporating cognitive behaviour
therapy improved considerably over the course of one year. However, the predictors
investigated accounted for only 10% and 15% of pain and disability outcomes, respectively.
This information on prognostic outcome is important for patients and clinicians as it helps to
set realistic expectations and can be used to guide decision making regarding the need for
additional interventions. It is likely that prognosis depends on multiple factors (HAYDEN et
al., 2009). Further investigation of important and novel predictors are needed (e.g. stress, job
satisfaction, beliefs). Advanced phases of investigation are needed to progress the low back
pain prognosis field, including confirmation studies for prognostic factors with more frequent
(e.g. monthly) and longer follow-up (e.g. longer than 12 months).
Selecting a representative cohort is a key consideration in designing studies on the
prognosis of back pain. For studies investigating the prognosis of low back pain, the ideal is
to assemble a sample that is at risk of developing chronic low back pain and then identifying
an inception cohort from incident cases (COSTA LDA et al., 2007). These inception cohorts
generally provide stronger evidence on prognosis than cohorts assembled from available
cases (e.g. survival cohorts) and are therefore recommended for future research. Lastly,
intervention strategies for low back pain should make greater use of prognostic data to
support the theoretical rationale for interventions and to identify the group of patients most
likely to benefit from it.
The effects of most clinical interventions for the management of low back pain
reported in trials are usually classified as small or moderate at best (HAYDEN et al., 2005).
There is always the argument that different patients will not respond similarly to the same
intervention and, therefore, subgroups should be considered (COSTA LDA et al., 2013). The
systematic review in Chapter Eight found eight trials that investigated 38 subgroup
interactions; one presented a significant effect modifier for low back pain and one for sciatica
populations. Although some statistically significant subgroup interactions were noted, it is
questionable if the estimates accurately represent the effect modification. This is largely due
199
to the limited number, heterogeneity and overall quality of studies found. Interestingly,
subgroup studies are a research priority in the low back pain field since 2007 (HENSCHKE
et al., 2007; COSTA LDA, KOES et al., 2013), however, there are only a few clinical trials
and most are underpowered. Therefore, well-designed, adequately powered trials are
required. Moreover, the general content and reporting of subgroup analyses is rather poor. It
is thus recommended, that authors use available guidelines when performing subgroup
analyses to ensure that they are reliable and of a good standard (ROTHWELL, 2005).
Another problem with subgroup analysis is that the sample size required is around
four times larger than if the only interest was the main effect of treatment (CUZICK, 1999).
Therefore, acquiring a reasonable sample size is always a challenge for subgroup studies. The
combination of data across multiple studies may be a practical option to gain power and
overcome some of the concerns reported in our review. However, data should be combined
only when studies are homogeneous. This is not always obvious and requires great caution.
10.3.3. Factors influencing recruitment rate
Identifying important factors that influence recruitment to observational studies is
required to improve the efficiency, impact and success of research studies (WILLIAMS et al.,
2014). Many of the factors investigated in Chapter Nine did not appear to influence
participant recruitment rate. The identification of factors that increase recruitment remains
challenging, providing a strong case for the urgent need for more studies in this area. For this
reason, future research should appropriately focus on identifying other variables that could be
incorporated with factors already known to improve participant recruitment rate.
Recruiting participants to research studies in primary care setting presents some
unique challenges as primary care studies often rely on clinicians to screen and enrol patients.
One possible way to optimise recruitment of patients to observational studies is the use of a
computerised pop-up prompts. Previous studies have reported that one of the main problems
in recruiting patients was that clinicians are time poor and normally forget about the study
due to the large amount of patients seen per day (SPAAR et al., 2009). This new method
reminds clinicians of potential eligible patients using computer prompts when patients’
information is entered into their electronic medical records. This approach could potentially
enhance recruitment to future research studies.
200
Finally, the series of studies described in this thesis provide new, important
information that lead to a better understanding of the mechanisms of low back pain. It is
hoped that the findings and recommendations that arise from this thesis are widely adopted in
future low back pain research.
201
10.4. References
COSTA LDA, C., N. HENSCHKE, C. G. MAHER, K. M. REFSHAUGE, R. D. HERBERT,
J. H. MCAULEY, A. DAS and L. O. COSTA, Prognosis of chronic low back pain: design of
an inception cohort study. BMC Musculoskelet Disord, 8, p. 11, 2007.
COSTA LDA, C., B. W. KOES, G. PRANSKY, J. BORKAN, C. G. MAHER and R. J.
SMEETS, Primary care research priorities in low back pain: an update. Spine (Phila Pa
1976), 38, 2, p. 148-156, 2013.
CUZICK, J., Interaction, subgroup analysis and sample size. IARC Sci Publ, 148, p. 109-
121, 1999.
HAMBERG-VAN REENEN, H. H., G. A. ARIENS, B. M. BLATTER, W. VAN
MECHELEN and P. M. BONGERS, A systematic review of the relation between physical
capacity and future low back and neck/shoulder pain. Pain, 130, 1-2, p. 93-107, 2007.
HAYDEN, J. A., R. CHOU, S. HOGG-JOHNSON and C. BOMBARDIER, Systematic
reviews of low back pain prognosis had variable methods and results: guidance for future
prognosis reviews. J Clin Epidemiol, 62, 8, p. 781-796 e781, 2009.
HAYDEN, J. A., K. M. DUNN, D. A. VAN DER WINDT and W. S. SHAW, What is the
prognosis of back pain? Best Pract Res Clin Rheumatol, 24, 2, p. 167-179, 2010.
HAYDEN, J. A., M. W. VAN TULDER, A. MALMIVAARA and B. W. KOES, Exercise
therapy for treatment of non-specific low back pain. Cochrane Database Syst Rev, 3, p.
CD000335, 2005.
HENEWEER, H., F. STAES, G. AUFDEMKAMPE, M. VAN RIJN and L. VANHEES,
Physical activity and low back pain: a systematic review of recent literature. Eur Spine J, 20,
6, p. 826-845, 2011.
HENSCHKE, N., C. G. MAHER, K. M. REFSHAUGE, A. DAS and J. H. MCAULEY, Low
back pain research priorities: a survey of primary care practitioners. BMC Fam Pract, 8, p.
40, 2007.
HOOGENDOORN, W. E., M. N. VAN POPPEL, P. M. BONGERS, B. W. KOES and L. M.
BOUTER, Systematic review of psychosocial factors at work and private life as risk factors
for back pain. Spine (Phila Pa 1976), 25, 16, p. 2114-2125, 2000.
HOY, D., P. BROOKS, F. BLYTH and R. BUCHBINDER, The Epidemiology of low back
pain. Best Pract Res Clin Rheumatol, 24, 6, p. 769-781, 2010.
202
JARVIK, J. J., W. HOLLINGWORTH, P. HEAGERTY, D. R. HAYNOR and R. A. DEYO,
The Longitudinal Assessment of Imaging and Disability of the Back (LAIDBack) Study:
baseline data. Spine (Phila Pa 1976), 26, 10, p. 1158-1166, 2001.
JENSEN, T. S., J. KARPPINEN, J. S. SORENSEN, J. NIINIMAKI and C. LEBOEUF-YDE,
Vertebral endplate signal changes (Modic change): a systematic literature review of
prevalence and association with non-specific low back pain. Eur Spine J, 17, 11, p. 1407-
1422, 2008.
KERR, M. S., J. W. FRANK, H. S. SHANNON, R. W. NORMAN, R. P. WELLS, W. P.
NEUMANN and C. BOMBARDIER, Biomechanical and psychosocial risk factors for low
back pain at work. Am J Public Health, 91, 7, p. 1069-1075, 2001.
KOPEC, J. A., E. C. SAYRE and J. M. ESDAILE, Predictors of back pain in a general
population cohort. Spine (Phila Pa 1976), 29, 1, p. 70-77; discussion 77-78, 2004.
LANG, J., E. OCHSMANN, T. KRAUS and J. W. LANG, Psychosocial work stressors as
antecedents of musculoskeletal problems: a systematic review and meta-analysis of stability-
adjusted longitudinal studies. Soc Sci Med, 75, 7, p. 1163-1174, 2012.
LINTON, S. J., Occupational psychological factors increase the risk for back pain: a
systematic review. J Occup Rehabil, 11, 1, p. 53-66, 2001.
MACDONALD, L. A., R. A. KARASEK, L. PUNNETT and T. SCHARF, Covariation
between workplace physical and psychosocial stressors: evidence and implications for
occupational health research and prevention. Ergonomics, 44, 7, p. 696-718, 2001.
MODIC, M. T. and J. S. ROSS, Lumbar degenerative disk disease. Radiology, 245, 1, p. 43-
61, 2007.
ROTHWELL, P. M., Treating individuals 2. Subgroup analysis in randomised controlled
trials: importance, indications, and interpretation. Lancet, 365, 9454, p. 176-186, 2005.
RUBIN, D. I., Epidemiology and risk factors for spine pain. Neurol Clin, 25, 2, p. 353-371,
2007.
SHIRI, R., J. KARPPINEN, P. LEINO-ARJAS, S. SOLOVIEVA and E. VIIKARI-
JUNTURA, The association between smoking and low back pain: a meta-analysis. Am J
Med, 123, 1, p. 87 e87-35, 2010.
SPAAR, A., M. FREY, A. TURK, W. KARRER and M. A. PUHAN, Recruitment barriers in
a randomized controlled trial from the physicians' perspective: a postal survey. BMC Med
Res Methodol, 9, p. 14, 2009.
203
TAYLOR, J. B., A. P. GOODE, S. Z. GEORGE and C. E. COOK, Incidence and risk factors
for first-time incident low back pain: a systematic review and meta-analysis. Spine J, p.
2014.
WANG, Y., T. VIDEMAN and M. C. BATTIE, ISSLS prize winner: Lumbar vertebral
endplate lesions: associations with disc degeneration and back pain history. Spine (Phila Pa
1976), 37, 17, p. 1490-1496, 2012.
WILLIAMS, C. M., C. G. MAHER, M. J. HANCOCK, J. H. MCAULEY, C. W. LIN and J.
LATIMER, Recruitment rate for a clinical trial was associated with particular operational
procedures and clinician characteristics. J Clin Epidemiol, 67, 2, p. 169-175, 2014.
204
APPENDIX
205
Appendix A: Media coverage of Chapter Five
Television:
1. Channel 9 News: http://buff.ly/U5R25m
2. ABC News:
Broadcasts:
1. 2UE
2. 2UE 954 News Talk
3. 6PR Perth
4. 4BC Brisbane
Online:
1. Wiley: http://au.wiley.com/WileyCDA/PressRelease/pressReleaseId-111044.html
2. News.com.au: http://www.news.com.au/national/breaking-news/back-pain-dont-blame-it-
on-the-rain/story-e6frfku9-1226984395748
3. Life hacker Australia: http://www.lifehacker.com.au/2014/07/why-your-back-pain-has-
nothing-to-do-with-the-weather/
4. Business insider Australia: http://www.businessinsider.com.au/low-back-pain-dont-blame-
the-weather-2014-7
5. The Washington Post: http://www.washingtonpost.com/news/to-your-
health/wp/2014/07/10/no-uncle-fred-the-weather-has-nothing-to-do-with-your-back-pain/
206
6. Channel 9 News: http://news.ninemsn.com.au/health/2014/07/10/14/08/back-pain-don-t-
blame-it-on-the-rain
7. Live Science: http://www.livescience.com/46740-back-pain-not-linked-weather.html
8. Vancouver Desi: http://www.vancouverdesi.com/lifestyle/dont-curse-weather-for-low-
back-pain/768630/
9. News Medical: http://www.news-medical.net/news/20140710/Acute-episodes-of-low-
back-pain-not-linked-to-weather-conditions.aspx
10. Northern Voices Online: http://nvonews.com/dont-curse-weather-for-low-back-pain/
11.TVNZ One News: http://tvnz.co.nz/world-news/back-pain-don-t-blame-rain-6024295
12. Science Codex: http://www.sciencecodex.com/low_back_pain_dont_blame_the_weather-
137261
13. Medical Daily: http://www.medicaldaily.com/lower-back-pain-not-made-worse-
inclement-weather-such-humidity-or-cold-292130
14. E Newspaper of India: http://www.eni.network24.co/lifestyle/dont-curse-weather-for-
low-back-pain-12574_13
15. EurekAletr: http://www.eurekalert.org/pub_releases/2014-07/w-lbp070814.php
16.MedicalXpress: http://medicalxpress.com/news/2014-07-pain-dont-blame-weather.html
17. Daily Mail: http://www.dailymail.co.uk/wires/aap/article-2687005/Back-pain-dont-
blame-rain.html
18. Yahoo News: http://news.yahoo.com/feel-bones-back-pain-not-linked-weather-
071628526.html
207
19. The Australian: http://www.theaustralian.com.au/news/latest-news/back-pain-dont-
blame-it-on-the-rain/story-fn3dxiwe-
1226984395748?nk=179f05082c5bbe67589cada8dbfdbe1d
20. TechieTonics: http://www.techietonics.com/health-tonics/back-pain-does-not-link-to-the-
weather-conditions-posture-is-to-be-blamed.html
21. Apple Balla: http://www.appleballa.com/2014/07/154959/dont-curse-weather-low-back-
pain
22. Nature World News: http://www.natureworldnews.com/articles/7988/20140710/lower-
back-pain-related-weather-study.htm
23. Web MD: http://www.webmd.boots.com/back-pain/news/20140710/weather-lower-back-
pain
24. Daijiworld.com: http://www.daijiworld.com/news/news_disp.asp?n_id=247590
25. Science World Report:
http://www.scienceworldreport.com/articles/15929/20140710/low-back-pain-not-linked-to-
weather-conditions.htm
26. Health Medicine Network: http://healthmedicinet.com/i/low-back-pain-dont-blame-the-
weather/
27. Business Standard: http://www.business-standard.com/article/news-ians/don-t-curse-
weather-for-low-back-pain-114071000586_1.html
28. Best Health: http://besthealth.bmj.com/x/news/758164/news-
item.html?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+bestheal
th%2Fnews+(Best+Health%3A+Latest+news)
208
29. Topix: http://www.topix.com/forum/health/back-pain/TTCM5SSIBICJR3OTE
30. The times of India: http://timesofindia.indiatimes.com/life-style/health-
fitness/health/Dont-curse-weather-for-low-back-pain/articleshow/38136126.cms
31. University Herald: http://www.universityherald.com/articles/10332/20140710/lower-
back-pain-weather-conditions-sydney-australia.htm
32. Huffington Post US: http://www.huffingtonpost.com/2014/07/10/weather-low-back-
pain_n_5573968.html
33. National Pain Report: http://americannewsreport.com/nationalpainreport/researchers-say-
weather-not-linked-to-back-pain-8824219.html
34. Daily RX: http://www.dailyrx.com/low-back-pain-onset-not-tied-weather-factors-
humidity-and-temperature
35. Upstart Magazine: http://www.upstartmagazine.com/weather-doesnt-impact-lower-back-
pain-says-study/295012/
36. NVO News: http://nvonews.com/weather-doesnt-cause-lower-back-pain/
37. Daily Mail Australia: http://www.dailymail.co.uk/health/article-2687631/Dont-listen-
granny-weather-NO-impact-state-bad-back.html
38. KSBY 6: http://www.ksby.com/news/study-finds-weather-does-not-affect-back-pain/
39. Bayou Buzz: http://www.bayoubuzz.com/healthcare/healthcare-news/item/702916-
medical-news-today-back-pain-not-brought-on-by-weather-except-for-trivial-wind-effect
40. KYTX 19: http://www.cbs19.tv/story/25984211/health-alert-back-and-neck-pain-not-
linked-to-weather
209
41. My Foxny: http://www.myfoxny.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
42. 13 ABC: http://www.13abc.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
43. Daily Digest News: http://dailydigestnews.com/2014/07/researchers-stop-blaming-the-
weather-for-your-lower-back-pain/
44. The Daily Express: http://www.express.co.uk/life-style/health/487969/Research-shows-
no-link-between-cold-weather-and-back-pain
45. Philly.com:
http://www.philly.com/philly/health/HealthDay689584_20140710_Don_t_Blame_Bad_Weat
he for_Your_Aching_Back.html
46. Fox News: http://www.foxnews.com/health/2014/07/10/feel-it-in-your-bones-back-pain-
not-linked-with-weather/
47. Design & Trend: http://www.designntrend.com/articles/16542/20140710/weather-does-
not-affect-lower-back-pain-latest-study-suggests.htm
48. Headlines & Global News: http://www.hngn.com/articles/35733/20140710/weather-
conditions-increase-low-back-pain-study.htm
49. Counsel & Heal: http://www.counselheal.com/articles/10419/20140710/weather-patterns-
not-tied-to-back-pain.htm
50. CBS Atlanta: http://atlanta.cbslocal.com/2014/07/10/study-low-back-pain-not-linked-to-
weather/
51. TIME: http://time.com/2970789/achy-back-dont-blame-the-weather/
210
52. Science Recorder: http://www.sciencerecorder.com/news/lower-back-pain-dont-blame-
the-weather/
53. Medical News Today: http://www.medicalnewstoday.com/articles/279435.php
54. Los Angeles Times: http://www.latimes.com/science/sciencenow/la-sci-sn-back-pain-
bad-weather-20140710-story.html
55. Red Orbit: http://www.redorbit.com/news/health/1113188840/low-back-pain-not-caused-
by-the-weather-071014/
56. Tech Times: http://www.techtimes.com/articles/10146/20140710/achy-back-due-bad-
weather.htm
57. IndiLeak: http://www.indileak.com/dont-curse-weather-for-low-back-pain/
58. Nelms Pharmacy: https://nelmspharmacy.com/article.php?id=689584
59. Health Magazine: http://news.health.com/2014/07/10/dont-blame-bad-weather-for-your-
aching-back/
60. Science Daily: http://www.sciencedaily.com/releases/2014/07/140710081200.htm
61. Arthritis Research UK: http://www.arthritisresearchuk.org/news/general-
news/2014/july/weather-conditions-do-not-affect-low-back-pain.aspx
62. Mental Help:
http://www.mentalhelp.net/poc/view_doc.php?type=news&id=165586&cn=72
63. Smile-on News: http://www.smile-onnews.com/news/view/weather-not-to-blame-for-
low-back-pain
64. India Today: http://indiatoday.intoday.in/story/low-back-pain-monsoon/1/370700.html
211
65. CVBT: http://www.centralvalleybusinesstimes.com/stories/001/?ID=26265
66. Kuam News: http://www.kuam.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
67. People Say About: http://peoplesayabout.com/dont-blame-bad-weather-for-your-aching-
back/
68. News Hub:
http://au.newshub.org/feel_it_in_your_bones_back_pain_not_linked_with_weather_1926696.
html
69. News 10 ABC: http://www.news10.com/story/25985267/dont-blame-bad-weather-for-
your-aching-back
70. NEWS 724 : http://news724.com/feel-it-in-your-bones-back-pain-not-linked-with-
weather/
71. WTVM 9: http://www.wtvm.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
72. Immunology: http://immunologynews.blogspot.com.au/2014/07/lower-back-pain-not-
triggered-by.html
73. Economy Lead: http://www.economylead.com/lifestyle/back-pain-linked-weather-22667
74. Isupon: http://isupon.com/dont-curse-weather-for-low-back-pain/
75. Celebrities Snitch: http://celebritiessnitch.com/bad-back-dont-blame-the-rain-research-
shows-no-link-between-cold-weather-and-back-pain/
76. VEOOZ: http://www.veooz.com/news/wHJyc4h.html
212
77. 6 Minutes: http://www.6minutes.com.au/news/latest-news/weather-link-to-back-pain-a-
lot-of-hot-air
78. RTT NEWS: http://www.6minutes.com.au/news/latest-news/weather-link-to-back-pain-a-
lot-of-hot-air
79. News Ledge: http://www.newsledge.com/back-pain-blues-study-refutes-weather-link-
7672
80. Health Central:
http://www.healthcentral.com/dailydose/cf/2014/07/10/study_finds_lower_back_pain_not_tie
d_to_weather
81. Betty Hardwick Center:
http://www.bhcmhmr.org/poc/view_doc.php?type=news&id=165586&cn=72
82. Regular News Update: http://regularnewsupdate.com/?p=48887
83. 6 WLNS: http://www.wlns.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
84. Delhi Daily News: http://www.delhidailynews.com/news/Weather-does-not-cause-back-
pain-1405011439/
85. Biocompare: http://www.biocompare.com/Life-Science-News/165005-Low-Back-Pain-
Don-t-Blame-The-Weather/
86. Breaking News: http://palashbd.com/tag/says-study/
87. Fox 23: http://www.myfoxmaine.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
213
88. Chicago Tribune: http://www.chicagotribune.com/health/la-sci-sn-back-pain-bad-
weather-20140710,0,4484041.story
89. Silo Breaker: http://news.silobreaker.com/bad-weather-is-not-affecting-your-back-pain--
but-high-winds-might-5_2268078554707132465
90. Khaleej Times: http://www.khaleejtimes.com/kt-article-display-
1.asp?section=health&xfile=/data/health/2014/July/health_July10.xml
91. Rheumatology: http://www.rheumatologyupdate.com.au/latest-news/weather-link-to-
back-pain-a-lot-of-hot-air
92. Z News: http://zeenews.india.com/news/health/fitness/don-t-curse-weather-for-low-back-
pain_28709.html
93. Ethiopia News Hub:
http://et.newshub.org/don_t_curse_weather_for_low_back_pain_1938312.html
94. Science News Line: http://www.sciencenewsline.com/summary/2014071011150015.html
95. Health Living: http://healthylng.blogspot.com.au/2014/07/don-blame-bad-weather-for-
your-aching.html
96. Health Day – News for Healthier living: http://consumer.healthday.com/bone-and-joint-
information-4/backache-news-53/don-t-blame-bad-weather-for-your-aching-back-
689584.html
97. News Max – Health: http://www.newsmaxhealth.com/Health-News/backache-pain-
symptoms-weather/2014/07/10/id/581893/
98. NBC News: http://www.nbcnews.com/id/55615058
214
99. The Advertiser – Adelaide: http://www.adelaidenow.com.au/news/breaking-news/back-
pain-dont-blame-it-on-the-rain/story-fni6ul2m-
1226984395748?nk=f1339b0422d39b4ed34178ee98d4198a
100. Deccan Herald: http://www.deccanherald.com/content/418918/dont-curse-weather-low-
back.html
101. Fox 5 – Las Vegas: http://www.fox5vegas.com/story/25985267/dont-blame-bad-
weather-for-your-aching-back
102. Yotta Fire: http://yottafire.com/2014/07/does-weather-affect-back-pain-no-new-study-
finds/
103. ANI News: http://www.aninews.in/newsdetail9/story175283/weather-doesn-039-t-
cause-low-back-pain-say-scientists.html
104. The Morung Express: http://www.morungexpress.com/health/118511.html
105. The Free Press Journal: http://freepressjournal.in/dont-curse-weather-for-low-back-pain/
106. The University of Sydney:
http://sydney.edu.au/news/84.html?newscategoryid=1&newsstoryid=13764
107. 12 WBoy: http://www.wboy.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
108. Perth Now: http://www.perthnow.com.au/news/breaking-news/back-pain-dont-blame-it-
on-the-rain/story-fnhrvfuw-1226984395748?nk=f1339b0422d39b4ed34178ee98d4198a
109. Herald Sun Melbourne: http://www.heraldsun.com.au/news/breaking-news/back-pain-
dont-blame-it-on-the-rain/story-fni0xqi4-
1226984395748?nk=0f0749c3e80365b2b3cc4dc0e5f26705
215
110. Medicine Net: http://www.medicinenet.com/script/main/art.asp?articlekey=179416
111. Bright Surf:
http://www.brightsurf.com/news/headlines/98424/Low_back_pain_Dont_blame_the_weather
.html
112. New Kerala: http://www.24dunia.com/english-news/shownews/8/Don-t-curse-weather-
for-low-back-pain/19150408.html
113. Armenian Medical Network: http://www.health.am/ab/more/low-back-pain-dont-blame/
114. Eye Witness News: http://www.wfsb.com/story/25985267/dont-blame-bad-weather-for-
your-aching-back
115. Womens Health:
http://www.womenshealth.gov/news/healthday/en/2014/jul/10/689584.html
116. The Siasat Daily: http://www.siasat.com/english/news/dont-curse-weather-low-back-
pain
117. ABC News 4: http://www.abcnews4.com/story/25985267/dont-blame-bad-weather-for-
your-aching-back
118. KHQ: http://www.khq.com/story/25985267/dont-blame-bad-weather-for-your-aching-
back
119. InteliHealth: http://www.intelihealth.com/news/dont-blame-bad-weather-for-your-
aching-back?level=0
120. KMPH Fox 26: http://www.kmph.com/story/25985267/dont-blame-bad-weather-for-
your-aching-back
216
121. MedBroadcast:
http://www.medbroadcast.com/health_news_details.asp?news_id=31673&news_src=1&news
_channel_id=1007#.U7-TsvmSx8E
122. My Fox Houston: http://www.myfoxhouston.com/story/25985267/dont-blame-bad-
weather-for-your-aching-back
123. Mangalorean:
http://www.mangalorean.com/news.php?newstype=local&newsid=494792
124. The Daily Telegraph: http://www.dailytelegraph.com.au/news/breaking-news/back-pain-
dont-blame-it-on-the-rain/story-fni0xqi3-
1226984395748?nk=179f05082c5bbe67589cada8dbfdbe1d
125. Geelong Advertiser: http://www.geelongadvertiser.com.au/news/national/back-pain-
dont-blame-it-on-the-rain/story-fnjbnvyf-1226984395748
126. Spire Healthcare: http://www.spirehealthcare.com/patient-information/health-
news/orthopaedic-surgery/801734511-low-back-pain-cannot-be-linked-to-weather-
conditions-/
127. Health Canal: http://www.healthcanal.com/disorders-conditions/pain/52954-low-back-
pain-don-t-blame-the-weather.html
128. Wonder woman: http://wonderwoman.intoday.in/story/low-back-pain-
monsoon/1/111692.html
129. Terra Daily:
http://www.terradaily.com/reports/Low_back_pain_Dont_blame_the_weather_999.html
217
130. Fox 42: http://www.fox42kptm.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
131. Fox 2127: http://www.fox2127.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
132. People’s Media: http://peoplesmedia24.com/dont-blame-bad-weather-for-your-aching-
back/
133. The George Institute: http://www.georgeinstitute.org.au/media-releases/rain-and-back-
pain-not-
linked?utm_content=buffer4669e&utm_medium=social&utm_source=facebook.com&utm_c
ampaign=buffer
134. Harvard Medical School: http://www.health.harvard.edu/blog/bad-weather-isnt-blame-
aching-back-201407117262
135. Guelph Mercury: http://www.guelphmercury.com/living-story/4627655-study-finds-no-
link-between-weather-and-lower-back-pain/
136. TV 3: http://www.tv3.ie/entertainment_article.php?locID=1.803.1098&article=139873
137. Montlhly Prescribing Reference: http://www.empr.com/back-pain-dont-blame-the-
weather/article/360458/
138. Health Professionals Network: http://www.hcplive.com/articles/Weather-Conditions-
Not-Associated-With-Lower-Back-Pain
139. Doctors Lounge: http://www.doctorslounge.com/index.php/news/pb/48085
140. The Record: http://www.therecord.com/living-story/4627655-study-finds-no-link-
between-weather-and-lower-back-pain/
218
141. The Baltimore Sun: http://www.baltimoresun.com/health/la-sci-sn-back-pain-bad-
weather-20140710,0,2527158.story
142. 8 News Now: http://www.8newsnow.com/story/25985267/dont-blame-bad-weather-for-
your-aching-
back?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+lasvegasnow
%2Fhealth+(8NewsNOW.com+-+Health+News)
143. Start at 60: http://www.startsatsixty.com.au/health/stop-blaming-it-on-the-weather
144. Your News Now: http://www.hometownstations.com/story/25985267/dont-blame-bad-
weather-for-your-aching-back
145. WMBB Northwest Florida: http://www.wmbb.com/story/25985267/dont-blame-bad-
weather-for-your-aching-back
146. GTN News: http://www.mygtn.tv/story/25985267/dont-blame-bad-weather-for-your-
aching-back
147. Central Coast News: http://health.keyt.com/story/25985267/dont-blame-bad-weather-
for-your-aching-back
148. Health e Galaxy: http://www.hegalaxy.com/weather-conditions-not-associated-with-
low-back-pain/
149. The Hamilton Spectator: http://www.thespec.com/living-story/4627655-study-finds-no-
link-between-weather-and-lower-back-pain/
150. Australian News:
http://www.australiannews.net/index.php/sid/223696183/scat/88f7d0d02bea1b33/ht/Weather-
doesnt-cause-low-back-pain-say-scientists
219
151. 7 News Denver: http://www.thedenverchannel.com/news/study-finds-no-link-between-
certain-weather-conditions-lower-back-pain
152. Record Search Light: http://www.redding.com/news/national/study-finds-no-link-
between-certain-weather-conditions-lower-back-pain
153. Health News Digest: http://www.healthnewsdigest.com/news/weather0/Low-Back-Pain-
Don-t-Blame-the-Weather_printer.shtml
154. WBKO: http://wn.wbko.com/story/25985267/dont-blame-bad-weather-for-your-aching-
back
155. NBC 40: http://www.nbc40.net/story/25985267/dont-blame-bad-weather-for-your-
aching-back
156. 760 KFMB: http://www.760kfmb.com/story/25985267/dont-blame-bad-weather-for-
your-aching-back
157. Action 3 News: http://health.kmtv.com/story/25985267/dont-blame-bad-weather-for-
your-aching-back
158. Bio-Medicine: http://www.bio-medicine.org/medicine-news-1/Low-back-pain-3F-Dont-
blame-the-weather-127490-1/
159. Israel Foreign Affairs News: http://israelforeignaffairs.com/dont-attribute-inclemency-
for-the-aching-back/
160. Live 5 News: http://www.live5news.com/story/25985267/dont-blame-bad-weather-for-
your-aching-back
161. Tulsa’s Channel: http://www.ktul.com/story/25985267/dont-blame-bad-weather-for-
your-aching-back
220
162. Walb News: http://www.walb.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
163. Kusi News: http://www.kusi.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
164. Drugs.com: http://www.drugs.com/news/don-t-blame-bad-weather-your-aching-back-
52308.html
165. Medline Plus: http://www.nlm.nih.gov/medlineplus/news/fullstory_147239.html
166. Wrex: http://www.wrex.com/story/25985267/dont-blame-bad-weather-for-your-aching-
back
167. Yahoo Health: http://health.yahoo.net/news/s/hsn/don-t-blame-bad-weather-for-your-
aching-back
168. Healthy Living: http://healthyliving.msn.com/diseases/back-pain/dont-blame-bad-
weather-for-your-aching-back
169. Weekly Times Now: http://www.weeklytimesnow.com.au/news/national/back-pain-
dont-blame-it-on-the-rain/story-fnjbnvyg-1226984395748
170. NBC Right Now: http://www.nbcrightnow.com/story/25985267/dont-blame-bad-
weather-for-your-aching-back
171. News Net 5: http://www.newsnet5.com/news/national/study-finds-no-link-between-
certain-weather-conditions-lower-back-pain
172. WAFB: http://www.wafb.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
221
173. KSFY: http://www.ksfy.com/story/25985267/dont-blame-bad-weather-for-your-aching-
back
174. WAFF: http://www.waff.com/story/25985267/dont-blame-bad-weather-for-your-aching-
back
175. The Courier Mail Brisbane: http://www.couriermail.com.au/news/breaking-news/back-
pain-dont-blame-it-on-the-rain/story-fnihsfrf-
1226984395748?nk=179f05082c5bbe67589cada8dbfdbe1d
176. Black Christian News: http://www.blackchristiannews.com/2014/07/if-you-have-pain-
in-your-lower-back-dont-blame-the-weather/
177. KSLA News: http://www.ksla.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
178. News West 9: http://www.newswest9.com/story/25985267/dont-blame-bad-weather-for-
your-aching-back
179. Healing Well: http://news.healingwell.com/index.php?p=news1&id=689584
180. KTRE: http://www.ktre.com/story/25985267/dont-blame-bad-weather-for-your-aching-
back
181. My Fox Orlando: http://www.myfoxorlando.com/story/25985267/dont-blame-bad-
weather-for-your-aching-back
182. WCAX: http://www.wcax.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
183. Sify News: http://www.sify.com/news/weather-doesn-t-cause-low-back-pain-say-
scientists-news-news-ohlmaBahdgccf.html
222
184. Fox Oregon: http://www.kptv.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
185. KXXV: http://www.kxxv.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
186. WPSD Local: http://www.wpsdlocal6.com/story/25985267/dont-blame-bad-weather-
for-your-aching-back
187. My Fox Los Angeles: http://www.myfoxla.com/story/25985267/dont-blame-bad-
weather-for-your-aching-back
188. Wnem: http://www.wnem.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
189. KEYC TV Mankato: http://www.keyc.com/story/25985267/dont-blame-bad-weather-
for-your-aching-back
190. WHLT 22: http://www.whlt.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
191. KATV: http://www.katv.com/story/25985267/dont-blame-bad-weather-for-your-aching-
back
192. CBS 5 AZ: http://www.kpho.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
193. KTIV: http://www.ktiv.com/story/25985267/dont-blame-bad-weather-for-your-aching-
back
194. WAOW: http://www.waow.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
223
195. Oklahoma’s Own: http://www.newson6.com/story/25985267/dont-blame-bad-weather-
for-your-aching-back
196. Kotatv: http://www.kotatv.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
197. Valley News Live: http://www.valleynewslive.com/story/25985267/dont-blame-bad-
weather-for-your-aching-back
198. My Fox Memphis: http://www.myfoxmemphis.com/story/25985267/dont-blame-bad-
weather-for-your-aching-back
199. WXYZ Detroit: http://www.wxyz.com/news/national/study-finds-no-link-between-
certain-weather-conditions-lower-back-pain
200. Independent Mail: http://www.independentmail.com/news/national/study-finds-no-link-
between-certain-weather-conditions-lower-back-pain
201. Irish Health: http://www.irishhealth.com/article.html?id=23849
202. The Indy Channel: http://www.theindychannel.com/news/study-finds-no-link-between-
certain-weather-conditions-lower-back-pain
203. WKRG News: http://ww2.wkrg.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
204. ABC 6: http://www.abc6.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
205. News Plex: http://wn.newsplex.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
224
206. My 13 LA: http://www.my13la.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
207. Be Live: http://phucanpc.com/8120/dont-blame-bad-weather-for-your-aching-back/
208. Lycos News: http://news.lycos.com/entertainment/weather-not-related-to-back-ache-
9ab8817dbfd88f499f11b5e88f498903/
209. WIFR Rockford: http://wn.wifr.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
210. KKTV Sothern Colorado: http://wn.kktv.com/story/25985267/dont-blame-bad-weather-
for-your-aching-back
211. Capital Gazette: http://www.capitalgazette.com/parade/health/does-weather-cause-
aches/article_3ced89f1-7c0c-5259-817b-a13c0e94cdb8.html
212. Cinema Blend: http://www.cinemablend.com/pop/Scientists-Claim-Link-Between-Cold-
Weather-Back-Pain-Nonexistent-65185.html
213. Fox 16: http://www.fox16.com/story/d/story/back-pain-not-caused-by-the-
weather/30094/RvNSiTKnf06Hlp3Tkkr6MA
214. FM News Talk: http://www.971talk.com/news/health/weather-doesnt-cause-aggravate-
back-pain
215. Value Based Care in Rheumatology: http://www.valuebasedrheumatology.com/vbcr-
news/news-feed/1172-back-pain-not-brought-on-by-weather-except-for-trivial-wind-effect
216. Joint Pain 101: http://jointpain101.com/achy-back-pain-isnt-due-to-bad-weather-latest-
study-finds-tech-times/
225
217. India News Hub: http://indianewshub.com/weather-cause-back-pain/
218. Faraday’s Natural Foods and Supplements:
http://www.faradaysnaturalfoods.com/common/news/news_results.asp?task=Headline&id=1
5368&StoreID=EADB2AA619684A9AB9AF9A7D0A20FF81
219. Wild by Nature:
http://www.wildbynature.com/common/news/news_results.asp?task=Headline&id=15368&S
toreID=D272A3B93180420D908E136E9D7E775D
220. Lovelock Pharmacy: https://lovelockpharmacy.com/article.php?id=689584
221. My Center Pharmacy: https://mycenterpharmacy.com/article.php?id=689584
222. US News: http://health.usnews.com/health-news/articles/2014/07/10/dont-blame-bad-
weather-for-your-aching-back
223. Wate: http://www.wate.com/story/25985267/dont-blame-bad-weather-for-your-aching-
back
224. Clinical Research: http://www.clinicalresearch.com/NewsDetail.aspx?id=689584
225. WMBF News: http://www.wmbfnews.com/story/25985267/dont-blame-bad-weather-
for-your-aching-back
226. Jose Marcos – Doencas Reumaticas:
http://doencasreumat.blogspot.com.au/2014_07_11_archive.html
227. 1 Click News: http://1clicknews.com/is-the-weather-to-blame-for-lower-back-pain/
228. The Malay Mail Online: http://m.themalaymailonline.com/features/article/dont-blame-
the-weather-for-lower-back-pain-study-says
226
229. Gulf Bend Center:
http://www.gulfbend.org/poc/view_doc.php?type=news&id=165586&cn=72
230. Priyo News: http://news.priyo.com/2014/07/13/dont-curse-weather-low-back-pain-
113952.html
231. Bakersfield Now: http://wn.bakersfieldnow.com/story/25985267/dont-blame-bad-
weather-for-your-aching-back
232. 0 Hag: http://www.0hag.com/dont-listen-granny-weather-impact-state-bad-back/
233. WLTZ First News: http://www.wltz.com/story/25985267/dont-blame-bad-weather-for-
your-aching-back
234. Daily Health Headlines: http://www.dailyhealthheadlines.com/article/health-
headlines/feel-it-in-your-bones-back-pain-not-linked-with-weather
235. The Health Site: http://www.thehealthsite.com/news/weather-to-blame-for-lower-back-
pain/
236. CTV News: http://www.ctvnews.ca/health/is-the-weather-to-blame-for-lower-back-pain-
1.1911889
237. Astro Awani: http://english.astroawani.com/news/show/is-the-weather-to-be-blamed-
for-lower-back-pain-39770
238. Free Malaysia Today:
http://www.freemalaysiatoday.com/category/leisure/2014/07/14/is-the-weather-to-blame-for-
lower-back-pain/
239. Malaysian Digest: http://malaysiandigest.com/features/509026-don-t-blame-the-
weather-for-lower-back-pain-study-says.html
227
240. International Business Times: http://au.ibtimes.com/articles/559112/20140714/back-
pain-backache-weather-world-health-association.htm#.U8OTEPmSx8E
241. Iafrica: http://lifestyle.iafrica.com/wellness/949058.html
242. The New Age: http://thenewage.co.za/131503-12-53-
Is_the_weather_to_blame_for_lower_back_pain
243. The Roger Hedgecock Show: http://www.rogerhedgecock.com/story/25985267/dont-
blame-bad-weather-for-your-aching-back
244. Reuters UK: http://uk.reuters.com/article/2014/07/14/us-weather-back-pain-
idUKKBN0FJ1SI20140714
245. Huffington Post Canada: http://www.huffingtonpost.ca/2014/07/14/back-pain-causes-
weather_n_5584538.html
246. Ciencias Medicas News: http://elbiruniblogspotcom.blogspot.com.au/2014/07/dont-
blame-bad-weather-for-your-aching.html
247. ABC 40 KRHD: http://www.abc40.com/story/25985267/dont-blame-bad-weather-for-
your-aching-back
248. WITN: http://wn.witn.com/story/25985267/dont-blame-bad-weather-for-your-aching-
back
249. WBTV: http://www.wbtv.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
250. Hon News: http://www.hon.ch/News/HSN/689584.html
228
251. WOWKRV: http://www.wowktv.com/story/25985267/dont-blame-bad-weather-for-
your-aching-back
252. WDAM: http://www.wdam.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
253. Newsday: http://www.newsday.com/news/health/don-t-blame-bad-weather-for-your-
aching-back-1.8755826
254. 14 News: http://www.14news.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
255. WSAV: http://www.wsav.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
256. KPLCTV: http://www.kplctv.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
257. WLOX 13: http://www.wlox.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
258. WGEM: http://www.wgem.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
259. My Fox Nepa: http://www.myfoxnepa.com/story/25985267/dont-blame-bad-weather-
for-your-aching-back
260. WDRB: http://www.wdrb.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
261. WSPA 7: http://www.wspa.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
229
262. Winnipeg Free Press: http://www.winnipegfreepress.com/arts-and-life/life/health/dont-
blame-bad-weather-for-your-aching-back-266581831.html
263. My Fox Wausau: http://www.myfoxwausau.com/story/25985267/dont-blame-bad-
weather-for-your-aching-back
264. KCBD: http://www.kcbd.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
265. News Channel 12: http://www.wjtv.com/story/25985267/dont-blame-bad-weather-for-
your-aching-back
266. News R India: http://newsr.in/n/Health/750jc4162/Weather-to-blame-for-lower-back-
pain.htm
267. WKOW Madison: http://www.wkow.com/story/25985267/dont-blame-bad-weather-for-
your-aching-back
268. Herald Whig: http://www.whig.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
269. West Virginia Illustrated: http://www.wvillustrated.com/story/25985267/dont-blame-
bad-weather-for-your-aching-back
270. The Mercury: http://www.themercury.com.au/news/breaking-news/back-pain-dont-
blame-it-on-the-rain/story-fnj6ehgr-1226984395748
271. WRCB Chattanooga: http://www.wrcbtv.com/story/25985267/dont-blame-bad-weather-
for-your-aching-back
272. Hawaii News Now: http://www.hawaiinewsnow.com/story/25985267/dont-blame-bad-
weather-for-your-aching-back
230
273. KWWL: http://www.kwwl.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
274. ABC Kait 8: http://www.kait8.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
275. My Fox Phoenix: http://www.myfoxphoenix.com/story/25985267/dont-blame-bad-
weather-for-your-aching-back
276. My Fox DC: http://www.myfoxdc.com/story/25985267/dont-blame-bad-weather-for-
your-aching-back
277. WTHR Indiana’s News Leader: http://www.wthr.com/story/25985267/dont-blame-bad-
weather-for-your-aching-back
278. My Fox Boston: http://www.myfoxboston.com/story/25985267/dont-blame-bad-
weather-for-your-aching-back
279. CBS 8: http://www.cbs8.com/story/25985267/dont-blame-bad-weather-for-your-aching-
back
280. My Fox Dallas-Fort Worth: http://www.myfoxdfw.com/story/25985267/dont-blame-
bad-weather-for-your-aching-back
281. WSFA 12: http://www.wsfa.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
282. My Fox Tampa Bay: http://www.myfoxtampabay.com/story/25985267/dont-blame-bad-
weather-for-your-aching-back
283. WSET-TV Lynchburg Danville Roanoke: http://www.wset.com/story/25985267/dont-
blame-bad-weather-for-your-aching-back
231
284. WKRN-TV Nashville: http://www.wkrn.com/story/25985267/dont-blame-bad-weather-
for-your-aching-back
285. Fox 51 WOGX: http://www.wogx.com/story/25985267/dont-blame-bad-weather-for-
your-aching-back
286. News Channel 5: http://www.newschannel5.com/story/25985267/dont-blame-bad-
weather-for-your-aching-back
287. Fox 29 WFLX: http://www.wflx.com/story/25985267/dont-blame-bad-weather-for-
your-aching-back
288. Yahoo! News India: https://in.news.yahoo.com/dont-curse-weather-low-back-pain-
090004253.html
289. 9&10 Northern Michigan’s News Leader:
http://www.9and10news.com/story/25985267/dont-blame-bad-weather-for-your-aching-back
290. The Courant: http://www.courant.com/health/sns-rt-us-weather-back-pain-
20140714,0,296648.story
291. KTBS 3: http://www.ktbs.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
292. Townsville Bulletin: http://www.townsvillebulletin.com.au/news/breaking-news/back-
pain-dont-blame-it-on-the-rain/story-fnjbnvyi-1226984395748
293. KLTV 7: http://www.kltv.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
294. Rocket News: http://www.rocketnews.com/2014/07/feel-it-in-your-bones-back-pain-not-
linked-with-weather/
232
295. Yahoo! News UK and Ireland: https://uk.news.yahoo.com/feel-bones-back-pain-not-
linked-weather-071628526.html?.tsrc=lgwn#iELc3Jm
296. WAVE 3 News: http://www.wave3.com/story/25985267/dont-blame-bad-weather-for-
your-aching-back
297. Gold Coast Bulletin: http://www.goldcoastbulletin.com.au/news/breaking-news/back-
pain-dont-blame-it-on-the-rain/story-fnjbnvyk-1226984395748
298. KVVU-TV Fox 5 Las Vegas: http://www.fox5vegas.com/story/25985267/dont-blame-
bad-weather-for-your-aching-back
299. Web India 123:
http://news.webindia123.com/news/Articles/India/20140711/2422516.html
300. WVVA – The two Virginias: http://www.wvva.com/story/25985267/dont-blame-bad-
weather-for-your-aching-back
301. WFMJ: http://www.wfmj.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
302. Truth Dive: http://truthdive.com/2014/07/11/Weather-doesn-t-cause-low-back-pain-say-
scientists.html
303. KTVN 2 News: http://www.ktvn.com/story/25985267/dont-blame-bad-weather-for-
your-aching-back
304. NBC 2: http://www.nbc-2.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
305. KTEN 10 Texoma: http://www.kten.com/story/25985267/dont-blame-bad-weather-for-
your-aching-back
233
306. WRBL: http://www.wrbl.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
307. WTOC 11: http://www.wtoc.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
308. KFVS 12: http://www.kfvs12.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
309. Prokerala News: http://www.prokerala.com/news/articles/a472570.html
310. KSWO 7 News Lawton/ Wichita Falls: http://www.kswo.com/story/25985267/dont-
blame-bad-weather-for-your-aching-back
311. ABC 2 WBAY: http://www.wbay.com/story/25985267/dont-blame-bad-weather-for-
your-aching-back
312. Mizo News: http://www.mizonews.net/world/dont-curse-weather-for-low-back-pain/
313. ABC 10 News: http://www.10news.com/news/national/study-finds-no-link-between-
certain-weather-conditions-lower-back-pain
314. Neuro Talk:
http://neurotalk.psychcentral.com/showthread.php?s=77a5572aa77f20b8e90925adf927a025&
p=1082100#post1082100
315. Latest News Link: http://latestnewslink.com/2014/07/weather-not-tied-to-back-pain-
study/
316. Big News Network: http://www.bignewsnetwork.com/index.php/cat/eb75a2fd5e16e873/
234
317. Personal Liberty Digest: http://personalliberty.com/study-finds-link-certain-weather-
conditions-lower-back-pain/
318. Cliprender: http://www.cliprender.com/clip/Is-The-Weather-To-Be-Blamed-For-Lower-
Back-Pain%3F
319. Turn to 10: http://ww2.turnto10.com/story/25985267/dont-blame-bad-weather-for-your-
aching-back
320. Focus Italy: http://www.focus.it/ADNKronos/salute-sfatato-legame-meteo-dolore-clima-
non-influenza-mal-di-schiena_C65.aspx
321. Meteo e scienze del cielo e della terra: http://www.meteoweb.eu/2014/07/salute-sfatato-
legame-meteo-dolori-clima-non-influenza-mal-schiena/298772/
322. Australian Doctor: http://www.australiandoctor.com.au/news/latest-news/weather-not-a-
barometer-for-back-pain
323. ABLX Boston: http://www.manewsday.com/national/65203-don-t-listen-to-granny-the-
weather-has-no-impact-on-the-state-of-your-bad-back.html
324. Sina Women Eladies – China: http://eladies.sina.com.tw/getnews.php?newsid=97932
325. Viet Times: http://www.viet-times.com.au/gia-dinh/suc-khoe/1300534-thoi-tiet-khong-
anh-huong-den-chung-dau-lung?device=desktop
326. Tien Phong Online: http://khoe360.tienphong.vn/gia-dinh-suc-khoe/khong-co-bang-
chung-dau-lung-do-thoi-tiet-734237.tpo
327. Path Finder:
http://www.pathfinder.gr/stories/3752169/%CF%80%CE%BF%CE%BD%CE%BF%CF%82
-%CF%83%CF%84%CE%B7-%CE%BC%CE%B5%CF%83%CE%B7-
235
%CE%BC%CE%B7%CE%BD-
%CE%B1%CE%BA%CE%BF%CF%85%CF%84%CE%B5-%CF%84%CE%B7-
%CE%B3%CE%B9%CE%B1%CE%B3%CE%B9%CE%B1-%CF%83%CE%B1%CF%82/
328. AArgauer Zeitung: http://www.aargauerzeitung.ch/leben/gesundheit/ist-das-schlechte-
wetter-schuld-am-hexenschuss-128166931
329. Anteka: http://www.apteka.ua/article/299054
330. RMF 24: http://www.rmf24.pl/nauka/news-bole-w-krzyzu-nie-przez-
pogode,nId,1467274
331. Tiscali: http://lifestyle.tiscali.it/salute/feeds/14/07/11/t_16_ADN20140711130058.html
332. TVN Meteo: http://tvnmeteo.tvn24.pl/informacje-pogoda/ciekawostki,49/bole-w-
krzyzu-to-nie-przez-pogode,127818,1,0.html
333. Sante Log: http://www.santelog.com/news/rhumatologie/arthrite-et-lombalgie-une-
question-de-meteo-_12595_lirelasuite.htm
334. Time Turk: http://www.timeturk.com/tr/2014/07/10/buyukanneler-yaniliyor-
olabilir.html#.U8TruPmSx8E
335.Wissenschaft: http://www.wissenschaft-
aktuell.de/artikel/Hexenschuss__Das_Wetter_ist_nicht_schuld1771015589598.html
336. Gazete A24: http://www.gazetea24.com/yerel-basin-haber/buyukanneler-yaniliyor-
olabilir_12387770.html
337. Aponet: http://www.aponet.de/aktuelles/kurioses/20140710-kein-wettereinfluss-auf-
rueckenschmerzen.html
236
Dr Daniel Steffens - Curriculum Vitae Page 1 of 4
EDUCATION
DOCTOR OF PHILOSOPHY (2011 - 2015), The George Institute for Global Health, Sydney Medical School, The University of Sydney, Australia. Thesis title: Mechanisms of low back pain. Supervisor: Professor Chris G Maher Main projects: Clinicians’ views on factors that trigger a sudden onset of low back pain. Factors predicting recruitment of participants to an observational study of low back pain
conducted in primary care. Prognosis of chronic low back pain in patients presenting to a private community-based group
exercise program. Does magnetic resonance imaging predict future low back pain? A systematic review. Triggers of an acute onset of low back pain – results of a case-crossover study. Does the weather affect back pain? A case-crossover study. Do MRI findings identify patients with low back pain who respond best to particular
interventions? A systematic review. Triggers for an episode of sudden onset low back pain: Study protocol. BACHELOR OF PHYSIOTHERAPY - HONOURS (2001 - 2005), University of Santa Cruz do Sul, Brazil.
EXPERIENCE (ACADEMIC)
LECTURER, Macquarie University, Department of Chiropractic, Faculty of Science, Australia (2014-present). Subject: Chiropractic 2 – CHIR 311 (Research Methods). Designing, preparing and developing teaching materials. Delivering lectures. Setting and marking assignments.
EXPERIENCE (RESEARCH)
CLINICAL RESEARCH ASSISTANT, Neuroscience Research Australia, University of New South Wales (2015 - present). Project: Standing Tall - A home-based balance exercise program. NHMRC-funded randomised controlled trial involving 500 participants. Administering participants comprehensive physical assessment. Maintaining study database. Delivering study intervention to participants. Developing study materials. RESEARCH ASSISTANT, The George Institute for Global Health, The University of Sydney, Australia (2010 – 2011). Project: Paracetamol for low back pain (PACE). NHMRC-funded randomised controlled trial involving 1650 participants. Recruited and enrolled study clinicians and participants. Provided additional administrative support and carried out general clerical duties. Administered participant’s interviews and prepared assessments. Wrote research manuscript, presentations, reports and ethical submissions. Developed and maintained research databases (Excel, FileMaker Pro). Achievement: Received a discretionary bonus for recognition and reward of exceptional performance.
Address: 4/18 Market Street | Rockdale, Sydney NSW 2216 Mobile: + 61 2 0423 786 695 | E-mail: [email protected]
Dr Daniel Steffens CURRICULUM
VITAE
237
Dr Daniel Steffens - Curriculum Vitae Page 2 of 4
EXPERIENCE (RESEARCH)
RESEARCH ASSISTANT, Faculty of Health Science, The University of Sydney, Australia (2009 – 2010). Project: Prognosis of chronic back pain. One year follow-up study that involved 118 participants presenting to private care. Performed face-to-face and telephone data collection. Performed systematic literature searching. Liaised with data collection sites. Performed data entry and statistical analysis (SPSS). Wrote protocols, ethical documents and scientific papers. Achievement: Completion of the study on time with minimal loss to follow-up. Published
study in relevant scientific journal.
SUPPORT OF JUNIOR RESEARCH STUDENTS
Keira BEILKEN and Vicky DUONG - Does weather affect daily pain levels in patients with acute low back pain? A longitudinal cohort study. Honours Students , Macquarie University - 2015.
Matthew STEVENS - Patients’ and clinicians’ views on triggers for low back pain. Doctor of Philosophy, The University of Sydney – 2014.
Patricia PARREIRA – Nominating triggers for low back pain patients. Doctor of Philosophy, The University of Sydney – 2014.
PUBLICATIONS (FULL PAPER)
DANIEL STEFFENS, Manuela L Ferreira, Jane Latimer, Bart W Koes, Fiona M Blyth, Paulo H Ferreira, Christopher G Maher. What triggers an episode of acute low back pain? A case-crossover study. Arthritis Care & Research, 2015; 67(3):403-10. DANIEL STEFFENS, Chris G Maher, Manuela L Ferreira, Mark J Hancock, Leani SM Pereira, Christopher M Williams, Jane Latimer. Clinician characteristics and operational factors have limited influence on participant recruitment in primary care: Results from an observational study. Journal of Manipulative and Physiological Therapeutics, 2015; xx:1-8. DANIEL STEFFENS, Chris Maher, Qiang Li, Manuela Ferreira, Leani Pereira, Bart Koes, Jane Latimer. Weather does not affect back pain: results from a case-crossover. Arthritis Care & Research, 2014; 66(12):1867-72. DANIEL STEFFENS, Chris Maher. Effectiveness of extracorporeal shock wave therapy in chronic plantar fasciitis. American Journal of Physical Medicine and Rehabilitation, 2014; 2:1-2. DANIEL STEFFENS, Chris Maher, Manuela Ferreira, Mark Hancock, Timothy Glass, Jane Latimer. Clinicians’ views on factors that trigger a sudden onset of low back pain. European Spine Journal, 2014; 23(3):512-9. DANIEL STEFFENS, Mark Hancock, Chris Maher, Jane Latimer, Rob Satchill, Manuela Ferreira, Paulo Ferreira, Melissa Partington, Anna-Louise Bouvier. Prognosis of chronic low back pain in patients presenting to a private community-based group exercise program. European Spine Journal, 2014; 23(1):113-9. DANIEL STEFFENS, Mark Hancock, Chris G Maher, Ciaran Williams, Tue Secher Jensen, Jane Latimer. Does magnetic resonance imaging predict future low back pain? A systematic review. European Journal of Pain, 2013; 18(6):755-65.
238
Dr Daniel Steffens - Curriculum Vitae Page 3 of 4
PUBLICATIONS (FULL PAPER)
DANIEL STEFFENS, Paula R Beckenkamp, Mark Hancock, Dulciane Nunes Paiva, Jennifer A Alison, Sergio S Menna-Barreto. Activity level predicts 6-minute walk distance in healthy older females: an observational study. Physiotherapy, 2013; 99(1):21-6. DANIEL STEFFENS, Manuela L Ferreira, Christopher G Maher, Jane Latimer, Bart W Koes, Fiona M Blyth and Paulo H Ferreira. Triggers for an episode of sudden onset low back pain: study protocol. BMC Musculoskeletal Disorders, 2012; 13:7. DANIEL STEFFENS, Chris Maher. Conflicting findings on effectiveness of low level laser therapy for tendinopathty. British Journal of Sports Medicine, 2011; 45:459. Antonio MV Silva, Luis U Signori, Guilherme C Torres, DANIEL STEFFENS, Rodrigo DM Plentz. Neuromuscular electrical stimulation versus strength training in elderly women. Geriatria & Gerontologia, 2008; 2(1):12-16 [Portuguese]. DANIEL STEFFENS, Paula R Beckenkamp, Isabella M Albuquerque, Dulciane N Paiva, Serigio SM Barreto. Occupational exposure to tobacco dust – effects on the respiratory system. Pulmão RJ, 2007; 16:86-90 [Portuguese].
PUBLICATIONS (PROCEEDINGS)
DANIEL STEFFENS, Manuela Ferreira, Jane Latimer, Paulo H Ferreira, Bart W Koes, Fiona Blyth, Qiang Li, Chris Maher. What triggers an episode of low back pain? Results of a case-crossover study. Proceedings XIII International Back Pain Forum. Campos do Jordao, Brazil, 2014. p52. DANIEL STEFFENS, Chris Maher, Qiang Li, Manuela Ferreira, Leani Pereira, Bart W Koes, Jane Latimer. Could the weather triggers an episode of low back pain? A case-crossover study. Proceedings XIII International Back Pain Forum. Campos do Jordao, Brazil, 2014. p81. DANIEL STEFFENS, Mark Hancock, Chris G Maher, Ciaran Williams, Tue S Jensen, Jane Latimer. Does magnetic resonance imaging predict future low back pain? A systematic review. Proceedings Pain in Europe VIII. Florence, Italy, 2013. p1117. DANIEL STEFFENS, Manuela Ferreira, Chris Maher, Jane Latimer, Bart Koes, Fiona Blyth, Paulo Ferreira. Does the method of training of recruiting clinicians influence recruitment to a low back pain case-crossover study. Proceedings Odense International Forum XII. Odense, Denmark, 2012. p.178. DANIEL STEFFENS, Manuela Ferreira, Chris Maher, Jane Latimer, Bart Koes, Fiona Blyth, Paulo Ferreira. Clinician’s views on triggers for sudden onset low back pain. Proceedings Odense International Forum XII. Odense, Denmark, 2012. p.195. DANIEL STEFFENS, Paula R Beckenkamp, Mark Hancock, Dulciane N Paiva, Sergio S Menna-Barreto, Jennifer A Alison. Six minute walk distance in healthy elderly active and sedentary female. Proceedings Australian Physiotherapy Association Biennial Conference 2011. Brisbane, Australia, 2011. p.126. DANIEL STEFFENS, Mark J Hancock, Rob Satchill, Manuela Ferreira, Paulo Ferreira, Chris G Maher, Melissa Partington, Ana-Louise Bouvier. Prognosis of patients with chronic low back pain presenting to a private functional group exercise program. Proceedings Australian Physiotherapy Association Biennial Conference. Brisbane, Australia, 2011. p.146.
239
Dr Daniel Steffens - Curriculum Vitae Page 4 of 4
RESEARCH GRANTS AND AWARDS
COTUTELLE AWARD (2011 – 2015), jointly awarded degree between The University of Sydney (Australia) and the Federal University of Minas Gerais (Brazil). TRAVEL GRANT (2014), Research Student Grant Scheme (RSGS), School of Public Health, Sydney Medical School, The University of Sydney (AUD$ 2602.00). TOP BEST ABSTRACT (2013), EFIC-Pain in Europe VII Congress. Florence, Italy. TRAVEL GRANT (2013), Research Student Grant Scheme (RSGS), School of Public Health, Sydney Medical School, The University of Sydney (AUD$ 1200.00). TRAVEL GRANT (2012), Postgraduate Research Support Scheme (PRSS), School of Public Health, Sydney Medical School, The University of Sydney (AUD$ 1020.74).
REVIEWER (SCIENTIFIC ARTICLES)
JOURNAL OF PHYSIOTHERAPY MANUAL THERAPY WORLD CONFEDERATION FOR PHYSICAL THERAPY BMC MUSCULOSKELETAL DISORDERS JOURNAL OF MEDICAL INTERNET RESEARCH PROTOCOLS
REFEREES
PROF. CHRIS G MAHER (PhD Supervisor) Director, Musculoskeletal Division. The George Institute for Global Health, The University of Sydney Telephone: +61 2 9657 0382 E-mail: [email protected]
A/PROF. MARK HANCOCK (Previous employer) Senior Lecturer, Musculoskeletal physiotherapy. Macquarie University Telephone: +61 2 9850 6622 E-mail: [email protected]
240