7/21/2019 Cordeiro,2003

1/5

See discussions, stats, and author profiles for this publication at: http://www.researchgate.net/publication/8999401

Depression, Insomnia, and Memory Loss in aPatient With Chronic Intoxication by Inorganic

Mercury

ARTICLE in JOURNAL OF NEUROPSYCHIATRY FEBRUARY 2003

Impact Factor: 2.77 DOI: 10.1176/appi.neuropsych.15.4.457 Source: PubMed

CITATIONS

2

DOWNLOADS

5

VIEWS

252

3 AUTHORS, INCLUDING:

Quirino Cordeiro

Santa Casa de So Paulo144PUBLICATIONS 763CITATIONS

SEE PROFILE

Renerio Fraguas

Hospital das Clnicas da Faculdade de Medici35PUBLICATIONS 436CITATIONS

SEE PROFILE

Available from: Quirino Cordeiro

Retrieved on: 12 August 2015

http://www.researchgate.net/profile/Quirino_Cordeiro?enrichId=rgreq-7111eeb0-8273-4d21-b5c7-2bb29c5b2623&enrichSource=Y292ZXJQYWdlOzg5OTk0MDE7QVM6MjU2NzA2OTk5NDg0NDE2QDE0MzgyMTUxMjYxNjA%3D&el=1_x_4http://www.researchgate.net/profile/Quirino_Cordeiro?enrichId=rgreq-7111eeb0-8273-4d21-b5c7-2bb29c5b2623&enrichSource=Y292ZXJQYWdlOzg5OTk0MDE7QVM6MjU2NzA2OTk5NDg0NDE2QDE0MzgyMTUxMjYxNjA%3D&el=1_x_4http://www.researchgate.net/institution/Hospital_das_Clinicas_da_Faculdade_de_Medicina_da_Universidade_de_Sao_Paulo?enrichId=rgreq-7111eeb0-8273-4d21-b5c7-2bb29c5b2623&enrichSource=Y292ZXJQYWdlOzg5OTk0MDE7QVM6MjU2NzA2OTk5NDg0NDE2QDE0MzgyMTUxMjYxNjA%3D&el=1_x_6http://www.researchgate.net/?enrichId=rgreq-7111eeb0-8273-4d21-b5c7-2bb29c5b2623&enrichSource=Y292ZXJQYWdlOzg5OTk0MDE7QVM6MjU2NzA2OTk5NDg0NDE2QDE0MzgyMTUxMjYxNjA%3D&el=1_x_1http://www.researchgate.net/profile/Renerio_Fraguas?enrichId=rgreq-7111eeb0-8273-4d21-b5c7-2bb29c5b2623&enrichSource=Y292ZXJQYWdlOzg5OTk0MDE7QVM6MjU2NzA2OTk5NDg0NDE2QDE0MzgyMTUxMjYxNjA%3D&el=1_x_7http://www.researchgate.net/institution/Hospital_das_Clinicas_da_Faculdade_de_Medicina_da_Universidade_de_Sao_Paulo?enrichId=rgreq-7111eeb0-8273-4d21-b5c7-2bb29c5b2623&enrichSource=Y292ZXJQYWdlOzg5OTk0MDE7QVM6MjU2NzA2OTk5NDg0NDE2QDE0MzgyMTUxMjYxNjA%3D&el=1_x_6http://www.researchgate.net/profile/Renerio_Fraguas?enrichId=rgreq-7111eeb0-8273-4d21-b5c7-2bb29c5b2623&enrichSource=Y292ZXJQYWdlOzg5OTk0MDE7QVM6MjU2NzA2OTk5NDg0NDE2QDE0MzgyMTUxMjYxNjA%3D&el=1_x_5http://www.researchgate.net/profile/Renerio_Fraguas?enrichId=rgreq-7111eeb0-8273-4d21-b5c7-2bb29c5b2623&enrichSource=Y292ZXJQYWdlOzg5OTk0MDE7QVM6MjU2NzA2OTk5NDg0NDE2QDE0MzgyMTUxMjYxNjA%3D&el=1_x_4http://www.researchgate.net/profile/Quirino_Cordeiro?enrichId=rgreq-7111eeb0-8273-4d21-b5c7-2bb29c5b2623&enrichSource=Y292ZXJQYWdlOzg5OTk0MDE7QVM6MjU2NzA2OTk5NDg0NDE2QDE0MzgyMTUxMjYxNjA%3D&el=1_x_7http://www.researchgate.net/institution/Santa_Casa_de_Sao_Paulo?enrichId=rgreq-7111eeb0-8273-4d21-b5c7-2bb29c5b2623&enrichSource=Y292ZXJQYWdlOzg5OTk0MDE7QVM6MjU2NzA2OTk5NDg0NDE2QDE0MzgyMTUxMjYxNjA%3D&el=1_x_6http://www.researchgate.net/profile/Quirino_Cordeiro?enrichId=rgreq-7111eeb0-8273-4d21-b5c7-2bb29c5b2623&enrichSource=Y292ZXJQYWdlOzg5OTk0MDE7QVM6MjU2NzA2OTk5NDg0NDE2QDE0MzgyMTUxMjYxNjA%3D&el=1_x_5http://www.researchgate.net/profile/Quirino_Cordeiro?enrichId=rgreq-7111eeb0-8273-4d21-b5c7-2bb29c5b2623&enrichSource=Y292ZXJQYWdlOzg5OTk0MDE7QVM6MjU2NzA2OTk5NDg0NDE2QDE0MzgyMTUxMjYxNjA%3D&el=1_x_4http://www.researchgate.net/?enrichId=rgreq-7111eeb0-8273-4d21-b5c7-2bb29c5b2623&enrichSource=Y292ZXJQYWdlOzg5OTk0MDE7QVM6MjU2NzA2OTk5NDg0NDE2QDE0MzgyMTUxMjYxNjA%3D&el=1_x_1http://www.researchgate.net/publication/8999401_Depression_Insomnia_and_Memory_Loss_in_a_Patient_With_Chronic_Intoxication_by_Inorganic_Mercury?enrichId=rgreq-7111eeb0-8273-4d21-b5c7-2bb29c5b2623&enrichSource=Y292ZXJQYWdlOzg5OTk0MDE7QVM6MjU2NzA2OTk5NDg0NDE2QDE0MzgyMTUxMjYxNjA%3D&el=1_x_3http://www.researchgate.net/publication/8999401_Depression_Insomnia_and_Memory_Loss_in_a_Patient_With_Chronic_Intoxication_by_Inorganic_Mercury?enrichId=rgreq-7111eeb0-8273-4d21-b5c7-2bb29c5b2623&enrichSource=Y292ZXJQYWdlOzg5OTk0MDE7QVM6MjU2NzA2OTk5NDg0NDE2QDE0MzgyMTUxMjYxNjA%3D&el=1_x_2

7/21/2019 Cordeiro,2003

2/5

456 J Neuropsychiatry Clin Neurosci 15:4, Fall 2003

LETTERS

The Preservation of

Consciousness, Automatism,and Movement Control

SIR:The paper by Devinsky etal.1 contains important laterality in-dexed information concerning thepreservation of consciousness, au-tomatism, and movement control,which deserve to be put in a morecohesive perspective. This in turncould have helped to present thedata in a more scientific manner.Specifically, I am referring to the

works of Serafetinides2 on the roleof the major hemisphere in preser-vation of consciousness and Serafe-tinides and Falconer3 on the role ofthe right (minor) hemisphere inspeech automatism. The results ofthese large numbered and meticu-lously conducted studies have beenconfirmed in more recent times,4,5

all indicating that when a seizureoccurs with speech arrest, loss ofconsciousness, and presence ofmemory of preictal events, the le-sion is in the major hemisphere. Asthese authors recorded epileptiformEEG activity in such patients theprocess is epileptic by definition,and calling the process convulsiveis appropriate in those in which ac-tual convulsion is seen (majority oc-curring in major hemispheric le-sions). To a neurologist,nonepileptic seizure is an oxy-moron. Of course, hysterical sei-zures do occur, but if the behavior

is associated with the rest of theitems enumerated above and isseen with a brain lesion in eitherhemisphere, one must avoid usingthat confused and confusing termi-nology.

The role of laterality of move-ment control (alluded to above, andcodified in handedness) in main-

taining the stream of consciousawareness is becoming clearer. The

activating neuronal aggregate de-voted to voluntary movements(otherwise called the command cen-ter in the major hemisphere) has

been recently the subject of an in-vestigation based on a review of theliterature and my own data. Thisensemble mediates interlimb coor-dination, guaranteeing the existenceof a cohesive self in a brain consist-ing of two hemispheres. It is onlywhen this asymmetrical interhemi-spheric relationship is disturbed,such as in surgical callosotomy,Marchiafava-Bignami disease, andtraumatic or vascular callosotomy,that the cohesion is lost forever.Cases of ictal automatism, as men-tioned above, are instances repre-senting temporary disruption ofthis cohesion. All references citedindicate that only when the activat-ing moiety (within the major hemi-sphere) is involved in the epilepto-genesis will the person loseconsciousness, as the disruptiveprocess is conveyed to the remain-ing hemisphere via the callosum.Epileptic activity generated withinthe minor hemisphere is the sourceof automatisms only, as mentionedabove. It cannot be generalized be-cause the callosal traffic for move-ment is one-way only. This recentlydescribed anatomy forms the neural

basis for handedness. 6 One of itsmanifestations is the melody lead ofthe piano players that has been

known to musicologists for morethan a century. The reason for thedelay of all effectors on the left side(in right handers) is the time takenfor the command in the majorhemisphere to reach the motor cor-tex on the right via the callosum.

Iraj Derakhshan

Charleston, WV

References

1. Devinsky O, Mesad, S, Alpers K. Non-dominant hemisphere lesions and con-version nonepileptic seizures. J Neuro-psychiatry Clin Neurosci 2001; 13:367373

2. Serafetinides EA, Hoare RD, Driver MV.Intracarotid sodium amobarbitone andcerebral dominance for speech and con-sciousness. Brain 1965; 88:107130.

3. Serafetinides, EA, Falconer MA. Speechdisturbances in temporal lobe lesions: Astudy in hundred epileptic patients sub-mitted to anterior temporal lobectomy.Brain 1963; 86:333346

4. Ebner A, Dinner DS, Noachtar S, Luders

H. Automatism with preserved respon-siveness: A lateralizing sign in psycho-motor seizures. Neurology 1995; 45:6164

5. Karlov VA, Selitskii GV, SviderskayaNE: The trigger role of the left cerebralhemisphere in the generalization of epi-leptic activity. Neurosci Behav Physiol.1993; 23:280-289

6. Derakhshan I. In defense of the sinis-trals: Anatomy of handedness and thesafety of prenatal ultrasound. ObstetGynecol 2003; 21:209-212

In Reply

SIR: Dr. Derakshan accuratelysummarizes the literature on tem-poral lobe seizures and impairmentof verbal consciousness and speechautomatism. Verbal consciousnessis impaired by dominant temporallobe seizures and automatic speech(resulting from preserved dominantspeech cortex) occurs most often

with nondominant temporal lobeseizures. However, our study con-cerned nonepileptic conversion sei-zures.

I strongly disagree with his asser-tion that one should never diagnoseconversion symptoms or conversiondisorder in a patient with a neuro-logical disorder. Indeed, there is

7/21/2019 Cordeiro,2003

3/5

J Neuropsychiatry Clin Neurosci 15:4, Fall 2003 457

LETTERS

extensive literature suggesting thatpatients with structural brain le-sions (e.g., tumor, stroke, multiplesclerosis, trauma) or neurophysio-logical disorders such as epilepsyhave an increased incidence of con-

version disorder.14

I would alsodisagree about any data on laterali-zed ictal motor automatisms andhemispheric dominance. Rather,partial seizures with lateralized ictalmotor automatisms usually startfrom the ipsilateral hemisphere.5

Orrin Devinsky, M.D.

Neurology, Neurosurgery, andPsychiatry, New York Univer-sity School of Medicine, NewYork, NY

References

1. Barry E, Krumholz A, Bergey GK, et al.Nonepileptic posttraumatic seizures.Epilepsia. 1998;39:42731

2. Eames P. Hysteria following brain in-jury. J Neurol Neurosurg Psychiatry1992;55:10461053

3. Caplan LR, Nadelson T. Multiple sclero-sis and hysteria. JAMA 1980;243:418421

4. Devinsky O, Mesad S, Alper K. Hemi-sphere lesions and conversion nonepi-leptic seizures. J Neuropsychiatry ClinNeurosci 2001;13:36773

5. Chee MW, Kotagal P, Van Ness PC, et

al. Lateralizing signs in intractable par-tial epilepsy: blinded multipleobserveranalysis. Neurology 1993;43:2519-25

Depression, Insomnia, andMemory Loss in a PatientWith Chronic Intoxication byInorganic Mercury

SIR:Conditions of chronic poison-

ing by inorganic mercury (hydrar-gyrism) have been described in per-sons who habitually handle thismaterial. Besides the physicalsymptoms, the patients present im-portant neuropsychiatric features

because the central nervous system(CNS) is the main target of mer-cury1-5.

Cognitive evaluations of individ-uals with hydrargyrism show dis-turbances that persist over theyears, even after interruption of ex-posure to mercury1-4. Insomnia is asymptom that also persists as a se-

quelae5

. Here, the case of a patientwith depression, insomnia, and re-cent memory loss related to thechronic intoxication by inorganicmercury is discussed.

Case Report

About 5 years ago, a 45-year-oldpatient without personal or familialhistory of psychiatric disordersstarted to work in a lamp factory,where he handled inorganic mer-cury. Some 6 months after daily

contact with the metal, he started topresent with gingival hemorrhage,headache, tremors of the extremi-ties, loss of the recent memory, in-somnia, and severe depression (lackof pleasure, social withdrawal, psy-chomotor retardation, depressivemood, feelings of worthlessness andinappropriate guilt, irritability).Even exhibiting such a condition,the patient continued to performthe same function for 1 more year.In this way, his symptoms becamemore intense. After a high metaldosing in his urine (only at thatmoment he was submitted to thisexam), 105 mg/L (nl: 25mg /L), thepatient was dismissed from work.Subsequent to withdrawal from ex-posure, the physical symptoms dis-appeared; however, the neuropsy-chiatric symptoms continued. For 3years, the patient remained withoutmedical care, and he was then re-ferred to our outpatient unit. At

that time, the patient did not showdetectable levels of mercury in hisurine. As the patient exhibited sig-nificant depressive symptoms, hewas administered sertraline. Whilehis changes of mood improved, thedose of antidepressant was in-creased until it reached 250 mg/day. With this dose, the patient no

longer presented with depression;however, recent memory impair-ment and the insomnia persisted.

Comment

Diagnosis of hydrargyrism for thispatient seems unquestionable, tak-ing into account the characteristicsof the symptoms (physical and neu-ropsychiatric) and mercury dosingin his urine. Further evidences arethe onset of the symptoms after theexposure to inorganic mercury,worsening related to the time of ex-posure, and improvement of thephysical symptoms soon after inter-ruption of the exposure. Neverthe-less, the neuropsychiatric symptoms

continued, even after exposureended and mercury levels in theurine became normal. This phenom-enon suggests that neuropsychiatricsymptoms associated with poison-ing by mercury are not restricted tothe acute stage of intoxication butpersist as sequelae1-5.

With antidepressant drug treat-ment, the patient presented remis-sion of the depression symptoms.Notwithstanding remission of thedepressive condition, insomnia andloss of memory did not improvewith the use of the antidepressant.The continuation of these symp-toms in this situation minimizes thepossibility that they may be the out-come of the depression disorder,thus memory loss and insomniaseem to be related to the chronicpoisoning by mercury in this case.

Quirino Cordeiro Junior, M.D.

Psychiatrist at the Consulta-tion-Liaison Group, Institute of

Psychiatry, Hospital das Clni-cas, School of Medicine, Uni-versity of Sao Paulo

Marclia de Araujo Medrado

Faria, M.D.

Professor at the Department ofSocial Medicine, School ofMedicine, University of SaoPaulo

7/21/2019 Cordeiro,2003

4/5

458 J Neuropsychiatry Clin Neurosci 15:4, Fall 2003

LETTERS

Renerio Fraguas Junior, M.D.

Coordinator of the Consulta-tion-Liaison Group, Institute ofPsychiatry, Hospital das Clni-cas, School of Medicine, Uni-versity of Sao Paulo

References

1. OCarroll RE, Masterton G, Dougall N,et al: The neuropsychiatric sequelae ofmercury poisoning: the Mad Hattersdisease revisited. Br J Psychiatry 1995;167:9598

2. Soleo L, Urbano ML, Petrera V, et al: Ef-fects of low exposure to inorganic mer-cury on psychological performance. Br JInd Med 1990; 47:105109

3. Powell TJ: Chronic neurobehavioral ef-fects of mercury poisoning on a groupof Zulu chemical workers. Brain Inj

2000; 14:7978144. Tirado V, Garcia MA, Moreno J, et al:

Neuropsychological disorders after oc-cupational exposure to mercury vaporsin El Bagre (Antioquia, Colombia). RevNeurol 2000; 31:741742

5. Rossini SRG, Reimao R, Lefevre BH, etal: Chronic insomnia in workers poi-soned by inorganic mercury: psycholog-ical and adaptatives aspects. Arq Neu-ropsiquiatr 2000; 58(1):3238

Ziprasidone-Induced Pisa

Syndrome after ClozapineTreatment

SIR:Pleurothotonus or Pisa syn-drome is a rare dystonia, whichwas first described by Ekbom andco-workers in the early 1970s.1 Thedevelopment of Pisa syndrome ismost commonly associated withprolonged treatment with typicalantipsychotics. However, the illness

has also been reported, althoughless frequently, in patients who arereceiving other medications (e.g.,cholinesterase inhibitors and antie-metics), in those not receiving med-ication (idiopathic Pisa syndrome),and in those with neurodegenera-tive disorders. Drug-induced Pisa

syndrome develops predominatelyin females and older patients withorganic brain disorder. 2 It some-times occurs following the additionof another antipsychotic drug to anestablished regimen of antipsychot-

ics, or it insidiously arises in anti-psychotic-treated patients for no ap-parent reason. Recently, thisadversity has been associated withatypical antipsychotics, such as clo-zapine, sertindole, olanzapine, andrisperidone.3 Clinical characteristicssuggest that the underlying patho-physiology of drug-induced Pisasyndrome is complex. A dopami-nergic-cholinergic imbalance or se-rotonergic or noradrenergic dys-function may be implicated. 2 Pisa

syndrome during ziprasidone ther-apy has not been documented inthe literature. Herein, we present acase of ziprasidone-induced Pisasyndrome.

A 38-year-old female patient withschizophrenia (meeting DSM-IV cri-teria) developed side effects (seda-tion, weight gain, salivation) duringclozapine treatment (275 mg/day).Because of the persisting side ef-fects, the clozapine therapy was dis-continued, and ziprasidone, 20 mgtwice daily, was started. After 2weeks, the ziprasidone dose was in-creased to 40 mg twice daily. Onday 18, the patient developed acutetruncal dystonia, with predomi-nantly unilateral distribution thatled to a left-sided lean and back-ward rotation, classically referred toas the Pisa syndrome. Ziprasidonewas reduced to 20 mg twice daily atday 20 and discontinued on day 24,without improvement in motor ab-

normality. Successively, treatmentwith amisulpride began (day 21, 50mg; day 24, 100 mg). Blood tests, anelectroencephalogram, and a to-mography (CT) of the brain re-vealed no abnormal findings. Afteran additional 14 days, the patient

began responding to withdrawal;

and symptoms disappeared.A constellation of putative risk

factors for development of Pisa syn-drome was found in this case: fe-male gender and previous treat-ment with typical and atypical

neuroleptics (the medical history re-vealed an approximately 9-year-long previous treatment with typi-cal and atypical neuroleptics). Wehypothesize that clozapine medica-tion that was subsequent to a longtreatment with typical neurolepticsled to dopaminergic hypersensivity.In the cortices of rat brains, ziprasi-done and clozapine are capable ofincreasing dopamine (DA) release4,and ziprasidone is an agonist at the5-HT1A receptor, which is believed

to occur pre- and postsynaptically. 5These mechanisms might play arole in our patient, and we recom-mend cautious use of neurolepticdrugs in patients with risk factors.

Marc Ziegenbein, M.D.

Social Psychiatry and Psycho-therapy, Medical School Han-nover, Hannover, Germany

Georg Schomerus, M.D.

Neurology and Clinical Neuro-physiology, Medical SchoolHannover, Hannover, Germany

Stefan Kropp, M.D.

Clinical Psychiatry and Psycho-therapy, Medical School Han-nover, Hannover, Germany

References

1. Ekbom K, Lindholm H, Ljungberg I:New dystonic syndrome associated withbutyrophenone therapy. Z Neurol 1972;202:94103

2. Suzuki T, Matsuzuka H: Drug-induced

Pisa syndrome (pleurothotonus): epide-miology and management. CNS Drugs2002; 16(3):165174

3. Stubner S, Padberg F, Grohmann R,Hampel H, Hollweg M, Hippius H,Moller HJ, Ruther E: Pisa syndrome(pleurothotonus): report of a multicenterdrug safety surveillance project. J ClinPsychiatry 2000; 61:569574

7/21/2019 Cordeiro,2003

5/5

J Neuropsychiatry Clin Neurosci 15:4, Fall 2003 459

LETTERS

4. Rollema H, Lu Y, Schmidt AW, SporesJS, Zorn SH: 5-HT1A receptor activationcontributes to ziprasidone-induced do-

pamine release in the rat prefrontal cor-tex. Biol Psychiatry 2000; 48:229237

5. Barnes NM, Sharp T: A review of cen-

tral 5-HT receptors and their function.Neuropsychopharmacology 1999;38:10831152