NEURO CASE3

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    Case

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    Case

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    Case

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    Subarachnoid hemorrhage (SAH)

    Most common cause is rupture of saccularaneurysm.

    Others: bleeding from vascular formation andextension from a primary intracerebralbleeding.

    Most unruptured intracranial aneurysms are

    asymptomatic. Symptoms are usually due to rupture and

    resultant SAH.

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    Subarachnoid hemorrhage (SAH)

    At rupture, ICP rises.

    Sudden transient loss of consciousness

    Excruciating headache, worst headache of mylife, generalized, change in usual headachepattern, most important is the sudden onset ofheadache

    Neck stiffness

    Vomiting

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    Subarachnoid hemorrhage (SAH)

    Prodromal symptoms suggest location ofenlarging aneurysm.

    3

    rd

    cranialnerve

    palsy- j

    unction of PC

    Aand IC

    A

    6th nerve palsy- cavernous sinus

    Occipital and cervicalpain- PICA or AICA aneurysm

    Pain in or behind the eye and in the low temple-

    MCA aneurysm

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    Vasospasm

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    Vasospasm

    Pathological constriction of cerebral arteries

    which can cause ischemia or stroke from 4 to21 days after SAH

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    Fisher Grading

    Classifies SAH according to how they appearon CT scan

    To check for vasospasms most dreadedcomplication ofSAH

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    Fisher Grading

    Grade 1- No hemorrhage evident

    Grade 2- Subarachnoid hemorrhage less than1mm thick

    Grade 3- Subarachnoid hemorrhage more than1mm thick

    Grade 4- Subarachnoid hemorrahge of any

    thickness with intra-ventricular hemorrhage(IVH) or parenchymal extension

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    Management

    Maintenance of optimalperfusion withhypertension & mild hypovolemia

    Administration of Nimodipine, a CCB that may

    decrease the incidence % degree of spasm

    Neurointerventional options for treatingsymptomatic vasospasm include intra-arterialpapaverine or nicardipine, and ballon angioplastyfor larger caliber vessels

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    Etiology & Presentation

    Treatment option & Timing of surgeryOutcome & Prognosis

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    Hunt-Hessclinical gra ing syste f r S H

    0- Assy pt atic; unrupture aneursy

    1- Awake; assy pt atic r ild headache, ildnuchal rigidity

    2- Awake, derate t severe headache, cranialnever palsy (e.g. CN3 r 4), nuchal rigidity

    3- Lethargic; ild f calneur logic deficit (e.g.pronator drift)

    4- Stupurous; significant neurologic deficit (e.g.he iplegia)

    5- Comatose; posturing

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    Treatment option& Timing of surgery

    Diagnosis

    Lumbar puncture

    CT scan MRI scan

    4-vessel cerebral angiography

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    Patients suspected with SAH should have CT immediately. If

    CT is (-), lumbar puncture (LP) should be performed. An LP with xantochromia and high RBC counts (usually

    100,000/mL), which do not decrease between tubes 1 and 4,is consistent with SAH

    (-) CT and LP essentially rules out SAH

    Patients diagnosed with SAH require 4 vessel cerebralangiography within 24 hours to assess for aneurysm or othervascular malformation

    Catheter angiography is the gold standard for assessing thepatients cerebral vasculature, relevant anomalies andpresence, location, and morphology of the cerebral

    aneurysms SAHpatients should be admitted to the neurologic ICU Hunt-Hess grade 4 or 5 require intubation and hemodynamic

    monitoring and stabilization. The current standard of care forruptured aneursyms requires early aneurismal occlusion

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    There are 2 options for occlusion: Craniotomy & Coiling

    The patient may undergo craniotomy with microsurgicaldissection and placement of a titanium clip across the

    aneurysm neck to exclude the aneurysm from the circulationand reconstitute the lumen of the parent vessel

    The 2nd option is to coil the aneurysm via an endovascularapproach. The patient is taken to the interventionalneuroradiology suite for placement oflooped titanium coils

    inside the aneurysm dome

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    The coils support thrombosis & prevent blood flow into the aneurysm

    Factors favoring craniotomy & clipping:

    Young age

    Good medical condition

    Broad aneurysm necks Factors favoring coiling:

    Age

    Medical comorbidities

    Narrow aneurysm necks

    Due to coil migration or compaction overtime, surgical clipping is believedto result in a more definitive cure

    Long term outcomes may be better in younger patient with clippedaneurysms

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    Outcome

    Mortality rate of50% in the 1st month

    Approximately 1/3 of survivors return to pre

    SAH function, and the remaining 2/3s havemild to severe disability

    Most require rehabilitation afterhospitalization

    Long term outcomes may be better in youngerpatient with clipped aneurysms

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    References

    Schwartzs Principle ofSurgery. 9th ed

    Harrisons Principle of InternalMedicine. 17th ed

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    ClassificationEtiology

    Clinical PresentationTreatmentOutcome

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    Classification

    Congenital

    Arterio-venousMalformation

    Venous Malformation

    Capillary Telangiectasias

    cquired

    Cavernous angioma (cavernousMalformation)

    DuralArteriovenous Fistula (Dural Venous Fistula)

    Harrisons InternalMedicine 17th

    ed

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    Vascular Malformations

    Hemorrhage to subarachnoid space- picturealmost identical to ruptured saccularaneurysm (SA)- less severe

    Most AVMs in cerebral tissue- intracerebralbleeding more than likely

    1/10 as common as SA

    Avm and SA associated with 5% of cases Association increases with size ofAVM and age ofpatient

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    Arterio-Venous Malformation

    Tangle of dilated vessels forming an abnormalcommunication bet arterial and venous systemsacross the cortical surface or within the brain

    substance. Vary in size and blood vessels usually thin and do

    not have normal structures.

    Occur in allparts of Cerebral hemispheres

    brainstem, and Spinal cord. Largest at posterior half of hemispheres- wedge

    shaped lesion extending from cortex to ventricle

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    ClinicalFeatures

    Bleeding & seizures

    Present at birth; Onset 10-30 y/o

    First clinical manifestation 50%- cerebral subarachnoid hemorrhage

    30%- seizure

    20%- headache

    10%- progressive hemiparesis and FND

    Chronic recurrent headache- migraine-like headaches- parieto-occipital

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    Huge AVM- progressive FND due tocompression of neighboring structures Enlarging mass of vessels & shunting ofblood to

    dilated vessels (intracerebral steel) Hydrocephalus- enlarged vein of Galen-

    drainage of adjacent AVM

    Pulsating carotid arteries on neck, mastoidprocess or eyeballs- pathognomonic ofAVM

    Fundoscopy- retinal vascular malfomation

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    DIAGNOSIS

    CT- contrast infusion- 90%

    MRI- shows previous bleeding AVM

    Arteriography/Conventional Xray-angiography- gold standard

    Autopsy- dissecting microscope

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    Treatment Surgical Excision

    20-40% block dissection

    Endovascular Embolization- Ligation of feeding arteries

    Radiosurgery Single dose of subnecrotizing stereotactically directedproton radiation.

    Photon radiation, linear accelerator, gamma knife Slow scelerosis of arterial channels for 2-3 years

    Complication: delayed radiation necrosis & venouscongestion

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    Venous Malformation

    Consist purely of distended veins deep in thewhite matter and results in an abnormalcerebral, cerebellar, or brainstem drainage.

    Functional venous channels Vs AVM

    Mostly seizures and headache

    Little significance- ignored

    Surgical resection- venous infarction andhemorrhage

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    Capillary telangiectasia

    True capillary malformation that formsextensive vascular networks on normalbrainstructure.

    Common: Pons, deep cerebral white matter Osler-Rendu-Webber- HereditaryHemorrhagic telangiectasia

    Rarely produces mass effect/ significantsymptoms

    No treatment options

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    Classification

    Congenital

    Arterio-venousMalformation

    Venous Malformation

    Capillary Telangiectasias

    cquired

    Cavernous angioma (cavernousMalformation)

    DuralArteriovenous Fistula (Dural Venous Fistula)

    Harrisons InternalMedicine 17th

    ed

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    DuralAV Fistula

    May be Cranial and Spinal

    Cranial- nidus of abnormal atrteries and veinswith AV shunting contained entirely within theleaflets of dura

    Origin oflesion not settled- not developmental

    Arise adjacent to venous sinus thrombosis or in

    association with vascular atresia Transverse sigmoid sinus/ adjacent cavernous sinus

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    DuralAV Fistula

    Acquired connection of dural sinus todural artery

    Manifestations Pulse-synchronous cephalic bruit (pulsatile

    tinnitus)

    Headache

    Cortical ischemia, venous hypertension- >subarachnoid hemorrhage

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    DuralAV Fistula

    After forceful injury- remote to site of contact

    Klippel-trenaunay or osler-weber rendusyndromes

    Subdural hemorrhage is infrequent- dramatic mode ofpresentation

    Large fatal clot

    Cerebral-subarachnoid hemorrhage- antcranial fossa, tentorial incisura.

    Seizures uncommon

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    DuralAV Fistula

    Pseudomotor cerebri- headache, vomitting,papilledema ( highflow)

    High-flow shunt0- cause CHF

    DX- CT & MRI- thickening or enhancement ofregion of dura generally close to a large duralvenous sinus

    Injection of Gadolinium TX: Surgery- smalllesions ;Endovascular

    Embolization-larger and inaccessible lesions

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    Cavernous Malformation

    Small hemorrhages- clinically silent

    Small hamartomatous lesions of multiple

    juxtaposed endothelium- lined cavites withoutinterposed neural tissues

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    Cavernous Malformation

    Diagnosis Clinical

    MRI- cluster if vessels surrounded by zone of

    hypodense ferritin on T1 weighted images-product ofprevious small episodes ofbleeding Mostly in brainstem, pons, cerebral hemispheres

    and adjacent venous anomalies

    Treatment: Surgical resection of cavernous angioma Low-dose proton-radiation

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    Prognosis

    With an overall risk of intracerebral hemorrhage of 2-4% per year,angiographic assessment is recommended to further defineprognosis for patients with AVM.

    Those with superficial, moderate-sized AVMs have a good long-term prognosis and may not have any additionalbenefit with

    interventional treatment. Lifetime risk of hemorrhage may be substantial for young patients

    with AVM. Prognosis after AVM hemorrhage is generally better than that after

    intracerebral hemorrhage from other causes. Better prognosis maybe due to the relatively younger age ofpatients and a greaterpotential for reorganization ofbrain function. More accurateprognosis awaits the results of currently active, long-term,population-based outcome studies.

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    Management ofSAH

    Early aneurysm repair prevents rupture and allows the safeapplication of techniques to improve blood flow (e.g. inducedhypertension & hypervolemia) should symptomaticvasospasm develop

    An aneurysm can be clipped by a neurosurgeon or coiledby an endovascular surgeon

    Medical management ofSAH focuses on protecting theairway, managing the BP before and after the aneurysmtreatment, prevent rebleeding prior to treatment, mnageing

    vasopasm, treating hydrocephalus, treating hyponatremia &preventing pulmonary embolus