Brain StrokeBrain Stroke

Bacterial endocarditis

Atrial fibrillation

Ball thrombus

Mitral valve stenosis

Mural thrombi

Myocardial infarction

Embolus

Common carotid a.

Common Sites ofPlaque Formation

Vertebral a.

Internal carotid a.

Basilar a.

Anterior cerebral a.

Middle cerebral a.

Posterior cerebral a.

Anterior inferiorcerebellar a.

Posterior inferiorcerebellar a.

WHAT IS A BRAIN STROKE?

Ischemia(75%)

Haemorrhage(25%)

CLINICAL PROFILE

Thrombotic stroke :

Embolic stroke :

Hemorrhagic stroke :

A Brain stroke is a focal neurological deficit caused by disruption of the cerebral circulation.

It should be considered as a symptom of an underlying process

• thrombosis

• embolism

About 70% of strokes present with hemiplegia

About 20% present with aphasia.

Second leading cause of death after myocardial infarction

• Gradual and stepwise progression.

• Occur during sleep and patient often awakens with thedeficit.

• Caused by insitu thrombosis of an atheroscleroticintracranial or neck vessel.

• Sudden onset

• Often during usual daily activities.

• Deficit is maximal at onset. Improves shortly as the embolusbreaks up and portions travel further out into more distal branchesof the affected artery.

• Signs of raised intra cranial pressure.

• Hypertension with bradycardia (Cushing reflex).

• Common sites of hypertensive, Intracerebral haemorrhage areputamen, thalamus, pons, cerebellum, hemispheric lobes.

• Hemorrhagic stroke can result from ruptured cerebral aneurysmscompounded with subarachnoid hemorrhage(SAH), rupturedarteriovenous malformations(AVM) or angiopathy

• Major symptoms of a vascular event affecting

• Hemiparesis, aphasia

• Face and arm affected more than leg - cortical localization

• Face, arm and leg equally involved - subcortical localization

• Aphasia, apraxia, neglect, seizures are usually cortical abnormalities

• Visual field defect suggest subcortical abnormalities

• “ The four D's ” diplopia, dysarthria, dysphagia and dizziness(vertigo).

a. Anterior circulation

b. Posterior circulation

Left Occipital AVM

CT showing Haematoma

DSA showing AVM

ANATOMIC SYNDROMES IN CEREBROVASCULAR DISEASE

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Internal carotid artery (ICA) supplies frontal lobes, parietal lobes, most oftemporal lobes, basal ganglia and internal capsule - ANTERIORCIRCULATION

Vertebro basilar (VB) system supplies brainstem, cerebellum, thalamus,occipital lobes and mesial and inferior temporal lobes - POSTERIORCIRCULATION

VASCULAR TERRITORIES OF BRAIN

Medial & Tentorial Surfaces of Left Cerebral Hemisphere

Supero-lateral Surface of Left Cerebral Hemisphere

Inferior Surface of Left Cerebral Hemisphere

MCA

ACA

PCA

ACA

PCAMCA

MCAACA

PCA

• • • PCA : Posterior Cerebral a.ACA : Anterior Cerebral a. MCA : Middle Cerebral a.

• Crossed findings, facial weakness or numbness combined withcontralateral extremity weakness or numbness.

Most important causes of stroke in anterior circulation

• ICA stenosis

• Cardiac embolism.

• Atherothrombotic disease of major intra-cranial branches, and

• Small vessel disease of penetrating arteries

Most important causes of stroke in posterior circulation

• Atherosclerosis of vertebrobasilar A.

• Small vessel disease in penetrating branches.

• Cardiac embolism to V.B.circulation.

• Posterior circulation is relatively sensitive to drops in cardiac output.Therefore, cardiac evaluation is important in investigating suspectedVB insufficiency.

1. History

• To localize the stroke

• To know the extent of stroke

• To find out the cause of stroke

• To collect clues regarding pathogenesis of event

2. Physical exam

• Asessment of patient's CVS for presence of heart murmurs, CCF,cardiac arrhythmias, carotid bruits and signs of Peripheral vascular disease.

3. Neurological exam

• Focus on major deficit and associated signs which aid in localization

CBC, platelet count, prothrombin time, partial thromboplastin time,electrolytes, calcium, glucose, BUN, creatinine

Chest radiograph, ECG

• lipid profile

• thyroid profile:

Hyperthyroidism is associated with AF.

Hypothyroidism is associated with hypercholesterolemia.

Basic evaluation of suspected stroke

A) Initial lab studies for patients with a stroke

B) Subsequent analysis

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C) In selected cases

Initial imaging in acute stroke

• Antithrombin III

• Protein C andprotein S inherited hyper coagulable state

• Activated protein C resistance

• Anti cardiolipin antibody

• Lupus anti Coagulant

• Homocysteine atherosclerosis, thrombosis

• Blood culture suspected endocarditis

• ESRAntinuclear antibody if vasculitisRheumatoid factor suspected

non contrast CT

• hemorrhagic stroke readily detected

• picks up SAH better than MRI

• more readily available

• can be performed more rapidly

• requires less patient cooperation

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antiphospholipid syndrome

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MRI performed later if necessary to assist with uncertain diagnosis anddiffcult localization

MR angiography(MRA) helpful in establishing mechanism of particular stroke

Transesophageal echo(TEE) is more sensitive than transthoracic echo fordiagnosing atrial and aortic abnormalities

Carotid Doppler may be used to evaluate the carotid circulation, the VBsystem, the circle of Willis, and the anterior, middle and posterior cerebralarteries and their branches.

Contrast cerebral angiography (DSA) provides the most detailed andreliable information about the presence of carotid and intracranial vasculardisease.

Most important established risk factor is age.

Second is hypertension

Other well established risk factors:

Risk factors

CT Scan in SAH

Blood in sub arachnoid space seen as hyper dense shadows

Gender[M>f], family history, diabetes mellitus, cardiac disease, prior stroke,transient ischemic attacks, carotid bruits, smoking, increased hematocrit(polycythemia), increased fibrinogen level, hemoglobinopathy, dehydration.

Lipid lowering therapy with statins results in 30 percent reduction inincidence of strokes.

Very low cholesterol may be a risk factor for haemorrhagic stroke.

Risk of stroke reverts to that of nonsmokers by 5years after smokingcessation.

Before starting therapy, most vital is to confirm by CT / MR whether the stroke is ischemic or hemorrhagic for / as the therapy for one is contraindicated for the other.

Treatment for Ischemic Stroke

Intra arterial thrombolysis : more effective than intravenous, but limitedindications.

Intra venous t-PA given with in the first 3 hours of an acute ischemic strokesignificantly improves neurologic outcome. Other antithrombotic drugs such asaspirin and heparin should be withheld in the first 24 hours in those cases.

Neuroprotective agents.

If patient presents after 3 hours of onset heparin is given in first 24 hoursfollowed by aspirin and antiplatelet agent.

Coumadin[warfarin] should be considered in all patients with cardiogenic emboli.

If TIA or non disabling stroke is due to an ICA stenosis of 70% or greater,carotid endarterectomy reduces the risk of a subsequent stroke. This is oneof the commonest operations done in USA.

Therapy: TIME IS BRAIN

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Before carotid endarterectomy

After carotid endarterectomy

The plaqueremoved from carotid bifurcation

Stenosis

Plaque from internal carotid a.

Plaque from common carotid a.

Plaque from external carotid a.

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Angioplasty or stenting of distal internal carotid or MCA lesions can be done.

Leading causes of death in the first month after a stroke are pneumonia,pulmonary edema, cardiac disease or stroke itself.

Thus treatment for a completed stroke is largely a matter of treating its medical complications

Estimated 15-20% of strokes are due to hemorrhage.

Half of these are due to SAH.

SAH can be due to trauma, ruptured aneurysm, ruptured AVM.

About 80 percent of aneurysms occurs in anterior circulation.

About 20 percent of aneurysm occur in posterior circulation.

Most common location - Anterior Communicating a. (A com) 30%

P com : ICA junction 25%

ICA/MCA bifurcation 20%

TIA is a warning of a brain stroke as angina is to heart attack. It must betaken seriously to avert lifelong misery associated with a full blown stroke.

SUB ARACHNOID HEMORRHAGE (SAH)

Basilar top aneurysm

Left Middle Cerebral aneurysm

A com

CINICAL PROFILE OF SAH

Explosive, first time ever, sudden, severe headache with or withoutneurological deficit often with altered mental status must be SAH unlessproved otherwise.

Aneurysmal SAH may also evolve over days, beginning with a moderatelysevere headache caused by initial episode, the sentinel bleed. Clinicaldeterioration due to re-bleeding may follow in 3-5 days.

Initial test in suspected SAH is a non-contrast CT scan of the brain revealingblood in cistern (s), sylvian fissure or sulci around the convexities orintraparenchymal blood depending on the location of ruptured aneurysm.

Aneurysm itself may be visible

CT scan may be negative in 10% of SAHs !

Cerebral angiography is necessary for identification of site of bleeding. It may be negative in 10-20% of all cases of SAH ! Hence must be repeated after2-3 weeks.

Surgical clipping of the aneurysm is the primary definitive & reliable treatment.

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Surgery must be performed with in first 48 hours from onset of symptomsbut some surgeons may choose to operate after 10 to 14 days because of risk ofvasospasm.

Thrombosis of the responsible aneurysm using thrombogenic coils placedvia catheter during cerebral angiography may be another option in somecases. However it has limitations resulting in lower long term occlusion rate.

DSA after Clipping the aneurysm

DSA before Clipping A-COM aneurysm

Aneurysm

Neck of being dissected before clipping

aneurysm

Neck of aneurysm

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Basic medical management of SAH centers on prevention of rebleeding bycareful blood pressure control and prevention of vasospasm using oralnimodipine and triple 'H' therapy. (Hypertension, Hypervolemia, Hemodilution)

1) Intraparenchymal extension cause focal deficits due to mass effect, includingdevelopment of cerebral edema and herniation.

2) Vasospasm occurs with aneurysmal SAH, leading to local ischemic injuryand infarction

3) Acute hydrocephalus, usually communicating hydrocephalus due toobstruction of pachyonian granulations in the venous sinuses bysubarachnoid blood. It may be treated temporarily by ventriculostomy orpermanently by V. P shunt.

4) Seizures: because blood is an irritant that can induce neuronal firing.

Characterised by confusion or decreased level of conciousness with focalneurological deficit [ speech or motor depending on the vascular territoryinvolved]

Onset ; almost never before day 3 post SAH

Maximal frequency of onset during 6-8 days post-SAH

Onset is usually insidious

Blood clots are especially spasmogenic when in direct contact with theproximal 9cm of the ACA and MCA

Not all patients with SAH develop spasm, and spasm can follow other insultsbesides SAH [Head injury without SAH]

The Hunt and Hess grade on admission correlates with the risk of CVS

Higher incidence with increasing age of patients.

Active cigarette smoking is an independent risk factor

Diagnosis of cerebral vasospasm

Delayed onset or persisting neuro deficit

Deficit appropriate to involved arteries

Rule out other causes of deterioration

• Hydrocephalus • Cerebral edema • Seizure • Hyponatremia • Hypoxia • Sepsis

Ancillary tests

• Trans cranial Doppler • Cerebral blood flow studies • SPECT • DSA

CNS complications in SAH

CLINICAL VASOSPASM(CVS)

TreatmentPreventive

Curative

DISSECTION OF CEREBRAL VESSELS

Triple H therapy

Early surgery with clipping will permit safe use of hyperdynamic therapy

Chemical angioplasty

• Intra arterial calcium channel blockers

• Intra arterial papaverine

Transluminal balloon angioplasty

Indirect arterial dilatation utilizing hyperdynamic therapy

Surgical removal of blood clot

CSF drainage via serial lumbar punctures, continous ventricular drainage

Dissection means extravassation of blood between the Intima & media, creatingluminal narrowing or occlusion.

Whether spontaneous or traumatic, may result in stroke

Dissection occurs at the transition between where the artery is mobile andwhere it is fixed in the bony canal

Dissection may be evidenced on an angiogram by an actual intimal tear or flapor by stenosis, irregularity, occlusion, or an associated pseudoaneurysm

Internal carotid artery tends to dissect atthe junction between the upper cervicalportion and petrous portions

Vertebral artery tends to dissect justbelow the skull base,usually at the C1C2 level

Both the dissections may be seen inassociation with emboli in distal branches

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a b c

a. Left MCA territory infarct due to embolus from partly occluded vessel

Treatment

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Anticoagulation

Vessel occlusion

• Indication progressive stroke despite anticoagulation

• Aimed at totally occluding a vessel that is partially occluded by dissection

• Good intracranial crossflow must be demonstrated prior to undertaking it

Stenting

• Reopens partly occluded vessels

• Indicated in short segment dissections

• Contraindicated in complete vessel occlusion

• Antiplatelet drugs - lifelong

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Left ICA dissectionProximal occlusion of (L) ICA

Good cross flow from (R) ICA ‘GIANTURCO’ THROMBOGENIC COIL

Commonly used self expandable stents

The outlook & outcome of neuroscience practise is completely revolutionized

by the advent of microsurgical techniques in neurosurgery in the last 3 decades.

Advances in neurosciences has been propelled by simultaneous advances in

neuroradiology, neuroanaesthesia & intensive care management. The technology

drive experienced in the field of medicine during the last 2 decades have propelled

neurosciences to the forefront of medical practise. The current scenario is full of

excitement and future can only be mind boggling.

- Dr. Keki E. Turel