CEREBRAL VASCULAR ACCIDENT/STROKE

WILSON MTWANA4TH YEAR MBchB

Definition of termsStroke• A stroke is the acute neurologic injury that occurs as a result of brain ischemia or

brain hemorrhage pathologic processes. or• Clinical syndrome of rapid onset of focal deficits of brain function lasting more

than 24 hours or leading to death.

Transient ischemic attack (TIA)• The sudden onset of a focal neurologic symptoms and/or sign that lasts less than

24 hours and is presumably brought on by a transient decrease in blood supply, which renders the brain ischemic in the area producing the symptom.

Def. continuedProgressive Stroke A stroke in which the focal neurological deficits worsen with time. Also called stroke in evolution

Completed StrokeA stroke in which the focal neurological deficits persist and do not worsen with time

Epidemiology• Third most common cause of death after cancer and ischemic heart disease• Most common cause of severe physical disability• Prevalence of stroke in India is about 1.54 per 1000• Prevalence in Africa 81.2 /100,000 (2009)• Death rate is about 0.6 per 1000• Incidence and prevalence of stroke is on the rise due to increasing adoption of

unhealthy lifestyle & an increasing life expectancy

Stroke Risk Factors

Non modifiable• Age• Gender (Male>Female)• Race (Afro-

Caribbean>Asian>European)• Heredity• Previous vascular event eg. MI,

peripheral embolism• High fibrinogen

Modifiable• Hypertension• Heart disease (Atrial fibrillation,

endocarditis)• Diabetes mellitus• Hyperlipidemia• Smoking• Excess alcohol consumption• Oral contraceptives

Classification & EtiologyStroke is classified into two major types:

• Brain ischemia: Due to thrombosis, embolism, or systemic hypoperfusion • Brain hemorrhage: Due to intracerebral hemorrhage or subarachnoid

hemorrhage

Approximately 80 percent of strokes are due to ischemic cerebral infarction and 20 percent to brain hemorrhage

Cont…

• Ischemic• Hemorrhagic

Ischemic Stroke• 80% of strokes• Arterial occlusion of an intracranial vessel leads to hypoperfusion of the

brain region it supplies• Three etiological types

• Thrombosis• Embolism• Systemic hypoperfusion

Thrombosis• Generally refers to local in situ obstruction of an artery.

• The obstruction may be due to disease of the arterial wall, such as arteriosclerosis, dissection, or fibromuscular dysplasia; there may or may not be superimposed thrombosis.

• Thrombotic strokes are those in which the pathologic process giving rise to thrombus formation in an artery produces a stroke either by reduced blood flow distally (low flow) or by an embolic fragment that breaks off and travels to a more distant vessel (artery-to-artery embolism).

• Thrombotic strokes can be divided into either large or small vessel disease.Large vessel disease: Large vessels include both the extracranial (common and internal carotids, vertebral) and intracranial arterial system (Circle of Willis and proximal branches)• Intrinsic lesions in large extracranial and intracranial arteries cause symptoms

by reducing blood flow beyond obstructive lesions, and by serving as the source of intraarterial emboli.

• Pathologies affecting large extracranial vessels include: Atherosclerosis, Dissection, Takayasu arteritis, Giant cell arteritis, Fibromuscular dysplasia

• Pathologies affecting large intracranial vessels include: Atherosclerosis, Dissection Arteritis/vasculitis, Noninflammatory vasculopathy, Moyamoya syndrome & Vasoconstriction

• Atherosclerosis is by far the most common cause of in situ local disease within the large extracranial and intracranial arteries that supply the brain.

Small vessel disease: Small vessel disease affects the intracerebral arterial system, specifically penetrating arteries that arise from the distal vertebral artery, the basilar artery, the middle cerebral artery stem, and the arteries of the circle of Willis. These arteries thrombose due to: • Lipohyalinosis (a lipid hyaline build-up distally secondary to hypertension)

and fibrinoid degeneration • Atheroma formation at their origin or in the parent large arteryThe most common cause of obstruction of the smaller arteries and arterioles that penetrate at right angles to supply the deeper structures within the brain (e.g. basal ganglia, internal capsule, thalamus, and pons) is lipohyalinosis, blockage of an artery by medial hypertrophy, and lipid admixed with fibrinoid material in the hypertrophied arterial wall.

Cont…A stroke due to obstruction of these vessels is referred to as a lacunar stroke.

Lacunar strokes represent 20% of all ischemic strokes

• Lipohyalinosis is most often related to hypertension, but aging may play a role• Microatheromas can also block these small penetrating arteries, as can

plaques within the larger arteries that block or extend into the orifices of the branches (called atheromatous branch disease)

• Penetrating artery occlusions usually cause symptoms that develop during a short period of time, hours or at most a few days, compared with large artery-related brain ischemia, which can evolve over a longer period.

Embolism: Refers to particles of debris originating elsewhere that block arterial access to a particular brain region Embolic strokes are divided into four categories. • Those with a known source that is cardiac • Those with a possible cardiac or aortic source based upon transthoracic and/or

transesophageal echocardiographic findings • Those with an arterial source (artery to artery embolism) • Those with a truly unknown source in which tests for embolic sources are

negativeThe embolus suddenly blocks the recipient site so that the onset of symptoms is abrupt and usually maximal at the start Unlike thrombosis, multiple sites within different vascular territories may be affected when the source is the heart (e.g. left atrial appendage or left ventricular thrombus) or aorta.

Systemic hypoperfusion• It is a more general circulatory problem, manifesting itself in the brain and

perhaps other organs• The reduced perfusion can be due to cardiac pump failure caused by

cardiac arrest or arrhythmia, or to reduced cardiac output related to acute myocardial ischemia, pulmonary embolism, pericardial effusion, or bleeding.

• Hypoxemia may further reduce the amount of oxygen carried to the brain.

• Blood supply to the brain is auto regulated.• Blood flow

• If zero leads to death of brain tissue within 4-10min • <16-18ml/100g tissue/min infarction within an hour(50 to 54 milliliters of blood per

100 grams of brain tissue per minute)

• Ischemia leads to development of an ischemic core and an ischemic penumbra

Pathophysiology of Ischemic Stroke

Ischemic Penumbra• Tissue surrounding the core region of infarction

which is ischemic but reversibly dysfunctional• Maintained by collaterals• Can be salvaged if reperfused in time• Primary goal of revascuralization therapies.

ATP depletion

Hypoperfusion

Failure of Na+/K+ ATPase membrane ionic pump

Calcium entryGlutamate release

Activation of lipid peroxidases, proteases & NO synthase

Destruction of intracellular organelles, cell membrane & release of free radicals

Free fatty acid release

Activation of pro-coagulant pathways

Liquefactive necrosis

Thrombus/embolus

Membrane depolarization & cytotoxic cellular edema

Hemorrhagic Stroke• Two types

• Intracerebral hemorrhage(ICH)

• Subarachnoid hemorrhage(SAH)

• Higher mortality rates when compared to ischemic stroke

Intracerebral Hemorrhage• Result of chronic hypertension• Small arteries are damaged due to hypertension• In advanced stages vessel wall is disrupted and leads to leakage• Other causes: amyloid angiopathy, anticoagulant therapy, cavernous

hemangioma, cocaine, amphetamines

Subarachnoid Hemorrhage• Most common cause is rupture of saccular or Berry aneurysms• Other causes include arteriovenous malformations, angiomas, mycotic

aneurysmal rupture etc.• Associated with extremely severe headache

Pathophysiology Of Hemorrhagic Stroke• Explosive entry of blood into the brain parenchyma structurally disrupts

neurons• White matter fibre tracts are split• Immediate cessation of neuronal function• Expanding hemorrhage can act as a mass lesion and cause further

progression of neurological deficits• Large hemorrhages can cause transtentorial coning and rapid death

CLINICAL FEATURES

History• Ask for onset and progression of neurological symptoms –

completed stroke or stroke in evolution

• History of previous TIAs & amaurosis fugax

• History of hypertension & diabetes mellitus

• History of heart conditions like arrhythmias, RHD & prosthetic valves

• History of seizures & migraine

• History of anticoagulant therapy

• History of oral contraceptive use

• History of any hypercoagulable disorders like sickle cell anemia & polycythemia vera

• Substance abuse: cocaine, amphetamines

History

Examination of a stroke patient• The neurological examination is highly variable and depends on the location

of the vascular lesion.• Skin: look for xanthelasma,rashes (arteritis,splinter haemorrhages,livedo

reticularis),limb ischemia(DVT)• Eyes:look for diabetic changes,retinal emboli,hypertensive changes.

Examination of a stroke patient• CVS: hyper/hypotension, abnormal rhythm(atrial

fibrillation),murmurs(valvular anomaly),raised JVP(heart failure),peripheral pulses and bruits(generalised arteriopathy)

• Respiratory system: pulmonary edema, infection• Abdomen: urinary retention• Locomotor system: injuries sustained during collapse with stroke,

comorbities which influence functional abilities.

General feature• Most cerebrovascular diseases are manifested by the abrupt onset of

a focal neurologic deficit, as if the patient was "struck by the hand of God.”

• The clinical manifestations of stroke are highly variable because of the complex anatomy of the brain and its vasculature.

CLINICAL CLASSIFICATION

STROKE

PROGRESSING/EVOLVING COMPLETED TIA

Stroke Syndromes• Stroke syndromes are divided into: (1) large-vessel stroke within the anterior circulation (2) large-vessel stroke within the posterior circulation,and (3) small-vessel disease of either vascular bed.

Stroke Within the Anterior Circulation• The internal carotid artery and its branches comprise the anterior

circulation of the brain i.e the anterior and middle cerebral arteries

Middle cerebral artery• Signs and symptoms: Structures involved• Paralysis of the contralateral face, arm, and leg; sensory

impairment over the same area: Somatic motor area• Motor aphasia: Motor speech area of the dominant

hemisphere• Central aphasia:Central, suprasylvian speech area and

parietooccipital cortex of the dominant hemisphere• Conduction aphasia: Central speech area (parietal

operculum)

Cont….

• Homonymous hemianopia (often homonymous inferior quadrantanopia): Optic radiation deep to second temporal convolution

• Paralysis of conjugate gaze to the opposite side: Frontal contraversive eye field or projecting fibers

• Central aphasia:Central, suprasylvian speech area and parietooccipital cortex of the dominant hemisphere

• Conduction aphasia: Central speech area (parietal operculum)• Homonymous hemianopia (often homonymous inferior

quadrantanopia): Optic radiation deep to second temporal convolution

Cont..• Apractognosia(agnosia +apraxia) of the nondominant

hemisphere:Nondominant parietal lobe (area corresponding to speech area in dominant hemisphere); loss of topographic memory is usually due to a nondominant lesion, occasionally to a dominant one.

• Apraxia is a neurological disorder characterized by loss of the ability to execute or carry out learned purposeful movements, despite having the desire and the physical ability to perform the movements. It is a disorder of motor planning.

• Agnosia (a-gnosis, "non-knowledge", or loss of knowledge) is a loss of ability to recognize objects, persons, sounds, shapes, or smells while the specific sense is not defective nor is there any significant memory loss

Deficits Due To ACA Occlussion

• Occlusion of the anterior cerebral artery may result in the following defects:• If stroke occurs prior to the anterior communicating artery it is usually well tolerated

secondary to collateral circulation • Paralysis of the contralateral foot and leg • Sensory loss in the contralateral foot and leg • Left sided strokes may develop transcortical motor aphasia • Gait apraxia • Urinary incontinence which usually occurs with bilateral damage in the acute phase

Internal Carotid Artery• The clinical picture of internal carotid occlusion varies depending on

whether the cause of ischemia is propagated thrombus, embolism, or low flow. The cortex supplied by the MCA territory is affected most often. With a competent circle of Willis, occlusion may go unnoticed.

Internal Carotid Artery• If the thrombus propagates up the internal carotid artery into the MCA

or embolizes it, symptoms are identical to proximal MCA occlusion.• Sometimes there is massive infarction of the entire deep white matter

and cortical surface.

Internal Carotid Artery• When the origins of both the ACA and MCA are occluded at the top of

the carotid artery, abulia or stupor occurs with hemiplegia, hemianesthesia, and aphasia or anosognosia. When the PCA arises from the internal carotid artery (a configuration called a fetal posterior cerebral artery), it may also become occluded and give rise to symptoms referable to its peripheral territory

Internal Carotid Artery• In addition to supplying the ipsilateral brain, the internal carotid

artery perfuses the optic nerve and retina via the ophthalmic artery. In ~25% of symptomatic internal carotid disease, recurrent transient monocular blindness (amaurosis fugax) warns of the lesion. Patients typically describe a horizontal shade that sweeps down or up across the field of vision

Internal Carotid Artery• A high-pitched prolonged carotid bruit fading into diastole is often

associated with tightly stenotic lesions. As the stenosis grows tighter and flow distal to the stenosis becomes reduced, the bruit becomes fainter and may disappear when occlusion is imminent.

Posterior Circulation• DYSARTHRIA & FACIAL NUMBNESS• ATAXIA & HORNER’S SYNDROME• FACIAL WEAKNESS(LMN)• HEMIPARESIS• HEMISENSORY LOSS• HEMIANOPIA• LOSS OF CONSCIOSNESS• DIPLOPIA, VERTIGO, VOMITING

CLASSICAL PRESENTATIONSTHROMBOTIC• H/O TIA• STROKE IN EVOLUTION• USUALLY HAPPENS EARLY

MORNING

EMBOLIC• PATIENTS WITH KNOWN HEART

DISEASE LIKE IHD, VALVULAR HEART DISEASE

• RAPID RECOVERY

HAEMORRHAGIC STROKE IN

HYPERTENSIVE PATIENTS

ASSOCIATED WITH EMOTIONAL EXCITEMENT

HEADACHE & VOMITING

DIFFERENTIAL DIAGNOSIS• SPACE OCCUPYING LESION(TUMOR)• SEIZURE• MIGRAINE• SUBDURAL HAEMATOMA• METABOLIC DISTURBANCE LIKE HYPOGLYCAEMIA

Hypoglycemia• That transient hypoglycemia may produce a

stroke like picture with hemiplegia and aphasia has been known for years.

• The wide use of bedside rapid laboratory testing for glucose now makes this easily detectable and treatable. The hemiplegia may resolve immediately with the administration of intravenous glucose but resolution over a hours is also reported

Space Occupying Lesions• Subacute or chronic duration of symptoms, however

some patients may present with acutely probably due to bleeding into a tumour

• Associated with deep seated bursting headache, projectile vomiting due raised ICT

SEIZURES AND POST ICTAL STATES• Traditional thought is that these postictal symptoms are

manifestations of seizure-induced alterations in neuronal function that are reversible; structural neuronal alterations are not present. The postictal weakness or Todd’s paralysis usually follows partial motor seizures but may follow generalized seizures as well. Duration is usually brief but may last 48 hours

MIGRAINE• Migraine may actually precipitate a stroke, but there is also a variant of migraine,

hemiplegic migraine, where unilateral hemiparesis outlasts the headache. This is difficult if not impossible to diagnose correctly at first presentation when it must be regarded as a diagnosis of exclusion; only with recurrent, stereotypic attacks can this be suspected. Cases with alternating hemiplegia have been reported. At times this disorder has been shown to be familial.

SUMMARY• Rapid onset focal deficit of brain function confirms stroke• Onset and progression will decide the aetiology• Precise history of deficit will decide the site of lesion

MANAGEMENT OF STROKE

INVESTIGATION OBJECTIVES

• To confirm the vascular nature of the lesion

• The pathological type of the vascular lesion

• The underlying vascular disease

• Risk factors present

INVESTIGATION MODALITIES: BRAIN

NON-INVASIVE• CT Scan• MRI Scan• MR Angiography• Doppler Ultrasound• EEG• PET• SPECT

INVASIVE• Lumbar Puncture• Contrast Angiography (Cerebral Arteriography)• CT Angiography

CT SCAN• Mandatory initial investigation• Haemorrhage appears instantly as a hyperdense area• Infarct appears as a hypodense area• Infarct may not appear before 48 hrs• MRI may be done instead but ct scan is more sensitive for

detecting haemorrhage• Diffusion weighted MRI is good for identifying ischaemic lesion

HAEMORRHAGIC LESION

ISCHAEMIC LESION

STROKE PATIENT

CT SCAN/MRI

VASCULAR NATURE CONFIRMED

HAEMORRHAGE ISCHAEMIA

Cont’d…

SEARCH FOR SOURCE

CEREBRAL ARTERIOGRAPHY MRA/CTA DOPPLER PET/SPECT

SEARCH FOR SOURCE

Cont’d…

NORMAL CT SCAN

HAEMORRHAGESUSPECTED

LUMBAR PUNCTURE

CSF WITH BLOOD/XANTHOCHROMIA

HAEMORRHAGE CONFIRMED

TREATMENT OBJECTIVES

1. MINIMIZE VOLUME OF BRAIN IRREVERSIBLY DAMAGED

2. PREVENT COMPLICATIONS

3. REHABILITATION

4. REDUCE RISK OF RECCURENCE

MANAGEMENT OF A TRANSIENT ISCHAEMIC ATTACK (TIA)

MEDICAL MANAGEMENT (if diffuse atherosclerotic disease or poor operative candidates)

1. Stop smoking2. Concurrent medical problems to be addressed:

• Emboli from heart and other parts of cardiovascular system

(a) anti coagulants: Heparin(IV), Warfarin(oral)(b) anti platelet drugs: Aspirin(oral), Ticlopidine

• Diabetes, Hypertension, Hyperlipidemia

MANAGEMENT OF A TRANSIENT ISCHAEMIC ATTACK(TIA) – Cont’d

SURGICAL MANAGEMENT

• CAROTID AND CEREBRAL ARTERIOGRAPHY

STENOSISMild to Moderate Severe

Regular Follow Up Carotid Endarterectomy

• All above can be done only if there is relatively little atherosclerosis elsewhere in cerebrovascular system.

MANAGEMENT OF AN ACUTE EPISODE OF STROKE

• AIRWAY - Maintain airway, prevent aspiration, keep nil per oral

• BREATHING - Maintain oxygen saturation > 97%

- Supplementary oxygen

• CIRCULATION - Adequacy of pulse and BP

- Fluid, Anti Arrhythmics, Ionotropes

• HYDRATION - Prevent dehydration ; give adequate fluids

- Parenteral or via nasogastric tube

• NUTRITION - Nutritional supplements and Nasogatric feeding

• MEDICATION - Administer medication also by routes other than oral

MANAGEMENT OF AN ACUTE EPISODE OF STROKE Cont’d

• BLOOD PRESSURE - unless indicated (heart or renal failure,hypertensive encephalopathy or aortic dissection) it should not be lowered for the fear of expansion of infarct.

Ischaemic stroke - maintain 180/110 mm Hg

Haemorrhagic stroke – keep MAP <115 mm Hg• BLOOD GLUCOSE - INSULIN to treat hyperglycaemia(can increase infarct size) - maintain < 200mg%• TEMPERATURE - early use of antipyretics• PRESSURE AREAS – To prevent occurrence of decubitus ulcers• INCONTINENCE

EARLY MANAGEMENT

ISCHAEMIC STROKE

• THROMBOLYTICS and REVASCULARISATION - - tPA (alteplase)-0.9mg/kg(max 90mg) 10% of dose – initial IV bolus remainder infused over one hour - to be used < 3 hrs of onset of symptoms (for maximum efficacy) - haemorrhage to be ruled out

• NEUROPROTECTIVE AGENTS

ANTI PLATELET THERAPY• Asprin, Clopidogrel - act by inhibiting platelet aggregation and adhesion. - aspirin 300mg single dose to be given immediately

following diagnosis. - if alteplase given it can be with held for 24 hrs. - later aspirin at a dose of 75 mg in combination with

clopidogrel 75 mg daily for about one year duration.

ANTI COAGULANTS• HEPARINS , WARFARIN -heparins act by accelerating the inhibition of factor II and factor X of coagulation

cascade -warfarin antagonises vitamin K to prevent activation of clotting factors -decrease risk of recurrence and venous thromboembolism -intra cranial haemorrhage to be excluded before therapy -more useful if stroke is evolving

ANTI COAGULANTS - Cont’d• HYPEROSMOLAR AGENTS - reduce cerebral oedema - 20% mannitol IV – 100ml TID - oral glycerol if swallow is normal• Concurrent medical problems such as atrial fibrillations to be tackled• OTHERS: - PENTOXYPHYLLINE (hemorrheology modifier) to be used within 12 hrs -NEUROPROTECTIVE AGENTS

HAEMORRHAGIC STROKE

• Control of hypertension• Control coagulation abnormalities (esp due to oral anticoagulants)• Surgical decompression• Surgery for aneurysms and arterio-venous malformations• Anti platelet and anti coagulants are contraindicated

REHABILITATION• PHYSIOTHERAPY - as early as possible - initially passive moments - later active movements - in every case early mobilization - prevents contractures, spasticity and

atrophy

• OCCUPATIONAL THERAPY

REHABILITATION - Cont’d

• SPEECH THERAPY

• IMPROVE QUALITY OF LIFE WITH MOTOR AIDS -leg brace, toe spring , cane , walking stick

STROKE UNITS – A MULTIDISCIPLINARY APPROACH• Immediate resuscitation , prevent complications and recurrence• Emergency 24 hr evaluation and comprehensive care • Improves neurological outcome• Reduces mortality• 1000 patients admitted to stroke units saves the lives of atleast 5o

patients at end of 6 months

SECONDARY PREVENTION• Blood pressure control• Diabetes Management• Lipid Management• Smoking Cessation• Alcohol Moderation • Weight Reduction/Physical

Activity• Carotid Artery

Interventions

• Anti platelet agents / Anti coagulants

• Statins• Diuretics +/- ACE

inhibitors

COMPLICATIONS• Due to cortical brain injury(immediate) - Epilepsy/seizures - Cerebral oedema • Residual deficits from stroke - Paralysis - Aphasia

COMPLICATIONS – Cont’d • Due to immobility - Chest infections - Pressure sores - Deep vein thrombosis / pulmonary embolism - Painful shoulder - Urinary infection/constipation - Depression and anxiety

PROGNOSISISCHAEMIC STROKE

• Mortality rate in first 30 days is 8-12% • Can vary depending upon size, location, symptoms of stroke • Time that elapses from the event to medical intervention• First 3 hrs after stroke - GOLDEN PERIOD

PROGNOSIS – Cont’dINTRACEREBRAL HAEMORRHAGE

• Mortality rate in first 30 days is almost 50%• Site and extent of hematoma also plays a role in determining the prognosis• Hamorrhagic strokes have a poor prognosis compared to ischaemic type .

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