Ashwin HaridasAsem Ali AshrafAdam Ebrahim

DefinitionsStroke

Clinical syndrome of rapid onset of focal deficits of brain function lasting more than 24 hours or leading to death

Transient Ischemic attack (TIA)Clinical syndrome of rapid onset of focal

deficits of brain function which resolves within 24 hours

Amaurosis fugax

DefinitionsProgressive 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

EpidemiologyThird most common cause of death after

cancer and ischeamic heart diseaseMost common cause of severe physical

disabilityPrevalence of stroke in India is about 1.54

per 1000Death rate is about 0.6 per 1000Incidence and prevalence of stroke is on the

rise due to increasing adoption of unhealthy lifestyle & an increasing life expectancy

Stroke Risk Factors

FixedAgeGender

(Male>Female)Race (Afro-

Caribbean>Asian>European)

HeredityPrevious vascular

event eg. MI, peripheral embolism

High fibinogen

ModifiableHypertensionHeart disease

(Atrial fibrillation, endocarditis)

Diabetes mellitusHyperlipidaemiaSmokingExcess alcohol

consumptionOral contraceptives

Anterior Circulation

Posterior Circulation

Middle Cerebral Artery

Anterior Cerebral Artery

Posterior Cerebral Artery

Types of StrokeIschemicHemorrhagic

Ischemic Stroke80% of strokesArterial occlusion of an intracranial vessel

leads to hypoperfusion of the brain region it supplies

Two etiological typesThromboticEmbolic

Etiology of ischemic strokeThrombotic

Lacunar strokeLarge vessel

thrombosisHypercoagulable

disorders

EmbolicArtery to artery

Carotid bifurcation Aortic arch

Cardioembolic Atrial fibrillation Myocardial infarction Mural thrombus Bacterial endocarditis Mitral stenosis Paradoxical embolus

Thrombotic Stroke

Atherosclerosis is the most common pathology leading to thrombotic occlusion of blood vessels

Hypercoagulable disorders – uncommon causeAntiphospholipid syndromeSickle cell anemiaPolycythemia veraHomocysteinemia

Vasculitis: PAN, Wegener’s granulomatosis, giant cell arteritis

Lacunar strokeAccounts for 20% of all strokesResults from occlusion of small deep

penetrating arteries of the brainPathology: lipohyalinosis & microatheromaThrombosis leads to small infarcts known as

lacunesClinically manifested as lacunar syndromes

Thrombotic Stroke

Embolic StrokeCardioembolic stroke

Embolus from the heart gets lodged in intracranial vessels

MCA most commonly affectedAtrial fibrillation is the most common causeOthers: MI, prosthetic valves, rheumatic heart disease

Artery to artery embolismThrombus formed on atherosclerotic plaques gets

embolized to intracranial vesselsCarotid bifurcation atherosclerosis is the most common

sourceOthers: aortic arch, vertebral arteries etc.

Etiology of ischemic stroke

Blood supply to the brain is autoregulatedBlood flow

If zero leads to death of brain tissue within 4-10min

<16-18ml/100g tissue/min infarction within an hour

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 collateralsCan be salvaged if reperfused in

timePrimary 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 typesIntracerebral

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 HemorrhageMost common cause is rupture of saccular or

Berry aneurysmsOther 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 splitImmediate cessation of neuronal functionExpanding 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

HistoryAsk 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 patientThe 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,arcus senilis(refer to ophthalmologist)

Examination of a stroke patientCVS: 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 retentionLocomotor system: injuries sustained

during collapse with stroke, comorbities which influence functional abilities.

General featureMost cerebrovascular diseases are manifest

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.

‘HAND OF GOD’

CLINICAL CLASSIFICATION

Stroke SyndromesStroke 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 CirculationThe internal carotid artery and its branches

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

Middle cerebral arterySigns and symptoms: Structures involvedParalysis 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 OcclussionOcclusion 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 ArteryThe 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 ArteryIf 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 ArteryWhen 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 ArteryIn 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 ArteryA 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 CirculationDYSARTHRIA & FACIAL

NUMBNESSATAXIA & HORNER’S SYNDROMEFACIAL WEAKNESS(LMN)HEMIPARESISHEMISENSORY LOSSHEMIANOPIALOSS OF CONSCIOSNESSDIPLOPIA, VERTIGO, VOMITING

CLASSICAL PRESENTATIONSTHROMBOTICH/O TIASTROKE IN

EVOLUTIONUSUALLY HAPPENS

EARLY MORNING

EMBOLICPATIENTS WITH

KNOWN HEART DISEASE LIKE IHD, VALVULAR HEART DISEASE

RAPID RECOVERY

HAEMORRHAGIC STROKE IN

HYPERTENSIVE PATIENTS

ASSOCIATED WITH EMOTIONAL EXCITEMENT

HEADACHE & VOMITING

DIFFERENTIAL DIAGNOSISSPACE OCCUPYING LESION(TUMOR)SEIZUREMIGRAINESUBDURAL HAEMATOMAMETABOLIC DISTURBANCE LIKE

HYPOGLYCAEMIA

HypoglycemiaThat 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 LesionsSubacute 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 STATESTraditional 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

MIGRAINEMigraine 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.

 

SUMMARYRapid onset focal deficit of brain function

confirms strokeOnset and progression will decide the

aetiologyPrecise history of deficit will decide the site

of lesion

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-INVASIVECT ScanMRI ScanMR AngiographyDoppler UltrasoundEEGPETSPECT

INVASIVELumbar PunctureContrast Angiography (Cerebral

Arteriography)CT Angiography

PATHOLOGICAL TYPES

STROKE

HAEMORRHAGIC ISCHAEMIC

CT SCANMandatory initial investigationHaemorrhage appears instantly as a hyperdense

areaInfarct appears as a hypodense areaInfarct may not appear before 48 hrsMRI may be done instead but ct scan is more

sensitive for detecting haemorrhageDiffusion weighted MRI is good for identifying

ischaemic 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…

Carotid Artery Ultrasound Showing a Completely Calcified Atherosclerotic Plaque

3-D reconstruction of CT angiogram showing stenosis at the carotid bifurcation

Intra-arterial angiography showing arteriovenous malformation

MR angiogram showing giant aneurysm at the middle cerebral artery bifurcation

NORMAL CT SCAN

HAEMORRHAGESUSPECTED

LUMBAR PUNCTURE

CSF WITH BLOOD/XANTHOCHROMIA

HAEMORRHAGE CONFIRMED

UNDERLYING DISEASECerebral vasculature

Abnormalities like aneurysms orAV malformations

Cerebral angiographyVascular imaging – MRA/CTA or doppler (non

invasive)

CARDIOVASCULAR

Like MI, atrial fibrillation, valvular diseases etc.

ElectrocardiogramChest X-RayEchocardiographyTransesophageal ultrasoundHolter monitoring(paroxysmal nocturnal

arrhythmia)Blood cultures

UNDERLYING DISEASE

UNDERLYING DISEASESerum lipids for hyperlipidemiaANA for SLEMR Angiography for arterial dissectionLupus anticoagulant for antiphospholipid

antibody syndromeESR, CRP, ANCA for vasculitisPT, aPTT, Platelet count for bleeding

disordersProteins C & S for hypercoagulability

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 THERAPYAsprin, 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 COAGULANTSHEPARINS , 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’dHYPEROSMOLAR AGENTS - reduce cerebral oedema - 20% mannitol IV – 100ml TID - oral glycerol if swallow is normalConcurrent medical problems such as atrial

fibrillations to be tackledOTHERS: - PENTOXYPHYLLINE (hemorrheology modifier) to be used within 12 hrs -NEUROPROTECTIVE AGENTS

HAEMORRHAGIC STROKE

Control of hypertensionControl coagulation abnormalities (esp due to

oral anticoagulants)Surgical decompressionSurgery for aneurysms and arterio-venous

malformationsAnti platelet Anti platelet and anti coagulants anti coagulants are

contraindicated

REHABILITATIONPHYSIOTHERAPY - as early as

possible

- initially passive moments

- later active movements

- in every case early mobilization

- prevents contractures, spasticity and atrophy

OCCUPATIONAL THERAPY

REHABILITATION - Cont’dSPEECH THERAPY

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

STROKE UNITS – A MULTIDISCIPLINARY APPROACHImmediate resuscitation , prevent

complications and recurrenceEmergency 24 hr evaluation and

comprehensive care Improves neurological outcomeReduces mortality1000 patients admitted to stroke units

saves the lives of atleast 5o patients at end of 6 months

SECONDARY PREVENTIONBlood pressure controlDiabetes ManagementLipid ManagementSmoking CessationAlcohol Moderation Weight

Reduction/Physical Activity

Carotid Artery Interventions

Anti platelet agents / Anti coagulants

StatinsDiuretics +/- ACE

inhibitors

COMPLICATIONSDue 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

interventionFirst 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 .