DefinitionStroke or “brain attack” is an acute CNS

injury that results in neurologic S/S brought on by a reduction or absence of perfusion to a territory of the brain. The disruption in flow is from either an occlusion (ischemic) or rupture (hemorrhagic) of the blood vessel.

Terms used in stroke:• Cerebral Ischemia: reduction in blood flow

lasts longer than several seconds. As neurons lack glycogen so energy failure is rapid and neurological symptoms manifest within seconds.

• Infarction: cessation of blood for more than a few minutes.

• Focal Ischemia or Infarction is caused by thrombosis of a cerebral vessels themselves or by emboli from a proximal

Arterial source of heart.• INFARCTION results when:

– Cerebral blood flow of 0 (zero) in 4 – 10 mins– CBF <16-18 ml/ 100g tissue per min in 1 hour

• CBF <20ml/100g tissue per min = ischemiaTransient Ischemic Attack(TIA):in this blood

flow is quickly restored and brain tissue recovers fully and patients symptoms are only transient.

The brain requires 20 % of the total blood pumped by the heart.No storage in the brain for either fuel or oxygenRequires constant supply of oxygen and glucose.

Blood Supply to the BrainCarotid arteries – anterior neck

LargeFrequently congested with plaqueCan be cleaned out surgically

Vertebral arteries Pass through cervical vertebraeWell protectedNot accessible for surgical cleaning

Circle of WillisBoth blood supplies (carotid and

vertebral) join on the under surface of the brain.

CAUSES OF STROKEDisruption of blood flow to the brain

Plaque – build up of cholesterol in interior of blood vessel

Foreign debris– blood clot bubble of fluid airBroken vessel

RISK FACTORS FOR STROKE(NON MODIFIABLE)AgeGender

MALE>FEMALE except at extremes off ageRace

African American high riskPrevious vascular eventEg.MI,STOKE,Peripheral vasc.ds.HeredityHigh fibrogen

Modifiable risk factorsHigh BPCigarette smokingExcessive Alcohol intakeHeart disease Atrial fibrillation,CCF,IEUncontrolled DiabetesHyperlipidemiaOestrogen containing drugsLike Oral contraceptive pills .

Sedentary lifestyleObesityStress

Ischemic STROKECaused by blockage of blood flow to brainProgressive Thrombus -- growing

Plaque deposit – similar to process in heart with coronary artery disease

Cerebral Emboli –Clot arises from somewhere else -- floating debrisBlood clotAir bubbleBubble of amniotic fluidBone marrow from a fracture

PATHOPHYSIOLOGY OF ISCHAEMIC STROKEArterial occlusion of an intracranial vessel

causes reduction in blood flow to the brain region supplied by it.

Tissue surrounding the region of infarction is ischemic but revesibaly dysfunctional and is referred as ISCHEMIC PENUMBRA.

The ischemic penumbra will eventually infarct if no change in the flow oocurs , so saving this ischemic penumbra is goal of revascularisation therapies.

PathophysiologyIschemia produces necrosis by starving

neurons of glucose.No glucose means no ATP production.No ATP, the neurons start to depolarize

which in turn increases intracellular calcium levels to rise and glutamate to accumulate.

This excess of extracellular glutamate produces neurotoxicity as it activates postsynaptic glutamate receptors which

Inc neuronal calcium influxo Free radicals produced buy memb. Lipid

degeneration and mitochondrial damage will result in cellular dysfunction and death.

CASCADE OF CCEREBRAL ISCHEMIA :

ARTERIAL OCCLUSION

NO GLUCOSE AND OXYGEN SUPPLY TO NEURONS

MITOCHONDRIA FAILS TO PRODUCE ATP

NEURONS DEPOLARISE WITHOUT ATP

Calcium and sodium influx Glutamate release

Glutamate receptorsProteolysis

Memb.and cytoskeletal breakdown

Cell death

Free radical form.

ETIOLOGY OF ISCHEMIC STROKEThrombosis-• Lacunar stroke (small vessel)• Large vessel thrombosisEmbolic occlusion• Cardioembolic (atrial fibrillation,mural

thrombosis,MI,valvular lesions like MITRAL STENOSIS AND BACTERIAL ENDOCARDITIS,Paradoxical embolus)

• Artery to artery: carotid bifurcation,aortic arch

OTHER UNCOMMON CAUSES :

• Hypercoagulable disorders:protein C&S def., antiphospholipid syndrome

• Sickle cell disease• Venous sinous thrombosis• Fibromuscular dysplasia• Vasculitis:Takayasu ,giant cell arteritis etc.

Causes of Ischemic Stroke

Thrombotic StrokeThrombus causes

occlusion of large vessel

Seen more commonly in Older population

Rapid event, but slow progression (usually reach max deficit in 3 days)

Embolic StrokeEmbolus becomes lodged in

vessel and causes occlusionBifurcations are most

common site for embolus lodgement

Sudden in onset with immediate deficits

Cardioembolic StrokeThese are responsible for 20% of all ischemic

strokes.Stroke is caused by embolism of thrombotic

material forming on the atrial or ventricular wall or the left heart valves

thrombi then detach and embolize into the arterial circulation

Embolic strokes tend to be sudden in onset, with maximum neurologic deficit at once

Cardioembolic StrokeEmboli from the heart most often lodge in the

MCA, PCA, and very rarely ACA territory is involved.

Nonrheumatic atrial fibrillation is the most common cause of cerebral embolism overall.

Patient’s with atrial fibrillation have an average annual risk of 5%

Left atrial enlargement is an additional risk factors for the formation of atrial thrombi

Cardioembolic Stroke causes:nonrheumatic atrial fibrillationMIprosthetic valvesrheumatic heart diseaseischemic cardiomyopathy

Artery to artery embolic stroke:Thrombus formation on atherosclrotic plaque

embolizes to intracranial arteries producing an artery to artery embolism

Any diseased vessel can be an embolic source like aortic arch,common carotid, internal carotid , vertebral or basal artery.

Carotid bifurcation atherosclerosis is most common source of artery to artery embolus

Carotid AtherosclerosisResponsible for 10% of all ischemic strokesfrequently within the common carotid

bifurcation and proximal internal carotid artery

RISK FACTORS: Male gender, older age, smoking,

hypertension, diabetes, and hypercholesterolemia

Plaques develop in an area of high turbulence

Platelets and fibrin aggregate or collect on the surface of the plaque.

Parts of the plaque breaks off and travel to a narrower distal artery leading to production of artery to artery emboli.

Carotid disease can be classified by whether stenosis is symptomatic or asymptomatic and by degree of stenosis.

Symptomatic carotid disease implies that pt. had experinced a stroke within vascular distribution of artery and is associated with greater risk of subsequent stroke.

Greater degrees of arterial narrowing are associated with greater risk of stroke.

Other causes of artery to artery embolic stroke:Intracranial atherosclerosis: it produses

stroke either by embolic mech. Or by in situ thrombosis of a diseased vessel.

Dissection of internal carotid or vertebral artery: it is usually painful and precedes stroke by several hours.

SMALL VESSEL STROKE - 20% of all stokes Lacunar infarction is infarction following atherothrombotic

or lipohyalinotic occlusion of small artery in brain.Small, deep penetrating arteries are involved in small vessel

strokeHigh incidence:

Chronic hypertension Elderly

Clinical manifestations1. Pure motor hemiparesis: from an infarct in

posterior limb of internal capsule or base of pons. In this arms ,face , legs are always involved.

2. Pure sensory stroke:due to infarct in ventral thalamus.

3. Ataxic hemiparesis:infarct in ventral pons or internal capsule.

4. Dysarthria:due to infarction in ventral pos or in genu of internal capsule.

RECOVERY FROM SMALL VESSEL STROKE IS MORE RAPID AND COMPLETE THAN RECOVERY FROM ALARGE VESSEL STROKE

Signs and Symptoms of ISCHEMIC STROKE

Weakness in one sideFacial droopingNumbness and tinglingLanguage disturbanceVisual disturbance

WEAKNESS : Unilateral weakness is classical presentation of stroke .

1.Sudden in onset2.Progresses rapidly3.Follows a hemiplegic pattern4.Reflexes are initially reduced but latter

become inc. with a spastic pattern5.Upper motor neuron weakness of face is

often present

SPEECH DITURBANCEDysphasia and dysarthria are common

presentations.DYSPHASIA – indicates damage to dominant

frontal or parietal lobe.DYSARTHRIA – indicates weakness of face ,

pharynx , lips, tongue or palate

VISUAL DEFICIT:Visual loss can be due to unilateral optic

ischemia (called amaurosis fugax if transient), caused by disturbance of bld. Flow in internal carotid artery and ophthalamic artery that leads to monocular blindness

Left Brain StrokeRight side paralysisSpeech and language disturbanceBehavioral changesSwallowing problems

Right Brain DamageLeft side paralysisSpatial perceptionCoordination problemsPerception

Recognition of familiar objects

Transient Ischemic Attack (TIA) Or MINI STROKE

These are episodes of stroke symptoms that last only briefly.

Duration < 24 hrs.May arise from emboli to the brain or from in

situ thrombosis of an intracranial vessel.Amaurosis fugax – transient monocular

blindness occurs from emboli to the central retinal artery of the eye and it is a specific TIA symptom .

Transient Ischemic Attack (TIA)• Risk of stroke after a TIA is 10-15% in the

first 3 months with most events occurring in the first 2 days.

• So urgent evaluation and treatment is vey important.

Transient Ischemic Attack (TIA) TreatmentAntiplatelet agents

Aspirin: Can prevent platelet aggregation Acetylates cyclooxygenase whicg irreversibly

inhibits the formation in platelets of thromboxane A2

Effect is permament and lasts for the usual 8-day life of the platelet

Also inhibits endothelial prostacyclin, and antiaggregating and vasodilating prostaglandin

50-325 mg/day is recommended for stroke prevention

Transient Ischemic Attack (TIA) Treatment• Antiplatelet agents

– Clopidogrel:• Blocks the ADP receptor on platelets blocking the

platelet aggregation

– Dypiridamole:• Inhibits the uptake of adenosine by a variety of cells• Adenosine = inhibitor of aggregation• Also potentiates the anti aggregatory effects of

prostacyclin and nitric oxide by inhibiting platelet phosphodiesterase

• Prinicpal side effect is headache

Approach to the patientRapid evaluation is essential for use of

time sensitive treatments such as thrombolysis

Most patients with acute stroke do not seek medical attention because they are rarely in pain and they experience anosognosia(deficit of self awareness)

Important clues pointing to stroke:HemiparesisChanges in visionChanges in gaitDisturbance in the ability to speak or

understandSudden severe headache

OTHER CAUSES OF SUDDEN ONSET NEUROLOGICAL SYMPTOMS THAT MIMIC STROKESEIZURES:History of convulsive activity can be

asked INTRACRANIAL TUMOUR:cause neurological

symptoms due to haemorrhage , seizure, hydrocephalus.

MIGRAINEMETABOLIC ENCEPHALOPATHY

Migraine can mimic strokeThe sensory and motor deficit tend to

migrate slowly across a limb over minutes rather than seconds as with stroke

Once diagnosis of stroke is made, brain imaging study is necessary to determine the cause of the stroke whether ischemic or hemorrhagic

CT imaging is the standard imaging procedure

Management of Acute Ischemic StrokeFirst goal is to prevent or reverse brain

injury.Check ABCs and treat hypoglycemia or

hyperglycemia.Perform an emergency noncontrast head CT

to determine whether stroke is ischemic or hemorrhagic.

STROKE Check ListSecuring A B CsStroke identificationUse of FAST ScreenEKG monitoring if ableOxygen saturation of > 94%Management of blood glucoseIV access (ILS/ALS)Blood specimens obtained (ILS/ALS)Head of Bed elevated 15 degreesEarly communication with PhysicianUrgent transport to CT Scan

Use a “FAST” STROKE Assessment

FaceArmSpeechTime of onset

FACELook for Facial Droop

Have the patient smile or show his/her teethNORMAL Both sides of the face move equally ABNORMAL One side of the patient’s face droops or does not move

ARMSMotor Weakness: Look for arm drift by

asking the patient to close eyes and lift arms

NORMAL- arms remain extended equally or drift downward equallyABNORMAL – One arm drifts down compared to the other

Problem with gripping handsMany elderly have arthritis in handsHurts to grip handsMay mimic weakness

SPEECHAsk the patient to say “You can’t teach an old

dog new tricks”Lots of t’s, k’s and c’s

NORMAL –Phrase repeated clearly and plainly

ABNORMAL – Words slurred, abnormal or unable to speak

Abnormal SpeechSlurring of speechUnable to think of wordsInappropriate wordsExpressive aphasia – unable to speak words

Area of brain where words are created is damaged

Receptive aphasia – unable to understand wordsArea where words are interpreted is damaged

TIME OF ONSETThe window of opportunity to effectively treat

STROKE is 3 hours (180 minutes)May be extended to 4 ½ hours in some cases

Need to know “ last known well”.Difficult when

Patient lives aloneWoke up with symptoms

Management of Acute Ischemic Stroke6 categories to improve clinical outcome

Medical supportIntravenous thrombolysisEndovascular techniquesAntithrombotic treatmentNeuroprotectionrehabilitation

Management of Acute Ischemic StrokeMedical Support

Immediate goal is to optimize cerebral perfusion in sorrounding penumbra

Prevent complications such as infections, DVT, and bedsores

Maintain euglycemiaTreat feverManage hypertensionWater restriction and use of IV Mannitol to raise

serum osmolarity and prevent brain edema

Management of Acute Ischemic StrokeIntravenous Thrombolysis: There is a benefit of IV rTPA(recombinant

Tissue Plasminogen Activator) in selected patients with acute strokeGolden period is within 3 hrs of the onset of

ischemic stroke (0.9 mg/kg – 10% as bolus and remainder over 1 hr)

The time of onset of stroke is defined as the time patient’s symptoms began or the time the patient was last seen normal

Management of Acute Ischemic StrokeIndications for rTPA

Clinical diagnosis of strokeOnset < 3 hrsCT scan shows no hemorrhage or edema of >

1/3 of the MCA territoryAge > 18 yrs of ageconsent

Management of Acute Ischemic Stroke• Contraindications

– Sustained BP > 185/110 despite treatment– Plt < 100,000, hct < 25%, glucose <50 or >400 mg/dl– Use of heparin within 48 hrs, prolonged PTT, or

elevated INR– Rapidly improving symptoms– Prior stroke or head injury within 3 months– Major surgery in preceding 14 days– Minor stroke symptoms– GI bleeding in preceding 21 days– Recent MI– Coma or Stupor

Management of Acute Ischemic StrokeEndovascular Techniques

Usually done in occlusions of large vessels such as MCA, internal carotid artery, and basilar artery

Procedure is done intraarteriallyIn this thrombolytics are given by intra arterial

route to inc. the conc. Of drug at site of clot.Mechanical thombectomy can be used as an

alternative to this in which a device is used to restore patency of an occluded vesselwithin 8 hrs of stroke symptoms.

Management of Acute Ischemic StrokeAntithrombotic Treatment

Platelet inhibition Aspirin is the only antiplatelet agent that has been

proven effective for the acute treatment of ischemic stroke

Usually given within 48 hrs of stroke onsetAnticoagulation

Has shown no benefit in the primary treatment of atherothrombotic cerebral ischemia

Management of Acute Ischemic StrokeNeuroprotection

To provide a treatment that prolongs the brain’s tolerance to ischemia

Most common neuroprotective drug: Citicoline – reduces the rate of death and disability

Management of Acute Ischemic StrokeRehabilitation

to improve neurologic outcomes and reduce mortality

Directed towards educating the patient and family about the patient’s neurologic deficit, preventing complications of immobility and providing encouragement and instruction in overcoming the deficit

Goal is to return the patient home and to maximize recovery

STROKE SYNDROMES

Stroke Within the Anterior CirculationMiddle Cerebral ArteryAnterior Cerebral ArteryAnterior Choroidal ArteriesInternal Carotid ArteryCommon Carotid Artery

Middle Cerebral ArteryOcclusion of the proximal MCA or

one of its major branches is most often due to an embolus rather than intracranial atherothrombosis

The cortical branches of the MCA supply the lateral surface of the hemisphere

Middle Cerebral Artery• The proximal MCA (M1 segment) supplies the

following:– Putamen– Outer globus pallidus– Posterior limb of the internal capsule– Corona radiata– Most of the caudate nucleus

• In the sylvian fissure, the MCA divides into the superior and inferior divisions (M2 branches)– Inferior division supplies

• Inferior parietal and temporal cortex– Superior division supplies

• Frontal and superior parietal cortex

Middle Cerebral Arteryentire MCA is occluded at its origin :

contralateral hemiplegia, hemianesthesia, homonymous hemianopia(due to invovement of optic radiation)

Dysarthria is common because of facial weakness

global aphasia(diff.in both using words and understanding words)

Anosognosia(deficit of self awareness), constructional apraxia(inability to draw or correctly copy an image), and neglect

• Middle Cerebral Artery: Partial Syndromes– Brachial syndrome : embolic occlusion of a

single branch include hand, or arm and hand, weakness alone

– Frontal Opercular Syndrome: facial weakness with nonfluent (Broca) aphasia, with or without arm weakness

– Lacunar stroke within internal capsule - pure motor stroke or sensory-motor stroke contralateral to the lesion

Anterior Cerebral ArteryDivided into 2 segments:

Precommunal Circle of Willis (A1) Connects the internal carotid artery to the anterior

communicating arteryPostcommunal segment (A2)distal to anterior

communicating artery

Anterior Cerebral Artery• Supplies the anterior limb of the internal

capsule, the anterior perforate substance, amygdala, anterior hypothalamus, and the inferior part of the head of the caudate nucleus

• Occlusion of the proximal ACA is usually well tolerated because of collateral flow through the anterior communicating artery and collaterals through the MCA and PCA

Anterior Cerebral Artery

Anterior Cerebral Artery• Paralysis of opposite foot and leg:

Motor leg area• A lesser degree of paresis of

opposite arm: Arm area of cortex or fibers descending to corona radiata

• Cortical sensory loss over toes, foot, and leg: Sensory area for foot and leg

• Urinary incontinence: Sensorimotor area in paracentral lobule

Anterior Cerebral Artery• Abulia (akinetic mutism)ie. Pt. is not able to move

nor speak, slowness, delay, intermittent interruption, lack of spontaneity, whispering, reflex distraction to sights and sounds: Uncertain localization—probably cingulate gyrus and medial inferior portion of frontal, parietal, and temporal lobes

• Impairment of gait and stance (gait apraxia): Frontal cortex near leg motor area

• Dyspraxia of left limbs(failure of coordination of movements), tactile aphasia in left limbs: Corpus callosum

Stroke within the Posterior Circulation

Posterior Cerebral ArteryVertebral ArteryPosterior Inferior Cerebellar ArteryBasilar Artery

Stroke within the Posterior CirculationPosterior Cerebral Artery

result from atheroma formation or emboli that lodge at the top of the basilar artery

May also be caused by dissection of the vertebral

artery or fibromuscular dysplasia

Posterior Cerebral Artery(1) P1 syndrome: midbrain, subthalamic, and

thalamic signs, which are due to disease of the proximal P1 segment of the PCA or its penetrating branches

(2) P2 syndrome: cortical temporal and occipital lobe signs, due to occlusion of the P2 segment distal to the junction of the PCA with the posterior communicating artery.

Posterior Cerebral ArteryP1 Syndromes

third nerve palsy with contralateral ataxia (Claude's syndrome) or with contralateral hemiplegia (Weber's syndrome)

contralateral hemiballismus ie. Undesired movement of limbs (if subthalamic nucleus is involved)

thalamic Déjerine-Roussy syndrome - contralateral hemisensory loss followed later by an agonizing, searing or burning pain in the affected areas

Posterior Cerebral Artery• P2 Syndromes

• Occulsion of the PCA causes infarction of the medial temporal and occipital lobes

• Contralateral homonymous hemianopia with macula sparing is the usual manifestation

• acute disturbance in memory (hippocampus)• peduncular hallucinosis - visual hallucinations of

brightly colored scenes and objects• infarction in the distal PCAs produces cortical

blindness • Anton's syndrome – unaware of blindness and

denial

Basilar Artery• Atheromatous lesions are most frequent in the

proximal basilar and the distal vertebral segments• Supplies base of pons,superior cerebellum• Complete basilar occlusion :

• a constellation of bilateral long tract signs (sensory and motor) with signs of cranial nerve and cerebellar dysfunction

• “locked-in" state of preserved consciousness with quadriplegia and cranial nerve signs suggests complete pontine and lower midbrain infarction

Basilar Artery• TIAs in the proximal basilar distribution may

produce vertigo• Occlusion of the superior cerebellar artery results

in– Ipsilateral cerebellar ataxia, nausea and vomiting,

dysarthria, contralateral loss of pain and temp sensation

• Occusion of the anterior inferior cerebellar artery results in– Ipsilateral deafness, facial weakness, vertigo,

nausea and vomiting, nystagmus, tinnitus and contralateral loss of pain and temperature sensation

ImagingCT Scan

identify or exclude hemorrhage as the cause of stroke

the infarct may not be seen reliably for 24–48 h may fail to show small ischemic strokes in the

posterior fossa

MRI reliably documents the extent and location of

infarction in all areas of the brain less sensitive than CT for detecting acute blood

ImagingCerebral Angiography

"gold standard" for identifying and quantifying atherosclerotic stenoses of the cerebral arteries

used to deploy stents within delicate intracranial vessels

intraarterial delivery of thrombolytic agents Carries the risk for arterial damage, groin hemorrhage,

embolic stroke, embolic stroke, and renal failure

Carotid Doppler

REMEMBER IN STROKE -Race Against Time