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CEREBROVASCULAR

DISEASES : STROKE

B y : E i l e e n K r i s t i n e S . A b a r r a

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CVD

ISCHEMIC

STROKE

HEMORRHAGIC

STROKE

CEREBROVASCULAR

ANOMALIES

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Causes ~200,000 deaths each year in US

& are a major cause of disability.

Struck by the hands of God Defined by this abrupt onset of a

neurologic deficit that is attributable to a

focal vascular cause.

Cerebrovascular Diseases

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. .

DEFINE. Cerebral ischemia caused by a reductionin blood flow that lasts longer thanseveral seconds.

Infarction death of brain tissue Transient ischemic attack (TIA) all

neurologic signs and symptoms resolvewithin 24 h regardless of whether there isimaging evidence of new permanentbrain injury

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APPROACH PATIENT Rapid evaluation is essential for use of time

sensitive treatments such as thrombolysis

Most patients with acute stroke do not seekmedical attention because they are rarely in painand they experience anosagnosia

Important clues pointing to stroke:Hemiparesis

Changes in visionChanges in gait

Disturbance in the ability to speak or understand

Sudden severe headache

To The

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APPROACH PATIENT Common causes of sudden-onset

neurologic symptoms that may mimicstroke:

Seizure Intracranial tumor

Migraine

Metabolic encephalopathy CT imaging of the brain standard

imaging modality

To The

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HEMORRHAGIC STROKE

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Hemorrhages are classifiedby location and underlying

vascular pathology

Bleeding into subdural andepidural spaces is

principally produced bytrauma

SAHs are produced bytrauma and rupture ofintracranial aneurysms

Often identified by CT scan

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INTRAPARENCHYMAL HEMORRHAGE

Most common type of intracranial

hemorrhage

Accounts for ~10% of all strokes; 50% case

fatality rate

Causes: Hypertension, trauma, and cerebral

amyloid angiopathy

Advance age, heavy alcohol consumption, and

cocaine increases the risk

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INTRAPARENCHYMAL HEMORRHAGE

Clinical Manifestations:

Almost always occur while the patient is

awake or sometimes when stressed Seizures are uncommon

Worsens over 30-90 mins

Diminishing level of consciousness, headache,and vomiting

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ISCHEMIC STROKE

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Acute occlusion of an intracranial vesselcausing reduction in blood flow to the brainregion

The magnitude of flow reduction is a functionof collateral blood flow

INFARCTION results when:Cerebral blood flow of 0 (zero) in 4 10 mins

CBF

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Produces necrosis by

starving neurons of glucose

ISCHEMIA

Failure of mitochodriato produce ATP

NOGLUCOSE

Membrane ion pumps stopfunctioning and neurons depolarizeallowing an increase in intracellular

calcium & glutamate to accumulate

NO ATP

Produced in this process willresult in cellular dysfunction and

death

FREERADICALS

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MANAGEMENT OFACUTE ISCHEMIC

Attend to the A-B-

Cs and treathypoglycemia/hyperglycemia

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MANAGEMENT OF ACUTE

6 categories toimprove clinical

outcome

Medical support

Intravenousthrombolysis

Endovasculartechniques

Antithrombotictreatment

Neuroprotection

Stroke centersand rehab

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1) Medical Support

Immediate goal is to optimize cerebral

perfusion

Prevent complications such as infections,DVT, and bedsores

Treat fever

Manage hypertension

Use of IV Mannitol to raise serum

osmolarity and prevent brain edema

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2) Intravenous Thrombosis

NINDS rTPA stoke study showed benefitfor IV rTPA in selected patients with acute

stroke

Golden 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 patients symptoms began or

the time the patient was last seen normal

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INDICATIONS

Clinical diagnosis of stroke

Onset of symptoms to time ofdrug administration 3 h

CT scan showing nohemorrhage or edema of >1/3of the MCA territory

Age 18 years

Consent by patient orsurrogate

CONTRAINDICATIONS

Sustained BP >185/110 despitetreatment

Platelets

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3) Endovascular Techniques

Usually done in occlusions of large

vessels such as MCA, internal carotid

artery, and basilar arteryProcedure is done intraarterially

Endovascular mechanical thrombectomy

is an alternative

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4) Antithrombotic 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 onset

Anticoagulation Numerous clinical trials have failed to

demonstrate any benefit in the treatment of

atherothrombotic cerebral ischemia

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5) Neuroprotection

Providing a treatment that prolongs the

brains tolerance to ischemia

Hypothermia powerful neuroprotectivetreatment in patients with cardiac arrest

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6) Stroke Centers and

Rehabilitationto improve neurologic outcomes and

reduce mortality

Directed towards educating the patient

and family about the patients neurologicdeficit, preventing complications ofimmobility and providing encouragement

and instruction in overcoming the deficitGoal is to return the patient home and to

maximize recovery

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ETIOLOGY OF ISCHEMIC STROKE

establishing a cause is essential in reducing the

risk of recurrence

Particular focus on atrial fibrillation and carotidatherosclerosis

30% of strokes remain unexplained despite

extensive evaluation Clinical examination focus: peripheral & cervical

vascular system, heart, extremities, and retina

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CARDIOEMBOLIC STROKE

Responsible for 20% of all ischemic strokes

embolism of thrombotic material forming

on the atrial or ventricular wall or the left

heart valves

Embolic strokes tend to be sudden inonset, with maximum neurologic deficit at

once

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Emboli from the heart most often lodge in the

MCA, PCA, and infrequently ACA

Nonrheumatic atrial fibrillation is the mostcommon cause of cerebral embolism overall

Patients with atrial fibrillation have an average

annual risk of 5% Left atrial enlargement and CHF are additional

risk factors for the formation of atrial thrombi

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CAUSES:

nonrheumatic atrial fibrillation

MI prosthetic valves

rheumatic heart disease

ischemic cardiomyopathy

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CAROTID ATHEROSCLEROSIS

10% of all ischemic strokes

frequently within the common carotid

bifurcation and proximal internal carotid artery RISK FACTORS:

Male gender, older age, smoking,

hypertension, diabetes, andhypercholesterolemia

Mx: Carotid endarterectomy, endovascular

therapy, bypass surgery

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Other Causes of

Intracranial Atherosclerosis

Dissection of Internal Carotid Artery

Hypercoagulability

Venous sinus thrombosis

Fibromuscular dysplasia Sickle cell anemia

Temporal arteritis

Necrotizing atreritis

Drugs

Reversible posterior leukoencephalopathy

Leukoariosis

CADASIL

ST

R

OKE

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Transient Ischemic Attack (TIA)

Episodes of stroke symptoms that last

briefly

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

in situ thrombosis

Amaurosis fugax or transient monocularblindness - occurs from emboli to the

central retinal artery of the eye

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Risk of stroke after a TIA is ~10-15% in the first 3months with most events occurring in the first 2 days

Acute antiplatelet therapy is effective and

recommended

Atherosclerotic risk factors:

Older age

Family history of thrombotic stroke

DM

Hypertension most significant risk factor

Tobacco smoking

Abnormal blood cholesterol


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Other risk factors:

Prior stroke or TIA

Certain cardiac conditionsOral contraceptives

Hormone replacement therapy


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Antiplatelet agents

Aspirin:

Can prevent platelet aggregation

Aspirin acetylates cyclooxygenase, which irreversiblyinhibits the formation in platelets of thromboxane A2

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

platelet

Also inhibits endothelial prostacyclin, and anti-aggregatingand vasodilation of prostaglandin

50-325 mg/day is recommended for stroke prevention

TIA Treatment

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Antiplatelet agents

Clopidogrel:

Blocks the ADP receptor on platelets blocking the platelet

aggregation

Dipyridamole:

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

TIA Treatment

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Anticoagulation therapies

The decision to use anticoagulation for

primary prevention is based on risk factors(rheumatic heart disease, atrial fibrillation,

and prosthetic valve implantation)

TIA Treatment

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STROKE

SYNDROME

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Stroke Within the Anterior Circulation

Middle Cerebral Artery

Anterior Cerebral Artery

Anterior Choroidal Arteries

Internal Carotid Artery

Common Carotid Artery

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Occlusion 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

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The proximal MCA (M1 segment) suppliesthe following:

Putamen

Outer globus pallidus

Posterior limb of the internal capsule

Corona radiata

Most of the caudate nucleus


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In the sylvian fissure, the MCA divides intothe superior and inferior divisions (M2

branches)

Inferior division supplies

Inferior parietal and temporal cortex

Superior division supplies Frontal and superior parietal cortex


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If entire MCA is occluded at its origin :

contralateral hemiplegia, hemianesthesia,

homonymous hemianopia, and a day or two of

gaze preference to the ipsilateral side

Dysarthria is common because of facial

weakness

global aphasia

anosognosia, constructional apraxia, and

neglect


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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


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Divided into 2 segments:

Precommunal Circle of Willis (A1)

Connects the internal carotid artery tothe anterior communicating artery

Postcommunal segment (A2)

Distal to the anterior communicatingartery

ANTERIOR Cerebral Artery

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Supplies the anterior limb of the internalcapsule, the anterior perforate substance,

amygdala, anterior hypothalamus, and the

inferior part of the head of the caudatenucleus

Occlusion of the proximal ACA is usually

well tolerated because of collateral flowthrough the anterior communicating artery

and collaterals through the MCA and PCA


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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


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Abulia (akinetic mutism), slowness, delay,intermittent interruption, lack of spontaneity,

whispering, reflex distraction to sights and

sounds: Uncertain localizationprobably

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, tactile aphasia in left

limbs: Corpus callosum


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Stroke Within the Anterior Circulation

Posterior Cerebral Artery

Vertebral Artery

Posterior Inferior Cerebellar

Artery

Basilar Artery

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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

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(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 withthe posterior communicating artery.


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P1 Syndromes third nerve palsy with contralateral ataxia

(Claude's syndrome) or with contralateral

hemiplegia (Weber's syndrome)

contralateral hemiballismus (if subthalamic

nucleus is involved)

thalamic Djerine-Roussy syndrome -

contralateral hemisensory loss followed later byan agonizing, searing or burning pain in the

affected areas


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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 (hippocampal involvement)

peduncular hallucinosis - visual hallucinations of brightly

colored scenes and objects infarction in the distal PCAs produces cortical blindness

(blindness with preserved pupillary light reaction)

Anton's syndrome unaware of blindness and in denial


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Atheromatous lesions are most frequent in

the proximal basilar and the distal vertebral

segments

locked-in" state of preserved

consciousness with quadriplegia and cranial

nerve signs suggests complete pontine andlower midbrain infarction

BASILAR Artery

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TIAs in the proximal basilar distribution mayproduce vertigo

Other symptoms that warn of basilar thrombosis

Diplopia, dysarthria, facial or cirumoralnumbness, and hemisensory symptoms

Occlusion of a branch of the basilar artery

Causes unilateral signs and symptomsinvolving motor, sensory, and cranial

nerves

BASILAR Artery

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Occlusion of the superior cerebellar artery results in Ipsilateral cerebellar ataxia, nausea and vomiting,

dysarthria, contralateral loss of pain and

temperature sensation Occusion of the anterior inferior cerebellar artery

results in

Ipsilateral deafness, facial weakness, vertigo,

nausea and vomiting, nystagmus, tinnitus,

cerebellar ataxia and contralateral loss of pain

and temperature sensation

BASILAR Artery

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Imaging

CT Scan

identify or exclude hemorrhage as the

cause of stroke the infarct may not be seen reliably for

2448 h

may fail to show small ischemic strokes inthe posterior fossa

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Imaging

MRI

reliably documents the extent andlocation of infarction in all areas of the

brain

less sensitive than CT for detecting acuteblood

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Imaging

Cerebral Angiography

"gold standard" for identifying and

quantifying atherosclerotic stenoses of thecerebral arteries

used to deploy stents within delicate

intracranial vessels Carries the risk for arterial damage, groin

hemorrhage, embolic stroke, embolic

stroke, and renal failure

mf3 - stroke

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