Stroke

Stroke

Second important cause of death

Physical and pshychosocial handicap

Lesions of brain parenchima due to pathology of cerebral circulatory system that leads to hemorrhageae or ichemic lesions

Cerebral Anatomy

Vascular circulation: Anterior and Posterior Anterior circulation

– Origin: carotid system– supplies 80% brain- optic nerve, retina,

frontoparietal and anterotemporal lobes of brain Posterior circulation:

– supplies 20% of brain– Derived from vertebral arteries– Supplies brainstem, cerebellum, thalamus, auditory

centers and visual cortex

Important arteries of the brain

Blood supply of the brain

Anastomosys of main arterial systems

Circle of Willis– 2 anterior

cerebral arteries

– Anterior communicating artery

– Postrior communicating arteries

– Posterior cerebral arteries

Anatomosys

Compensation via1. Aortic arch2. Subclavian – vertebral aa3. Internal – external carotis

communications4, 5 Willis polygone6. Cortical and meningean

anastomosys

Extracranial Intracranial

Cerebral perfusion

Blood flow: 50-55 ml/100g/min (20% of the heart output)

Values above 20 ml/100g/min no consequences

Values below 12 ml/100g/min cell death

Flow regulation – Mechanisms are active at an

average BP under 60 mmHg, or above 160 mmHg

– Quick acting

Stroke

Sudden onset (seconds- minutes, rarely 1-2 days) of a focal neurological deficit

Evolution towards stabilization or remission

Risk factors for vascular disease: arterial hyoertension, embolic conditions, etc

Stroke Types

80% ischemic– Thrombosis– Embolism– Hypoperfusion

20% hemorrhagic– Intracerebral– Subarachnoid

Ischemic Strokes

Thrombosis-most common cause

Etiology – Atherosclerotic disease-

most common– Vasculitis– Dissection– Polycythemia– Hypercoagulable states– Infectious Diseases-HIV,

TB, syphilis Evolution of mural thrombi:

– Lysis – fragmentation (eventally emboli formation) or resorbtion

– Fibrous evolution– Extension

Ischemic stroke – other type of vascular obstruction

Inflamatory angeitis – Takayasu disease, Horton temporal arteritis, Lupus erithematosus, granulomatous angeitis)

Infectious angeitis (lues, tuberculosys, AIDS)

Arterial dissection Radiotherapy associated

stenosys

Ischemic Strokes

1/5th due to Embolism Etiology

– Cardiac More often in the carotidian system Valvular Vegetations Mural thrombi- caused by A-fib, MI, or dysrhythmias Paradoxical emboli – from ASD, VSD Cardiac tumors-myxoma

– Arterial emboli (trombi, atheroma plaque fragments)– Fat emboli– Particulate emboli – IV drug injections– Septic Emboli

Spontaneous lysis and clinical remission may happen, depending of the nature of the embolus

Usually multiple ischemic lesions of different ages More often secondary hemorrhageae

Hemorrhageae in the infarctus area

Ischemic Strokes

Hypoperfusion- less common mechanism– Typically caused by cardiac failure– More diffuse injury pattern vs thrombosis or

embolism– Usually occur in watershed regions of brain

– Focal hypoperfusion – arterial stenosis; collateral circulation may compensate

– Global hypoperfusion – consequences depend on the dynamics of the flow reduction (duration, intensity)

Systolic AT <7 mmHg Watershed infarct

Cerebral infarctus

Flow decrease increase of oxygen extraction Celular death dramatic decrease of oxygen

extraction, vasoplegia (due to acidosys, release of other substances) increase of flow

Penumbra:– Critical flow, enough for

some of the processes required for cell survival

– Not enough for cell function

– Recovery if blood flow increases

Atherosclerosis

Arteries with a diameter above 1 mm

Potentiated and caused by the risk factors

Main cause of ischemic stroke

Is thought to start around the age of 40

General Comments

Arteriosclerosis– Thickening and loss of elasticity of

arterial walls – Hardening of the arteries– Greatest morbidity and mortality of all

human diseases

Two major processes in plaque formation:– Intimal thickening– Lipid accumulation

Non-Modifiable Risk Factors

Age– A dominant influence– Atherosclerosis begins in the young, but does

not precipitate organ injury until later in life Gender

– Men more prone than women, but by age 60-70 about equal frequency

Family History– Familial cluster of risk factors– Genetic differences

Modifiable Risk Factors(potentially controllable)

Hyperlipidemia Hypertension Cigarette smoking Diabetes Mellitus Elevated Homocysteine Factors that affect hemostasis and

thrombosis Infections: Herpes virus; Chlamydia

pneumoniae Obesity, sedentary lifestyle, stress

Normal Artery

                                                                                                   

  

                                               

Summary of Atherosclerotic Process

Multifactorial process (risk factors) Initiated by endothelial dysfunction Up regulation of endothelial and leukocyte

adhesion molecules Macrophage diapedesis LDL transcytosis LDL oxidation Foam cells Recruitment and proliferation of smooth muscle

cells (synthesis of connective tissue proteins) Formation and organization of arterial thrombi

Fibrous Plaques Complicated Lesions

Complicated Lesions

Types of stroke

Transitory ischemic attacs– Neurologic deficits are completelly and

spontaneously reversible in less than 24 hours Stroke “in evolution”

– Defficit aggravates during hours, but lasts more than 24 h

– Pathologic process continues: tromobsys/bleeding;

– Cerebral oedema may lead to dangerous intracranian hypertension

Stroke

Cerebral Arteries Areas

1. anterior cerebral

2. Middle cerebral

3. Penetrating branches of middle cerebral

4. anterior choroidal

5. Posterior cerebral

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Anterior cerebral artery syndrome

Anatomy – Initial part – before

the anterior communicating artery

– Anterior communicating A – near the genu of the corpus calosum

– Curved portion (anterior convexity) over the corpus calosum

– Pericalosal artery (deep in the interhemisferic fissure)

Anterior Cerebral Artery

Surface branches supply cortex and white matter of :– inferior frontal lobe– medial surface of the frontal

and parietal lobes (and a narrow territory of the lateral surface along the margin)

– anterior 4/5 of the corpus callosum

Penetrating branches supply:– deeper cerebrum– limbic structures– head of caudate– inferior part of the anterior

limb of internal capsule – anterior part of the lenticulate

nucleus– anterior hypothalamus

Anterior Cerebral Artery Infarction

Clinical picture:– Contralateral weakness/numbness greater in leg than arm– Dyspraxia (apraxia of left arm (sympathetic apraxia) if anterior

corpus callosum is affected)– Speech perseveration– Slow responses

In 10% of cases stroke is bilateral due to common origin of both ACA– Akinetic muteness (apathy, inertia, suppresion of verbal,

emotional and gestual expression) – Forced prehension reflex bilaterally– Paraparesis/paraplegia– Urinary incontinence

Middle cerebral artery syndrome

Middle Cerebral Arteries Surface branches supply

– Most of the cortex & white matter of hemispheric convexity

(all four lobes and insula). Penetrating branches

– deep white matter (including the upper part of anterior and posterior limbs of the internal capsule, external capsula)

– some diencephalic structures – Basal ganglia – putamen, caudate, external pallidus)

(Netter, Part II, p. 58)

Middle cerebral artery occlusion

contralateral motor and sensory deficits in the face and arm > leg, and aphasia in the dominant (left) hemisphere.

Middle cerebral artery occlusion

Most common stroke syndrome. – Dominant Hemisphere (usually the left)

Contralateral weakness/numbness in arm and face greater than leg

Contralateral hemianopia Gaze preference toward side of infarct Aphasia (Wernicke’s -receptive, Broca’s –expressive, or

complete) Dysarthria

– Nondominant hemisphere Contralateral weakness/numbness in arm and face greater

than in the leg Constructional Apraxia Dysarthria Inattention, neglect, or extinction

Middle cerebal artery stroke

Stroke in the surface branches’ territory– Hemiplegia (facio-brachial)– Hemihipestesia (sometimes limited to astereognosia); – Homonime lateral hemianopia (temporal radiations); also

(space agnosia in nondominant hemisphere involvement) – Impaired spatial perception, spatial neglect, anosognosia

or hemiasomatognosia (nondominant hemisphere) – aphasia – dressing apraxia, constructional apraxia(dominant

hemisphere) Stroke in the deep branches’ territory

– Severe complete hemiplegia (destruction of the internal capsula)

– Hemianopia, sensory damage, speech problems

Middle cerebal artery stroke

Complete MCA obstruction– Frequent– Controlateral: hemiplegia;

sensory loss; hemianopia; – anosognosia/global

aphasia– Eyes and head deviated

towards the lesion– Early counsciousness

problems– Massive oedema ->

herniation risk –> death

Posterior communicating artery– Joins the MCA with the PCA– Branches for the hypothalamus, thalamus, posterior limb

of the IC, Luys body

Long, small diameter Goes backward around the cerebral peduncles,

following the optic bandelete until the geniculate body

Supplies for the anterior hippocampus, posterior limb of the internal capsule

Stroke in the territory of the anterior choroidian artery:– Massive controlateral hemiplegia, hemianopia (optic

hemianopsie homonimă laterală (bandeleta optică sau fibrele geniculo-calcarine)

Anterior Choroidal Arteries

Posterior cerebral artery syndrome

Vertebral Arteries

Rise from subclavian artery Branches

– anterior spinal arteries & – posterior inferior cerebellar arteries.

2 vertebral arteries join at the junction of the pons and medulla – form basilar artery – basilar divides into 2 posterior cerebral arteries

Posterior Cerebral Artery

Is born from the basilary artery around the cerebral peduncles inferior face of hemispheres (occipital lobe) calcarine fissure

Surface branches supply – cortex and white matter of medial

occipital lobes– inferior temporal lobes– posterior corpus callosum

Penetrating branches supply: – parts of the thalamus,

hypothalamus, geniculate bodies– parts of the midbrain

Posterior cerebral artery (PCA) supplies:

midbrain diencephalon temporal and occipital

lobes

(Netter, Part II, p. 65)

Posterior Cerebral Artery

Complete proximal occlusion– contralateral hemisensory loss, and

hemiplegia spontaneous pain and dysesthesia if thalamus

affected (thalamic pain syndrome) contralateral severe proximal chorea

(hemiballism) (red nucleus)– Hemianopia– Cerrebelar disturbances– Sensory aphasia (dominant hemisphere)– Vertical gaze palsy, nerve III palsy

Posterior Cerebral Artery

Visual disturbances– Contralateral homonymous hemianopsia

(central vision is often spared) May be associated to visual agnosia, alexia

– Bilateral lesions: cortical blindness patients unaware they cannot see Possible sparing of central vision; light pupilary reflexes are

maintained Usually associated with halucinations, agnosia, colour

blindness, other psychic disorders

Memory impairment if temporal lobe is affected

Posterior Cerebral Artery stroke

Basilar artery

Arises from the jcn of paired vertebral arteries– Supplies: occipital lobe, medial temporal lobe,

medial thalamus, posterior limb of internal capsule, entire brainstem and cerebellum

– Clinical Presentation: Often results in death; bilateral neurological signs Occlusion involving the dorsal/tegmentum portion of

the pons– Uni or bilateral CN VI palsy, vertical nystagmus, pupils

constricted but are reactive to light,h emi or quadroplegia

– Coma - common Occlusion involving the ventral portion of the pons:

remains conscious, but quadriplegic; locked-In Syndrome

Clinical picture of TIA

TIA is usually characterized by focal neurological symptoms. The last usually dominate over general brain symptoms. Thus TIA is regional DCBCD. They are usually acute and develop suddenly.

There are 2 main groups of TIA’s symptoms: General - usually manifest as headache,

dizziness, short loss of consciousness Focal symptoms depend on the vessel

territory

TIAs in carotid distribution

30 % of all TIAs subjective sensory disorders motor disorders transient aphasia blindness or reduction of vision Focal Jackson motor or sensory

epileptic attacks

TIAs in vertebrobasilar distribution

70 % of all TIAs Vestibular syndrome Brainstem – cerebellum syndrome Paresis of oculomotor muscles Bulbar syndrome Alternate syndromes Cortical vision disorders Atonic – adynamic syndrome - “drop –

attacks “ Paroxysmal hypersomnic and katalepsic

syndromes temporal epilepsy

Diagnostic tests

Diagnosis-Critical Pathway

Initial orders– ECG, Cardiac Enzymes– Haemogram (blood cell count) – Coagulation tests – NIR;

For etiologic diagnosis: genetic conditions - test for C protein, S protein, factor V, factor VIII, fibrinogen, etc

– Blood proteins; electrophoresis – glucose, Renal function studies, +/- drug

screen,

Diagnostic Tests

Noncontrast CT of head– Differentiate hemorrhage vs ischemia

MOST ischemic strokes are negative by CT for at least 6 hrs

– Hypodensity indicating infarct seen 24-48 hrs Can identify hemorrhage greater than 1cm, and

95% of SAH If CT is negative, but still considering SAH may

do lumbar punction

Diagnostic Tests

Depending on circumstances, other helpful tests– Echocardiogram – identifies mural

thrombus, tumor, valvular vegetations in suspected cardioembolic stroke

– Echography of arteries in the neck (Doppler, duplex)

finds out the absence or presence of stenosis and occlusions of magistral arteries of head and neck.

dissection

– Angiography – “gold standard” identifies occlusion or stenosis of large and small vessels of head/neck, dissections and aneurysms

Angio CT, MRA scan – identifies large vessel occlusions – may replace angiography in the future

– MRI scan – identifies posterior circulation strokes better and ischemic strokes earlier than CT

Emergent MRI- considered for suspected brainstem lesion or dural sinus thrombosis

– MRI techniques for recent ischemic stroke – allow rapid confirmation for thrombolysis

Additional methods of medical examination

Ultrasonic evaluation of carotids, verteral arteries – Absence or presence of stenosis and occlusions– Degree of obstruction of the blood vessel – Type of plaques, risk of emboli formations

Ischemic Stroke Management

General Management– General support measures

IV, oxygen, monitor, elevate head of bed slightly Treat dehydration and hypotension Avoid overhydration – cerebral edema Avoid IVF with glucose – except if hypoglycemic Fever – worsens neurologic deficits

Hypertension– Treatment indicated for SBP > 220 mm Hg or mean

arterial pressure > 130 mm Hg Lowering BP too much reduces perfusion to

penumbra converting reversible injury to infarction Use easily titratable Rx (labetalol or enalaprilat) SL Ca-channel blockers should be avoided

Management of HTN cont.

Thrombolytic candidates- use NTG paste or Labetalol to reduce BP < 185/115 to allow tx

Requirements for more aggressive treatment exclude the use of tissue plasminogen activator.

Thrombolysis Background

NIH/NINDS study– 624 patients, trial with I.V. tPA vs placebo

Treatment w/in 3 hrs of onset– At 3 months, pts treated with tPA were at least 30%

more likely to have minimal/no disability; absolute favorable outcome in 11-13 percent

– 6.4% of patients treated with tPA developed symptomatic ICH compared with 0.6% in placebo group

– Mortality rate at 3 months not significantly different– tPA group had significantly less disability– FDA approved in 1996

tPA Dose and Complications

IV tPA –Total dose 0.9 mg/kg, max. 90mg– 10% as bolus, remaining infusion over 60

min.– BP and Neuro checks q 15 min x 2 hrs

initially Treatment must begin w/in 3 hrs of

symptoms and meet inclusion and exclusion criteria

No ASA or heparin given x 24 hrs after thrombolysis

Thrombolysis Criteria in Ischemic Stroke

Inclusion criteria– Age 18 years or older– Time since onset well established to be < 3 hrs– Clinical diagnosis of ischemic stroke

Exclusion criteria– Minor/rapidly improving neurologic signs– Evidence of intracranial hemorrhage on

pretreatment noncontrast head CT– History of intracranial hemorrhage– High suspicion of SAH despite normal CT– GI or GU bleeding within last 21 days

Exclusion criteria– Known bleeding diathesis

Platelet count < 100,000 /mm3 Heparin within 48 hours and has an elevated PTT Current use of anticoagulation or PT > 15 seconds or INR > 1.7

– Intracranial surgery, serious head trauma or previous stroke within 3 months

– Major surgery within 14 days– Recent arterial puncture at non compressible site– Lumbar puncture within 7 days– Seizure at onset of stroke– History of ICH, AVM or aneurysm– Recent MI– Sustained pretreatment systolic pressure > 185 mmHg or

diastolic pressure > 110 mmHg despite aggressive treatment to reduce BP to within these limits

– Blood glucose < 50 or > 400 mg/dL

Criteria for IV Thrombolysis

Drug Therapy in Ischemic Stroke

Majority of the patients are not thrombolysis candidates– secondary prevention

Antiplatelet agents– ASA: ↓ risk 20-25% vs placebo

50-300 mg dose and will not interfere with tPA therapy

– Dipyridamole: alone (200mg BID) ↓ risk 15% Dipyridamole + ASA (Assasantin, Aggrenox)

– Clopidogrel: (75 mg qd) 0.5% absolute annual risk reduction when compared to ASA

Good Rx for pts who cannot tolerate or fail ASA

Heparin: unproven– Pts may expect fewer strokes but benefit is

offset by increased ICH– Similar results with low molecular weight

heparin– Use of heparins or heparinoids to tx a specific

stroke subtype or TIA cannot be recommended based on available evidence.

– Prevention of decubitus complications

Anticoagulants

Drug Therapy in Ischemic Stroke

Cerebral vasodilators: – vincamine, vinpocetine, nicergoline,

pentoxifylline– Ginkgo biloba

Cerebral trophic agents– Pyracetam, pramiracetam– Cerebrolysin, Actovegin