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
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