STROKE

KAMAU, JOY W. MED VI

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OBJECTIVES

Define stroke Epidemiology of stroke Neuroanatomy of the brain

Blood supply Functions of various areas of the brain

Aetiology of stroke Pathophysiology of stroke

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Presentation

STROKE/ CVA Is an acute neurological deficit due to a vascular lesion which persists for longer than 24hours Characterized by loss of circulation to an area (s) of the brain, resulting in a corresponding loss of neurological Click to edit Master subtitle style function. Can be Focal or Global TIA

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acute focal neurological deficit due to cerebral ischaemia that completely resolves within 24hours

LOBAR FUNCTIONS

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Cerebru m

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Korbinian Broadmann - Learn about the man who divided the Cerebral Cortex into 52 distinct regions: 7/5/12 http://en.wikipedia.org/wiki/Korbinian_Brodmann
Modified from:

Cerebru m

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Some important Subcortical structures

Hippocampus Amygdala Thalamus Hypothalamu s Nucleus accumbens MedulLa

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Blood Supply of the BRAIN

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Anterior Cerebral Artery

The ACA extends upward and forward from the ICA. It supplies frontal lobes, parts of the brain that control logical thought, personality, and voluntary movement, especially the legs. Stroke results in opposite leg weakness. If both ACA territories are affected, profound mental symptoms may result 7/5/12 (akinetic mutism).

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ACA Territory

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Middle Cerebral Artery

The MCA is the largest branch of the ICA. The artery supplies part of the frontal lobe, lateral surfaces of the temporal and parietal lobes, including the primary motor and sensory areas of the face, throat, hand and arm and in the dominant hemisphere, the areas for speech.

The middle cerebral artery is the artery most often occluded in stroke. 7/5/12

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MCA Territory

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PCA

The PCA supplies the temporal and occipital lobes. PCA stroke is usually secondary to embolism from segments of the vertebral basilar system or heart. Clinical symptoms depend on site of occlusion and may include thalamic syndrome, contralateral hemiplegia, hemianopsia and other symptoms e.g, colour blindness, verbal dyslexia, and hallucinations. The most common finding is occipital lobe infarction leading to an 7/5/12 opposite visual field defect.

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PCA Territory

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Lacunar strokes (20%)

Small, deep penetrating arteries lenticulostriate arteries from MCA

basal ganglia and internal capsule

Penetrating arteries from basilar and PCA

brainstem &thalamus. caused by chronic

Mechanisms:
lipohyalinosis hypertension 7/5/12

Watershed infarcts

Also known as border zone infarcts They develop from relative hypoperfusion in the most distal arterial territories and can produce bilateral symptoms They are frequently associated with surgical procedures

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Dses of cerebral vessels -3rd most common cause of death in developed countries-After cancer & IHD Annual incidence of CVA in UK-350/100,000 (about 700,000 annual cases in the US)

EPIDEMIOLOGY: globally

30% of strokes are fatal 15-30% severely disabled 50-70% cause mild disability

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U.S.A

Third leading cause of death in the US 750,000 strokes occur yearly in the US, 500,000 are ischaemic. There are 4.4 million current stroke survivors in the US Similar global picture with increasing incidence as population gets older
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Morbidity and Mortality

Mortality:

Approximately 29% of patients die within 1 year percentage rises in patients older than 65 years In 1990 CVdx caused 4.3 million deaths worldwide

Stroke is the leading cause of disability in the US

31% need help in taking care of themselves 20% need some assistance for walking placed in assisted living institution

16% 7/5/12

Race

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Young blacks have 2-3 times risk compared to white population of the same age Blacks are 2.5 times more likely to die of a stroke Their age adjusted risk for death is 1.49 times that of whites Hispanics have a lower incidence of stroke than both, but a higher incidence of lacunar strokes and stroke at an early age Higher incidence in the black than white population

Age

It can occur in all ages including children SCD was noted to be the commonest cause of stroke in children (J. Makani, Tanzania 2004) Risk increases with age, esp >65 years in whom 75% of strokes occur

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TANZANIA

Incidence of stroke in tanzania amongst children is 1.29/100000(J. Makani,2004) Commonest cause is SCD 20 to 25% of sicklers get a stroke Other risk factors found from the study included cerebral malaria, TB, IE, CHDx, congenital blood vessel anomalies

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Joshi et al found commonest cardiovascular risk factors included DM, dyslipidemia, age, male sex, hypertension Yonga et al found high prevalence rate of obesity, hyperchole, smoking in Nairobi Cohen et al (2001) at MTRH found hypertension to be the commonest discharge diagnosis at 15.9% and diabetes at 6.9% 7/5/12

KENYA

EPIDEM.

Risk factors (non modifiable)

Age-risk increases with increasing age Gender-Males at higher risk than females (except very young/old) Race-Blacks,Hispanics,Latinos & Asians Family Hx of stroke & heart dse Prior stroke/TIA/MI/PE

>Whites

Risk factors ( modifiable)

Hypertension Diabetes Heart dse- Chronic AF, CAD, LVH, HF Smoking Excess Alcohol intake Hyperlipidaemia

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CLASSIFICATION OF STROKE
ISCHAEMIC STROKE Thrombotic occlusion Large vessels (major cerebral arteries) Small vessels (lacunar stroke) Venous occlusion Embolic Artery to artery Cardioembolic Hypoperfusion Vasospasm HEMORRHAGHIC STROKE Intraparenchymal hemorrhage Subarachnoid hemorrhage Subdural hemorrhage Epidural hemorrhage 7/5/12 Hemorrhagic ischemic infarction

ISCHAEMIC STROKE MECHANISMS

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Normal vessel Fatty streak formation Leukocyte recruitment Foam cell formation Inflammation Microvessel infiltration Plaque evolution and rupture 7/5/12

Factors modulating atherosclerosis

Dyslipidemias: LDL Vs HDL Diabetes: nonenzymatic glycation of apolipoproteins-promoting atherogenesis Smoking: elevated fibrinogen, homocysteine Hypertension: Homocysteinemia: increased thrombogenesis 7/5/12

Common Causes of Ischemic Stroke Thrombosis Lacunar stroke (20%) Large vessel thrombosis Dehydration Embolic occlusion Artery-to-artery Carotid bifurcation Aortic arch Arterial dissection Cardioembolic (20%) Atrial fibrillation Mural thrombus Myocardial infarction Dilated cardiomyopathy Valvular lesions Mitral stenosis Mechanical valve Bacterial endocarditis Paradoxical embolus Atrial septal defect Patent foramen ovale Atrial septal aneurysm Spontaneous echo contrast 7/5/12

Uncommon causes of Ischemic Stroke Hypercoagulable disorders Venous sinus thrombosisb Protein C deficiency Fibromuscular dysplasia Protein S deficiency Vasculitis Antithrombin III deficiency Systemic vasculitis (PAN, Wegener's, Antiphospholipid syndrome Takayasu's, giant cell arteritis) Factor V Leiden mutationa Primary CNS vasculitis Prothrombin G20210 mutationa Meningitis (syphilis, tuberculosis, Systemic malignancy fungal, bacterial, zoster) Sickle cell anemia Cardiogenic Thalassemia Mitral valve calcification Polycythemia vera Atrial myxoma Systemic lupus erythematosus Intracardiac tumor Homocysteinemia Marantic endocarditis Thrombotic thrombocytopenic purpura Libman-Sacks endocarditis Disseminated intravascular coagulation Subarachnoid hemorrhage vasospasm Dysproteinemias Drugs: cocaine, amphetamine Nephrotic syndrome Moyamoya disease Inflammatory bowel disease Eclampsia Oral contraceptives 7/5/12

PATHOPHYSIOLOGY OF ISCHEMIC STROKE

Only 2% of the body's mass but needs 15-20% of the total resting cardiac output to provide the necessary glucose and oxygen for its metabolism. Acute occlusion of intracranial vessel(s). blood flow to the brain region it supplies. Collateral blood flow/Homeostatic responses(vasodilation; oxygen extraction). Q of zero - death of brain tissue 4 -10 min. Q <18 to 16 mL/100 g tissue/min- infarction in one hour. Click to edit Master subtitle style

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Pathophys Contd.

Q 18-20 mL/100 g tissue/min - ischemia without infarction, unless prolonged for several hours or days. If blood flow is restored prior to a significant amount of cell death transient symptoms, i.e. a TIA. Umbra; region of infarction & permanent damage. Ischemic penumbra; the surrounding 7/5/12 ischemic & reversibly dysfunctional

Pathophys Contd.
Cascade of cerebral ischemia:
v Infarction

by two pathways:

Necrotic Apoptotic

v Necrotic
o

Pathway:

glucose & O2 supply Failure of mitochondria to produce ATP Membrane pumps stop functioning Neurons depolarize :ca2+, Na+, water influx and K+ efflux cytotoxic oedema. Glutamate release exacerbates the depolarization Ca2+ activates intracellular lytic enzymes that

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Pathophys Contd.
o

Free radicals produced by membrane lipid degradation & mitochondrial dysfxn, cause catalytic destruction of cells. Release of inflammatory mediators by microglia & astrocytes causes death of all cell types in area of maximal ischaemia.

Apoptotic pathway: occurs in:

o o

Areas of lesser ischaemia e.g. Penumbra. Cellular death in days or weeks later.

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Pathophys Contd.

Factors that worsen the ischaemia

demands):

(by incr. O2

Fever Hyperglycemia >11.1 to 16.7mmol/L (200300mg/dL) Lactic acidosis - pH caused by anaerobic met.
(from ischemic to

Haemorrhagic transformation hrgic stroke):

Ischaemic damage to vascular endothelium Restoration of blood flow (violent refill) esp. in large infarcts. 7/5/12

Causes:

Pathophysiology of Haemorrhagic Stroke.

Primary intra-cerebral hemorrhage Sub-Arachnoid Hemorrhage Hemorrhagic transformation

Damage Via:
q

Explosive entry of blood Structural disruption of white matter fibre tracts thus immediate cessation of function. Haematoma & associated rim of cerebral oedema: behaves like an SOL:

Progressive neurological deficits

Shifts of intracranial contents e.g. trans-tentorial coning & 7/5/12 death

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Net effects of Excitotoxicity

The net effect of these events is a tremendous influx of Na+ and Ca2+ into neurons through glutamate- & voltage-gated ion channels. The resultant overload in intracellular Ca2+ appears to be especially toxic & may exceed the ability of the neuron to extrude or sequester the cation. This results in sustained activation of a variety of calcium-sensitive enzymes, including proteases, phospholipases, and endonucleases, leading to cell death. Animal studies demonstrate a reduction in the size of ischemic lesions after treatment with 7/5/12 glutamate receptor antagonists

Causes of Intracranial HaemorrhageLocation Cause

Head trauma Hypertensive hemorrhage

Transformation of prior ischemic infarction Metastatic brain tumor

Coagulopathy

Drug

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Comments Intraparenchymal: frontal lobes, Coup and contracoup anterior temporal lobes; injury during brain subarachnoid deceleration Putamen, globus pallidus, Chronic hypertension thalamus, cerebellar hemisphere,produces hemorrhage from pons small (~100 m) vessels in these regions Basal ganglion, subcortical Occurs in 16% of ischemic regions, lobar strokes with predilection for large hemispheric infarctions Lobar Lung, choriocarcinoma, melanoma, renal cell carcinoma, thyroid, atrial myxoma Any Uncommon cause; often associated with prior stroke or underlying vascular anomaly Lobar, subarachnoid Cocaine, amphetamine, phenylpropranolamine

Causes of Intracranial Haemorrhage(cont)

Arteriovenous malformation Aneurysm Amyloid angiopathy Lobar, intraventricular, subarachnoid Subarachnoid, intraparenchymal, rarely subdural Lobar Risk is ~24% per year for bleeding Mycotic and nonmycotic forms of aneurysms Degenerative disease of intracranial vessels; linkage to Alzheimer's disease, rare in patients <60 Multiple cavernous angiomas linked to mutations in KRIT1, CCM2, and PDCD10 genes Produces bleeding by venous hypertension Rare cause of hemorrhage

Cavernous angioma

Intraparenchymal

Dural arteriovenous fistula Capillary telangiectasias

Lobar, subarachnoid Usually brainstem

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MANAGEMENT
Initial assessment and management Subsequent hospital care History Physical examination Labs Imaging

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Initial assessment and management

ABCDE (primary survey) Serum glucose Noncontrast head CT Hemorrhage -Medical and surgical management Tumor or other CNS process -Treat as indicated Normal or hypo dense area consistent with acute ischemic stroke
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-Consider thrombolysis- for thrombosis/

Subsequent management

Establish cause of stroke and risk factors (in-depth history, physical exam, special imaging CTA) Plan for secondary prophylaxis (drugs, risk factor modifications) Provide supportive management

Obtain physical, occupational, and speech therapy consultation and social work as appropriate Provide nutrition

Prevent onset of complications Plan for discharge, including prescriptions for risk factor reduction e.g. when to institute antihypertensive treatment, and antithrombotic 7/5/12 medication prophylaxis

History taking goals

Establish timeframe: onset of symptoms progression of symptoms and severity Deficits resulting hence localise the lesion Risk factors: modifiable & nonmodifiable
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hypertension and drug compliance, diabetes mellitus, tobacco use, high cholesterol,

Symptoms
Fever - endocarditis and resulting embolic stroke

Seizures

- Intracerebral hemorrhage (ICH) , brain embolism Severe headache - Subarachnoid hemorrhage (SAH) Gradual onset of neurological signs, decreased consciousness, vomiting Intracranial hemorrhage 7/5/12

Symptoms ctd.
Reduced alertness + presence of haemorrhage : with focal neurological signs =ICH whereas without focal signs =SAH Thrombotic , embolic stroke of post. circulation, large arterial ischaemia of tegmentum of Pons Hypotension- blood loss, CCF, trauma, dehydration Previous transient ischaemic attack >
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Physical examination
Five major areas; 1. assessment of ABCs 2. define severity of the patients neurological deficits 3. identify potential causes of the stroke 4. identify potential stroke mimics 5. identify co morbid conditions

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ABCs and vital sign monitoring need to be frequent as these patients may deteriorate rapidly eg in haemorrhagic stroke or need airway protection and ventilation A rapid neurological assesment is mandatory and may indicate the aggressiveness of therapy Examination of the head and neck may point towards trauma as a cause of the symtoms
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Measuring BP bilaterally may reveal rare causes such as aoric dissection Check for carotid bruit, renal bruit, atrial fibrillation A useful tool in measuring neurological impairment is the National Institutes of Health Stroke Scale (NIHSS). This scale can be used easily, is reliable and valid, provides insight to the location of vascular lesions, and can be correlated with outcome in patients with ischemic 7/5/12 stroke..

It focuses on 6 major areas of the neurologic examination: (1) level of consciousness, (2) visual function, (3) motor function, (4) sensation and neglect, (5) cerebellar function, and (6) language

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NEUROLOGICAL FINDINGS
Neurological Findings: finding the lesion Weakness of the face, arm, and leg (one side of the body) without sensory, visual, or cognitive abnormalities (pure motor stroke) = thrombotic stroke in penetrating arteries or a small ICH. Large focal neurologic deficits that begin abruptly or progress quickly = embolism or ICH. Vertigo, staggering, diplopia, deafness, crossed symptoms (one side of the face and other side of the body), bilateral motor and/or sensory signs, and hemianopia (auditory & visual symptoms/signs)= posterior circulation. Abnormalities of language , presence of motor & sensory signs on the same side of the body. = anterior circulation disease. Sudden onset of impaired consciousness in absence of focal neurologic s & s = SAH. Click to edit Master subtitle style

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STROKE- DOMINANT HEMISPHERE

Left (Dominant) Hemisphere Stroke

Aphasia Right hemiparesis Right-sided sensory loss Right visual field defect Poor right conjugate gaze Dysarthria

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STROKE- NONDOMINANT HEMISPHERE Right (Nondominant) Hemisphere Stroke

Left hemiparesis Left-sided sensory loss Left visual field defect Poor left conjugate gaze Dysarthria Spatial disorientation 7/5/12

Internal capsule & thalamic lesions

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Brain Stem / Cerebellum / Posterior Hemisphere Stroke: Common Patterns

Motor or sensory loss in all four limbs Crossed signs Limb or gait ataxia Dysarthria Dysconjugate gaze Nystagmus Amnesia
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Bilateral visual field defects

Examination of other systems

General exam and vitals: already done CVS: Afib, arrythmias, left ventriular hypertrophy, signs of ccf, murmurs suggesting site of embolic origin, carotid bruit ascultation Pulmonary: features of PTE Musculoskeletal: fractures ? Fat embolism, DVT, neurological deficits 7/5/12 etc

Acute stroke- differential diagnoses

Migraine Intracerebral hemorrhage Head trauma Brain tumor /

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INVESTIGATIONS
q

COMPUTED TOMOGRAPHY SCAN : done!

CT Radiographic images identify or exclude > stroke, extrapyramydial haemorrhages, abscesses Contrast enhanced CT scan> add specificity (contrast enhancement of subacute infarcts) > visualization of venous structure
q q

Magnetic Resonance Imaging Cerebral Angiography > Gold standard for vasculopathies; artherosclerotic stenosis of cerebral art. , aneurysms, vasospasms, intraluminal thrombi, vasculitis, state of collateral channels of bloodflow Ultrasound techniques > stenosis of Int. carotid artery

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IMAGING

CT scan remains the commonest modality used Not very sensitive for ischaemia in the first 6 hours Findings that can suggest ischemic changes relatively early include loss of the gray-white matter interface, loss of sulci, and loss of the insular ribbon are subtle signs of early ischemia.
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Early mass effect and areas of hypodensity suggest irreversible injury and identify patients at higher risk of hemorrhage if given thrombolytics. Significant hypodensity on the baseline scan should prompt the physician to question the time of onset. Hypodensity in an area greater than one third of the MCA distribution is considered by some a relative contraindication for thrombolytics.
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CT-early infarction

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CT scan may demonstrate other causes of the patient's symptoms including; -neoplasm -epidural -subdural hemorrhage -aneurysm -abscess -arteriovenous malformation -hydrocephalus.
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CT angiography can demonstrate the vascular occlusion and areas of perfusion deficits Digital subtraction angiography is considered the definitive method for demonstrating vascular lesions, including occlusions, stenoses, dissections, and aneurysms. Cerebrovascular angiography provides useful information on the extracranial and intracranial vasculature It also allows for intra-arterial therapies, both intraarterial thrombolytics and investigational catheter devices.
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Angiography requires special facilities and a skilled operator and it carries a stroke risk of 1-2%.

MR spectroscopy Carotid duplex scanning Transcranial Doppler ultrasonography. The use of single-photon emission computed tomography (SPECT) in stroke is still relatively experimental and available only at select institutions; it can define areas of altered regional blood flow ECHO, ECG, CXR
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Patient work up

Glucose and electrolyte tests: Hypoglycemia is the most common electrolyte abnormality that produces strokelike symptoms. Electrolyte disorders Complete blood count: CBC aids in evaluating for anemia. Additionally, sickle cell disease, polycythemia, and thrombocytosis increase the risk for stroke. Prothrombin time (PT) and activated partial thromboplastin time (aPTT) tests

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Cardiac enzymes: Not infrequently patients with acute stroke also experience acute myocardial ischemia. Arterial blood gas (ABG) analysis: In patients with suspected hypoxemia, ABG will define the severity of hypoxemia and may detect acid-base disturbances.

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Additional laboratory tests are tailored to the individual patient. They may include

rapid plasma reagent (RPR), toxicology screen, fasting lipid profile, ESR, pregnancy test, antinuclear antibody (ANA), rheumatoid factor, and homocysteine.

In select patients with possible hypercoagulable states, protein C, protein S, antithrombin III, and Factor V Leiden testing may be required. 7/5/12

Treatment
Begin after 1st TIA- dont wait 4 STROKE! Control stroke risk factors: - Pt education VERY IMPORTANT! -Smoking, BP, lipids, DM etc. Drug therapy: - Anti platelets- low dose ASPIRIN - + dipyridamole for 2 years - PUD pts use CLOPIDOGREL or TICLOPIDINE

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Anticoagulation; generally no benefit (may lead to worse outcome in acute phase due to increased incidence of hemorrhage) Warfarin indications-prophylactic: Heart emboli

Afib with age above 65 or age below 65 but with other risk factors eg hptn, DM etc

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General management
Click icon to add table Treat hypoglycemia with D50 Blood glucose Treat hyper if >11mmol/l Blood pressure Next table

Cardiac monitor

Continous monitoring for a fib and ischaemia Intravenous fluids Avoid D5w and overhydration, n saline not more than 50ml/hr Oral intake NPO Oxygen Temperature Supplement if necessary Avoid hyperthermia

Blood pressure Treatment

Click icon to Pretreatment Candidate add table lysis SBP>185 or DBP>110

Labetalol 10-20mg IVP 1or 2 Enalapril 1.25mg IVP Na nitroprusside 0.5mcg/kg/min labetalol 1-2mg/min or nicardipine 5mg/h Labetalol 10mg may repeat n *2 to max 150 every 10 mins

Post treatment DBP>140 SBP>230 or DBP>120 SBP>180 or DBP>105

Non DBP>140 candidat SBP>220 or Click icon to add table DBP>120 or MAP>130

Na nprusside 0.5mcg/kg/min Labetalol 10mg may repeat n *2 to max 150 every 10 mins or nicardipine 5mg/h Antihypertensive therapy SBP<220 or only indicated if AMI, aortic DBP>105 or dissection, severe CHF or hypertensive MAP<130 encephalopathy

thrombolytic therapy

Intravenous t-PA for appropriate patients within 3 hours from symptom onset remains a Class I recommendation by the American Stroke Association. Symptom onset:

Acute onset of symptoms Last time patient was normal If patient was asleep; time when pt fell asleep

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The protocol for treatment is as follows:

(1) IV tPA (0.9 mg/kg) is administered (maximum of 90 mg). (2) The first 10% is given as a bolus over 1 minute. The remaining 90% is delivered over the next hour. (3) No anticoagulants or antiplatelet agents are used for the next 24 hours.

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(4) BP is monitored closely over the next 24 hours and aggressively managed (5) Opportunities for neurosurgical consultation and reversal of bleeding (eg, with cryoprecipitate, fresh frozen plasma) should be available if intracerebral hemorrhage complicates treatment.

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Prourokinase is also known as recombinant prourokinase or r-proUK. This intra-arterial therapy requires the involvement of a skilled interventionist. The time window is 6 hours from symptom onset.

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Surgical intervention
Endarterectomy with thrombolysis Balloon angioplasty with/ without stenting Bypass ineffective Hemicraniotomy to treat life-threatening ICP Surgical evacuation of the hematoma

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Rehabilitation

The American Stroke Association guidelines for rehabilitation focus on 6 major areas, as follows;

Preventing, recognizing, and managing comorbid conditions and medical complications Training for maximum independence Facilitating maximum psychosocial coping and adaptation by patient and family Preventing secondary disability by promoting community reintegration, including resumption of home, family, recreational, and vocational activities Enhancing quality of life in view of residual disability Preventing recurrent stroke and other vascular conditions

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Complications

Chest infection Epileptic seizures DVT/ PE Painful shoulder Pressure sores Urinary infection Constipation Depression and anxiety
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