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Stroke
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- 2. Definition • Abrupt onsetof neurological deficit that is attributable to a focal vascular cause. • Incidence increases with age • Common medical emergency
- 3. • Ischemic strokeaccounts for 85% cases • As a result of obstruction within a blood vessel supplying blood to brain • Hemorrhagic accounts for 15% cases • It results from weakened vessel that rupture and bleeds into surrounding area
- 4. Risk factors • Fixedrisk factors ● Modifiable risk factors 1. Age 2. Gender 3. Race 4. Previous vascular event: • MI • Peripheral vascular disease 5. Heredity 6. Sickle cell disease 7. High fibrinogen 1. Hypertension 2. Cigarette smoking 3. Hyperlipidemia 4. DM 5. Heart Disease : Atrial fibrillation, CCF, IE 6. Excessive alcohol intake 7. OCPs, HRT 8. Polycythemia
- 5. Pathophysiology Cerebral infarction • Mostlycaused by thromboembolic disease secondary to atherosclerosis • Acute occlusion -> reductn in blood flow to brain • The magnitude of flow reduction is function of collateral blood flow and this depends on individual vascular anatomy, the site of occlusion and systemic BP. • As cerebral blood flow declines -> neuronal function fails • Blood flow below threshold -> neuronal deficit develops
- 6. • If bloodflow is retained prior to significant amount of cell death -> transient symptoms -> TIA • Between ischemic core and normally perfused brain at periphery lies the ischemic penumbra, zone of moderately reduced cerebral blood flow • If blood falls further, hypoxia->ATP decreases -> sodium & water influx -> glutamate release-> Ca influx; release of free radicals and ultimately cellular destruction.
- 7. Intracerebral hemorrhage • Bleedingwithin the brain caused by rupture of vessel • Explosive entry of blood -> cessation of functions, as neurons are disrupted and white matter fibre tracts are split apart • Hematoma growth -> neurological deterioration • Perihematoma brain edema, primary cause of neurological deterioration after first day of bleed
- 9. Transient ischemic attack •Abrupt onset focal neurological deficit of presumed vascular etiology not lasting longer than 24hrs • Most TIAs resolve in less than 30mins • TIA implies an active plaque in the major feeding artery & is a warning sign of stroke Features Carotid territory • I/L mono ocular blindness • Weakness & heaviness of C/L arm, face leg • Numbness & paraesthesia • Bradykinesia, dysphagia Vertebro basilar territory • Vertigo • Tinnitus • Ataxia • Dysarthria • Hemianopia • diplopia • Sudden fall • Dysphagia
- 10. RISK ASSESSMENT OF STROKE Highestincidence of stroke in TIA occurs within first 48hrs 0 -3 low risk 4-5 moderate risk 6-7 high risk Score 7 -> 22% chance of developing stroke
- 11. Symptoms suggestive ofTIA/ Stroke • Sudden onset of facial weakness • Arm weakness • Speech deficit • Time delay implies max damage to neurons
- 12. Investigations • Full bloodcount, ESR • Blood glucose, urea, proteins • CXR, ECG • Echocardiography • Lipid profile • Carotid doppler • Homocysteine Treatment • DAPT – Dual antiplatelet theraphy Aspirin 75mg to 300mg Clopidogrel 75mg to 300mg • Noval oral anticoagulants -> Rivaroxaban, Dabigatrin Carotid territory TIA, >70% stenosis in carotid imaging • Carotid endarterectomy • Carotid stenting
- 13. CORTICAL STROKE Cerebral cortexinvolvement -> • Aphasia • Apraxia (Altered voluntary movement) • Visual field defect • Memory deficits -> temporal lobe involvement • Hemi neglect -> parietal lobe involvement • Disorganised thinking, confusion -> frontal lobe involvement • Anosognosia( inability to appreciate severity of cognition defect)
- 14. PARIETAL LOBE In righthanded person dominant lobe is left and non dominant lobe is right. • Nondominant parietal lobe -> Visuospatial skills • Right parietal lobe lesion leads to loss of visuospatial skills -> Constructional Aparxia • Dominant parietal lobe lesion -> • Acalculia • Agraphia • Left to Right disorientation • Finger agnosia • Global aphasia Gertsmann syndrome
- 15. TEMPORAL LOBE • Hippocampus-> short term memory • Neo cortex-> long term memory • Temporal lobe lesion • Antegrade amnesia – loss of short term memory • Prosopagnosia – impaired memory of faces • Complex hallucination – smell of rotten fish/dead rat, metallic taste in mouth, hearing music • Deja vu – undue familiarity • Jamai vu - unfamiliarity
- 16. FRONTAL LOBE • Frontallobe damage • Aggressive ,antisocial behaviour • Personality changes • Urge incontinence ( damage to paracentral lobule) • Apathy(lack of interest in self care) • Abulia (lack of desire to speak) • Primitive reflexes present- grasp reflex, rooting reflex
- 17. OCCIPITAL LOBE • Visualhallucination • Palinopsia- persistence of an image even when the object is removed • Asimultagnosia- Simultaneous visual information is not processed by brain • Homonymous hemianopia Anton syndrome -> B/L distal PCA obstruction -> cortical blindness -> Gun barrel vision
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- 23. Medullary syndromes 1. Medialmedullary syndrome • Vessel involved – vertebral artery, anterior spinal artery • Structures affected – Corticospinal tract Medial lemniscus Medial longitudinal fasciculus Hypoglossal nucleus • Clinical features- C/L hemiplegia C/L loss of position and vibration Internuclear ophthalmoplegia I/L 12th nerve palsy( deviation of tongue towards same side of lesion)
- 24. 2. Lateral medullarysyndrome • Vessel involved – Posterior inferior cerebellar artery • Structures affected – Inferior cerebellar peduncle Vestibular nucleus Trigeminal nucleus Nucleus Ambiguus Lateral spinothalamic tract Descending fibres of Sympathetic chain • Clinical features – I/L ataxia I/L nystagmus and vertigo I/L facial numbess I/L palatal palsy Horners syndrome C/L loss of pain, touch and temperature
- 25. LACUNAR STROKE • Internalcapsule -> Anterior limb, genu, Posterior limb • Corticospinal tract conducts impulse from brain to spinal cord • Due to occlusion of lenticulo striate artery(small penetrating artery) • Lipohyalinosis of small vessels feeding the internal capsule • Pure motor stroke- Lesion of posterior limb of internal capsule hemiparesis or hemiplegia typically affects face,arms and leg equally motor aphasia-> lesion in genu & anterior capsule
- 26. • Ataxic hemiparesis-combination of cerebellar & motor symptoms-> weakness & clumsiness on I/L side of body Most frequent site of infarction – posterior limb, basis pontis, corona radiata • Pure sensory stroke- persistent/ transient numbness and/or tingling on 1side of body Frequent site of infarction- thalamus • Mixed sensorimotor stroke- hemiparesis/hemiplegia with I/L sensory impairment Infarct usually in thalamus and adjacent posterior internal capsule
- 28. Investigations • Initial evaluation •BP, Cardiac function and ECG • Degree of neurological deficit and vascular territory involved • Metabolic status -> Blood sugar, hypoxia, RFT, Electrolyte status • Hematological parameters-> Hb, coagulation parameters • Other investigations • CT- to confirm infarct • MRI • CT angiography & MR angiography • CXR
- 29. Treatment • General measures •Adequate airway • Give O2 if saturation <95% • Treat hyperglycemia with insulin if serum glucose>200mg/dL • Avoid hyperthermia • Skincare by changing position once in 2hrs to prevent bed sore • Assess nutritional status and provide supplements if needed, nasogastric tube if unable to swallow • Signs of dehydration give fluids parenterally or via nasogastric tube • Bladder catheterisation if continence or retention has occurred • Passive movements of limbs to prevent contractures, edema of limb,venous stasis and pulmonary embolism
- 30. • Blood pressure •Urgent reduction is required only if • SBP>220mmHg • DBP>120mmHg • MAP>130mmHg • BP not elevated to that extent but patient has pulmonary edema, renal failure, acute MI etc, antihypertensives required • Candidates of thrombolytic therapy, Antihypertensives are recommended if SBP>185mmHg or DBP>110mmHg • Anti edema measures • Mannitol 20% iv over 20mins, 3 to 4 times daily • Glycerol 30ml orally 3 to 4 times daily • Furosemide 20mg iv 3 times a day
- 31. • Thrombolytic therapy •Reteplase, Alteplase • Intravenoulsy within 4.5hrs of onset of symptoms • Dissolve blood clot and restore blood flow • Dose 0.9mg/kg with 10% of tot dose bolus and rest over 1 hour • Intra arterial rTPA can be given in selected patients • Anticoagulant • Aspirin, heparin, warfarin • Subcutaneous administration is recommended for treatment of immbolised patients to prevent DVT If patient presents, 4.5 -6hrs after onset of symptoms -> mechanical thrombectomy
- 32. Prevention • Cessation ofsmoking • Control of diabetes • Diet (low fat, high fiber) • Lowering SBP by 10mmHg is associated with a reduction in the risk of stroke by about 1/3rd, irrespective of baseline BP levels • Antiplatelet agents and anticoagulants in patients with atrial fibrillation • Reducing LDL cholesterol to 100mg/dL using statin • For asymptomatic patients who are detected to have carotid artery stenosis of 60-99%, carotid endarterectomy may be considered.
- 33. • Later managementincludes rehabilitation, adequate control and maintenance of risk factors • Rehabilitation should involve family members, and includes motor sensory, cognitive and psychological measures and attempts at occupational rehabilitation.
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