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stroke; cerebrovascular accident (CVA)

Cerebrovascular accident (CVA) or stroke is the rapid onset of a neurological deficit that persists for at least 24 hours. Etiology: - strokes are caused by (15%) or subarachnoid hemorrhage (10%) or the - see specific type of stroke - hemorrhagic stroke - intracerebral hemorrhage (15%) - subarachnoid hemorrhage (10%) - ischemic stroke (75%) - embolic stroke - also see risk factors for ischemic stroke - cryptogenic stroke [4] - cervical artery dissection - hypercoagulability - autoimmune disease - patent foramen ovale* - shared risk factors (hemorrhagic stroke & ischemic stroke) a) hypertension b) cocaine abuse c) tobacco abuse d) malignancies [46] - lung cancer (RR=4.2) - pancreatic cancer (RR=2.6) - colorectal cancer (RR=2.5) - breast cancer (RR=1.4) * may be likely cause in younger patients; unlikely to cause subsequent stroke in the absence of hypercoagulability [4] Epidemiology: 1) 4% of individuals (mean age 75 years) will suffer from stroke within 4 years [10] 2) 7% of individuals ((baseline age 45-64 years)) will suffer stroke within 24 years [43] 3) no association with dietary fat [16] 4) incidence of stroke is declining, but severity is not [19,43] 5) worldwide, death from stroke is declining, but incidence is increasing [37] a) lower income countries account for the increase b) incidence of stroke in high-income countries has declined 6) worldwide, children & adults < 65 years of age account for 1/3 of strokes [37] 7) incidence of stroke worldwide will increase by 50% by 2050 if action is not taken to reduce risk factors [69] Pathology: - blockage of a blood vessel supplying or draining the brain (75%) . elapsed time changes 6 hrs. no changes 8-48 hrs. swelling > 48 hrs. soft, friable 2 weeks liquefaction > 3 weeks cavitation (~1mL/3 months) cell sensitivity to ischemia: - neurons > oligodendrocytes > astrocytes > microglia > blood vessels brain region sensitivity to ischemia: - hippocampus (CA1) > extrapyramidal layer (3) of neocortex > cerebellar Purkinje cells > inferior olivary neurons > subthalamic nucleus Microscopic Pathology: . elapsed time changes 8 - 12 hrs. classic ischemic changes* 12 - 48 hrs. macrophages appear 48 hrs. macrophages become foamy 3rd day proliferating astrocytes, gemistocytes 7th day capillary wall thickening > 30 days astrocytes only remaining (depends on size) * classic ischemic changes: eosinophilic degeneration, glassy cytoplasm, loss of Nissl substance, hyperchromatic nuclei, neuronal shrinkage & increase in perineuronal space) History: - onset, improvement or progression of symptoms, anatomic location of deficit, activity prior to onset, headache, nausea/vomiting, loss of consciousness, brisk neck movement, visual aura, scotoma, vertigo, seizure, trauma, confusion, dysarthria, incontinence, dysphagia, palpitations, prior TIAs or strokes, amaurosis fugax, HTN, diabetes, CAD, hyper- lipidemia, IVDA, cocaine, valvular heart disease, migraine, anticoagulants, oral contraceptives, tobacco, alcohol Clinical manifestations: 1) focal or multifocal neurologic deficit evolving over second to minutes, persisting > 24 hours a) carotid or vertebrobasilar artery territories - involvement of upper &/or lower extremity &/or face on opposite side, opposite visual field or eye onsame side - motor dysfunction: - dysarthria; weakness; clumsiness; pronator drift - sensory: numbness; paresthesias - blindness - monocular blindness (same side) - Hollenhorst plaque - homonymous hemianopia (opposite visual field) b) carotid artery territory - paresthesias of hand, arm & face (contralateral) - hemiparesis more common with ischemic stroke - weakness of hand, arm & face (contralateral) - aphasia (dominant hemisphere) - dysarthria - unilateral neglect - loss of vision (ipsilateral eye) - carotid bruit c) lacunar TIAs - hemibody sensory loss or paresthesias - pure motor hemiparesis d) vertebrobasilar territory: - dysarthria - dysphagia - vertigo - ataxia - diplopia - visual field loss - homonymous hemianopia - perioral paresthesias - acute confusional state - profound general weakness 2) nonfocal symptoms suggest increased intracranial pressure a) common with: - hemorrhagic stroke - major ischemic stroke with cerebral edema b) headache c) nausea & vomiting d) impaired consciousness - restlessness - drowsiness - coma e) elevated systolic blood pressure [15] Laboratory: 1) all patients [4] - serum glucose - electrolytes: serum K+ < 4.0 meq/L confers 2.5 fold increased risk of stroke in patients taking diuretics - serum creatinine, BUN - markers of myocardial infarction - complete blood count (CBC) - prothrombin time, INR, aPTT 2) selected patients - liver function tests - toxicology screen - blood alcohol level - pregnancy test - arterial blood gas [4] 3) CSF analysis for xanthochromia if hemorrhagic stroke suspected [36] Special laboratory: 1) all patients - electrocardiogram - pulse oximetry 2) selected patients a) echocardiography b) cerebral angiography - determines localization & degree of carotid stenosis - necessary prior to carotid endarterectomy - identifies aneurysms & arteriovenous malformations (AVM) c) lumbar puncture - CT negative for blood - subarachnoid hemorrhage suspected - CSF analysis for xanothochromia [36] 4) electroencephalography (EEG) if seizures suspected [4] Radiology: 1) all patients a) computed tomography (CT) of head - obtained within 24 hours distinguishes hemorrhagic stroke from ischemic stroke [36] - CT changes in ischemic stroke appear after 24 hours b) MRI [18,20] alternative to CT - can detect early ischemic strokes not seen by CT - can detect hemorrhagic strokes not seen on CT - proposed standard of care [20] - not as fast as CT - patient in less monitored environment than CT [4] 2) selected patients - carotid artery ultrasound (Doppler) - chest X-ray (if lung disease suspected) [4] Complications: 1) anxiety (27-40%) develop clinically significant anxiety [8] 2) depression is common after stroke or TIA (14% at 1 year) [30] - major depression with psychosis is a further complication 2) cognitive impairment: [21] a) more common in hemorrhagic stroke than ischemic stroke b) more common with left hemisphere stroke, cortical stroke c) cognitive decline immediately after stroke & continued for at least 6-years thereafter [50] d) cognitive decline can occur both before & after a stroke [60] 3) delirium occurs in 12% of patients admitted to stroke unit; associated with poor prognosis [28] 4) residual focal neurologic deficits 5) seizures early after stroke* a) more common with hemorrhagic stroke than ischemic stroke (15% vs 4%) [29] b) more common with cortical stroke than subcortical stroke (19% vs 10%) c) do not predict mortality or function at 6 months [29] 6) risk of pneumonia is highest in the 1st week after stroke [68] 7) PTSD in 25% of survivors within 1 year after stroke [34] 8) fatigue after stroke due to depression, sleep apnea, heart failure [4] 9) reemergence or recrudescence of stroke symptoms in the setting of an intercurrent illness [61] 10) stroke often compromises well-being of family caregivers [48] - spouses of stroke survivors have reduced health-related quality-of-life many years after stroke [51] 11) 1/6 of patients will have another stroke within 5 years [9] * among anticonvulsants used as monotherapy in poststroke epilepsy, lamotrigine is associated with the lowest risk for mortality, valproate the highest [66] Differential diagnosis: 1) migraine headache (prodrome) 2) head trauma - subdural hematoma 3) seizure disorder with postictal hemiparesis 4) arteritis 5) multiple sclerosis (MS) 6) central nervous system (CNS) infection 7) intracranial mass lesion: brain tumor, brain abscess (evolution over hours to days) 8) dementia (with subacute worsening of cognitive impairment) 9) conversion disorder 10) cardiac arrhythmia 11) drug overdose 12) hypertensive encephalopathy 13) myasthenia gravis 14) syncope 15) systemic infection unmasking prior stroke-related deficit 16) Bell's palsy - facial droop with dysarthria may suggest stroke [56] - paralysis of the forehead muscles suggests Bell's palsy - most strokes that cause facial weakness have other neurologic signs, such as ipsilateral arm numbness or muscle weakness [56] Management: 1) see ACLS algorithm for suspected stroke - prehospital intravenous magnesium sulfate of no value [45] 2) NIH stroke scale recommended during emergency evaluation [4] 3) general a) nothing by mouth (NPO) for the 1st 24 hours b) provide supplemental oxygen - supplemental oxygen in patients with normal SaO2 increases mortality [4] c) control excessively high blood pressure - withhold antihypertensive treatment (2-7 days) if - systolic blood pressure < 220 mm Hg and - diastolic BP < 120 mm Hg [25] - lower threshold (systolic blood pressure 180-200 mm Hg) recommended in patients with hemorrhagic stroke [26] - target blood pressure is 160/90 mm Hg [4] - initial goal is to lower systolic blood pressure by 25% - aggressive control of blood pressure not indicated except in: - myocardial infarction - hypertensive encephalopathy - labetolol nay be agent of choice - negligible effect on intracranial pressure - ARB not helpful [27] d) avoid hypotonic fluids (i.e. D5W) which may exacerbate cerebral edema e) avoid glucose containing solutions in diabetic patients f) serial neurologic examination g) DVT prophylaxis h) control of blood glucose; elevated blood glucose may induce increased intracranial pressure i) mechanical ventilation as needed for severe stroke - early tracheostomy does not improve 6 month outcome [65] j) positioning, mobilization - avoid mobilization within 24 hours [49] - of no benefit, possibly harmful - supine vs sitting up has no effect on disability or mortality after acute stroke [58] k) early physical therapy l) dysphagia screening [23,41] - clinically assess swallowing before initiating diet - beside swallowing evaluation with 97% sensitivity & -90% specificity for dysphagia [12] - prophylactic antibiotics do not prevent pneumonia in post-stroke patients with dysphagia & may result in harm [53] m) patient education: - expectations - neurorehabilitation 4) specific therapy under ischemic stroke & hemorrhagic stroke 5) decompressive craniotomy or craniectomy for intracranial mass lesion effect 6) stroke units (neurorehabilitation) a) proposed standard of care [20] b) neurorehabilitation begins when the patient is medically stable c) neurorehabilitation is provided in inpatient stroke units d) in-home or nursing home rehabilitation is generally reserved for patients requiring a slower pace of neurorehabilitation [12] e) inpatient care in a stroke unit associated with diminished mortality 1 year after stroke [54] 7) telestroke systems of benefit for rural areas (see telehealth) 8) cervical spinal cord stimulation for post-stroke upper extremity paresis investigational [67] 9) follow-up: a) depression is common after stroke - treatment of depression can improve recovery [5] - nortriptyline is superior to fluoxetine [12] - citalopram & trazodone have been shown beneficial [12,22] - antidepressants may improve survival in patients with or without depression [17] b) anxiety is common after stroke (27-40%) [8] - depression & anxiety often coexist (74%) - treatment of anxiety may improve recovery - relaxation theraoy is standard [63] c) deconditioning in common - fatigue associated with lower extremity weakness [42] d) occupational therapy - routine occupational therapy of no benefit [47] e) exercise of no benefit in subacute phase after stroke [63] f) caregiver training - no benefit to training caregivers [35] g) risk factor modification* - hypertension: systolic BP < 140 mm Hg noninferior to < 120 mm Hg [62] - smoking - diabetes - alcohol abuse - hypercholesterolemia - dietary K+ may reduce risk of stroke in patient NOT taking diuretics [12] - use of chlorthalidone vs HCTZ associated with lower cardiovascular morbidity & mortality [70] h) ACE inhibitor may reduce risk* - combination of perindopril (Aceon) + indapamide (Lozol) found to reduced risk of recurrent stroke in patients with & without hypertension [7, 9] - ramipril >= 10 mg/day reduced stroke risk 31% & fatal stroke risk 61%, with BP reduction of 3.8/2.8 mm Hg [11] i) screening for osteoporosis with bone mineral density suggested [59] j) wait at least 9 months after ischemic stroke prior to elective non-cardiac surgery [44] k) horse-riding & music-&-rhythm therapies may help improve function & perceived recovery in patients years after a stroke [57] 10) prognosis a) degree of long-term cognitive impairment after stroke cannot be determined for at least 3 months [12] b) some patients with transient ischemic attack & minor stroke become disabled within 3 months, even without having a recurrent vascular event [32] - predictors of disability include: - baseline CT or CT angiography abnormalities - symptoms at presentation - female gender - diabetes mellitus - severity of initial neurologic deficit is the strongest predictor of long-term disability [4] c) ref [31] discusses reduction in early mortality by aggressive management vs severe long-term disability d) a first stroke relatively early in adulthood is associated with a higher mortality risk up to 20 years later [33] * * Follow-up - neurorehabilitation

Interactions

disease interactions

Related

ACLS algorithm for suspected stroke hospice guidelines for determining prognosis, stroke & coma National Institutes of Health (NIH) Stroke Scale; (NIHSS score) neurorehabilitation reversible ischemic neurologic deficit (RIND) transient ischemic attack (TIA)

Specific

brainstem infarction cerebellar infarction hemorrhagic stroke ischemic stroke silent brain infarct stroke, pre & postpartum (antenatal stroke) Weber-Gubler syndrome; hemiparesis alternans oculomotoria; superior alternating hemiplegia

General

cerebrovascular disease/disorder

Database Correlations

OMIM 601367

References

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