Acute neurologic injury that occurs as a result of ischemic infarction or bleeding into part of the brain manifested by rapid onset of focal CNS signs and symptoms with or without a focal higher cerebral dysfunction (e.g. aphasia, hemisensory loss, visual defect) lasting >24 hours.
It is a common medical emergency with an annual incidence of between 180 – 300 per 100,000
Stroke is the third most common cause of death in the developed world after cancer and ischemic heart disease
In US stroke has a higher incidence in the black population than in the white population. Hispanics have a lower overall incidence of stroke
In patients younger than 60 years, the incidence of stroke is greater in males (3:2 ratio).
Stroke can occur in patients of all ages, including children.
Risk of stroke increases with age, especially in patients older than 64 years, in whom 75% of all strokes occur.
It classifies ischemic strokes into 5 subtypes using clinical features & ancillary diagnostic studies including neuro-imaging
Large artery atherosclerosis (LAA)
Small vessel occlusion
Strokes of other determined etiology
Strokes of other undetermined etiology (cryptogenic) which can be due to; negative evaluation, Incomplete evaluation
Pathophysiology of Ischemic Stroke
Acute occlusion of vessel> reduction in blood flow to brainà> ischemia / infarction
A fall in cerebral blood flow to zero causes death of brain tissue within 4–10 min
Values <16–18 mL /100 g tissue / min cause infarction within an hour; & values <20 mL/100 g tissue / min cause ischemia without infarction unless prolonged for several hours or days.
NB – tissue surrounding the core region (umbra) of infarction is ischemic but reversibly dysfunctional and is referred to as ischemic penumbra
Pathways of Focal Cerebral Infarction in ischemic strokes
Necrotic pathway in which cellular cytoskeleton breakdown is rapid, due principally to energy failure of the cell. Occur in umbra region.
Apoptotic pathway in which cells become programmed to die. Occur in the penumbra.
Necrotic pathway: ischemic cascade
Ischemia produces necrosis by starving neurons of glucose, which results in failure of mitochondria to produce ATP. Without ATP, membrane ion pumps fail & neurons depolarize, allowing intracellular calcium to raise ↑.
Cellular depolarization also cause glutamate release from synaptic terminals; ↑ EC glutamate induce neurotoxicity by activating postsynaptic glutamate receptors that increase neuronal calcium influx.
Free radicals are produced by membrane lipid degradation & mitochondrial dysfunction: cause catalytic destruction of membranes & likely damage other vital functions of cells
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.
Intra – cerebral (ICH) / parenchymal
Subarachnoid Hemorrhage (SAH)
Hypertension (about 60%)
Illicit drug use (cocaine, amphetamin)
Less frequent causes: bleeding into tumor, aneurysmal rupture & Vasculitis
The bleeding is directly into the brain, forming a localized hematoma that spreads along white matter pathways.
Accumulation of blood occurs over minutes or hours; the hematoma gradually enlarges by adding blood at its periphery.
Headache, vomiting, and a decreased level of consciousness develop if the hematoma becomes large enough to increase intracranial pressure or cause shifts in intracranial contents.
Diagnosis involves the following;
Symptoms include the following:
Sudden numbness or weakness of face, arm, or leg, especially on one side of the body.
Confusion of sudden onset, difficulty in speaking or understanding.
Progressive sudden deterioration of vision of one or both eyes.
Sudden difficulty in walking, dizziness, and loss of balance or coordination.
Severe headache with no known cause.
Establish the time the patient was last normal is especially critical when thrombolytic therapy is an option.
Rule out risk factors for atherosclerosis and CVS D’SES e.g. hypertension and diabetes( DM).
Also rule out history of smoking, alcohol, high cholesterol levels. History of drugs, trauma.
Physical examination is directed toward 5 major areas:
Assessing the airway, breathing, and circulation (ABCs),
Defining the severity of the patient’s neurologic deficits
Head and neck exam; Contusions, lacerations, and deformities may suggest trauma as the cause for the patient’s symptoms. Auscultation of the neck may elicit a bruit, suggesting carotid disease as the cause of the stroke.
Cardiac: Cardiac arrhythmias, such as atrial fibrillation, are found commonly in patients with stroke.
The neurologic examination must be thorough; able to localise which site has been affected based on neurological deficits.
A useful tool in quantifying neurological impairment is the National Institutes of Health Stroke Scale (NIHSS).
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. The NIHSS is used most by stroke teams.
Management of stroke include the following measures;
CBC- anemia, SCD, polycythemia, thrombocytosis,
RBS- hypoglycemia may mimic stroke
Cardiac enzymes- MI may occur concurrently
ABG(Arterial blood gas test)
Renal function tests
CT scan remains the commonest modality used
Not very sensitive 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
CT scan may demonstrate other causes of the patient’s symptoms including;
CT angiography can demonstrate the vascular occlusion and areas of perfusion deficits .
Diffusion-weighted MRI (DW-MRI) can detect areas of ischemic brain injury earlier in the evolution of ischemia than standard T1/T2-weighted MRI images or CT scan by detecting changes in water molecule mobility
Observe ABCs principles
Stabilize the patient
1)Do Blood glucose levels
Correct hypoglycemia if present.
Treat hyperglycemia if rbs >11mmol/l because it may increase the infarct volume therefore use insulin to normalize levels.
2)Correct BP- see below.
3)Cardiac monitor- continuous monitoring for ischemic changes or Atrial fibrillation.
4)Hydration; intravenous fluids- avoid D5W and excess fluid admin- use normal saline ( not >50ml/h).
Nil per oral initially due to risk of aspiration; avoid oral intake until swallowing is assessed because dysphagia is common after stroke.
6) Oxygen therapy if SaO2 <90% or patient is hypotensive.
Hypertensive ischemic stroke patients with a moderate elevation of Bp (up to 180/110 mmHg) may not require antihypertensive therapy. Early BP reduction may decrease cerebral perfusion and increase infarction.also the BP normalizes with few
If any of the following is present treat HTN regardless of BP; hypertensive encephalopathy, aortic dissection, acute renal failure, acute pulmonary edema, acute myocardial infarction, severe hypertension ( > 220/120 mmHg).
Avoid >10% reduction in diastolic blood pressure or >25% reduction in systolic blood pressure within first 24%hrs unless values exceed SBP >220, DBP >115
Drugs of choice: labetalol, Enalapril, Sodium nitroprusside, Nicardipine
The Chinese Acute Stroke Trial (CAST) and the International Stroke Trial (IST) are 2 large studies in which investigators evaluated aspirin 160-300 mg/d within 48 hours of ischemic stroke symptom onset.
Compared with no treatment, aspirin resulted in a 1% absolute reduction in risk of stroke and death in the first few weeks.
At later time points (e.g. 6 months), aspirin had absolute reduction of approximately 1% for death or dependence.
Aspirin reduces the risk of early recurrence .
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
Types of stroke rehabilitation
Physical Therapy (PT)
Walking, range of movement
Occupational Therapy (OT)
Taking care of one’s self
Speech Language Therapy
Communication skills, swallowing, cognition
10% of stroke survivors recover almost completely
25% recover with minor impairments
40% experience moderate to severe impairments requiring special care
10% require care within either a skilled-care or other long-term care facility
15% die shortly after the stroke
Written by Doc Bob
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