Acute ischemic stroke is a sudden neurological deficit caused by an interruption of blood flow to a part of the brain due to thrombotic or embolic occlusion of cerebral arteries. It accounts for approximately 85–90% of all strokes, making it significantly more common than hemorrhagic stroke (which accounts for 10–15%).
A stroke refers to a spectrum of diseases characterized by the abrupt onset of neurological dysfunction due to brain injury caused by:
- Ischemia : Inadequate blood supply to the brain tissue (ischemic stroke).
- Hemorrhage : Bleeding into the brain parenchyma or surrounding spaces (hemorrhagic stroke).
A transient ischemic attack (TIA) is a transient episode of neurological dysfunction caused by focal brain ischemia without acute infarction, lasting less than 24 hours.
Etiology and Causes of Ischemic Stroke
- Thrombotic stroke : Caused by in situ thrombosis over atherosclerotic plaques that narrow cerebral arteries, commonly at carotid bifurcation or large intracranial vessels.
- Embolic stroke : Arises from emboli traveling from cardiac sources (e.g., mural thrombi after myocardial infarction, infective endocarditis vegetations, atrial fibrillation).
- Paradoxical emboli : Venous emboli bypass pulmonary circulation via right-to-left shunts (e.g., patent foramen ovale).
- Other causes : Vasculitis, arterial dissection, hypercoagulable states.
Risk Factors for Stroke
Non-modifiable:
- Age >55 years (stroke risk doubles every decade after 55)
- Male sex (30% higher risk than females)
- Genetic predisposition influencing atherosclerosis and cardiac disease
Modifiable:
- Hypertension (most important risk factor)
- Diabetes mellitus
- Hyperlipidemia
- Cigarette smoking
- Obesity and sedentary lifestyle
- Cardiac diseases (atrial fibrillation, coronary artery disease)
- Substance abuse (e.g., cocaine, amphetamines)
Pathophysiology
Ischemic stroke results from vascular occlusion leading to ischemia and hypoxia in brain tissue. The loss of oxygen supply causes:
- Failure of ATP-dependent ion pumps (Na+/K+ ATPase)
- Cellular depolarization and calcium influx
- Cytotoxic edema due to intracellular water accumulation
- Release of excitatory neurotransmitters (glutamate) causing excitotoxicity
- Generation of free radicals and activation of apoptotic pathways
- Irreversible neuronal injury can occur within minutes (~5 min) in vulnerable brain areas (e.g., hippocampus, neocortex)
The infarct core undergoes necrosis, surrounded by the ischemic penumbra, a region of potentially salvageable tissue targeted by reperfusion therapies.
Clinical Features
The clinical presentation depends on the brain area affected but generally includes:
- Sudden focal neurological deficits :
- Hemiparesis or monoparesis
- Hemisensory loss
- Aphasia (dominant hemisphere involvement)
- Dysarthria
- Visual field deficits (homonymous hemianopia)
- Facial droop
- Ataxia and vertigo (brainstem or cerebellar involvement)
- Diplopia, nystagmus
- Sudden decrease in consciousness may occur in large strokes.
Diagnostic Evaluation
History and Physical Examination:
- Onset and progression of neurological symptoms
- Stroke risk factors and comorbidities
Neuroimaging:
- Noncontrast CT scan : First-line to exclude hemorrhage; may be normal early in ischemic stroke.
- MRI with diffusion-weighted imaging (DWI) : Most sensitive for early ischemia detection.
- CT or MR angiography : To identify vascular occlusions.
- Cerebral angiography : Reserved for intervention planning.
Laboratory Studies:
- Complete blood count (CBC): Detect polycythemia or infection.
- Basic metabolic panel: Rule out metabolic mimics (hypoglycemia, hyponatremia).
- Coagulation profile: Identify coagulopathies.
- Cardiac biomarkers: Evaluate for concurrent myocardial ischemia.
- ECG and echocardiography: Assess cardiac sources of emboli.
Additional tests:
- Lumbar puncture: If suspicion for subarachnoid hemorrhage with negative CT or meningitis.
Management of Ischemic Stroke
Initial stabilization:
- ABCs (Airway, Breathing, Circulation)
- Supportive care including oxygen, fluids, and blood pressure management
Reperfusion therapy:
- Intravenous thrombolysis (IV tPA) within 3-4.5 hours of symptom onset (Alteplase 0.9 mg/kg; max 90 mg)
- Mechanical thrombectomy for large vessel occlusion within 6-24 hours in selected patients
Antiplatelet therapy:
- Aspirin initiated 24–48 hours post thrombolysis to reduce recurrent stroke risk
- Alternatives: Clopidogrel or dipyridamole if aspirin contraindicated
Secondary prevention:
- Control hypertension, diabetes, and hyperlipidemia
- Smoking cessation and lifestyle modification
- Statins for atherosclerotic disease
- Anticoagulation for cardioembolic sources (e.g., atrial fibrillation)
Neuroprotection (investigational):
- Targeting glutamate excitotoxicity, free radicals, calcium influx, and apoptotic pathways to preserve the ischemic penumbra (currently experimental)
High-Yield Notes for NCLEX/USMLE
- Ischemic stroke accounts for ~85% of strokes; hemorrhagic for ~15%.
- Stroke risk doubles every decade after 55 years of age.
- Sudden onset focal neurological deficit lasting >24 hours is stroke; <24 hours is TIA.
- Most common cause: thrombotic occlusion over atherosclerotic plaques.
- Reperfusion with IV tPA must be initiated within 3-4.5 hours.
- Mechanical thrombectomy is for large vessel occlusions and can extend treatment window.
- Early aspirin reduces recurrent ischemic stroke risk but is delayed until 24 hours after thrombolysis.
- Neuroimaging is essential to rule out hemorrhage before thrombolysis.
- Penumbra: ischemic brain tissue at risk but potentially salvageable with timely treatment.
- Control modifiable risk factors aggressively to prevent primary and secondary stroke.
