Ischemic stroke
Ischemic stroke is sudden focal neurologic deficit from arterial occlusion confirmed by infarction on neuroimaging. Diagnosis relies on urgent noncontrast head CT to exclude hemorrhage; treatment is IV alteplase within 4.5 hours and mechanical thrombectomy for large-vessel occlusion within an extended window, followed by antiplatelet therapy and risk-factor control.
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What this article covers
- Overview
Definition: stroke is sudden-onset focal neurologic deficit from dysfunction in the brain, retina, or spinal cord due to occlusion or rupture of a cerebral or spinal artery; ischemic stroke, from…
- Epidemiology
Burden: incidence rises each decade of life, though a minority occur in younger patients with a cardioembolic or hypercoagulable cause.
- Risk factors
Hypertension: the single most important modifiable risk factor for both ischemic and hemorrhagic stroke.
- Pathophysiology
Large-artery atherosclerosis: plaque rupture with artery-to-artery embolism, most often in the extracranial carotid and vertebral arteries and the intracranial carotid, middle cerebral, and vertebral-basilar junction arteries.
- Clinical features
Focal neurologic deficit of sudden onset: hemiparesis, aphasia, ataxia, loss of balance, visual field loss, and unilateral sensory loss, corresponding to the vascular territory involved.
- Differential diagnosis
Hemorrhagic stroke (intracerebral hemorrhage): headache and impaired consciousness are more prominent, and blood is visible on the noncontrast head CT obtained before any treatment decision, unlike…
- Diagnosis
Stroke is a clinical diagnosis confirmed by neuroimaging; the exam alone cannot reliably distinguish ischemic from hemorrhagic stroke, so imaging is required before any treatment decision.
- Management
First, assess airway, breathing, and circulation and check point-of-care glucose; correct hypoglycemia immediately, since it can mimic or worsen a focal deficit.
- Complications
Symptomatic intracranial hemorrhage after alteplase: occurs in up to 6% of treated patients, with mortality as high as 50% when it occurs; the main risk factors are treatment beyond 4.5 hours and uncontrolled hypertension.
- Prognosis
Time to reperfusion predicts outcome: earlier alteplase, and earlier thrombectomy for large-vessel occlusion, is associated with better functional outcomes and less disability at 3 months.
- Prevention
Blood pressure control: the single most impactful modifiable target for primary and secondary prevention; hypertension treatment reduces both ischemic and hemorrhagic stroke risk.
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Related articles
- Lacunar stroke
Small subcortical infarct, under 1.5 cm, from occlusion of a single penetrating artery, most often caused by hypertensive lipohyalinosis, producing one of five classic pure motor, pure sensory, ataxic hemiparesis, dysarthria-clumsy hand, or mixed sensorimotor syndromes without cortical signs, diagnosed by MRI and managed with the standard acute stroke pathway plus aggressive antiplatelet, statin, and blood pressure secondary prevention.
- Cerebellar stroke
Cerebellar stroke, ischemic or hemorrhagic infarction of the cerebellum, presents with vertigo, truncal ataxia, dysarthria, and limb incoordination and is diagnosed with brain MRI when CT is falsely reassuring. Its defining danger is delayed swelling that compresses the brainstem and fourth ventricle, which is treated with emergent decompressive suboccipital craniectomy.
- Basilar artery occlusion
Basilar artery occlusion is a posterior circulation large-vessel stroke that threatens the brainstem, cerebellum, and thalami, presenting with rapidly progressive quadriparesis, cranial nerve palsies, and impaired consciousness, up to locked-in syndrome or coma. Diagnosis requires urgent CT angiography, and management is emergent reperfusion with IV alteplase followed by mechanical thrombectomy in eligible patients.
- Intracerebral hemorrhage
Spontaneous bleeding into brain parenchyma, most often from chronic hypertension affecting deep penetrating vessels or from cerebral amyloid angiopathy in lobar locations, diagnosed by noncontrast CT and managed with acute blood pressure lowering, reversal of anticoagulation, and surgical evacuation for select cerebellar or deteriorating hemorrhages.
- Subarachnoid hemorrhage
Subarachnoid hemorrhage is sudden bleeding into the subarachnoid space, most often from a ruptured saccular (berry) aneurysm, presenting as the worst headache of a patient's life. Diagnosis is noncontrast head CT, then lumbar puncture if CT is negative, then catheter angiography to define the aneurysm; management is early aneurysm securement, blood pressure control, and nimodipine to reduce delayed cerebral ischemia from vasospasm.
- Carotid artery stenosis
Carotid artery stenosis is atherosclerotic narrowing of the extracranial internal carotid artery that raises ischemic stroke risk, graded by percent luminal narrowing on duplex ultrasound. Symptomatic stenosis of at least 50% warrants urgent revascularization; asymptomatic stenosis under 80% is managed with best medical therapy alone, including a high-intensity statin and antiplatelet agent.
- Carotid artery dissection
Carotid artery dissection is a tear in the wall of the internal carotid artery creating an intramural hematoma, typically presenting with unilateral head, face, or neck pain, partial Horner syndrome, and ischemic stroke or transient ischemic attack in a young or middle-aged patient. Diagnosis is by MRA or CTA of the neck, and most patients are treated with antiplatelet or anticoagulant therapy.
- Vertebral artery dissection
A tear in the vertebral artery wall, spontaneous or from neck trauma or manipulation, that causes posterior circulation ischemia through thrombus formation or direct luminal narrowing. Presents with posterior neck or occipital headache plus brainstem or cerebellar signs, most classically a lateral medullary (Wallenberg) syndrome; diagnosed with MRI/MRA or CT angiography of the neck and treated with antithrombotic therapy.
- Cerebral venous sinus thrombosis
Thrombosis of the dural venous sinuses or cortical veins that impairs cerebral venous drainage and CSF absorption, producing headache, papilledema, focal deficits, or seizures; MRI/MRV or CT venography establishes the diagnosis, and anticoagulation is first-line even when hemorrhagic venous infarction is present.