- Clinical science
Ischemic stroke is an acute neurologic condition caused by impaired cerebral blood flow (e.g., vascular occlusion or systemic hypoperfusion). Chronic systemic hypertension and cardiovascular disease are the most important risk factors. Clinically, ischemic stroke is characterized by the acute onset of focal neurologic deficits, which are dependent on the cerebral territory covered by the relevant vessel. A noncontrast head CT should immediately be performed to rule out intracranial hemorrhage. Revascularization of the vessels affected in ischemic strokes, for example via tissue plasminogen activator (tPA) or thrombectomy, is vital to preserving brain tissue. Secondary prevention is focused on managing modifiable risk factors (i.e., hypertension, atherosclerosis).
For more information, see, , and .
- Stroke: acute neurologic injury caused by ischemia or hemorrhage
- Ischemic stroke: cerebral infarction due to insufficient cerebral blood flow (hypoperfusion), which results in ischemia and neuronal injury
- Transient ischemic attack: temporary, focal cerebral ischemia; that results in neurologic deficits without acute infarction or permanent loss of function (previously defined as lasting < 24 hours) 
- Hemorrhagic stroke: cerebral infarction due to hemorrhage
- Intracerebral hemorrhage: bleeding within the brain parenchyma
- Subarachnoid hemorrhage: bleeding into the subarachnoid space
- Intraventricular hemorrhage: bleeding within the ventricles
- Ischemic strokes account for ∼ 85% of all strokes
- Nonmodifiable risk factors 
Modifiable risk factors 
- Systemic hypertension
- Diabetes mellitus
- Cardiovascular disease
- Coagulopathy , hyperhomocysteinemia
- Alcohol abuse
- Tobacco use
- Recreational drug use (e.g., cocaine can cause cerebral vasospasm)
- Oral contraceptive use
- Hormone replacement therapy
Epidemiological data refers to the US, unless otherwise specified.
Embolic strokes (∼ 20%)
- Most commonly affect the middle cerebral artery (MCA)
- Cardiac emboli
- Infectious emboli: bacterial endocarditis
- Paradoxical embolism: in patients with right-to-left cardiac shunt (e.g., persistent foramen ovale or atrial septal defect)
Thrombotic strokes (∼ 40%)
- Large vessel atherosclerosis (∼ 20%)
- Small vessel occlusion (e.g., ) (∼ 20%): see “Subtypes and variants” below.
Global cerebral ischemia
- Systemic hypoperfusion
- Hypoglycemia: repeated episodes of hypoglycemia (e.g., due to insulinoma) increase the risk of cerebral ischemia
- Severe and/or chronic hypoxia: hypoxemia (e.g., due to respiratory arrest) → global tissue hypoxia in the brain
- Other causes
- Definition: temporary, focal cerebral ischemia that results in neurologic deficits without acute infarction or permanent loss of function (previously defined as lasting < 24 hours) 
- Etiology: see “Etiology” above
- Risk factors: see “Epidemiology” above
- Acute transient focal neurologic symptoms
- Typically, symptoms last < 1 hour.
- Symptoms depend on the affected territory (see and ).
- Diagnosis: to identify areas of ischemia and rule out infarction
- Treatment: treatment of underlying etiology (e.g., management of hypertension, diabetes mellitus, carotid artery disease, atrial fibrillation)
- Prognosis: increased risk of future ischemic stroke
Lacunar infarct 
- Definition: noncortical infarcts characterized by the absence of cortical signs (e.g., no aphasia, hemianopsia, agnosia, apraxia)
- Risk factors
- Clinical features
- Pathology: results in a pale infarction at the periphery of the cortex
- Treatment: same as other ischemic strokes; see “Treatment” below
Infarction of the posterior limb of the internal capsule is the most common type of lacunar stroke and may manifest clinically with pure motor stroke, pure sensory stroke (rare), sensorimotor stroke, dysarthria-clumsy hand syndrome, and/or ataxic hemiparesis.
Watershed infarct 
- Definition: border-zone infarct in the region between the territory of two major arteries that supply the brain
- Etiology: sudden decrease in blood pressure or cessation of blood flow through both vessels → ischemia in the susceptible region between two vascular territories
- Signs of systemic hypoperfusion (e.g., tachycardia, low blood pressure, pallor, sweating)
- Diffuse neurologic deterioration
- Bilateral visual loss (cortical blindness)
- Proximal limb weakness with sparing of the face, hands, and feet
- Determine the time of onset of symptoms: The time of stroke onset is used to determine treatment options (thrombolytic therapy).
- Stabilize the patient if needed.
- Check serum glucose.
- Emergency imaging
- Immediate noncontrast head CT to evaluate for acute hemorrhage prior to administration of thrombolytic therapy
- Further choice of imaging depends on head CT findings.
The decision to obtain further imaging should not delay the administration of thrombolytic therapy in appropriate candidates!
- Ischemic changes can be detected ∼ 6 hours after stroke onset.
- Acute (within 12 hours of symptom onset)
- 12–24 hours after symptom onset: hypodense
- After 24 hours of symptom onset: hyperdense
- Ischemic changes can be detected ∼ 3 minutes after stroke onset, but MRI takes longer to perform.
- T1: hypointense signal
- T2: hyperintense signal
CT angiography (CTA)
- Allows identification of the exact location of the defect (in most cases)
- MRI angiography (MRA): indications similar to CTA
Laboratory evaluation 
- Initial evaluation: serum glucose
- Subsequent laboratory tests to consider (after emergent imaging is complete)
- Hypercoagulable workup: consider if patient is < 50 years old and/or has a history of thrombosis
Additional diagnostic workup
- ECG to rule out atrial fibrillation and myocardial ischemia
- Continuous cardiac rhythm monitoring for paroxysmal atrial fibrillation
- Transthoracic echocardiogram (TTE) and/or transesophageal echocardiogram (TEE) to evaluate for intracardiac thrombus and patent foramen ovale (PFO)
- Carotid ultrasound to evaluate for carotid artery stenosis
For more information on the diagnosis of other stroke types, see .
- General: infarction → liquefactive necrosis → cystic cavity formation
- Two main responses to brain tissue ischemia
- Irreversible neuronal injury begins ∼ 5 minutes after tissue hypoxia
- See .
- Definition: selective destruction of nerve cells with sparing of glial cells
- Transient ischemia → subsequent reperfusion (e.g., resuscitation following cardiac arrest) → increased metabolic demand, release of toxic excitatory neurotransmitters → ischemic injury
- Certain neurons are more susceptible to ischemic injury
- Histology: neuronal necrosis with viable glial cells (which can proliferate and cause a laminar or pseudolaminar tissue architecture)
- Definition: the death of all cell types in a given region of the brain, including neurons, glial cells, and vascular cells
- Mechanism: permanent ischemia
- Histology: cystic lesions and loss of tissue architecture
Histologic changes in the infarcted region 
|Time from start of ischemia||Histologic features|
|> 15 days|| |
- Goal is to prevent further tissue ischemia and irreversible infarction
- Should be administered as soon as possible in eligible candidates (see below for specific indications)
Reperfusion therapy should not be delayed – “time is brain”! However, intracranial hemorrhage is a contraindication for reperfusion therapy and must be ruled out first.
IV thrombolytic therapy 
- Definition: administration of intravenous recombinant tPA (e.g., alteplase, tenecteplase) to break down blood clots
- Intracranial and extracranial hemorrhage
- Current conditions
- Preexisting conditions
Intra-arterial thrombolysis 
- Definition: intra-arterial (not intravenous) administration of a thrombolytic agent (e.g., prourokinase)
- Indication: MCA stroke patients with onset of symptoms < 6 hours who are not eligible for IV thrombolytic therapy
- Definition: physical retrieval of the occluding thrombus via a catheter (usually through the femoral artery)
- Indications: proximal large artery occlusion in anterior cerebral circulation (usually in addition to intravenous thrombolytic therapy)
Blood pressure management 
- Elevated blood pressure is generally tolerated in acute ischemic stroke (permissive hypertension).
- For patients with severe hypertension (> 220 mm Hg / > 120 mm Hg)
- See “Treatment” in .
- Prevent post-stroke complications (see “Complications” in )
- Secondary prevention (see below)
- Early rehabilitation (physiotherapy, occupational and speech therapy) and mobilization
- Determine the time of onset of symptoms and assess score on stroke scale.
- Immediate neurology consult/stroke code
- Establish IV access.
- Immediate head CT without contrast (to rule out hemorrhage)
- Consider further imaging (e.g., MRI or CTA with or without perfusion protocol).
- Evaluate indications and contraindications for thrombolytic therapy.
- If indicated, administer thrombolytic therapy (e.g., alteplase ). 
- Blood pressure management
- Exclude high-grade stenosis of the brain-supplying arteries before reducing blood pressure.
- For patients with severe hypertension (> 220 mm Hg / > 120 mm Hg):
- Preferred agents 
- Evaluate indication for mechanical thrombectomy of proximal vessel occlusion.
- Identify and treat the underlying cause (e.g., TTE if concern for embolic stroke).
- Identify and treat any complications (e.g., seizures, ).
- Admit to neurology or medicine service.
- Make patient NPO and order dysphagia screening.
- Order physical therapy and occupational therapy.
- Close observation, GCS monitoring, and serial neurologic examination
- Euglycemia: Avoid hypoglycemia and hyperglycemia.
- Normothermia: antipyretics for fever
- Normovolemia: IV fluids for hypovolemia
- VTE prophylaxis
- : management of modifiable risk factors to decrease the likelihood of having a first stroke 
- aspirin or clopidogrel) (e.g.,
- Medical management of risk factors
- Medical management and/or carotid endarterectomy for