A stroke is an acute neurologic condition resulting from a disruption in cerebral perfusion, either due to ischemia (ischemic strokes) or hemorrhage (hemorrhagic strokes). Hemorrhagic strokes are further classified as intracerebral or subarachnoid. Systemic hypertension and other cardiovascular diseases are common risk factors for both ischemic and hemorrhagic strokes. Clinically, strokes are characterized by the acute onset of focal neurologic deficits, including hemiparesis, paresthesias, and hemianopsia. The pattern of clinical features is dictated by the affected vessel. Distinguishing between ischemic and hemorrhagic strokes based on physical examination is difficult and requires initial evaluation with a noncontrast head CT. Further neurovascular imaging may be required before deciding on treatment options. In ischemic strokes, immediate revascularization of the affected vessel is vital to preserve brain tissue and prevent further damage. Hemorrhagic strokes are treated with supportive measures and neurosurgical evacuation of blood. Long-term management of all types of stroke focuses on the management of modifiable risk factors (i.e., hypertension and atherosclerosis).
For more information, see respective articles “Ischemic stroke,” “Intracerebral hemorrhage,” and “Subarachnoid hemorrhage.”
- 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
The following table focuses on nontraumatic cerebral ischemia and intracranial hemorrhage.
|Ischemic stroke||Intracerebral hemorrhage||Subarachnoid hemorrhage|
|Epidemiology|| || || |
|Etiology|| || || |
|Risk factors|| || || |
|Clinical features|| || || |
|Findings on noncontrast head CT|| || || |
|Treatment|| || || |
For both ischemic and hemorrhagic strokes, age is the most important nonmodifiable risk factor and arterial hypertension is the most important modifiable risk factor.
- Stroke is the fourth leading cause of death and the leading cause of disability in the US. 
- Stroke is responsible for ∼ 5% of deaths in the US. 
- See ischemic stroke, intracerebral hemorrhage, and subarachnoid hemorrhage for specific risk factors.
Epidemiological data refers to the US, unless otherwise specified.
- Ischemic stroke (∼ 85%)
Hemorrhagic stroke (∼ 15%)
- Intracerebral hemorrhage (∼ 10%)
- Subarachnoid hemorrhage (∼ 5%)
Stroke symptoms by affected vessel
|Clinical features of stroke by affected vessel|
|Affected vessel||Clinical features |
Middle cerebral artery (MCA) (most commonly affected vessel)
|Anterior cerebral artery (ACA)|| |
|Posterior cerebral artery (PCA)|| |
|Posterior inferior cerebellar artery|| |
|Anterior inferior cerebellar artery|| |
|Lenticulostriate arteries (penetrating arteries)|| |
|Basilar artery|| |
|Extracranial arteries||Internal carotid artery|| |
|Common carotid artery|
|Vertebral artery|| |
|Anterior spinal artery|| |
Stroke symptoms by affected region
Lacunar syndromes 
- Lacunar strokes most commonly occur in ischemic stroke but can also arise as a result of microbleeds
- There are no cortical signs (e.g., neglect, aphasia, visual field loss) in any of the types of lacunar stroke.
|Overview of lacunar strokes|
|Lacunar stroke type||Location||Clinical features|
|Pure motor stroke|| |
|Pure sensory stroke|| || |
|Sensorimotor stroke|| || |
|Ataxic hemiparesis|| || |
|Dysarthria-clumsy hand syndrome|| || |
|Hemiballismus|| || |
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.
Brainstem syndromes 
- Brainstem syndromes involve the cranial nerves and/or their nuclei (produce symptoms ipsilaterally to the lesion) and major brainstem tracts (produce symptoms contralaterally to the lesion unless they are uncrossed or double-crossed).
- Disruption of reticular activating system, if present, results in decreased level of consciousness or coma.
Midbrain syndromes 
|Overview of midbrain syndromes|
|Syndrome||Affected vessel||Affected structures||Resulting symptom|
|Ventral midbrain syndrome (Weber syndrome)|| |
|Paramedian midbrain syndrome (Benedikt syndrome)|| |
|Dorsal midbrain syndrome (Parinaud syndrome)|| || || |
|Nothnagel syndrome|| |
|Overview of pontine syndromes|
|Syndrome||Affected vessel||Affected structures||Resulting symptom|
Ventral pontine syndrome (Millard-Gubler syndrome)
|Lateral pontine syndrome (Marie-Foix syndrome)|| || |
| || |
| || |
|Inferior medial pontine syndrome (Foville syndrome)|| |
|Locked-in syndrome|| |
Facial droop means AICA has swooped: involvement of facial nuclei (not the facial nerve as in other pontine syndromes) is characteristic of AICA stroke.
To remember the cause and the symptoms of the lateral medullary syndrome: Try not to pick a (PICA) horse (hoarseness) that can't eat (dysphagia).
Clinical features of strokes affecting other regions
|Overview of clinical features of strokes affecting other regions|
|Location of lesion||Clinical features |
|Watershed border-zone|| |
- Primary survey
Clinical assessment and history
- Identify risk factors for ischemic stroke or risk factors for hemorrhagic stroke, including the presence of carotid bruits.
- Identify signs (above) that indicate the affected vessel and/or region of the brain.
- Determine the time of onset of symptoms (e.g., “last known normal”): The time of stroke onset determines whether thrombolytic therapy is an option (see below).
- Noncontrast head CT to evaluate for acute hemorrhage
- Diffusion-weighted MRI to detect acute ischemia
- Consider further neurovascular imaging depending on the type of stroke
Noncontrast head CT (first-line imaging)
- Allows for detection of acute hemorrhage
- Allows for detection of ischemic changes that occur after 6–24 hours (cannot be used to reliably identify earlier ischemia)
- Indicated in all patients suspected of having an acute stroke to rule out intracranial hemorrhage before administering thrombolytic therapy
- Allows identification of ischemia earlier than a CT (within 3–30 minutes after onset) 
- Allows detection of hyperacute hemorrhage
- Evaluates reversibility of ischemic injury
- Perfusion-weighted imaging (PWI): visualizes areas of decreased perfusion and allows quantification of perfusion parameters, e.g., mean transit time (MTT), cerebral blood flow (CBF) and cerebral blood volume (CBV)
- Perfusion-diffusion mismatch MRI: allows identification of the penumbra (or “tissue-at-risk”)
- See ischemic stroke, subarachnoid hemorrhage, and intracerebral hemorrhage for specific imaging findings and other modalities.
- Initial: serum glucose
- Complete blood count, electrolytes
- Coagulation parameters (e.g., INR, PTT)
- Urine drug screen for recreational substances (e.g., cocaine), blood alcohol level
- Serum troponin
Laboratory studies should not delay imaging for patients with acute stroke. 
- Alcohol withdrawal
- Drug intoxication (e.g., heroin, barbiturates)
- Osmotic demyelination syndrome
- Paraneoplastic syndromes/autoimmune disorders
The differential diagnoses listed here are not exhaustive.
- See ischemic stroke, subarachnoid hemorrhage, and intracerebral hemorrhage for specific management.
If symptoms of a suspected ischemic stroke began less than 4.5 hours prior to presentation and there are no signs of intracranial bleeding, begin reperfusion therapy immediately.
Stabilization and monitoring 
See “Secondary brain injury and neuroprotective measures.”
- Maintain euvolemia with fluid replacement as needed.
- Maintain a sufficient oxygen supply and consider intubation if the patient shows signs of increased intracranial pressure (e.g., altered mental state).
- Maintain euglycemia (e.g., blood glucose levels within 140–180 mg/dL).
- Maintain normothermia (e.g., antipyretics).
- Cardiac monitoring (for at least 24 hours)
- Maintain a normal acid-base status.
- Electrolyte repletion as needed
- Analgesia as needed
- Monitor for signs of elevated intracranial pressure (see elevated intracranial pressure and brain herniation).
- Seizures should be treated pharmacologically.
- Evaluate for dysphagia.
Blood pressure management 
- Always treat hypotension (e.g., with fluid replacement, vasopressors).
Ischemic stroke: permissive hypertension
- See “Treatment” in “Ischemic stroke.”
- Only treat severe hypertension (> 220 systolic pressure and/or 120 mm Hg diastolic pressure).
- Reduce systolic blood pressure to approx. 140–160 mm Hg.
- See “Treatment” sections in ”Subarachnoid hemorrhage” and “Intracerebral hemorrhage.”
Nitrates should be avoided because they can increase intracranial pressure.
- Aspiration pneumonia
- Cardiac dysfunction (arrhythmias, myocardial infarction)
- Deep vein thrombosis and pulmonary embolism
- Urinary tract infections
- Bleeding (e.g., gastrointestinal bleeding)
- Poststroke bone fractures
Neurologic complications 
- Elevated intracranial pressure and brain herniation (Cushing triad)
- Syndrome of inappropriate secretion of antidiuretic hormone (SIADH)
- Persistent neurologic deficits (hemiparesis, aphasia) and disability 
Central poststroke pain 
- Affects < 10% of all stroke patients
- Can occur with thalamic lesions
- Unilateral facial pain and/or extremity pain associated with previous stroke
- Contralateral or ipsilateral initial paresthesia followed by neuropathic pain (e.g., allodynia, dysesthesia)
- Neuropathic pain
Hemorrhagic transformation: occurrence of hemorrhage in the same region as previous ischemia 
- Onset: usually 1–2 days after the inciting ischemic event
- Risk factors: thrombolytic medications (e.g., alteplase), antiplatelet therapy (e.g., aspirin, clopidogrel), and/or thrombosis prophylaxis (e.g., heparin, enoxaparin) within 24 hours of ischemic injury
- Management: discontinuation of anticoagulation and/or antiplatelet therapy, admission to a neurointensive care unit, and neuroprotective measures
- Vascular dementia
- Vasospasm (typically occurs 5–7 days after SAH) → ischemic stroke
- Recurrent hemorrhage
- Intraventricular hemorrhage
We list the most important complications. The selection is not exhaustive.
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Stroke prevention focuses on reducing modifiable risk factors and treating conditions that increase the risk of cerebrovascular ischemia and/or hemorrhage. In patients with risk factors for both ischemic and hemorrhagic stroke, the risks and benefits of each prevention strategy should be carefully weighed.
- General preventive measures (all stroke subtypes): Reduce modifiable risk factors for atherosclerosis. 
- Ischemic stroke prevention
Hemorrhagic stroke prevention: Address the risk of bleeding and risk factors for cerebral small vessel disease. 
- Optimize management of hypertension. 
- If possible, avoid medications that increase bleeding risk in patients with known cerebral small vessel disease.
- Avoid aspirin for primary prevention of ischemic stroke. 
- In patients with Afib , use DOACs instead of vitamin K antagonists or consider left atrial appendage closure. 
The two main modifiable risk factors for the primary prevention of hemorrhagic stroke are hypertension and the use of anticoagulants. 
Prevention of stroke recurrence
- Ischemic stroke: See “Secondary prevention of ASCVD.”
- Manage hypertension and address lifestyle risk factors.
- Treat hypercholesterolemia.
- Statin therapy increases the risk of recurrent hemorrhagic stroke but is nonetheless typically indicated. 
- PCSK9 inhibitors can be considered as an alternative. 
- Avoid long-term use of NSAIDs and use SSRIs with caution. 
Individuals often have overlapping risk factors for both ischemic stroke and hemorrhagic stroke; assess recurrence risk with a thorough history and examination, laboratory studies, and possibly imaging.