Nontraumatic intracerebral hemorrhage

Ravindra Kumar Garg MD (Dr. Garg of King George's Medical University in Lucknow, India, has no relevant financial relationships to disclose.)
Steven R Levine MD, editor. (

Dr. Levine of the SUNY Health Science Center at Brooklyn has no relevant financial relationships to disclose.

Originally released December 18, 2001; last updated April 6, 2020; expires April 6, 2023

This article includes discussion of nontraumatic intracerebral hemorrhage, acute spontaneous brain hemorrhage, deep intracerebral hemorrhage, intracerebral parenchymal hemorrhage, intracranial hematoma, parenchymal intracerebral hemorrhage, primary intracerebral hemorrhage, and spontaneous intracerebral hemorrhage. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.


Intracerebral hemorrhage is much less common than ischemic stroke but is associated with a significantly high mortality and morbidity. Intracerebral hemorrhage frequently affects the basal ganglia, thalamus, cerebral lobes, pons, and cerebellum. Hypertension, cerebral amyloid angiopathy, and anticoagulation are major causes of intracerebral hemorrhage. Cerebellum emerged as a frequent location of coagulant-associated intracranial hemorrhage. Statins are associated with only marginal risk of intracerebral hemorrhage. Non-vitamin K antagonist oral anticoagulants are associated with lesser frequency of intracerebral hemorrhage to that of smaller size. Alcohol consumption in moderate amounts decreases risk of both lobar and nonlobar intracerebral hemorrhage. Statins are associated with only marginal risk of intracerebral hemorrhage. Carriers of apolipoprotein E2 and E4 have an increased risk of intracerebral hemorrhage in lobar locations, presumably because of the effects of these gene variants on risk of cerebral amyloid angiopathy. Genetic studies identify 1q22 as a susceptibility locus for intracerebral hemorrhage. Hematoma expansion is an accurate predictor of poor outcome of intracerebral hemorrhage. "Spot sign" on CT angiography has been reported to predict hematoma expansion. Strict blood pressure control may prevent further enlargement of hematoma. Anticoagulation-related intracerebral hemorrhage is often fatal, and rapid reversal of anticoagulation is the most effective therapy currently available. Levetiracetam is a preferred drug for seizure control as it has a neuroprotective effect against posthemorrhagic stroke brain injury. Surgical evacuation of hematoma for supratentorial intracerebral hemorrhage was not shown to be beneficial. Considering a high rate of early neurologic deterioration in the first few hours, the American Heart Association recommends identifying patients at high risk of hematoma expansion. There is a substantial risk of incident dementia in dementia-free survivors of spontaneous intracerebral hemorrhage. In this article, the author reviews in detail the different aspects of intracerebral hemorrhage.

Key points


• Intracerebral hemorrhage is a common cause of stroke.


• It results from hypertensive damage to blood vessels, rupture of an aneurysm or arteriovenous malformations, cerebral amyloid angiopathy, altered hemostasis (like thrombolysis and anticoagulation), hemorrhagic necrosis (like tumor and infection), or substance abuse (cocaine).


• Common sites for involvement include the basal ganglia, lobes of cerebral hemispheres, thalamus, pons, cerebellum, and other brainstem sites.


• Computed tomography readily demonstrates acute hemorrhage.


• Initial management is focused on maintaining breathing, circulation, and fluid and electrolyte balance.


• Quick hemostasis to prevent hematoma expansion, surgical removal of clot, removal of intraventricular blood, and prompt blood pressure control improve outcomes.

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