Nontraumatic intracerebral hemorrhage is also known as or subsumes Acute spontaneous brain hemorrhage and Intracranial hematoma. -ed.
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. 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. Hematoma expansion is an accurate predictor of poor outcome of intracerebral hemorrhage. Hematoma volumes are substantially larger in patients who are older than 70 years. A newly-described "spot sign" on CT angiography has been reported to predict hematoma expansion. Strict blood pressure control may prevent further enlargement of hematoma. The hemostatic agent recombinant activated factor VII (rFVIIa) had been shown to reduce hematoma growth but this agent did not improve survival or functional outcome. Anticoagulation-related intracerebral hemorrhage is often fatal, and rapid reversal of anticoagulation is the most effective therapy available. Surgical evacuation of hematoma for supratentorial intracerebral hemorrhage was not shown to be beneficial in a large randomized trial of 1033 patients. Endoscopic hematoma evacuation may provide the quick, adequate decompression of intracerebral hemorrhage. In this clinical summary, Dr. Ravindra Kumar Garg, Professor of Neurology at Chhatrapati Shahuji Maharaj Medical University, Uttar Pradesh in Lucknow, India, reviews in detail the different aspects of intracerebral hemorrhage.