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pathologic basis for hemorrhage is probably the presence of microaneurysms that develop on perforating vessels of 100 300 mcm in diameter in hypertensive patients Hypertensive intracerebral hemorrhage occurs most frequently in the basal ganglia and less commonly in the pons, thalamus, cerebellum, and cerebral white matter Hemorrhage may extend into the ventricular system or subarachnoid space, and signs of meningeal irritation are then found Hemorrhages usually occur suddenly and without warning, often during activity In addition to its association with hypertension, nontraumatic intracerebral hemorrhage may occur with hematologic and bleeding disorders (eg, leukemia, thrombocytopenia, hemophilia, or disseminated intravascular coagulation), anticoagulant therapy, liver disease, cerebral amyloid angiopathy, high alcohol intake, and primary or secondary brain tumors There is also an association with advancing age and male sex Bleeding is primarily into the subarachnoid space when it occurs from an intracranial aneurysm or arteriovenous malformation (see below), but it may be partly intraparenchymal as well In some cases, no specific cause for cerebral hemorrhage can be identified

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Neurologic management is generally conservative and supportive, regardless of whether the patient has a profound deficit with associated brainstem compression, in which case the prognosis is grim, or a more localized deficit not causing increased intracranial pressure or brainstem involvement Such therapy may include ventilatory support, blood pressure regulation, seizure prophylaxis, control of fever, osmotherapy, and nutritional supplementation Intracranial pressure may require monitoring Ventricular drainage may be required in patients with intraventricular hemorrhage and acute hydrocephalus Decompression may be helpful when a superficial hematoma in cerebral white matter is exerting a mass effect and causing incipient herniation In patients with cerebellar hemorrhage, prompt surgical evacuation of the hematoma is appropriate, because spontaneous unpredictable deterioration may otherwise lead to a fatal outcome and because operative treatment may lead to complete resolution of the clinical deficit The treatment of underlying structural lesions or bleeding disorders depends on their nature Randomized trials of recombinant activated factor VII given within a few hours of onset are in progress, and preliminary reports are encouraging

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Mayer SA et al Treatment of intracerebral haemorrhage Lancet Neurol 2005 Oct;4(10):662 72 [PMID: 16168935]

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With hemorrhage into the cerebral hemisphere, consciousness is initially lost or impaired in about one-half of patients Vomiting occurs very frequently at the onset of bleeding, and headache is sometimes present Focal symptoms and signs then develop, depending on the site of the hemorrhage With hypertensive hemorrhage, there is generally a rapidly evolving neurologic deficit with hemiplegia or hemiparesis A hemisensory disturbance is also present with more deeply placed lesions With lesions of the putamen, loss of conjugate lateral gaze may be conspicuous With thalamic hemorrhage, there may be a loss of upward gaze, downward or skew deviation of the eyes, lateral gaze palsies, and pupillary inequalities Cerebellar hemorrhage may present with sudden onset of nausea and vomiting, disequilibrium, headache, and loss of consciousness that may terminate fatally within 48 hours Less commonly, the onset is gradual and the course episodic or slowly progressive clinical features suggesting an expanding cerebellar lesion In yet other cases, however, the onset and course are intermediate, and examination shows lateral conjugate gaze palsies to the side of the lesion; small reactive pupils; contralateral hemiplegia; peripheral facial weakness; ataxia of gait, limbs, or trunk; periodic respiration; or some combination of these findings

Sudden severe headache Signs of meningeal irritation usually present Obtundation is common Focal deficits frequently absent

Between 5% and 10% of strokes are due to subarachnoid hemorrhage Although hemorrhage is usually from rupture of an aneurysm or arteriovenous malformation, no specific cause can be found in 20% of cases

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CT scanning (without contrast) is important not only in confirming that hemorrhage has occurred but also in determining the size and site of the hematoma It is superior to MRI for detecting intracranial hemorrhage of less than 48 hours duration If the patient s condition permits further intervention, cerebral angiography may be undertaken thereafter to determine whether an aneurysm or arteriovenous malformation is present (see below)

Subarachnoid hemorrhage has a characteristic clinical picture Its onset is with sudden headache of a severity never experi-

enced previously by the patient This may be followed by nausea and vomiting and by a loss or impairment of consciousness that can either be transient or progress inexorably to deepening coma and death If consciousness is regained, the patient is often confused and irritable and may show other symptoms of an altered mental status Neurologic examination generally reveals nuchal rigidity and other signs of meningeal irritation, except in deeply comatose patients A focal neurologic deficit is occasionally present and may suggest the site of the underlying lesion

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