Pathophysiology And Pathology Intracerebral hemorrhage usually results from spontaneous rupture of a small penetrating artery deep in the brain. The most common sites are (1) the basal ganglia (putamen, thalamus, and adjacent deep white matter), (2) the deep cerebellum, and (3) the pons. When hemorrhages occur in other brain areas or in nonhypertensive patients, greater consideration should be given to hemorrhagic disorders, neoplasms, and other causes. The small arteries in these areas seem most prone to hypertension-induced vascular injury. The leak may be small, or a large clot may form and compress adjacent tissue, causing herniation and death. Rupture or seepage into the ventricular system often occurs. Primary intraventricular hemorrhage is rare. If the patient survives, the clot liquefies, is absorbed, and leaves only a small residual cleft. Most hypertensive intracerebral hemorrhages develop over 30 to 90 min, whereas those associated with anticoagulant therapy may evolve for as long as 24 to 48 h. Once bleeding stops, it generally does not start again. Within 48 h macrophages begin to phagocytize the hemorrhage at its outer surface. After 1 to 6 months, the hemorrhage is generally resolved to a slitlike orange cavity lined with glial scar and hemosiderin-laden macrophages.
Clinical Manifestations Although not particularly associated with exertion, intracerebral hemorrhages almost always occur while the patient is awake and sometimes when stressed. The clinical presentation is generally that of an abrupt onset of a focal neurologic deficit that typically worsens steadily over 30 to 90 min. The common clinical presentations are shown in Table 366-6 . The putamen is the most common site for hypertensive hemorrhage , and the adjacent internal capsule is invariably damaged. Contralateral hemiparesis is therefore the sentinel sign. When mild, the face sags on one side, speech becomes slurred, the arm and leg gradually weaken, and the eyes deviate away from the side of the hemiparesis. The paralysis may worsen until the affected limbs become flaccid or extend rigidly with a Babinski sign on the same side. When hemorrhages are large, drowsiness gives way to stupor as signs of upper brainstem compression appear. Coma ensues, accompanied by deep, irregular, or intermittent respiration; a dilated and fixed ipsilateral pupil; bilateral Babinski signs; and decerebrate rigidity. In milder cases, edema in adjacent brain tissue may cause progressive deterioration over 12 to 72 h. Thalamic hemorrhages also produce a hemiplegia or hemiparesis from pressure on, or dissection into, the adjacent internal capsule. A prominent sensory deficit involving all modalities is usually present. Aphasia, often with preserved verbal repetition, may occur after hemorrhage into the dominant (left) thalamus, and apractognosia or mutism occurs in some cases of nondominant hemorrhage . There also may be a transient homonymous visual field defect. Thalamic hemorrhages cause several typical ocular disturbances by virtue of extension medially into the upper midbrain. These include deviation of the eyes downward and inward so that they appear to be looking at the nose, unequal pupils with absence of light reaction, skew deviation with the eye opposite the hemorrhage displaced downward and medially, ipsilateral Horner's syndrome, absence of convergence, paralysis of vertical gaze, and retraction nystagmus. In pontine hemorrhages, deep coma with quadriplegia usually occurs over a few minutes. There is often prominent decerebrate rigidity and &quot;pin-point&quot; (1 mm) pupils that react to light. There is impairment of reflex horizontal eye movements evoked by head turning (doll's-head or oculocephalic maneuver) or by irrigation of the ears with ice water (see Chap. 24 ). Hyperpnea, severe hypertension, and hyperhidrosis are common. Death usually occurs within a few hours, but there are exceptional survivors. Cerebellar hemorrhages usually develop over several hours and are characterized by occipital headache, repeated vomiting, and ataxia of gait. In mild cases there may be no other neurologic signs; therefore it is imperative to test gait. Dizziness or vertigo may be prominent. There is often paresis of conjugate lateral gaze toward the side of the hemorrhage , forced deviation of the eyes to the opposite side, or an ipsilateral sixth nerve palsy. Less frequent ocular signs include blepharospasm, involuntary closure of one eye, ocular bobbing, and skew deviation. There may be little or no evidence of the usual signs of cerebellar disease, and only a minority of patients show nystagmus or limb ataxia. A mild ipsilateral facial weakness and a diminished corneal reflex are common. Dysarthria and dysphagia may occur. There are no Babinski signs until late in the evolution of the hemorrhage as it compresses or dissects into the ventral brainstem. As the hours pass, the patient often becomes stuporous and then comatose from brainstem compression. In summary, ocular signs have been highlighted as a method of rapidly localizing hemorrhages. In putamenal hemorrhage , the eyes are deviated to the side opposite the paralysis; in thalamic hemorrhage , the eyes are deviated downward and the pupils may be 2 to 3 mm and minimally reactive; in pontine hemorrhage , the reflex lateral eye movements are impaired and the pupils are 1 mm yet reactive; and in cerebellar hemorrhage , the eyes may be deviated laterally (to the side opposite the lesion) in the absence of paralysis.
TREATMENT Prevention Hypertension is the leading cause of primary cerebral hemorrhage . Prevention is primarily aimed at reducing hypertension, excessive alcohol use, and use of illicit drugs such as cocaine and amphetamines. Acute Management Approximately 75 percent of patients with a hypertensive intracerebral hemorrhage die. The size and location of the hematoma determine the prognosis. Supratentorial hematomas 5 cm in largest diameter have a poor prognosis, and infratentorial pontine hematomas 3 cm are usually fatal. Except possibly in patients with a bleeding disorder, nothing can be done about the hemorrhage itself. Treating severe hypertension seems reasonable, but harmful hypotension is a risk. Generally, the bleeding has stopped by the time the patient comes under medical care. General measures for treating intracranial hypertension secondary to mass effect are warranted. Evacuation of the hematoma usually is not helpful, except in cerebellar hemorrhages. For cerebellar hemorrhages, a neurosurgeon should be consulted immediately to assist with the evaluation, with a view to possible surgery. Most hematomas 3 cm in diameter will require surgical evacuation. If the patient is alert without focal brainstem signs and if the hematoma is 1 cm in diameter, surgical removal usually will not be necessary. Patients with hematomas between 1 and 3 cm require careful observation for signs of impaired consciousness, which usually mean surgery is required. If a patient survives the initial hemorrhage without signs of severe brain injury and subsequently fails to improve or insidiously worsens, surgical evacuation of the hematoma also should be considered. Tissue surrounding hematomas is displaced and compressed but not necessarily infarcted. Hence, in survivors, major improvement commonly results as the hematoma is reabsorbed and the adjacent tissue regains its function. Careful management of the patient during the acute phase of the hemorrhage can lead to considerable recovery. Mannitol and other osmotic agents reduce intracranial pressure that has been raised by the volume of the hematoma and edema (see Chap. 374 ). Glucocorticoids are not helpful for the edema from intracerebral hematoma. Both excessive hypo- and hypertension associated with acute hemorrhage should be treated cautiously to avoid excessive or precipitous blood pressure changes.
LOBAR INTRACEREBRAL HEMORRHAGE Pathophysiology And Pathology As control of hypertension in the general population has improved, the relative proportion of hemorrhages outside the basal ganglia and thalamus has increased. These &quot;lobar hemorrhages&quot; appear on CT scan as oval or circular clots in the subcortical white matter. The role of chronic hypertension in their genesis is controversial, but many occur without a history of increased blood pressure. A number of other underlying conditions are found in many cases. Cerebral amyloid angiopathy is a disease of the elderly in which arteriolar degeneration occurs and amyloid is deposited in the walls of the cerebral arteries, but not elsewhere in the body. Amyloid angiopathy causes both single and recurrent lobar hemorrhages and is probably the commonest cause of lobar hemorrhage in the elderly. This disorder can be diagnosed only by postmortem demonstration of Congo red staining of amyloid in cerebral vessels. Patients may have multiple hemorrhages over several months or years. Rarely, genetic causes are found as in mutation of the amyloid precursor peptide (see Chap. 363 ). Other causes are bleeding diatheses (often associated with warfarin administration), AVM , aneurysm, and tumor (often a melanoma or glioma). Often the cause remains undetermined even after extensive study, though amyloid angiopathy can not be excluded in the absence of brain histology. Some lobar hemorrhages may result from AVMs or venous angiomas that are obliterated by the hemorrhage or are angiographically occult.