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ings or prodromal symptoms; headache, dizziness, epistaxis, or other symptoms do not occur with any consistency There is no age predilection except that the average age of occurrence is lower than in thrombotic infarction, and neither sex is more disposed The incidence of hypertensive cerebral hemorrhage is higher in African Americans than in whites and seems recently to have been reported with increasing frequency in Japanese In the majority of cases, the hemorrhage has its onset while the patient is up and active; onset during sleep is a rarity There has long been a notion that acute hypertension precipitates the hemorrhage in some cases This is based on the occurrence of apoplexy at moments of extreme fright or anger or intense excitement, presumably as the blood pressure rises abruptly beyond its chronically elevated level The same has been described in relation to taking sympathomimetic medications such as phenylpropanolamine (Kernan et al), ephedra, or cocaine and to numerous other similar circumstances However, in fully 90 percent of instances, the hemorrhage occurs when the patient is calm and unstressed (Caplan, 1993) The level of blood pressure rises early in the course of the hemorrhage, but the preceding chronic hypertension is usually of the essential type Other causes of hypertension must always be considered renal disease, renal artery stenosis, toxemia of pregnancy, pheochromocytoma, aldosteronism, adrenocorticotropic hormone or corticosteroid excess and, of course, sympathetically active drugs There is ordinarily only one episode of hypertensive hemorrhage; recurrent bleeding from the same site, as happens with saccular aneurysm and arteriovenous malformation, is infrequent However, it is now recognized by serial CT scanning that in many instances, as the patient s condition worsens over a few hours, there may be slight enlargement of the hematoma In the series of Brott and colleagues, one-quarter of hematomas were found to have enlarged in the rst hour and another 12 percent in the rst day Blood that has extravasated into cerebral tissue is absorbed slowly, over a period of months, during which time symptoms and signs recede Hence the neurologic de cit is never transitory in intracerebral hemorrhage, as it so often is in embolism; for the same reason, one does not expect rapid improvement in the neurologic de cit from one examination to another The main types of cerebral hemorrhage are described below Putaminal Hemorrhage The most common syndrome is the one due to putaminal hemorrhage, with extension to the adjacent internal capsule (Fig 34-20) The neurologic symptoms and signs vary slightly with the precise site and size of the extravasation, but hemiplegia from interruption of the capsule is a consistent feature of medium-sized and large clots Vomiting occurs in about half the patients Headache is frequent but not invariable With large hemorrhages, patients lapse almost immediately into a stupor with hemiplegia, and their condition visibly deteriorates as the hours pass More often, however, the patient complains of headache or of some other abnormal cephalic sensation Within a few minutes the face sags on one side, speech becomes slurred or aphasic, the arm and leg gradually weaken, and the eyes tend to deviate away from the side of the paretic limbs These events, occurring gradually over a period of a few minutes to a half hour, are strongly suggestive of intracerebral bleeding The paralysis may worsen; a Babinski sign appears, at rst unilaterally and then bilaterally; the affected limbs become accid; painful stimuli are not appreciated; speaking becomes impossible; and confusion gives way to stupor The most advanced stages are characterized by signs of upper brainstem compression (coma); bilateral Babinski signs; deep, ir-.

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regular, or intermittent respiration; dilated, xed pupils, rst on the side of the clot; and occasionally by decerebrate rigidity The widespread use of CT scanning has disclosed the frequent occurrence of smaller putaminal hemorrhages, which in former times would have been misdiagnosed as embolic or thrombotic ischemic strokes (especially if the CSF was clear) With hemorrhages con ned to the anterior segment of the putamen, the hemiplegia and hyperre exia tend to be less severe and to clear more rapidly (Caplan) There is also prominent abulia, motor impersistence, temporary unilateral neglect, and with left-sided lesions non uent aphasia and dysgraphia With posterior lesions, weakness is also less and is attended by sensory loss, hemianopia, impaired visual pursuit to the opposite side, Wernicke-type aphasia (leftsided lesions), and anosognosia (right-sided) Caplan has also analyzed the effects of relatively pure caudate hematoma Those extending laterally and posteriorly into the internal capsule behave much like large putaminal hemorrhages Those extending medially into the lateral ventricle give rise to drowsiness, stupor, and either confusion and underactivity or restlessness and agitation Thalamic Hemorrhage The central feature here is severe sensory loss on the entire contralateral body If large or moderate in size, thalamic hemorrhage also produces a hemiplegia or hemiparesis by compression or destruction of the adjacent internal capsule (Fig 34-21) The sensory de cit is usually severe and involves all of the opposite side, including the trunk, and may exceed the motor weakness A uent aphasia may be present with lesions of the dominant side, and amorphosynthesis and contralateral neglect with lesions of the nondominant side A homonymous eld defect, if present, usually clears in a few days Thalamic hemorrhage, by virtue of its extension into the sub-

Figure 34-21 CT scan of a left thalamic hemorrhage that caused hemiplegia and hemisensory loss in a hypertensive patient A small amount of blood is seen in the adjacent posterior third ventricle

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