There has long been a notion that acute hypertension can precipitate the hemorrhage. This is based on the anecdotal occurrence of cerebral hemorrhage at moments of extreme fright or anger or intense excitement, presumably as the blood pressure rises abruptly beyond its chronically elevated level. Similarly, hemorrhages have been described in relation to taking sympathomimetic medications such as phenylpropanolamine (Kernan et al), ephedra, or cocaine, and to numerous other hypertensive circumstances. However, in fully 90 percent of instances, the hemorrhage occurs when the patient is calm and unstressed, according to 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. Nonetheless, causes of hypertension must always be considered—renal disease, renal artery stenosis, eclampsia, pheochromocytoma, hyperaldosteronism, adrenocorticotropic hormone or corticosteroid excess and, of course, sympathetically active drugs as mentioned.
It has been recognized by serial CT that in many instances, there is enlargement of the hematoma. In the series reported by Brott and colleagues (1997), 25 percent were found to have enlarged in the first hour and another 12 percent in the first day. Contrast extravasation into the adjacent brain after CTA was associated in a retrospective study with expansion of a hematoma, the aforementioned “spot sign” (Goldstein et al), but there are no other clear predictive factors of expansion of the clot. Blood in cerebral tissue is absorbed slowly over months during which time symptoms and signs recede. Hence the neurologic deficit is never transitory in intracerebral hemorrhage, as it so often is in TIA or embolism.
The main types and locations of cerebral hemorrhage are described below and shown in Fig. 33-24. Chronic hypertension is associated with bleeding into the putamen, thalamus, pons, and cerebellum. Intracerebral bleeding at other sites, “lobar hemorrhages,” has numerous causes.
The most common syndrome is the one caused by putaminal hemorrhage with extension to the adjacent internal capsule (see Fig. 33-24A). 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. As often, there is headache or some other abnormal cephalic sensation. Within a few minutes or less the face sags on one side, speech becomes slurred or aphasic, the arm and leg weaken and are flaccid, and the eyes tend to deviate away from the side of the paretic limbs. These events, occurring gradually over a period of several minutes or more, are strongly suggestive of intracerebral bleeding. More advanced stages are characterized by signs of upper brainstem compression (coma); bilateral Babinski signs; irregular or intermittent respiration; dilated, fixed pupils, first on the side of the clot; and decerebrate rigidity.