This usually develops over a period of 1 or more hours, and loss of consciousness at the onset is unusual. Repeated vomiting is a prominent feature, with occipital headache, vertigo, and inability to sit, stand, or walk. Often these are the only abnormalities, making it imperative to have the patient attempt to ambulate; otherwise the examination may erroneously seem to be normal. In the early phase of the illness other clinical signs of cerebellar disease are usually minimal or lacking; only a minority of cases shows nystagmus or cerebellar ataxia of the limbs, although these signs must always be sought. A mild ipsilateral facial weakness, diminished corneal reflex, paresis of conjugate lateral gaze to the side of the hemorrhage, or an ipsilateral sixth-nerve weakness occur with larger hemorrhages that compress the pons or extend into the cerebellar peduncle. Dysarthria and dysphagia may be prominent in some cases but usually are absent. Other infrequent ocular signs include blepharospasm, involuntary closure of one eye, skew deviation, “ocular bobbing,” and small, often unequal pupils that continue to react until very late in the illness. Contralateral hemiplegia and ipsilateral facial weakness occur if there is marked displacement and compression of the medulla against the clivus.
Occasionally at the onset there is a spastic paraparesis or a quadriparesis with preservation of consciousness. The plantar reflexes are flexor in the early stages but extensor later. When these signs occur, hydrocephalus is usually found and may require drainage. In the series collected by St. Louis and colleagues, patients with vermian clots and hydrocephalus were at the highest risk for rapid deterioration. As the hours pass, and occasionally with unanticipated suddenness, the patient becomes stuporous and then comatose or suddenly apneic as a result of brainstem compression, at which point reversal of the syndrome, even by surgical therapy, is seldom successful. As discussed further on, cerebellar hemorrhage is the most amenable to surgical evacuation with good results. A typical case is shown with imaging in Fig. 33-24D.
Bleeding in areas other than those listed above, specifically in the subcortical white matter of one of the lobes of the cerebral hemisphere, is not associated strictly with hypertension. Any number of other causes are usually responsible, the main ones being anticoagulation or thrombolytic therapy, acquired coagulopathies, cranial trauma, arteriovenous malformation (discussed further on), trauma, and, in the elderly, amyloidosis of the cerebral vessels. The role of antiplatelet agents in precipitating intracerebral hemorrhage has been a matter of contention with numerous surveys and studies giving divergent results regarding larger, expanding or more clinically destructive hematomas.
Most lobar hemorrhages are spherical or ovoid, but a few follow the contour of the subcortical white matter tracts and take the form of a slit (subcortical slit hemorrhage). It is our impression that many of these are the result of a bleeding diathesis, such as thrombocytopenia.