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thalamus and high midbrain, may cause a series of ocular disturbances pseudo-abducens palsies with one or both eyes turned asymmetrically inward and slightly downward, palsies of vertical and lateral gaze, forced deviation of the eyes downward, inequality of pupils with absence of light reaction, skew deviation with the eye ipsilateral to the hemorrhage assuming a higher position than the contralateral eye, ipsilateral ptosis and miosis (Horner syndrome), absence of convergence, retraction nystagmus, and tucking in (retraction) of the upper eyelids Extension of the neck may be observed Compression of the adjacent third ventricle leads to enlargement of the lateral ventricles, and this requires temporary drainage of the ventricles in a small proportion of patients Small and moderate-sized hemorrhages that rupture into the third ventricle are seemingly associated with fewer neurologic de cits and better outcomes, but early hydrocephalus is almost invariable Pontine Hemorrhage Here deep coma usually ensues in a few minutes, and the clinical picture is dominated by total paralysis, decerebrate rigidity, and small (1-mm) pupils that react to light Lateral eye movements, evoked by head turning or caloric testing, are impaired or absent Death usually occurs within a few hours, but there are rare exceptions in which consciousness is retained and the clinical manifestations indicate a smaller lesion in the tegmentum of the pons (disturbances of lateral ocular movements, crossed sensory or motor disturbances, small pupils, and cranial nerve palsies) in addition to signs of bilateral corticospinal tract involvement A small number of our patients with small tegmental hemorrhages and blood in the CSF have survived, with good functional recovery In a series of 60 patients with pontine hemorrhage reviewed by Nakajima, 19 survived (8 of these had remained alert) Similarly, Wijdicks and St Louis reported that 21 percent made a good recovery mostly those who were alert on admission Cerebellar Hemorrhage This usually develops over a period of one to several hours, and loss of consciousness at the onset is unusual Repeated vomiting is a prominent feature, along 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 stand and walk; otherwise the examination may be falsely normal In the early phase of the illness, other clinical signs of cerebellar disease may be minimal or lacking; only a minority of cases show nystagmus or cerebellar ataxia of the limbs, although these signs must always be sought A mild ipsilateral facial weakness and a diminished corneal re ex are common Dysarthria and dysphagia may be prominent in some cases but usually are absent Contralateral hemiplegia and ipsilateral facial weakness do not occur unless there is displacement and compression of the medulla against the clivus There is often paresis of conjugate lateral gaze to the side of the hemorrhage, forced deviation of the eyes to the opposite side, or an ipsilateral sixth nerve weakness Vertical eye movements are retained Other 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 Occasionally, at the onset, there is a spastic paraparesis or a quadriparesis with preservation of consciousness The plantar re exes are exor in the early stages but extensor later When these signs occur, hydrocephalus is present and may require drainage In the series of St Louis et al, those with vermian clots and hydrocephalus were at the highest risk for deterioration As the hours pass, and occasionally with unanticipated suddenness, the patient becomes stuporous and then comatose or suddenly apneic as a re-.

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sult of brainstem compression, at which point reversal of the syndrome, even by surgical therapy, is seldom successful Lobar Hemorrhage Bleeding in areas other than those listed above, speci cally in the subcortical white matter of one of the lobes of hemisphere, is not associated strictly with hypertension; it is presented here for ease of exposition Any number of other causes are usually responsible, the main ones being anticoagulation or thrombolytic therapy, arteriovenous malformation (discussed further on), trauma, and, in the elderly, amyloidosis of the cerebral vessels In a series of 26 cases of lobar hemorrhage, we found 11 to lie within the occipital lobe (with pain around the ipsilateral eye and a dense homonymous hemianopia); 7 in the temporal lobe (with pain in or anterior to the ear, partial hemianopia, and uent aphasia); 4 in the frontal lobe (with frontal headache and contralateral hemiplegia, mainly of the arm); and 3 in the parietal lobe (with anterior temporal headache and hemisensory de cit contralaterally) (Ropper and Davis) The smaller hematomas simulate an embolic stroke in the same territory The occurrence of a progressively worsening headache, vomiting, and drowsiness in conjunction with any one of these syndromes is virtually diagnostic, and, of course, a lobar hemorrhage is readily corroborated by an unenhanced CT scan Of our 26 patients, 14 had had normal blood pressure, and in several of the fatal cases there was amyloidosis of the affected vessels (see further on) Also, 2 patients were receiving anticoagulants, 2 had an arteriovenous malformation, and 1 had a metastatic tumor In a series of 22 patients with lobar clots reported by Kase and colleagues, 55 percent were normotensive; metastatic tumors, arteriovenous malformations, and blood dyscrasias were found in 14, 9, and 5 percent of the patients, respectively The role of amyloid angiopathy in lobar hemorrhage in the elderly patient is discussed further on In the localization of an intracerebral hemorrhage, ocular signs are particularly important In putaminal hemorrhage, the eyes are deviated to the side opposite the paralysis; in thalamic hemorrhage, the commonest ocular abnormality is downward deviation of the eyes and the pupils may be unreactive; in pontine hemorrhage, the eyeballs are xed and the pupils are tiny but reactive; and in large cerebellar hemorrhage, the eyes are deviated laterally to the side opposite the lesion and ocular bobbing may occur Although the proper interpretation of this array of clinical data allows the correct diagnosis to be established in most cases, the ancillary examinations described below are de nitive, especially in the diagnosis of small hemorrhages Laboratory Findings Among laboratory methods for the diagnosis of intracerebral hemorrhage, the CT scan occupies the foremost position This procedure has proved totally reliable in the detection of hemorrhages that are 10 cm or more in diameter Smaller pontine hemorrhages are visualized with less certainty At the same time, coexisting hydrocephalus, tumor, cerebral swelling, and displacement of the intracranial contents are readily appreciated MRI is particularly useful for demonstrating brainstem hemorrhages and residual hemorrhages, which remain visible long after they can no longer be seen by the CT scan (after 4 to 5 weeks) Hemosiderin and iron pigment have their own characteristic appearances, as described earlier In general, lumbar puncture is ill advised, for it may precipitate or aggravate an impending shift of central structures and herniation The white cell count in the peripheral blood may rise tran-.

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