A cute hydrocephalus after subarachnoid hemorrhage is not uncommon. The frequency depends on the criteria used for the diagnosis and ranges from 9%' to 67%.2 In a consecutive series of 174 subarachnoid hemorrhage patients admitted within 72 hours after the initial hemorrhage to the University Hospital Rotterdam's Department of Neurology, computed tomography (CT scanning) showed ventricular enlargement (defined as a bicaudate index exceeding the 95th percentile for age) in 20%. 3The decision to treat acute hydrocephalus may be difficult to make for several reasons. First, impaired consciousness on admission may result from either

Degos' disease, a rare multisystem vasculopathy of unknown etiology, only occasionally involves the nervous system. We report the Mayo Clinic experience of the neurologic features of Degos' disease in a series of 15 patients. All 15 patients had the typical skin lesions of Degos' disease, confirmed by skin biopsy. Ten patients developed neurologic manifestations including fatal hemorrhagic or ischemic strokes (n=5), disabling polyradiculoneuropathy (n=1), and nonspecific neurologic symptoms without objective findings (n=4). Results of laboratory tests varied but none were pathognomonic of the disease. Long-term follow-up revealed death in six patients; nine patients were nearly asymptomatic. Immunosuppressive and antiplatelet agents were not of benefit. CNS infarcts and hemorrhages with intravascular thrombi, but without evidence of vasculitis, were characterized features at autopsy.

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Cerebral aspergillosis is an important cause of mortality in organ transplant recipients and is typically associated with concomitant pulmonary infection. 1 Herein we describe two patients with insidious Aspergillus sinusitis leading to catastrophic CNS infection. Case reports Patient 1A 56-year-old man with pancreas and kidney transplant was transferred to our tertiary care facility with meningoencephalitis and cerebral infarction. He had a history of new onset headache of 6 weeks with fever. His immunosuppressive regimen consisted of mycophenolate mofetil, prednisone, and tacrolimus with prophylactic sulfamethoxazole/ trimethoprim and valganciclovir. He had a temperature of 38.9 °C, opened eyes to voice only but followed commands, and neurologic examination showed neck stiffness, dysarthria, right-sided anisocoria, and a left sided hemiparesis. Empiric antimicrobial therapy was started, including fluconazole. CT showed fluid and membrane thickening within paranasal sinuses. Cranial MRI demonstrated enhancement involving the basilar meninges and sphenoid sinus ( figure, A). Diffusion-weighted images demonstrated restricted diffusion in the right pons, right cerebellum, and right caudate head consistent with acute infarction (figure, B). Cerebral angiogram demonstrated narrowing of arteries around the basal cisterns and occlusion of the right superior cerebellar artery, consistent with vasculitis secondary to basal meningitis. Lumbar puncture (LP) revealed CSF leukocytes of 1,200/mm 3 (94% neutrophils), protein of 73 g/L, and glucose of 64 mg/dL. Fluconazole was changed to voriconazole. Cultures of CSF remained negative. The serum galactomannan antigen test was normal (0.39 index), but CSF galactomannan antigen titers were elevated (6.47 index). Otolaryngology evaluation showed cheesy material in the right sphenoid sinus; fungal smear of the specimen revealed septated hyphae and cultures grew Aspergillus fumigatus susceptible to voriconazole. Three weeks after admission, his level of consciousness suddenly worsened. CT showed right frontal cerebral hemorrhage with extension to the ventricles, and hydrocephalus. An external ventricular drain was inserted. The patient died 4 weeks after admission. Autopsy showed frontal hematomas with extension into the ventricular system resulting in midline midbrain herniation (figure, C figure, D). Patient 2A 62-year-old woman with kidney transplant was transferred to our tertiary care facility with chronic meningoencephalitis and altered consciousness. She had a history of headache of 6 months duration. LP 3 months prior to admission showed leukocytes of 101/mm 3 (27% neutrophils), protein of 47 g/L, and glucose of 40 mg/dL; empiric antimicrobial treatment was initiated. Diagnostic tests on serum and CSF had been negative. Her immunosuppressive regimen consisted of mycophenolate mofetil, prednisone, and tacrolimus with prophylactic sulfamethoxazole/trimethoprim. Neurologic examination showed disorientation to place and time but was otherwise normal. CT showed membrane thicken...

SUMMARY Hyponatraemia following aneurysmal subarachnoid haemorrhage is associated with an increased risk of cerebral infarction. Whether the development of hyponatraemia was related to enlargement of the third ventricle on the admission CT scan was investigated in a consecutive series of 133 patients who were seen within 72 hours of aneurysmal haemorrhage. Hyponatraemia occurred significantly more often in patients with enlargement of the third ventricle (with or without dilatation of the lateral ventricles) than in patients with a normal ventricular system (20/41 versus 24/92, p = 0-0 16). After ventricular drainage, the sodium levels returned to normal in two patients in whom the size of the third ventricle decreased and not in four patients with persistent enlargement of the third ventricle. The significant relationship between enlargement of the third ventricle and hyponatraemia remained after adjustment for the amount of cisternal blood, but not after adjustment for the amount of intraventricular blood. These results suggest that the size of the third ventricle is an important but not the only factor in the relationship between acute hydrocephalus and hyponatraemia in patients with aneurysmal subarachnoid haemorrhage.