Two hundred thirty-one cases of neurocysticercosis are reviewed. Diagnosis was established by cerebral computed tomography during a seven-year period (1983-1989). One hundred and fourty-four (62%) presented with symptom-related disease (symptomatic neurocysticercosis and in 87 the diagnosis was incidental (asymptomatic neurocysticercosis). In symptomatic neurocysticercosis the parasitosis was considered inactive in 115 cases and active in 29. Seizures occurred in 135 patients (96% of the symptomatic neurocysticercosis). In the active form we also found: meningitis (n = 15), intracranial hypertension (n = 12), hydrocephalus (n = 10) and arteritis (n = 2). Treatment included praziquantel (n = 21), albendazole (n = 4), dexamethasone (n = 18) and surgery (n = 10).
In this retrospective study we have analysed a series of 38 patients seen from 1983 to 1992 (mean follow-up, 4.5 years) with active neurocysticercosis (NCC), 23 (60.5%) with parenchymal and 15 (39.5%) with extraparenchymal NCC. Classification into these two forms of NCC was based on computed tomography and magnetic resonance imaging criteria. The enzyme-linked immunosorbent assay performed in cerebrospinal fluid, for anti-Taenia solium antibodies, was positive in 18 of 23 (78%) cases. Epilepsy and/or intracranial hypertension were the most common clinical presentation (92%). Twenty-three (60.5%) of 38 patients were treated with praziquantel and/or albendazole. In parenchymal NCC, the efficacy of medical therapy was complete in 13 of 16 (81%) and partial in 3 of 16 (19%) patients. In contrast, in all cases of extraparenchymal NCC treated with cysticidal drugs the results were disappointing. A ventriculoperitoneal shunt was performed in 9 of 13 patients with extraparenchymal NCC and hydrocephalus. Severe complications, including two deaths, associated with the natural evolution of the disease or with surgery, occurred only in extraparenchymal NCC. Therefore, we confirm the existence of the two forms of active NCC, parenchymal and extraparenchymal, which are strikingly different in clinical presentation, medical therapy response, complications, morbidity and mortality.
We present a retrospective study of 6 patients with spinal cord infarction in the territory of the Adamkiewicz artery. In all patients, the clinical picture was stereotyped: sudden onset of paraplegia and bilateral radicular pain, dissociated sensory loss below the level of infarction and sphincter dysfunction. Emergency neuroradiological investigation ruled out a compressive lesion in all cases. In one patient, spinal angiography was performed and identified an occlusion of the Adamkiewicz artery. Treatment was supportive and all patients had a substantial recovery over a period of weeks.
A case of type V intracranial dural arteriovenous fistula (DAVF) is reported because of its unusual rapidly progressive paraparesis. Despite this clinical presentation, the diagnosis of DAVF was made and precocious endovascular treatment was instituted. Angiographic normalization was obtained after embolisation and the patient significantly improved within the first weeks, although at the six month control MRI there still was a hyperintense signal of the cord in T2 weighted images, but less extensive than originally.
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