Arch Neurol Chicago
-
Arch Neurol Chicago · Mar 2004
Comparative StudyUtilization of intravenous tissue plasminogen activator for acute ischemic stroke.
Intravenous tissue plasminogen activator (tPA) is the only approved therapy for acute ischemic stroke, although only 2% of patients with stroke receive intravenous tPA nationally. ⋯ Only 15% of patients arrived within the 3-hour time window for intravenous tPA, making delay in presentation the most common reason patients were ineligible for i.v. thrombolysis. Neurologic criteria were the second most common group of exclusions. Overall tPA use was low, but it was used in nearly half of all patients with no documented contraindications. Intravenous tPA use in a community setting can compare favorably with the rate of use seen in academic medical settings.
-
Arch Neurol Chicago · Jan 2004
Multiminicore disease in a family susceptible to malignant hyperthermia: histology, in vitro contracture tests, and genetic characterization.
Histological anomalies associated with malignant hyperthermia (MH) have been scarcely reported. In some patients susceptible to MH (MHS), central cores have been identified and a genetic association has been proposed, but multiminicore lesions have not been systematically reported. ⋯ These results indicate that multiminicore lesions are observed in MHS patients with neither clinical signs related to multiminicore disease nor histological features of congenital myopathies. These multiminicore lesions may be secondary to mutations in the RYR1 gene. As a consequence, these patients must be distinguished from patients with multiminicore disease and from other MHS patients for whom multiminicores are not observed.
-
Arch Neurol Chicago · Dec 2003
Case ReportsMetronidazole-induced encephalopathy and inferior olivary hypertrophy: lesion analysis with diffusion-weighted imaging and apparent diffusion coefficient maps.
Although several cases of metronidazole-induced encephalopathy have been reported, to our knowledge, there is no previous report of brain changes in anterior commissure, basal ganglia, cerebellar white matter, and inferior olivary nuclei on magnetic resonance images. The precise mechanisms of action of metronidazole-induced encephalopathy have not been determined. ⋯ We describe a patient with metronidazole-induced encephalopathy involving reversible lesions in the anterior commissure, basal ganglia, and cerebellar white matter, which have not been reported previously. We observed inferior olivary hypertrophy, believed to be the result of lesions in the midbrain and cerebellar white matter rather than the result of lesions induced by metronidazole therapy. By using diffusion-weighted imaging and apparent diffusion coefficient maps, we found that metronidazole-induced encephalopathy might be caused by cytotoxic edema.