Background: Dalfampridine extended-release (ER) tablets, 10 mg twice daily, have been shown to improve walking in people with multiple sclerosis. We evaluated the safety and efficacy of dalfampridine-ER 5 mg compared with 10 mg.
Methods: Patients were randomized to double-blind treatment with twice-daily dalfampridine-ER tablets, 5 mg (n = 144) or 10 mg (n = 143), or placebo (n = 143) for 4 weeks.
Clin Neurol Neurosurg
February 2010
We report two patients with severe cardiac manifestations at the time of the initial presentation of polymyositis. Both cases are unusual in that they presented with predominant cardiac disturbances, associated with muscle weakness. One patient had a typical clinical syndrome of congestive heart failure, and the second mimicked an acute myocardial infarction in which coronary angiography was normal.
View Article and Find Full Text PDFHumans can generate and maintain relatively coherent trains of thought in natural discourse. The neural mediation of this ability and the phenomenology of its breakdown are not well understood. We report a case of a woman with paramedian thalamic strokes involving the mammillothalamic tract, intralaminar nuclei, parts of the dorsomedial and ventral lateral nuclei bilaterally.
View Article and Find Full Text PDFPatients with cobalamin deficiency may experience cognitive impairment or neuropsychiatric symptoms. Although abnormalities of central myelin are the presumed cause of these manifestations, there is a paucity of reports of white matter lesions as shown on neuroimaging studies, and the effects of cobalamin replacement on these lesions are not known. We report a man with subacute cognitive impairment associated with cobalamin deficiency and remarkable confluent white matter abnormalities on MRI, confirmed by biopsy.
View Article and Find Full Text PDFAs we have reported, calcium ionophore A23187 activates macrophages for tumor cell killing, and the activated macrophages produced a soluble cytotoxic factor (M phi-CF) that is similar, if not identical, to tumor necrosis factor. Based on these observations, we have investigated whether calcium is involved in the activation mediated by another potent macrophage activator, namely lipopolysaccharide (LPS). We first showed that A23187 caused uptake of extracellular calcium-45 by macrophage monolayers, whereas LPS did not.
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