Arch Neurol Chicago
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Arch Neurol Chicago · May 1984
Case ReportsRespiratory failure in myasthenia gravis due to vocal cord paresis.
Paroxysmal dyspnea and stridor in a patient with myasthenia were shown to be due to weakness of vocal cord abductors that improved with anticholinesterase therapy. Despite adequate inspiratory force, breathing was severely impaired by increased inspiratory resistance. The inspiratory flow-volume loop was useful in documenting the laryngeal obstruction and monitoring the effect of therapy. Reinterpretation of previous studies suggests that upper airway obstruction may often contribute to respiratory failure in patients with myasthenia.
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The records of 68 patients with hemoglobin SC disease and 68 age- and sex-matched control patients were reviewed for neurological problems. A significant increase in retinopathy, stupor/coma, and seizures was noted in the hemoglobin SC group. ⋯ Hemoglobin SC disease may often go unrecognized as a cause of stupor and coma in older patients without other obvious manifestations of a sickling hemoglobinopathy. Factors known to precipitate sickling crisis and the associated neurological complications should be avoided, especially in patients undergoing surgery or parturition.
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Arch Neurol Chicago · Nov 1983
Case ReportsDownbeat nystagmus. Long-term therapy with moderate-dose lithium carbonate.
Downbeat nystagmus developed in a 67-year-old hypomagnesemic woman while she was receiving lithium carbonate for depression. This nystagmus abated each time lithium carbonate therapy was withdrawn, and no alternative causes of nystagmus were demonstrated. However, this nystagmus occurred despite serum lithium carbonate levels in the nontoxic range. Total-body magnesium deficiency may have enhanced the toxic effect of lithium carbonate on cerebellomedullary connections.
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Arch Neurol Chicago · Sep 1983
Case ReportsThe effect of amantadine on arousal and EEG patterns in Creutzfeldt-Jakob disease.
In recent years, Creutzfeldt-Jakob disease (CJD) has been supposed to be of viral origin, and amantadine hydrochloride has been suggested as therapy because of its proved antiviral action. We studied nine patients with CJD (confirmed at autopsy in seven). Four were treated with amantadine hydrochloride, in dosages ranging from 3.5 to 15 mg/kg/day for an average period of 32 days. ⋯ The length of survival from the onset of clinical care did not differ significantly between the two groups. Nevertheless, a transient improvement in wakefulness and mentation was observed in three patients treated with amantadine, and EEG changes were observed in two, consisting above all of a reduction in the slow-wave activity and the periodic discharges (PDs). Amantadine administered intravenously did not induce any short-term changes in the PDs or the cyclic alternating pattern.
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Arch Neurol Chicago · Sep 1983
Case ReportsFoot deformity in myotubular myopathy. Pathology of intrinsic foot musculature.
An intrinsic foot muscle biopsy specimen was taken from a patient with myotubular myopathy who underwent surgical correction for orthopedic deformity. Pathologic findings were typical of primary muscle disease. Foot deformity in myotubular myopathy may result from abnormalities of intrinsic foot muscles, as well as those of more proximal musculature.