Biomedical subjects
N Langdon
Publications and source records attributed to N Langdon.
Selegiline in narcolepsy.
We examined the effect of the specific monoamine oxidase-B (MAO-B) inhibitor selegiline (deprenyl, Eldepryl), 20-30 mg p.o. daily, in 21 subjects with the narcoleptic syndrome for 4 weeks. Selegiline was compared to no treatment (7 subjects) or conventional central stimulant drugs, including dexamphetamine or mazindol (14 subjects). Severity and frequency of narcolepsy, accessory symptoms, and effects of selegiline on mood were measured. Selegiline, as well as causing MAO-B inhibition, is interconverted to amphetamine. Urinary amphetamine and methamphetamine excretion were determined in 18 subjects after 4 weeks on selegiline and the results were compared with amphetamine excretion in subjects on dexamphetamine. The effect of selegiline, 20-30 mg p.o., on alertness and mood was similar to that of dexamphetamine in the same dosage, with comparable sympathomimetic side effects. Selegiline, 20 mg p.o., caused a subjective increase in alertness for 4-8 h. Mean urinary amphetamine excretion on dexamphetamine, 15-70 mg daily (mean 29 mg) at pH 5.6-6.6, was 5,184 micrograms/24 h, and on selegiline, 20-30 mg daily (mean 22.5), was 4,127 micrograms/24 h. We conclude that selegiline, 20-30 mg daily, requires further evaluation in narcolepsy.
Breathing in Parkinson's disease.
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Fluoxetine in the treatment of cataplexy.
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Comparison of levodopa with carbidopa, and levodopa with domperidone in Parkinson's disease.
In a comparison of the effects of domperidone and carbidopa during levodopa treatment, 20 patients with idiopathic Parkinson's disease were treated with fixed dose regimens of either levodopa 500 mg-domperidone 20 mg or levodopa 100 mg-carbidopa 25 mg; each for 8 weeks. Clinical response, incidence of side effects, and plasma levodopa concentration resulting from each treatment were compared. Overall, in the dosages used, Parkinson's disease was less well controlled with levodopa-domperidone than with levodopa-carbidopa. In eight subjects there was a severe deterioration 2 to 7 days after changing from a fixed dose of levodopa-carbidopa to levodopa-domperidone. In nine subjects who completed the trial, the clinical response, occurrence of dyskinesias and of nausea and vomiting, were similar with both treatments, although peak plasma levodopa concentration and levodopa bioavailability were greater on levodopa-domperidone than on levodopa-carbidopa.
Immune factors in narcolepsy.
Most but not all subjects with the narcoleptic syndrome have the human leukocyte antigen (HLA) DR2 (and DQ1). The narcolepsy-DR2 association is the highest disease-HLA linkage known, and occurs in nonfamilial as well as familial cases of the narcoleptic syndrome. In other forms of daytime drowsiness, there is no relationship with a specific HLA, although some subjects considered to have "essential" hypersomnolence probably have the narcoleptic syndrome. The cause of the narcoleptic syndrome remains unknown, although in a few instances the condition follows infection. There is no evidence for a circulating sleep factor in the blood or in the cerebrospinal fluid of narcoleptic subjects, and no unequivocal marker of cellular immunity has yet been found. However, a few subjects with the narcoleptic syndrome have oligoclonal bands or raised immunoglobulin concentration in the cerebrospinal fluid. It is highly likely that the narcoleptic syndrome is an immune-mediated disorder, occurring in a genetically susceptible (DR2/DQ1-positive) subject.
Genetic markers in narcolepsy.
Narcolepsy has long been known to have a hereditary familial basis. All of 37 patients with narcolepsy expressed the major histocompatibility complex antigen HLA DR2 compared with 21.5% of 200 normal controls. This finding confirms the genetic basis for the disease, and furthermore links it with the short arm of chromosome 6. If the sleep disturbance in narcolepsy is due to a gene-determined defect in a neurotransmitter or receptor factor, the responsible agent may be DR2 itself or an enzyme determinant linked to DR2. This is the strongest HLA-disease association so far discovered.