Narcolepsy: a key role for hypocretins (orexins)
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Sleep abnormalities are frequently reported as possible etiopathogenic factor of fibromyalgia. We report 2 cases of fibromyalgia revealing a long-standing narcolepsycataplexy.
The aim of the study was to examine the influence of the blockade of group I metabotropic glutamate receptors (mGluRs) on the haloperidol-induced catalepsy and proenkephalin mRNA expression in the rat striatum. Bilateral, intrastriatal injection of AIDA ((RS)-1-aminoindan-1,5-dicarboxylic acid, 3-15 microg/0.5 microl), a selective antagonist of group I mGluRs, inhibited catalepsy induced by haloperidol (0.5 mg/kg i.p.). Repeated intrastriatal AIDA administrations (3 x 15 microg/0.5 microl, 3 h apart) counteracted the haloperidol-induced (3 x 1.5 mg/kg s.c., 3 h apart) increase in the proenkephalin mRNA expression in that structure. The present study indicates that the blockade of the striatal group I mGluRs may inhibit parkinsonian akinesia by normalizing the function of the striopallidal pathway.
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The responses of apparently healthy newborn foals to neurologic testing differ significantly from those of adult horses. These responses and the diagnostic techniques pertinent to neurologic problems are reviewed as a basis for evaluation of the compromised neonatal foal. The more frequently encountered neurologic diseases are discussed in a problem-oriented format. These clinical problems include behavioral abnormalities, convulsions, changes in consciousness, blindness, ataxia without loss of strength, ataxia with weakness and paralysis, and the floppy foal.
OBJECTIVES AND METHODS: To perform a video-polygraphic analysis of 11 cataplectic attacks in a 39-year-old narcoleptic patient, correlating clinical manifestations with polygraphic findings. Polygraphic recordings monitored EEG, EMG activity from several cranial, trunk, upper and lower limbs muscles, eye movements, EKG, thoracic respiration. RESULTS: Eleven attacks were recorded, all of them lasting less than 1 min and ending with the fall of the patient to the ground. We identified, based on the video-polygraphic analysis of the episodes, 3 phases: initial phase, characterized essentially by arrest of eye movements and phasic, massive, inhibitory muscular events; falling phase, characterized by a rhythmic pattern of suppressions and enhancements of muscular activity, leading to the fall; atonic phase, characterized by complete muscle atonia. Six episodes out of 11 were associated with bradycardia, that was maximal during the atonic phase. CONCLUSIONS: Analysis of the muscular phenomena that characterize cataplectic attacks in a standing patient suggests that the cataplectic fall occurs with a pattern that might result from the interaction between neuronal networks mediating muscular atonia of REM sleep and neural structures subserving postural control.
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Patients with sleep disorders present with a variety of complaints including excessive daytime sleepiness, daytime spells, inability to sleep, uncomfortable sensation in the extremities, and unusual night time behaviors. This article provides eight vignettes on patients with sleep disorders including narcolepsy, idiopathic hypersomnia, obstructive sleep apnea, restless legs syndrome, and rapid eye movement behavior disorder. The discussion provides data regarding the epidemiology, pathophysiology, and diagnostic approach for these conditions. The various treatment options for these sleep disorders are also identified.
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We found in a representative sample of 392 first hospital admissions for schizophrenia a higher mean age at onset in females by 3.2 to 3.9 years, whereas the lifetime risk was equal for both sexes. In males the rates of onset show a steep increase reaching the maximum value in the age group 15-24 years, followed then by a steady decrease. Females reach the first peak with a clear delay between 20 and 29 years. After the decrease a second smaller peak is observed consistently in females within the age group 45-49 years and over. After having excluded alternative explanations for this gender differences (for example, diagnosis artefacts, sociocultural factors), we hypothesized that the effect of oestradiol on the dopaminergic system enhances the vulnerability threshold for schizophrenia, which is lowered again during the menopause. Alternatively we assumed that testosterone reduces the vulnerability threshold and thus furthers the earlier onset of schizophrenia in males. We tested these hypotheses in animal models by investigating the effects of the gonadal hormones on haloperidol-induced catalepsy and on apomorphine-induced stereotypies in both neonatal and adult rats. Testosterone showed no clear influence on the tested dopamine-mediated behaviour. Oestradiol caused a significant reduction on both dopamine-agonist and dopamine-antagonist induced behaviour. These effects were stronger in neonatal animals. Since oestradiol caused a 2.8-fold reduction of dopamine receptor affinity for sulpiride, we assumed that the behavioural changes caused by oestradiol were accounted for by a down-regulation of the dopaminergic system.(ABSTRACT TRUNCATED AT 250 WORDS)
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