Clinical and polygraphic data reported by our group suggest that in hypersomnia with periodic apneas (HPA), diurnal sleepiness is not a consequence of the arousals induced by the apneic episodes and that obstructive apnea is the sole cause of hypersomnia (Lugaresi et al., 1978). It was therefore of interest to study whether the effect produced by obstructive apnea on the mechanisms which regulate seep and waking are linked to some biochemical alteration in the brain caused by the remarkable modifications of blood gas concentration produced by the obstructive apnea. In patients suffering from HPA with a documented obstruction of the upper respiratory tract, tracheostomy seems the only effective treatment, and results in a complete clinical remission of the syndrome (Lugaresi et al., 1970). We have therefore measured cerebrospinal fluid (CSF) concentrations of homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) in these patients before and after tracheostomy. It is generally accepted that acidic metabolites of monoamines in CSF may be taken as an expression of brain monoamine metabolism (Bowers, 1972). While CSF concentration of HVA and 5-HIAA have been studied in some other sleep disturbances in man (Mouret et al., 1976), to the best of our knowledge, HVA and 5-HIAA concentrations in CSF of patients with HPA before and after tracheostomy have not been reported in the literature. In this preliminary communication we also report HVA and 5-HIAA concentrations in a patient suffering from an idiopathic hypersomnia with excessive daytime sleepiness (EDS) and automatic behavior defined by other authors as neutral state syndrome (Guilleminault and Dement, 1977).
|Number of pages||3|
|Publication status||Published - 1980|
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