[The physiology of sleep and the physiopathology of insomnia]

After a review of the semiology and organization of normal sleep, the neuronal structures presently accepted as participating in sleep mechanisms are discussed. During a series of experiments designed to define the physiopathological role of slow wave sleep in chronic insomnia, we recorded in our laboratory normal subjects of both sexes and insomniacs whose predominant disorders was sleep maintenance. Sleep modifications as a function of aging chiefly involve stage 4, which is reduced by about one half between the ages of 19 and 30. Analyzing a large group of normal and insomniac subjects, it is possible to show a statistical association between very low values of slow wave sleep and short and fragile total sleep. This association cannot be explained simply by an increase in waking pressure. Comparison of a group of 16 insomniacs with 16 age and sex matched normal subjects shows in the insominacs a deficiency of production of slow wave sleep (stages 3 and 4), most probably linked to a disturbed waking/sleep balance, whereas the other parameters of sleep, especially paradoxical stage, remain unmodified. These results are consistent with the hypothesis of a physiopathological role of slow wave sleep deficiency in chronic primary insomnia; on the other hand, slow wave sleep may possibly be responsible for sleep induction and maintenance, playing the role of a physiological hypnogenic mechanism.