E. Lugaresi, F. Provini, P. Montagna
This review synthetizes the most important historical contributions in sleep anatomy and the pioneer discoveries in sleep medicine in the light of our clinical observations in Fatal Familial Insomnia (FFI), a genetic prion disease. Together with Morvan¿s chorea and Delirium Tremens, FFI is characterized by inability to sleep with severeloss of sleep spindles and delta sleep, with preserved presleep behaviour and abnormal REM sleep, associated with motor and autonomic overactivation. We labelled this pattern as Agrypnia Excitata (AE). AE is due to dysfunction in thalamolimbic circuits, which emphasizes the key role of the thalamus in sleep physiology and indicates that the anatomo-functional substrate of stage 1 non-REM sleep differs from that generating slow-wave-sleep (SWS, spindle and delta activity). Accordingly, the sleep-wake cycle in man should be conceptualized as consisting of 5 different behavioural and electrophysiological distinct states: active wakefulness, quiet wakefulness, drowsiness (or stage 1 non-REM), SWS (which incorporates spindle and delta sleep) and REM sleep. An intricate neuronal network extending from the caudal brainstem to the forebrain controls these different wake and sleep behaviours with several, at least three distinct generators.
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