We investigated the effects of the somatosensitive and sensory afferent inputs on the thalamic generators of sleep spindles (SS) in adult subjects affected by posterior funiculi lesions (five subjects), deafness (four subjects) or blindness (four subjects). The density, duration and frequency of SS, as well as the index of spindling, were analyzed during stage 2 NREM. The results show that the subjects with somatosensitive and sensorial lesions spent much more time on SS activity than the control group (eight subjects), and had a significantly increased density (< .0001), duration (< .0005) and index of spindling (< .0001). On the other hand, the frequency of spindling was little modified (< .05). Moreover, among the three groups of patients, those with somatosensitive deficits showed the greatest SS activity. In conclusion, our results suggest that the thalamic generators of SS are markedly modulated by peripheral inputs in man.

All-night polygraphic records (EEG, EOG and ECG) were performed on 9 subjects. Four of them were affected by Familiar Cerebellar Atrophy (FCA) whereas the others were their blood relatives without clinical signs of cerebellar deficit. In the former FCA was diagnosed clinically and the cerebellar atrophy was confirmed by computer tomography (CT). In all the latter except one who showed slight cerebellar atrophy, the CTs were negative. The EEG sleep records of the FCA patients were characterized by slowly changing phases between synchronized and desynchronized sleep, instability of the synchronized sleep with frequent modifications of EEG activity, subnormal measurement of both REM and slow-wave sleep and presence of spindles in REM sleep (only in 2 patients). The spindle activity was reduced in two FCA subjects. The electroencephalographic sleep records of two BRs, one of which with small cerebellar atrophy, showed qualitative and quantitative alterations similar to those of FCA patients, even if marked to a lesser degree. Increased spindle densities were present in the same BRs who showed sleep abnormalities. The EEG alterations observed in the two BR subjects could show small cerebellar injuries which would be insufficient to induce clinical signs.

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