[A polygraphic, haemodynamic and metabolic study of 2 cases of the "locked-in" syndrome (author's transl)].

The sleep-waking pattern, cerebral blood flow (CBF) and cerebral metabolism have been studied in 2 cases of the "locked-in" syndrome, one traumatic, the other vascular in origin. Studies were performed in the third week in the first case and the seventh in the second. A lesion of the ventral pons was suggested clinically and neuroradiologically. The waking EEG was composed of alpha and theta activity. Different stages of slow wave sleep were diminished in quantity (NREM) as was paradoxical sleep (REM). The basal cerebral blood flow (CBF) was increased by 30 p. 100 compared to normals. Cerebral oxygen consumption was normal. The cerebral hyperaemia was evenly distributed and was associated with a failure of autoregulation. The vascular response to CO2 was normal, however. The E.E.G. findings, haemodynamic and metabolic studies confirmed a pontine lesion as the cause of the "locked-in" syndrome in contrast to akinetic mutism where the lesion is in the mid-brain.