A middle-aged man was admitted to our department because of sleep-wake cycle disorders (alternating hypersomnia and sleeplessness), bipolar behavioural disturbances and marked fluctuations in blood pressure and heart rate. Neither evident precipitating stimuli nor an obvious cause for his illness were found. When tests that normally activate intrinsic autonomic responses were performed, two distinct circulatory patterns were recognized. During hypersomnia (phase A), cardiovascular reflex activity was blunted or abolished and orthostasis could not be maintained. The clinical, biochemical, behavioural pictures and the observed decrease in sympathetic outflow resembled the effects of clonidine administration. On the contrary, during sleeplessness (phase B) the autonomic pathways were functionally integral and orthostatic hypotension was not detected. The clinical, biochemical, behavioural features and cardiovascular overactivity closely mimicked the abrupt withdrawal syndrome encountered with clonidine. Three hypothetical mechanisms are advanced to explain this intriguing case as well as the acute and chronic relief of our patient's clinical problem following institution of clonidine therapy (phase C). The role played by central alpha adrenoceptors in integrating sleep-wake, cardiovascular and behavioural functions is also suggested.