AbstractAbnormalities of circadian rhythms in depressed patients have been noted, including decreased amplitude, distorted waveform, day-to-day instability, and unusual 48 hour periods. Consistent electroencephalographic sleep recording in these patients show a shortened rapid eye movement latency and slow-wave sleep (stages 3 and 4), resulting in an increase in rapid eye movement sleep. This phenomenon appears to be a dependable, measurable marker for diagnosing primary depression. Total sleep deprivation appears to significantly improve mood in a high percentage of depressed patients. Current pharmacological research suggests that drug treatment such as lithium would not affect the intra sleep cycles of the REM stagebut would shift the phase backward and lithium would also shift the phase of circadian rhythm of the daytime sleepiness backward. This paper highlights some of the new approaches for investigating the molecular substrate for the control of circadian rhythmicity and sleep in man and critically examines the hypothesis of the alteration of this mechanism in psychopathology, particularly depression. What is known of the endogenous clock mechanism is discussed with known molecular circadian mechanisms with a view towards understanding how circadian information is transmitted to the rest of the central nervous system and how it is affected in depression.
Connectivity differences between consciousness and unconsciousness in non-rapid eye movement sleep: a TMS–EEG study