Abstract
The hypothesis that greater perturbations of EEG-sleep architecture and continuity would occur in clinical depression contingent upon ∑stage shifts was tested. Duration of successive REM cycles was also evaluated in 16 young adult (17-25 years) nonpsychotic unipolar patients with primary depression and eight age-matched normal controls for 8 hr during 1-3 consecutive EEG recording nights (∑ N = 55). Two subgroups of eight patients were identified whose polysomnograms contained >100 versus <100 ∑sleep stage transitions. As predicted, sleep was shallow and fragmented to a significantly larger extent in depressives with: >100 stage shifts versus, <100 transitions, compared with controls. This was reflected by significantly longer delays in falling asleep, more intermittent wakefulness transitions into stage 1, increased ∑stage shifts, and more transitional stage 1 sleep. The depressed patients with <100 stage shifts (versus >100 transitions relative to the controls) accumulated significantly less total sleep (7.0 vs>7.6 hr), REM time; exhibited fewer REM episodes, and a slower REM cycle. Compared with controls both patient constituencies accumulated less REM time, showed a propensity for shallow NREM sleep reflected by significantly decreased stage 4, and more frequent transition into stage 1. REM time significantly increased progressively during sleep through the fourth cycle in both controls and depressives. The initial REM cycle was significantly longer among patients (N = 16), and the fourth proved to be shorter compared with controls. The longer first REM cycle in primary depression is construed to represent a disinhibition of neural processes that would normally either attenuate or delay this phenomenon. Accordingly, the possibility is raised that REM sleep disinhibition potentiates the mood disturbances and neurovegetative symptoms of endogenous/primary depression.