Rush A J, Erman M K, Giles D E, Schlesser M A, Carpenter G, Vasavada N, Roffwarg H P
Arch Gen Psychiatry. 1986 Sep;43(9):878-84. doi: 10.1001/archpsyc.1986.01800090068009.
Thirteen patients were examined by sleep polysomnograph (PSG) and the dexamethasone suppression test when clinically depressed and later when clinically remitted for six months and no longer receiving antidepressant medication for two to five weeks. None of the PSG variables (rapid eye movement [REM] latency, total sleep time, stage 1 through 4 times, REM time, and REM densities in periods 1 through 3) was significantly changed between symptomatic depression and symptom remission. While symptomatic, 11 of 13 patients exhibited a reduced REM latency (65 minutes or less). After clinical remission, eight of the 11 continued to exhibit reduced REM latencies, whereas the dexamethasone suppression test tended to show nonsuppression only during clinical depression. These data represent either longer-term (ie, slow to normalize) biologic consequences of a depressive episode or biologic antecedents of clinical depression that may herald a return of the depression in individuals vulnerable to recurrence. Whether PSG abnormalities identify clinically remitted patients who are prone to develop another depressive episode requires longitudinal follow-up studies.
对13名患者在临床抑郁时以及后来临床缓解6个月且不再接受抗抑郁药物治疗2至5周时进行了睡眠多导睡眠图（PSG）和地塞米松抑制试验检查。在症状性抑郁和症状缓解之间，PSG的任何变量（快速眼动[REM]潜伏期、总睡眠时间、1至4期睡眠时间、REM睡眠时间以及1至3期的REM密度）均无显著变化。在有症状时，13名患者中有11名的REM潜伏期缩短（65分钟或更短）。临床缓解后，11名患者中有8名继续表现出REM潜伏期缩短，而地塞米松抑制试验仅在临床抑郁期间倾向于显示无抑制。这些数据代表了抑郁发作的长期（即恢复正常缓慢）生物学后果，或者是临床抑郁的生物学先兆，可能预示着易复发个体的抑郁复发。PSG异常是否能识别出易于发生另一次抑郁发作的临床缓解患者，这需要进行纵向随访研究。
