Taillard J, Lemoine P, Boule P, Drogue M, Mouret J
Unité Clinique de Psychiatrie Biologique, Hôpital du Vinatier, Bron, France.
Chronobiol Int. 1993 Feb;10(1):63-72. doi: 10.3109/07420529309064483.
In order to determine whether a decrease in the amplitude of heart rate circadian rhythm (HRCR) could represent a chronobiological marker of depression and to answer the question of the possible role of this alteration in the reduction of rapid eye movement sleep latency (REM latency) observed in depression, 22 major depressed patients (DSM III R, Montgomery Asberg Depression Rating Scale) and 11 healthy volunteers entered this study, which included the simultaneous recordings of sleep and heart rate (HR) during two consecutive 24-h periods. After a smoothing procedure, the HR data, obtained from a portable device providing mean HR/min, were computed with the single cosinor method for the classical circadian parameters. We also determined the cosinor fitting index (CFI = percentage to fit). When studied as a single group and compared to the control group, the depressed patients, who had difficulties in sleep initiation and whose REM latencies were within normal limits, were characterized by a dampening of the amplitude HRCR and of the day-night HR difference. This was linked to a lesser increase of HR during the day and a reduced decrease at night. No significant phase modification of HRCR was observed in this group of depressives. In a second step, the depressives were divided into a depressed arrhythmic group (DAG, CFI < 50%, 11 patients) and a depressed rhythmic group (DRG, CFI > 50%, 11 patients) who did not differ on MADRS scores. Even though the amplitude of HRCR was reduced in the DAG only, with HR higher at night and lower during the daytime than for controls, both DAG and DRG significantly differed from controls on those items related to sleep induction and maintenance. In the DAG only was there a tendency toward a reduction of total sleep time and REM sleep time while REM latency was normal. This finding suggests that sleep problems are not responsible for the differences in HRCR parameters between the two depressed groups. These differences in HR and sleep parameters between two groups of similarly depressed patients also suggest that a short REM latency does not systematically imply a disruption of all circadian clocks.
为了确定心率昼夜节律(HRCR)幅度的降低是否可作为抑郁症的时间生物学标志物,并回答这种改变在抑郁症中观察到的快速眼动睡眠潜伏期(REM潜伏期)缩短中可能发挥的作用这一问题,22名重度抑郁症患者(DSM - III - R,蒙哥马利 - 阿斯伯格抑郁评定量表)和11名健康志愿者参与了本研究,该研究包括连续两个24小时期间同时记录睡眠和心率(HR)。经过平滑处理后,从提供平均每分钟心率的便携式设备获得的HR数据,采用单一余弦分析法计算经典的昼夜节律参数。我们还确定了余弦拟合指数(CFI = 拟合百分比)。当作为一个单一组进行研究并与对照组比较时,入睡困难且REM潜伏期在正常范围内的抑郁症患者,其特征为HRCR幅度以及昼夜HR差值减弱。这与白天HR升高较少以及夜间降低减少有关。在这组抑郁症患者中未观察到HRCR的显著相位改变。在第二步中,抑郁症患者被分为抑郁无节律组(DAG,CFI < 50%,11名患者)和抑郁有节律组(DRG,CFI > 50%,11名患者),两组在MADRS评分上无差异。尽管仅在DAG组中HRCR幅度降低,与对照组相比夜间HR较高而白天较低,但DAG组和DRG组在与睡眠诱导和维持相关的项目上均与对照组有显著差异。仅在DAG组中有总睡眠时间和REM睡眠时间减少的趋势,而REM潜伏期正常。这一发现表明睡眠问题并非两组抑郁症患者HRCR参数差异的原因。两组相似抑郁症患者在HR和睡眠参数上的这些差异还表明,较短的REM潜伏期并不一定意味着所有昼夜节律时钟都被破坏。