Bernier Denise, Bartha Robert, Devarajan Sivakumaran, Macmaster Frank P, Schmidt Matthias H, Rusak Benjamin
Department of Psychiatry, Dalhousie University, Halifax, NS.
J Psychiatry Neurosci. 2009 Sep;34(5):352-60.
Partial or total overnight sleep deprivation produces immediate mood improvement in about 50% of patients with depression, but not in healthy controls. Our objectives were to compare the neurochemical changes that accompanied partial overnight sleep deprivation in healthy and depressed participants, and to compare baseline neurochemical profiles and overnight neurochemical changes between those depressed participants who did and did not respond to sleep loss with mood improvement.
We studied 2 brain regions (left dorsal prefrontal area and pons) in 12 women with unipolar depression and in 15 healthy women using proton magnetic resonance spectroscopy acquired at 1.5 T. The scans took place at baseline and 24 hours later after a night with sleep restricted to a maximum of 2.5 hours (22:30-01:00). We assessed 3 neurochemical signals (referenced to internal water): N-acetylaspartate (NAA), choline compounds (Cho) and creatine-plus-phosphocreatine (tCr).
In both groups combined, sleep restriction caused a 20.1% decrease in pontine tCr (F(1-16) = 5.07, p = 0.039, Cohen's d = 0.54) and an 11.3% increase in prefrontal Cho (F(1-21) = 5.24, p = 0.033, Cohen's d = 0.46). Follow-up tests revealed that prefrontal Cho increases were significant only among depressed participants (17.9% increase, t(9) = -3.35, p = 0.008, Cohen's d = 1.06). Five depressed patients showed at least 30% improvement in mood, whereas 6 showed no change or worsening in mood after sleep restriction. Baseline pontine Cho levels distinguished subsequent responders from nonresponders to sleep restriction among depressed participants (z = 2.61, p = 0.008).
A limitation of this study is the relatively small sample size.
Sleep restriction altered levels of pontine tCr and prefrontal Cho in both groups combined, suggesting effects on phospholipid and creatine metabolism. Baseline levels of pontine Cho were linked to subsequent mood responses to sleep loss, suggesting a role for pontine phospholipid metabolism in mood effects of sleep restriction.
部分或完全夜间睡眠剥夺能使约50%的抑郁症患者的情绪立即改善，但对健康对照者则无此效果。我们的目标是比较健康参与者和抑郁症患者在部分夜间睡眠剥夺过程中伴随的神经化学变化，并比较那些对睡眠剥夺有情绪改善反应和无此反应的抑郁症患者之间的基线神经化学特征及夜间神经化学变化。
我们使用1.5T的质子磁共振波谱对12名单相抑郁症女性和15名健康女性的2个脑区（左侧背外侧前额叶区域和脑桥）进行了研究。扫描在基线时以及在睡眠限制为最多2.5小时（22:30 - 01:00）的一晚后的24小时进行。我们评估了3种神经化学信号（以内源性水为参照）：N - 乙酰天门冬氨酸（NAA）、胆碱化合物（Cho）和肌酸加磷酸肌酸（tCr）。
在两组合并分析中，睡眠限制导致脑桥tCr降低20.1%（F(1 - 16) = 5.07，p = 0.039，Cohen's d = 0.54），前额叶Cho增加11.3%（F(1 - 21) = 5.24，p = 0.033，Cohen's d = 0.46）。后续测试显示，前额叶Cho增加仅在抑郁症患者中显著（增加17.9%，t(9) = -3.35，p = 0.008，Cohen's d = 1.06）。五名抑郁症患者在睡眠限制后情绪改善至少30%，而六名患者在睡眠限制后情绪无变化或恶化。基线脑桥Cho水平区分了抑郁症患者中对睡眠限制有反应者和无反应者（z = 2.61，p = 0.008）。
本研究的一个局限性是样本量相对较小。
睡眠限制改变了两组合并后的脑桥tCr和前额叶Cho水平，提示对磷脂和肌酸代谢有影响。脑桥Cho的基线水平与随后对睡眠剥夺的情绪反应相关，提示脑桥磷脂代谢在睡眠限制的情绪效应中起作用。
