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Sleep deprivation has been used for exploring functions of sleep among healthy individuals and for treating patients suffering from depressive symptoms. Sleep deprivation is a rapid, effective and brief therapeutic alternative. Two types of sleep deprivation applications have been implemented; one is deprivation of sleep for whole night and the other is partial deprivation of sleep in the second part of the night. Although various hypotheses have been developed pertaining to the treatment potential of sleep deprivation in depression, the mechanisms underlying the process are still obscure (1). Early systematic research conducted by Pşug and Tolle proposed that patients characterized by endogenous depressive symptoms receptive to sleep deprivation have deficits in their circadian systems and sleep deprivation aids at ameliorating the dysregulation in the biological rhythm (2). Sleep deprivation and REM sleep deprivation act like antidepressants and some antidepressants have suppressing effects on REM sleep. Hence the role of REM sleep on the development of depression has received more attention. The reduction of REM latency and REM intensity are prominent features in patients with depression. Sleep deprivation reverses these two effects (3).
The psychological response to sleep deprivation seems to occur regardless of diagnostic category such as endogenous-reactive, psychotic, nonpsychotic, unipolar, bipolar, schizoaffective, or seasonal (4). Merely diurnal variation (soothing of affect is typical in patients with depression in the later hours of daytime) and chronobiological differences are substantial in the psychological response to sleep deprivation (5).
About 50-60 percent of patients with depression are prone to reşect antidepressant inşuences after one-night of sleep deprivation therapy. Deceleration in symptom severity as well as amelioration in suicidal thoughts occurs. The temporary antidepressant inşuence of the initial application does not predict inadequacy of further applications. If applications of sleep deprivation are continued one or two times per week, it has been claimed that it is likely to provide effective prophylaxis (6).
Although sleep deprivation provides a rapid psychological response and a potent inşuence, its application is not prominent in major depression. Sleep deprivation can be qualified as an awkward method, because the application requires constant monitoring and to ensure wakefulness of patients as well as carrying a relapse risk in fiesta. The most prominent advantage of sleep deprivation compared to other medications and ECT is that it causes rapid and apparent improvement in affect. Therefore the pros and cons of sleep deprivation should be taken into account in treatment planning.
References:
1. Rechtschaffen A. Current perspectives on the function of sleep. Perspect Biol Med 1998;41:359-390.
2. Pşug B, Tolle R. Disturbance of the 24 hour rhythm in endogenous depression and treatment of endogenous depression by sleep deprivation. Int Pharmacopsychiatry 1971;6:187-196.
3. Giedke H, Schwarzler F. Therapeutic use of sleep deprivation in depression. Sleep Med Rev 2002;6:361–377.
4. Wirz-Justice A. Biological rhythm disturbances in mood disorders. Int Clin Psychopharmacol 2006;21:11-5.
5. Selvi Y, Gulec M, Agargun MY, Besiroglu L. Mood changes after sleep deprivation in morningness–eveningness chronotypes in healthy individuals. J Sleep Res 2007;16:241–4.
6. Hemmeter UM, Hemmeter-Spernal J, Krieg JC. Sleep deprivation in depression. Expert Rev Neurother 2010;10(7):1101-15.