Sleep deprivation in depressionDR Doongaji, VN Vahia, PD Lakdawala, MD Parikh, AR Singh, Shubha S Thatte, Kamal D Lotlikar
Departments of Psychiatry, Medicine & Surgery-Statistics, K.E.M. Hospital and Seth G.S. Medical College, Parel, Bombay 400 012, India
Correspondence Address: Source of Support: None, Conflict of Interest: None PMID: 458741
Source of Support: None, Conflict of Interest: None
Ten patients diagnosed as suffering from depressive illness were treated with 2 consecutive nights of sleep deprivation. Sleep deprivation was effective in both types of depression viz. endogenous and reactive. The improvement was greater and seemed to last longer in endogenous depression as compared to reactive depression at the time of evaluation, 7 days after completion of sleep deprivation. Depressed mood, suicidal tendencies and retardation seemed to show the greatest improvement while insight and gastro-intestinal and somatic symptoms, improved the least.
In 1965, Schulte described a female patient who reported that her depression seemed to lessen after she had stayed awake all night.  It is well documented that the deprivation of sleep can induce a psychotic state. It seems remarkable therefore that sleeplessness, which often accompanies depression can also paradoxically be of benefit in depressive disorders. Following this report several workers have investigated the therapeutic value of sleep deprivation in depressed patients, notable among them being Pflug.  His results indicated that sleep deprivation had definite antidepressant effect, particularly where the depression was of the endogenous type. The improvement was noted specially in the variables: depressive mood, suicidal tendency and psychomotor inhibition. Further studies conducted by other investigators support these results also. ,,
It is not known how sleep deprivation therapy compares with the standard antidepressant therapies, under controlled conditions. It was as a prelude to investigating sleep deprivation as a therapeutic measure that we conducted this preliminary study.
The aim of the present study was to ascertain the effects of sleep deprivation in patients with depression.
This study was conducted in the inpatient services of the Department of Psychiatry, K.E.M. Hospital, Bombay.
Ten in-patients with a diagnosis of depression were admitted to this study. The age range was between 35 and 68 years (mean age 46.6 years). The duration of illness ranged between 1½ months to 10 years (mean duration 2.05 years). There were 6 males and 4 females. The diagnosis was endogenous depression in 8 patients and reactive depression in 2 patients. Eight out of ten patients had been under treatment with antidepressant drugs from 2 to 8 months without showing any improvement. There was a history of past episodes of depression in 4 patients which had been treated successfully with antidepressants and/or E,C.Ts. [Table 1]. As the range of the study sample included patients upto age of 60 years, all patients were examined clinically and were tested to exclude organic brain syndrome (Weschler's memory scale Bender-Gestalt visual motor perception test, Rorsach test) prior to inclusion in the study.
The study was conducted in an uncontrolled non-blind fashion. The patients were aware of the purpose of the therapy.
Immediately after hospitalisation a baseline evaluation of symptoms was made using the Hamilton Psychiatric Rating Scale for Depression (HPRSD) (period 1).  The patients were then kept completely awake from their usual time of arising till the lapse of 48 hours. They were fully ambulant and were kept awake by conversation, games, music, and simple diversions. At least one resident doctor and a nurse were present throughout the night to ensure complete wakefulness during this period. During day time the occupational therapists and the nursing staff took care that the patients on trial did not lie down or doze. off for a single moment. Clinical progress was assessed with the HPRSD at the end of 24 hours including one night of sleep deprivation (period 2), at the end of 48 hours which included 2 consecutive nights of sleep deprivation (period 3), following 2 consecutive nights of sleep deprivation and a night of permitted sleep, (period 4) and a week later (period 5). The patients were not assessed on item nos. 4, 5, 6 on HPRSD pertaining to sleep during the period of sleep deprivation i.e. periods 2 and 3. All ratings were done at the same time of the day and by the same rater.
The data was subjected to statistical analysis.
Sleep deprivation appeared to be effective in patients suffering from both endogenous and reactive depressions. As can be seen from [Figure 1], the HPR.SD
There was an increase in scores at period 5 in case of reactive depression indicating the temporary nature of improvement. The improvement in cases of endogenous depression seemed to last longer as the scores at period 5 remained more or less at the level obtained at period 4 [Figure 1].
Improvement on individual variables of the HPRSD was calculated by comparing the scores at period I and period V. The change scores were then converted into percentages. Maximum reduction in scores occurred for the variables: "Depressed. Mood, Suicide, Feelings of Guilt, Retardation, Agitation and Hopelessness." The percentage of improvement ranged from 90% for the variable, "depressed mood", to 72.73% for the variable "hopelessness". Least improvement was seen for the variables "Insight" (25%), "Somatic symptoms: Gastrointestinal" (28.57% ), and "Somatic symptoms" general" (35.71%) [Table 2].
Further analysis was carried out on the following five factors of the HPRSD by Freidman's two-way analysis of variance by ranks  viz; Factor I-"Anxiety Somatization", Factor III-"Cognitive Disturbance", Factor IV-"Diurnal Variation", Factor V-"Retardation" and Factor VI-"Sleep Disturbance". Significant differences between period 1 and period 5 could be demonstrated for all factors except Factor IV [Table 3] 
When between factor comparisons were made for period 1 and subsequent periods viz., periods 2, 3, 4 and 5, significant preferences could be domonstrated for factors I, III, V and VI indicating that sleep deprivation effectively reduced the initial scores for these factors.[Table 4].
Significant reduction was seen when the scores at periods 3, 4 and 5 were compared with the scores at period 1 for factors III, V and VI. The change in scores for factor I was significant when comparisons were made at period 3 and 4 with reference to period 1, but not at period 5. [Table 4].
Finally when the scores at each evaluation period were compared with the scores at successive periods, significant differences could be elicited at periods 2 and 3 for the factors, I, III and V. [Table 5]
No side effects were observed during the trial period and none of the patients had to be discontinued from the study.
The exact mechanism of action of sleep deprivation is unknown. Several theories have been proposed. According to Pflug,  sleep deprivation acts by bringing about resynchronisation of disturbed circadian rhythms by interrupting them. According to Vogel,  REM sleep deprivation and subsequent REM sleep pressure may be responsible for the beneficial effect of this procedure in depression. Both these hypotheses are in keeping with reports that continuous narcosis can also be of benefit in depression.  Another explanation assumes that patients with endogenous depression (both agitated and retarded) are in some way in a chronically over-aroused state.  There is a classical inverted "U" relationship between the level of arousal and the quality of behaviour. Thus in the overaroused depressive, the performance is poor. Sleep deprivation lowers the subjects' arousal level to a more adequate state, and thereby brings about improvement in behaviour.  This theory also explains the detrimental effects of sleep deprivation in normal subjects.  Animal studies suggest that sleep deprivation can increase brain monoamine levels. It seems likely that this is probably due to stress.  Quite possibly more than one mechanism may be operating. At this point we would like to submit an alternative explanation for the effects of sleep deprivation in depression.
Guilt feelings are commonly present as symptoms of depression. Patients with depression may interpret sleep deprivation as a form of self denial or punishment which, in turn, may alleviate the guilt feelings and thereby lift up the depressive mood.
The role of "TYAGA" (sacrifice) is mentioned in the Upanishads and in the Bhagawat Gita where Prayaschitta Karma (self punishment) is advocated as a means for atonement for past misdemeanours or sins. , However, all the improved patients in our series were not Hindus. Atonement for sins or performance of penance would also not explain the differential improvement between reactive and endogenous depression, unless it was granted that feelings of guilt are more frequent in endogenous than in reactive depression. This argument is supported by the fact that in our series the scores for the variable guilt feelings were greater in endogenous as compared to reactive depression, and the reducton in the scores after sleep deprivation was also larger. [Table 6].
Analysis of the 5 factors of the HPRSD showed that there was improvement in those variables which made up factor I (anxiety somatization) in addition to the variables which constituted Factors III, V and VI. The variables "suicide, depressed mood and psychomotor inhibition" are included in Factors III, V and VI and these symptoms have been reported to improve with sleep deprivation. ,
The improvement seen in this series for the variable constituting the factor "anxiety somatisation" may have been because the patients marked those variables which constituted Factor I more frequently as compared to other variables.
Perhaps patients in this culture somatise the symptoms of depression to a greater extent as compared to others. This possibility has been raised elsewhere. 
When the scores were compared between the initial evaluation and successive evaluation, with the initial evaluation as a point of reference, the improvement seen in the variables for the Factors III, V and VI lasted right upto period 5 i.e. 7 days after completion of sleep deprivation. This was not the case for Factor I, where the improvement failed to reach significance at period 5.
The successive factor scores at each evaluation period were compared serially among themselves. It was observed that no significant improvement occurred after one night of sleep deprivation. Significant improvement occurred only after two successive nights of sleep deprivation. This observation is contrary to what has been reported in the literature . ,
Most studies have reported the effects of a single night of sleep deprivation.. The difference between the findings reported here and those reported elsewhere may be due to the fact that in this study two consecutive nights of sleep deprivation was the rule for all patients in contrast to a single night of sleep deprivation as in the other studies. Quite possibly sleep deprivation for more than 2 consecutive nights, or for several nights interspersed with varying periods of permitted sleep may show different results altogether.
Factor II was not included in the analysis as this factor comprised of the actual and historical loss of weight. It is unlikely that this could have altered in such a short period of time.
Other extraneous variables which might have been responsible for some of the discrepancies between the present study and those reported elsewhere could be because of placebo effect such as is shown in trials of antidepressant medication and which cannot be discounted in our study. The distribution of patients in each group was uneven with reference to the type of depression, and the total number of patients treated was small. The patients were aware of our expectations and received extra amount of attention. Endogenous depression is known to remit spontaneously, although this seems unlikely in our patients. It could be argued that the apparent improvement during sleep deprivation period could have occurred directly or indirectly as a result of the patients' poor motivation and recourse to a ruse to end a treatment which had become an ordeal. This is unlikely because the patients entered the trial only after they had understood the procedure involved and had signified their willingness. Furthermore, as illustrated in [Figure 1], the scores increased differentially during the week following sleep deprivation. This would not have been the case if the decrease in scores during sleep deprivation was a function of the patients' effort to escape from an ordeal. The improvement could also have been due to the delayed result of medication given prior to commencement of sleep deprivation. However, most of our patients had been taking medication from 2 to 8 months and in adequate dose but without any benefit. A wash out period of 10 days was also allowed in between the termination of medication and commencement of sleep deprivation. Rater bias could be one more incriminating variable which was not controlled.
Finally, group processes could have been important. A feeling of well being might have been induced as a result of prevention of troublesome lonely wakefulness in bed. Some improvement may also have occurred due to the opportunity provided to the patients to express their psychological and social problems. However all patients who improved did not find this group therapeutic interaction helpful, or participate in it fully. All these variables will be accounted for in a future ongoing controlled study on sleep deprivation, which we are conducting in our department.
The authors thank Dr. C. K. Deshpande, Dean, K.E.M. Hospital & G.S. Medical College, Bombay for the permission to publish this paper.
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]