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  IN THIS Article
 ::  Abstract
 ::  Introduction
 ::  Material And Methods
 ::  Results
 ::  Discussion
 ::  Acknowledgement
 ::  References
 ::  Article Figures
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ARTICLE
Year : 1979  |  Volume : 25  |  Issue : 1  |  Page : 4-11

Sleep deprivation in depression


Departments of Psychiatry, Medicine & Surgery-Statistics, K.E.M. Hospital and Seth G.S. Medical College, Parel, Bombay 400 012, India

Correspondence Address:
D R Doongaji
Departments of Psychiatry, Medicine & Surgery-Statistics, K.E.M. Hospital and Seth G.S. Medical College, Parel, Bombay 400 012
India
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Source of Support: None, Conflict of Interest: None


PMID: 458741

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 :: Abstract 

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.



How to cite this article:
Doongaji D R, Vahia V N, Lakdawala P D, Parikh M D, Singh A R, Thatte SS, Lotlikar KD. Sleep deprivation in depression. J Postgrad Med 1979;25:4-11

How to cite this URL:
Doongaji D R, Vahia V N, Lakdawala P D, Parikh M D, Singh A R, Thatte SS, Lotlikar KD. Sleep deprivation in depression. J Postgrad Med [serial online] 1979 [cited 2017 Oct 20];25:4-11. Available from: http://www.jpgmonline.com/text.asp?1979/25/1/4/42097



 :: Introduction Top


In 1965, Schulte described a female patient who reported that her depression seemed to lessen after she had stayed awake all night. [9] 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. [7] 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. [2],[3],[11]

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.


 :: Material And Methods Top


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). [4] 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.


 :: Results Top


Efficacy

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 scores decreased substantially from period 1 to period 3.

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 [10] 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] [4]

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]

Side effects

No side effects were observed during the trial period and none of the patients had to be discontinued from the study.


 :: Discussion Top


The exact mechanism of action of sleep deprivation is unknown. Several theories have been proposed. According to Pflug, [7] sleep deprivation acts by bringing about resynchronisation of disturbed circadian rhythms by interrupting them. Accord­ing to Vogel, [13] 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. [2] Another explanation assumes that patients with endo­genous depression (both agitated and re­tarded) are in some way in a chronically over-aroused state. [5] 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. [3] This theory also explains the detri­mental effects of sleep deprivation in normal subjects. [3] Animal studies sug­gest that sleep deprivation can increase brain monoamine levels. It seems likely that this is probably due to stress. [8] 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. [1],[12] 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. [7],[11]

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. [6]

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 . [2],[7]

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.


 :: Acknowledgement Top


The authors thank Dr. C. K. Desh­pande, Dean, K.E.M. Hospital & G.S. Medical College, Bombay for the permis­sion to publish this paper.

 
 :: References Top

1.Bhagawat Geeta, Adhyaya 18, Verses 34, 39.  Back to cited text no. 1    
2.Bhanji, S. and Roy, G. A.: The treat­ment of psychotic depression by sleep deprivation: a replication study. Brit. J. Psychiat., 127: 222-226, 1975.  Back to cited text no. 2    
3.Burg, Van den W. and Hoofdakker Van den, R. H.: Total sleep deprivation on endogenous depression. Arch. Gen. Psychiat., 32: 1121-1125, 1975.  Back to cited text no. 3    
4.Hamilton, M.: Hamilton's psychiatric rating scale for depression, ECDEU Assessment manual, U.S. department of health education and welfare public health service, 1976, pp.: 179-183.  Back to cited text no. 4    
5.Kahneman, D.: "Attention and effort," Englewood Clip, New Jersey, Prentice Hall Inc., 1973.  Back to cited text no. 5    
6.Marfatia, J. C.: Editor "Proceedings of symposium on Sintamil" Ciba of India Limited (Bombay), 1972.  Back to cited text no. 6    
7.Pflug, B.: The effect of sleep deprivation on depressed patients, Acta. Psychiat. Scand., 53: 148-158, 1976.  Back to cited text no. 7    
8.Radulovacki, M.: Comparison of effects of paradoxical sleep deprivation and im­mobilization stress on 5 hydroxy-indolacetic acid in CSF, Brain Research, 60: 255-258, 1973.  Back to cited text no. 8    
9.Schulte, W.: Kombinierte psycho. used pharmakotheropie bei melancholikern. 1. Rothenburger Gesprach, Karger, Basel, New York 1965.  Back to cited text no. 9    
10.Siegel, S.: Nonparametric statistics for the behavioral sciences. International student edition. McGraw Hill Book Co. Inc. N.Y., 1956, p. 166.  Back to cited text no. 10    
11.Svendson, K.: Sleep deprivation therapy in depression. Acta. Psychiat. Scand., 54: 184-192, 1976.  Back to cited text no. 11    
12.Upanishad, Chandopanishad. Sarg II, Verse. No. 1.1.  Back to cited text no. 12    
13.Vogel, G. W., Thompson, F. C . , Thur­mond, A. and Rivers, B.: The effect of REM deprivation on depression. Psycho­somatics, 14: 104-107, 1973.  Back to cited text no. 13    


    Figures

  [Figure 1]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]



 

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