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Dépression et sommeil : aspects cliniques et polysomnographiques
Abstract
L'insomnie fait partie des critères diagnostiques de l'épisode dépressif majeur. Pourtant les relations qui existent entre ces deux entités sont loin d'avoir livré tous leurs secrets. Sur le plan clinique on observe en général une altération de la continuité du sommeil et un réveil précoce. La réduction du temps de sommeil s'accompagne d'une fatigue intense, maximum le matin. Cette fatigue ne correspond pas à une réelle somnolence et les patients restent bien souvent couchés sans dormir bien qu'ils soient persuadés du contraire. Grâce à la polysomnographie on met en évidence un déficit en sommeil lent profond et un raccourcissement de la latence du sommeil paradoxal dans les cas typiques. Certaines de ces anomalies, bien que non spécifiques, se retrouvent chez les parents du premier degré des dépressifs et persistent après la rémission de l'épisode. Ces éléments pourraient donc constituer des marqueurs de trait dépressif. Des données récentes permettent de penser que l'insomnie chronique, plus qu'un facteur de risque, pourrait être un facteur causal de la dépression. Cette hypothèse nous conduit à encourager la prise en charge pharmacologique et non pharmacologique de l'insomnie dans le cadre de la prévention et du traitement de la dépression. © 2007 Elsevier Masson SAS. Tous droits réservés.
Violent behavior in adolescents is a real social problem and a public health issue. It manifests in the form of violence against others or self-directed violence, and can be isolated or recurrent. The understanding of this behavior rests on a complex and multifactorial determinism including both psychiatric / psychopathological and educational / sociocultural dimensions. The aim of this paper is to examine the influence of sleep modifications during adolescence on this phenomenon of violence. Changes in processes of sleep regulation occurring at this age, which have both physiological and psychological origins, often lead to chronic sleep loss and to disruptions of the synchronization of biological rythms. These changes are likely to favour impulsive behavior, a hypothesis consistent with the results of numerous epidemiological studies. Sleep disorders could thus trigger and aggravate violent behavior in adolescents. In our opinion, this is strong evidence that sleep disturbances in adolescents should always be taken into consideration in clinical practice.
Depuis plusieurs années, de nombreux travaux scientifiques ont réaffirmé le rôle important du sommeil dans la régulation du comportement. Or, l'adolescent – chacun le sait – accorde peu d'importance à l'équilibre de son sommeil : il préfère souvent veiller et remettre son repos à plus tard, ce qui lui occasionne de nombreux cas de manque caractérisé de sommeil. Il est permis de se demander si, dans les cas les plus nets, le sommeil parvient encore à jouer son rôle restaurateur et si son insuffisance ne peut pas contribuer à la séquence qui aboutit, chez certains adolescents, à l'expression de comportements violents. La violence chez l'adolescent L'adolescence, période de maturation physique et psycholo-gique qui s'impose au grand enfant, évoque immédiatement les notions de crise, de conflit et donc de violence. Cette violence peut s'exprimer avec force et déterminer des comportements agressifs aux formes multiples, ce qui met en difficulté l'adolescent lui-même, son entourage et, bien souvent, le groupe social. Les comportements violents des adolescents, dont la fréquence et la typologie sont comparables dans l'ensemble des pays industrialisés (1), constituent à l'heure actuelle une question de société qui a d'importants échos dans le domaine de la santé publique. En témoignent plusieurs travaux récents réalisés sur demande institutionnelle (2, 3). D'une manière générale, toute expression extériorisée de violence mise à part, il faut signaler que l'adolescent vit ses émotions et ses sentiments avec une intensité telle qu'il éprouve souvent une certaine violence en lui et autour de lui. Ses comportements agressifs se situent donc fréquemment « en miroir » par rapport à une pression extérieure qu'il ressent et perçoit comme violente (4). Les rites qui étaient censés scander le passage à l'âge adulte, et qui ont quelque peu disparu de notre culture mais ont persisté dans des sociétés plus traditionnelles, utilisaient cette violence qu'ils canalisaient dans un but maturatif. Selon de nombreux ethnologues, les prises de risque de type ordalique chez les adolescents occidentaux en constitueraient un retour (5). Dans cet article, nous nous intéressons principalement à l'ex-pression comportementale de la violence adolescente, celle-ci se manifestant sous la forme de conduites agressives différen-ciables que l'on peut classer de la manière suivante (4) : • les conduites hétéro-agressives : – la violence contre les biens (vandalisme et conduites destructrices solitaires), – la violence contre les personnes (intra-ou extrafamiliale) ; • les conduites autoagressives : – le suicide et les tentatives de suicide violentes, – les équivalents suicidaires et les autres comportements de prise de risques, – les automutilations (impulsives ou chroniques). L'importance du phénomène suicidaire dans la population adolescente est bien connue : il constitue, en France, la deuxième cause de mortalité chez les 15-24 ans et les modes suicidaires les plus violents (pendaison, armes à feu ou arme blanche, défenestration…) sont à l'origine de la majorité des suicides accomplis (6). En ce qui concerne les comporte-ments hétéro-agressifs, une idée de leur fréquence apparaît à travers les statistiques judiciaires : même s'ils représentent une minorité des délits commis par des adolescents, ils sont en augmentation constante depuis plusieurs années, en particulier chez les garçons (7). Chaque type de violence peut s'exprimer ponctuellement ou de manière récurrente, la répétition des passages à l'acte indiquant le plus souvent la mise en place d'une organisation psychopathologique (2). Dans ce domaine, les comporte-ments hétéro-agressifs récurrents sont habituellement référés au diagnostic de « Trouble des conduites » (8, 9), entité qui renvoie, dans la classification française des troubles mentaux de l'enfant et de l'adolescent (10), essentiellement aux organisations psychopathique et perverse de la person-nalité. Les conduites autoagressives concernent, quant à elles, principalement les troubles de l'affectivité de type « États limites » et les dépressions de l'adolescent (4). Certaines parmi ces dernières surviennent dans le cadre de troubles bipolaires de l'humeur qui semblent favoriser chez l'adolescent à la fois les comportements auto-et hétéro-agressifs (11).
It has been well documented that depression can lead to insomnia. However, evidence from previous research and from clinical experience indicates that the reverse can also be the case: long-standing insomnia can often lead to depression. The aim of this study is to test the hypothesis that, for many people suffering from both depression and insomnia, treating the insomnia successfully without medication can lead the depression to lift as well. The sample consisted of 86 consecutive patients or clients who presented as suffering from chronic insomnia. Two thirds of these people were also suffering from depression at intake. During an initial hour-long interview, self-report estimates of key sleep parameters were recorded, and the Beck Depression Inventory was administered. Subjects were then introduced to the "Sleep Better Without Drugs" self-help program (a book and three audio cassettes, which they used at home to improve their sleep. At follow-up, six to eight weeks later, the sleep parameters were recorded again and the Beck Depression Inventory was re-administered. Results showed that 70% of the insomnia sufferers who were depressed before treatment and learned to sleep better were no longer depressed, or were significantly less depressed, once their sleep had improved. By contrast, among people who did not learn to sleep better, none experienced a significant reduction in depression. The conclusion is that, for many people who suffer from both depression and insomnia, treating the insomnia successfully without medication can eliminate or significantly reduce the depression.
Seasonal affective disorder (SAD) is a syndrome characterized by recurrent depressions that occur annually at the same time each year. We describe 29 patients with SAD; most of them had a bipolar affective disorder, especially bipolar II, and their depressions were generally characterized by hypersomnia, overeating, and carbohydrate craving and seemed to respond to changes in climate and latitude. Sleep recordings in nine depressed patients confirmed the presence of hypersomnia and showed increased sleep latency and reduced slow-wave (delta) sleep. Preliminary studies in 11 patients suggest that extending the photoperiod with bright artificial light has an antidepressant effect.
A growing body of research indicates that sleep disturbances may be specifically linked to suicidal behaviors. It remains unclear, however, whether this link is largely explained by depressive symptoms. The present study investigated the relationship between suicidality, depression, and sleep complaints in a clinical outpatient setting.
Upon admission, 176 outpatients completed measures on sleep disturbances, suicidal symptoms, and depression. Several sleep disturbances were evaluated with regard to suicidal ideation, including insomnia, nightmares, and sleep-related breathing symptoms.
Regression analyses revealed that insomnia and nightmare symptoms were associated with both depressive symptoms and suicidality. Sleep-related breathing symptoms were associated with depressive symptoms, but did not show an association with suicidal ideation. After controlling for depressive symptoms, only nightmares demonstrated an association with suicidal ideation. This relationship emerged as a nonsignificant trend (P = .06). Nightmares were particularly associated with suicidality among women compared with men. Posthoc analyses revealed that, after controlling for sex and depressive symptoms, nightmare symptoms were significantly associated with suicidality (P = .04).
Although insomnia and nightmares were significantly associated with depressive and suicidal symptoms, after controlling for additional variables, such as depression and sex, only nightmares remained associated with suicidality. This association was slightly stronger among women compared with men.
This study used empirically validated insomnia diagnostic criteria to compare depression and anxiety in people with insomnia and people not having insomnia. We also explored which specific sleep variables were significantly related to depression and anxiety. Finally, we compared depression and anxiety in (1) different insomnia types, (2) Caucasians and African Americans, and (3) genders. All analyses controlled for health variables, demographics, organic sleep disorders, and symptoms of organic sleep disorders.
Cross-sectional and retrospective.
Community-based sample (N=772) of at least 50 men and 50 women in each 10-year age bracket from 20 to more than 89 years old.
Self-report measures of health, sleep, depression, and anxiety.
People with insomnia had greater depression and anxiety levels than people not having insomnia and were 9.82 and 17.35 times as likely to have clinically significant depression and anxiety, respectively. Increased insomnia frequency was related to increased depression and anxiety, and increased number of awakenings was also related to increased depression. These were the only 2 sleep variables significantly related to depression and anxiety. People with combined insomnia (ie, both onset and maintenance insomnia) had greater depression than did people with onset, maintenance, or mixed insomnia. There were no differences between other insomnia types. African Americans were 3.43 and 4.8 times more likely to have clinically significant depression and anxiety than Caucasians, respectively. Women had higher levels of depression than men.
These results reaffirm the close relationship of insomnia, depression, and anxiety, after rigorously controlling for other potential explanations for the relationship.
In our 24-hour society, frequently disrupted and restricted sleep is a rapidly increasing problem that may contribute to the development of diseases such as depression. One of the proposed neurobiological mechanisms underlying depression is a disturbance in the brain's serotonergic neurotransmission, particularly a desensitization of the serotonin (5-HT)1A receptor system. However, a relationship between chronic sleep loss and changes in (5-HT)1A receptors has not been established yet. Therefore, in the present study, we experimentally tested the hypothesis that chronic sleep restriction leads to desensitization of the (5-HT)1A receptor system.
Rats were subjected to a schedule of restricted sleep allowing them 4 hours of sleep per day. Sleep restriction was achieved by placing the animals in slowly rotating wheels. The sensitivity of the (5-HT)1A receptor system was examined by measuring the hypothermic response to a standard injection of a 1A agonist.
After 2 days of restricted sleep, the sensitivity of the (5-HT)1A receptor system was not yet affected; however, after 8 days of sleep restriction, it was desensitized. Control experiments indicated that the effect of sleep restriction was not due to forced activity or stress. Importantly, the desensitization of the (5-HT)1A system persisted for many days even with unlimited recovery sleep. Normalization occurred gradually but required at least 7 days.
Chronic sleep restriction causes a gradual and persistent desensitization of the (5-HT)1A receptor system. This finding provides a link between chronic sleep loss and sensitivity for disorders that are associated with altered serotonergic neurotransmission.
• Using electroencephalographic sleep data from a sample of 235 elderly subjects, discriminant function analyses of sleep alterations in depression and dementia were performed. Overall, 80% of patients were correctly classified using a backward discriminant function analysis, and 81% with a general stepwise discriminant function analysis. Four measures contributed to the separation of depressed and demented patients: rapid eye movement (REM) sleep latency (lower in depressives); REM sleep percent (higher in depressives); indeterminate non-REM sleep percent (higher in demented patients, reflecting greater loss of spindles and K complexes); and early morning awakening (more marked in depressives). When both discriminant functions were subjected to cross-validation in independent subsamples, both procedures correctly identified 78% of patients. The classification functions derived from nondemented depressed and nondepressed demented patients were applied to a mixed-symptom group (n = 42). Overall, 27 patients (64%) with either depressive pseudodementia or dementia with depressive features were correctly classified using the same four predictor variables. These findings suggest that sleep physiological alterations of depression and dementia reflect between-group differences in sleep continuity, sleep architecture, and REM sleep temporal distribution, and that the differences are statistically reliable, in both diagnostically pure and mixed clinical presentations. These findings are discussed in the context of current hypotheses of sleep regulation and its mechanisms.
To develop further perspective on the psychophysiology of generalized anxiety disorder and primary depression, all-night electroencephalographic (EEG) sleep measures in outpatients with diagnoses of generalized anxiety disorder and primary (nondelusional) depression were compared. Both groups had difficulty initiating and maintaining sleep, and diminished amounts of slow-wave sleep. Compared to patients with generalized anxiety disorder, depressive had a shorter rapid eye movement (REM) latency, greater REM sleep percent and eye movement activity, and a different temporal distribution of REM sleep. Anxious patients showed few changes from first to second night, whereas depressives showed increases in several REM sleep indexes. The combination of REM sleep latency and REM percent correctly classified 86.7% of patients. These data may provide a more direct measure of central nervous system arousal and sleep / wake function than previous studies in the psychophysiology of anxiety. They also lend support to the clinical distinction between generalized anxiety disorder and primary depression and to the classification of anxiety states as disorders of initiating and maintaining sleep.
: The entire night's sleep of 6 patients with manic-depressive psychosis, depressive type, was studied electroencephalographically and compared with data similarly obtained from normal subjects. The categories for the electroencephalograms were waking or daytime and sleep, the latter being subdivided into low voltage, spindles, spindles plus random, and random.
There was considerable variability among the patients in the percentage of time that each electroencephalographic type appeared during the entire night's recording. This variability became less when the waking records were excluded and only the electroencephalographic patterns that occurred in sleep were considered.
In a comparison of the mean percentage of time each electroencephalographic sleep pattern appeared in the sleep records of patients and normal controls, it was found that the patients had almost twice as much low voltage activity as the normal controls (37.5 to 19 per cent respectively) and approximately one-half as much spindles plus random activity as the normal controls (23 to 40 per cent respectively).
In a comparison of the minute by minute fluctuations from one electroencephalographic pattern or level to another for the entire night's recording of patients and normal controls, it was found that the fluctuations were more frequent for the patients.
The percent of the minutes during the night's sleep which contained two or more of the electroencephalographic sleep levels was nearly twice as great for the patients as for the normal controls (52.7 to 28.5 per cent respectively).
Copyright (C) 1946 by American Psychosomatic Society
Data from all-night EEG sleep studies were used to distinguish normal subjects, primary depressed patients, and primary insomniac patients. In part 1, we compared 41 normal subjects, 56 depressed patients, and 18 insomniacs. In a univariate comparison with normal subjects, depressed patients showed less total sleep, longer sleep latency, more early morning awake time, more intermittent awake time, less delta sleep, less sleep efficiency, and shorter rapid eye movement (REM) latencies; compared with insomniacs, depressed patients showed greater early morning awake time, shorter REM latency, greater REM index, and greater REM density. Using multivariate discriminant analysis, 82% of the sample were correctly classified by diagnosis: 100% of the normal subjects, 72% of the depressed patients, and 77% of the insomniacs. Eight variables contributed to the multivariate separation of depressed individuals from insomniacs and normals: total sleep time, total recording period, sleep efficiency, sleep latency, early morning awake time, awake time, REM time and REM%. When the discriminant functions were applied to a second group of 18 primary depressed patients, 82% were correctly classified as depressed. These results suggest that primary depressed patients and primary insomniac patients may show relatively characteristic patterns of sleep abnormality.
Tested the hypothesis that manifest dysphoria indicates a special need for REM sleep; 127 undergraduates were Ss. Contrary to prediction, (a) dysphoric affect was not associated with heightened REM drive, (b) REM deprivation did not induce a greater increase in negative affect than did REM nondeprivation control awakenings, (c) postdeprivation sleep (recovery of REM) was not associated with a significant increase in positive affect, and (d) these predicted relationships were not more pronounced in sensitizers, individuals who are more apt to experience and report manifest dysphoria. The results provide no support for the hypothesis that REM sleep is especially important to the amelioration of dysphoric states. Nevertheless, the findings provide a framework for a critical reevaluation of the concept and operational definition of "REM need." (19 ref)
We reviewed the literature on sleep in psychiatric disorders and evaluated the data by meta-analysis, a statistical method designed to combine data from different studies. A total of 177 studies with data from 7151 patients and controls were reviewed. Most psychiatric groups showed significantly reduced sleep efficiency and total sleep time, accounted for by decrements in non-rapid eye movement sleep. Rapid eye movement sleep time was relatively preserved in all groups, and percentage of rapid eye movement sleep was increased in affective disorders. Reduction in rapid eye movement sleep latency was seen in affective disorders but occurred in other categories as well. Although no single sleep variable appeared to have absolute specificity for any particular psychiatric disorder, patterns of sleep disturbances associated with categories of psychiatric illnesses were observed. Overall, findings for patients with affective disorders differed most frequently and significantly from those for normal controls.
Alterations of nocturnal sleep have been widely described in affective disorders. However, little is known about putative daytime sleep and to what extent daytime sleep could interfere with nocturnal sleep. The goal of this study was to investigate 24-hr sleep patterns in 12 depressed patients hospitalized for a major depressive disorder and in 10 control subjects studied under the same experimental conditions. Patients and controls were free to sleep whenever they chose, and sleep recordings were performed using the Oxford Medilog System during 60 hr. Daytime sleep episodes were detected in 50% of the patients and in 60% of the controls. Patients took naps at various times of the day, whereas controls napped in the early afternoon, during the well-known "postlunch dip". Thus daytime sleep prevalence was similar in both groups; however, the biphasic distribution of sleep observed in controls disappeared in the patients. Napping did not affect subsequent nocturnal sleep in either group.
Earlier investigations have suggested that electroencephalographic (EEG) sleep may be altered as a function of the duration of an episode of depression. We compared the EEG sleep profiles in a group of recurrent depressives who had been depressed for less than 6 weeks with their sleep profiles as measured during their previous episode of depression. Findings in this sample of 32 patients point to the presence of specific rapid eye movement (REM) sleep abnormalities as being more pronounced earlier in the course of a depressive episode. Changes in REM latency and REM activity were also reflected in reductions in EEG spectral power in almost all bandwidths during the first REM period of the recurrent episode. These results are not easily explainable on the basis of traditional measures of clinical severity or the number of episodes.
In a cross-sectional design to address the effects of the course of depression on rapid-eye-movement (REM) latency, we have matched patients in their first-episode with (1) age-matched patients with recurrent depression, (2) onset-matched patients with recurrent depression, and (3) age-matched normal control subjects. Patients were also matched for sex and treatment site (inpatient or outpatient). No differences were found in REM latency for the three depressed groups, and all had lower REM latency than normals. This finding is taken as support for stable REM latency throughout the course of depression.
A substantial body of research in adults has established that certain sleep polysomnographic abnormalities are commonly found in depressed patients, including sleep continuity disturbances, reduced slow-wave sleep, shortened rapid eye movement (REM) latency, and increased REM density. To date, these abnormalities have not been documented in depressed children compared with age-matched controls. Three consecutive nights of polysomnographic recordings were obtained in 25 hospitalized depressed children and 20 age-matched healthy controls. The depressed patients had reduced REM latencies. The shortest single-night REM latency of each individual was the most sensitive discriminating value between depressed subjects and controls. The influence of different scoring criteria in distinguishing depressed children from healthy children is discussed. In addition, depressed children had an increased sleep latency and increased REM time but did not have stage 4 differences.
Psychobiological research has been used to validate subtypes of affective disorder. Nosologic separation of delusional from nondelusional depression has recently been aided by sophisticated analyses of sleep electrophysiology. In the present study, the sleep of elderly delusional and nondelusional depressed patients could be successfully distinguished from that of aged controls using standard sleep parameters. However, only a combination of manual and spectral analytic techniques separated the depressive subtypes. These results are preliminary and need replication in a larger sample.
Patients who met provincial criteria for atypical depression were contrasted with a group of patients who met RDC criteria for endogenous depression and a group of normal controls on a standard series of sleep variables. Atypical depressives were differentiated from normal controls by a shortened REMP latency. They did not, however, appear to have the sleep continuity disturbance exhibited by endogenous depressives. This preliminary work suggests that atypical depressives may have a unique pattern of sleep variables consisting of REM abnormalities without continuity disturbance. If this pattern is observed in additional studies, it would add to the validity of considering atypical depression a subtype of unipolar depressive illness.
Using electroencephalographic sleep data from a sample of 235 elderly subjects, discriminant function analyses of sleep alterations in depression and dementia were performed. Overall, 80% of patients were correctly classified using a backward discriminant function analysis, and 81% with a general stepwise discriminant function analysis. Four measures contributed to the separation of depressed and demented patients: rapid eye movement (REM) sleep latency (lower in depressives); REM sleep percent (higher in depressives); indeterminate non-REM sleep percent (higher in demented patients, reflecting greater loss of spindles and K complexes); and early morning awakening (more marked in depressives). When both discriminant functions were subjected to cross-validation in independent subsamples, both procedures correctly identified 78% of patients. The classification functions derived from nondemented depressed and nondepressed demented patients were applied to a mixed-symptom group (n = 42). Overall, 27 patients (64%) with either depressive pseudodementia or dementia with depressive features were correctly classified using the same four predictor variables. These findings suggest that sleep physiological alterations of depression and dementia reflect between-group differences in sleep continuity, sleep architecture, and REM sleep temporal distribution, and that the differences are statistically reliable, in both diagnostically pure and mixed clinical presentations. These findings are discussed in the context of current hypotheses of sleep regulation and its mechanisms.
In most research dealing with biological abnormalities in depression, the clinical diagnosis of depression is made and the occurrence of a biological abnormality, for example, reduced REM latency, is documented. In this study, that design was reversed; REM latency was used as a grouping variable to assess empirically the "biological" priority of Research Diagnostic Criteria endogenous symptoms. We found that terminal insomnia, pervasive anhedonia, unreactive mood, and appetite loss were most likely to discriminate among "reduced" and "nonreduced" REM latency depressions at various threshold values. Contrary to expectation, diurnal mood variation was found equivalently in all categories of REM latency studied. Implications for clinical decision making based on endogenous symptoms are discussed.
Thirteen patients were examined by sleep polysomnograph (PSG) and the dexamethasone suppression test when clinically depressed and later when clinically remitted for six months and no longer receiving antidepressant medication for two to five weeks. None of the PSG variables (rapid eye movement [REM] latency, total sleep time, stage 1 through 4 times, REM time, and REM densities in periods 1 through 3) was significantly changed between symptomatic depression and symptom remission. While symptomatic, 11 of 13 patients exhibited a reduced REM latency (65 minutes or less). After clinical remission, eight of the 11 continued to exhibit reduced REM latencies, whereas the dexamethasone suppression test tended to show nonsuppression only during clinical depression. These data represent either longer-term (ie, slow to normalize) biologic consequences of a depressive episode or biologic antecedents of clinical depression that may herald a return of the depression in individuals vulnerable to recurrence. Whether PSG abnormalities identify clinically remitted patients who are prone to develop another depressive episode requires longitudinal follow-up studies.
Electroencephalographic (EEG) sleep changes in affective disorders have been characterized by sleep continuity, slow wave sleep, and rapid eye movement (REM) abnormalities. The most commonly cited feature, however, has been shortened REM latency. Because the diagnostic and prognostic significance of shortened REM latency has been debated, this issue was reexamined in a group of 186 psychotic and nonpsychotic depressed inpatients and outpatients. The analyses suggest an increased frequency of sleep onset REM periods in psychotic depression and in elderly depressed patients (psychotic or nonpsychotic).
An analysis of electroencephalographic Summary sleep patterns in thirty-five consecutive patients admitted for the treatment of depression revealed that a single sleep characteristic—the interval between onset of sleep and the start of rapid-eye-movement (R.E.M.) sleep—is an objective indicator of depressive disease and correlates inversely with its severity. The mean R.E.M. latency for the entire group was 35 minutes; however, in patients with severe depression the R.E.M. latency averaged 18 minutes.
Studied 84 bipolar and unipolar depressed patients by means of a questionnaire to determine whether they showed symptoms of increased sleep time. It was found that hypersomnia is not an unusual symptom of depression. It is concluded that, if further confirmed, the finding has implications both for the classification of affective disorders and for biological research. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
SLEEP disturbance is a significant feature of most clinical descriptions of depression. Indeed, some authors attribute diagnostic or therapeutic implications to the nature of the sleep disturbance. Thus, for example, Mayer-Gross1 regarded early morning wakening as a feature of "endogenous depression," and onset sleep difficulty as a feature of "reactive depression." Noyes and Kolb2 reported that patients with severe depression (manic depressive psychosis) have characteristically little difficulty in falling asleep, but wake much earlier than when they are well. Kalinowsky3 reported that "sleeplessness" is an important diagnostic sign of "true depression" and an indication for electroconvulsive therapy (ECT). However, there are few systematic studies of the actual nature of sleep disturbance in depression.
Detre4 found sleep disturbance to be a feature in 70% of 295 newly admitted psychiatric patients. He claimed that early morning wakening correlated with the diag
The authors compare their laboratory measurements of the sleep of 21 depressed patients and 15 control subjects with similar data reported by others. All studies indicate less sleep and more wakefulness in depressed patients than in controls. The clinical impression of early morning awakening as a distinguishing feature of different types of depression is not borne out; it is not as definite a phenomenon as is generally suggested. The most consistent finding is a lack of Stage IV sleep among depressed patients.
In this clinical, psychometric and polysomnographic study, primary dysthymics (N = 20) were compared with anxious depressives (N = 22), and non-psychiatric controls (N = 11). Beck and MMPI depression scores were similar in the two affective groups. Prominent insomnia occurred in 82% of the anxious group; hypersomnia was more characteristic of the dysthymic group. On night 1, the anxious group had the poorest sleep efficiency (P less than 0.001), while dysthymics had the highest REM% (P less than 0.05) and shortest REM latency (P less than 0.01). On night 2, differences tended to be minimized, although the number of awakenings was still high (P less than 0.05) in the anxious group, and REM% was highest (P less than 0.01) and REM latency shortest (P less than 0.01) in the dysthymics. These findings suggest that patients with primary anxiety disorders experience greater sleep continuity difficulties on the adaptation night. Despite significant clinical overlap in depressive symptomatology between the two groups, REM% and REM latency appear as sturdy psychophysiological markers in differentiating primary dysthymics and anxious depressives on both nights. These data suggest that distinct anxious depressive and subaffective dysthymic subtypes can be distinguished within the universe of the atypical depressions.
Sleep was recorded in nine drug-free depressive patients and nine age- and sex-matched normal control subjects. All-night spectral analysis of the sleep electroencephalogram (EEG) showed a significantly reduced power density in the 0.25-2.50 Hz band in the depressive group. Power density values integrated over the entire frequency range (0.25-25.0 Hz) exhibited for both groups a decreasing trend over the first three non-REM/REM sleep cycles. In each cycle depressives had lower values than controls. The results are consistent with hypothesis that the build-up of a sleep-dependent process is deficient in the sleep regulation of depressive patients.
The possibility of characterizing subgroups of depressive disorders by biological markers was studied by means of the dexamethasone suppression test (DST), the 24-hr urinary free cortisol (UFC), the growth hormone response to the insulin tolerance test (ITT), and polygraphic sleep recordings. Forty-five hospitalized patients suffering from a moderate to severe nonpsychotic major depressive disorder were clinically subdivided into three groups: endogenous (n = 20), neurotic (n = 19), and "ambiguous" (n = 6). These clinical diagnoses were supplemented by operational diagnostic tools, namely, the Research Diagnostic Criteria (RDC) and the Newcastle Scale. The different diagnostic procedures exhibited a high degree of correspondence. Whereas the results of the ITT were normal in almost all patients, 20% of all patients were dexamethasone nonsuppressors and more than half of the patients showed a shortened REM latency. Both markers did not reveal any specificity for the endogenous subtype. A significant influence of weight loss on the DST and the excretion of UFC was evident.
Two processes play a dominant role in sleep regulation: a sleep-dependent process (Process S) and a sleep-independent circadian process (Process C). The time course of Process S was derived from the spectral analysis of slow wave activity in the human EEG. Its level shows an exponential decline during sleep and an increase during waking. The level of Process S at sleep onset is therefore a function of prior waking time. Process C is reflected by the rhythmic variation of sleep propensity during prolonged sleep deprivation, and is assumed to be controlled by a circadian oscillator. In the model, sleep propensity and the duration of sleep are determined by the combined action of the two processes. The model is able to simulate the variations of sleep duration as a function of sleep onset time. Since the amount of REM sleep is little influenced by prior sleep or waking and shows a marked circadian rhythmicity, it is assumed to reflect largely the level of Process C. The cyclic alternation of nonREM and REM sleep is assumed to result from a reciprocal interaction between the two sleep states. In contrast to previous models, only a single circadian oscillator is required to account for the sleep-wake cycle and the sleep organization under entrained and non-entrained schedules. The model also encompasses sleep regulation in animals and may provide indications as to the phylogenetic origin of sleep.
The persistence of a depressionlike sleep pattern in fully remitted depressed patients suggests that the pattern is a trait characteristic of sleep measurements. However, in the past, subjects have undergone investigation only after the onset of the disorder, and, therefore, the altered sleep pattern may merely represent a biological scar.
We polysomnographically investigated 54 healthy subjects who had no lifetime or current diagnosis of a psychiatric disorder but had at least one first-degree relative with major depression or a bipolar disorder and at least one further close relative with major depression, a bipolar disorder, or a schizophrenic disorder. Twenty unrelated control probands without a personal and family history of psychiatric disorders and 18 unrelated inpatients with major depression served as reference groups. Prior to investigation, all healthy subjects had been free of any prescription and nonprescription drug for at least 3 months. The depressed patients were free of drugs for at least 1 week. All subjects slept for 2 nights in the sleep research unit. The sleep of the second night was recorded and visually scored.
Analysis of the individual sleep cycles in these subjects revealed both a reduced amount of slow wave sleep and increased rapid eye movement density in the first sleep cycle. Discriminant analysis showed that 10 subjects (18%) had sleep patterns similar to those of depressed patients.
According to our observations, one fifth of the healthy subjects with a high genetic load for psychiatric disorders showed a conspicuous (depression-like) sleep pattern. The follow-up will determine whether this sleep pattern indeed represents a trait marker indicating vulnerability.
The current study was conducted to examine if recurrent depression is associated with more severe disturbances of all-night EEG sleep profiles than single-episode depressions. Unmedicated sex- and age-matched groups of 22 single-episode (SE) and 44 recurrent unipolar (RU) outpatients with DSM-III-R/SADS/RDC major depression underwent 2 consecutive nights of EEG sleep recording. Multivariate analyses of covariance (MANCOVAs) and/or analyses of covariance (ANCOVAs) were performed on six sets of sleep measures. Recurrent unipolar depression was associated with significantly increased phasic REM sleep, as well as increased REM counts on the second night of study. Recurrent depression also was associated with significantly poorer sleep efficiency, although the groups did not show consistent differences in sleep architecture or slow-wave sleep. Our findings generally support the hypothesis that recurrent depression is associated with a more severe neurophysiologic substrate than phenotypically similar SE cases. Results are, for the most part, compatible with Post's (1992) model of illness progression, particularly with respect to greater disturbances of state-dependent sleep abnormalities in the RU cases. Longitudinal studies are needed to confirm the evolution of such changes prospectively.
Limited evidence suggests that polysomnographic alterations may be more prominent early in a depressive episode. Whether the effects of episode duration extend beyond middle age and appear in late-life depression as well has important implications for treatment decisions and for understanding depressive illness across the life span. Furthermore, the impact of episode duration on sleep has not been examined in the context of other factors related to clinical history and psychosocial status.
Eighty-three persons aged 60 years or older with recurrent depression were studied: 34 had been depressed for 2 to 16 weeks and 49 for longer periods. An age- and gender-matched group of 48 persons with no history of major depression served as controls. Initial univariate analyses examined duration effects on electroencephalographic (EEG) sleep measurements. Multivariate analyses considered the combined effects of episode duration, clinical variables, and psychosocial variables on EEG sleep profile.
Episode duration was strongly associated with sleep continuity, architecture, and rapid eye movement: subjects who were earlier in their depressive episodes had their sleep impaired more than those later in their episodes, who, in turn, were more impaired than controls. Moreover, clinical characteristics of subjects' depressive illness, demographic variables, and psychosocial stressors and supports had unique effects on the EEG sleep profile.
Episode duration appears to be a potent factor to consider when evaluating sleep during depression. The additional contribution of clinical and psychosocial characteristics to the prediction of the EEG sleep profile demonstrates the importance of incorporating these variables into models of the psychobiologic characteristics of depression. The results are relevant to the timing and focus of therapeutic interventions.
Depressed patients often report problems sleeping, and epidemiologic evidence suggests that insomnia may precede the onset of depression. Insomnia is associated with marked impairment in quality of life and ability to function effectively. Many studies have indicated that patients with chronic sleep problems have impaired mood and that effective management of insomnia in depressed patients can markedly improve their depression. Diagnosis of insomnia is challenging because there can be many different causes and the clinical picture can be blurred by the presence of other psychiatric illnesses. Pharmacotherapy provides reliable and rapid relief from insomnia, whereas behavioral therapies help produce long-term improvement. For many years, benzodiazepines have been the mainstay of drug treatment for insomnia. However, these drugs have significant side effects, and tolerance and dependence have discouraged use. Many doctors use sedating antidepressants in low doses to treat chronic insomnia. However, there is little evidence supporting the efficacy of these agents, and many have adverse side effects, including impairment of sleep. The newer selective hypnotic drugs, including the imidazopyridines, may offer patients a better short-term alternative to benzodiazepines or sedating antidepressants.
The Wistar-Kyoto (WKY) rat exhibits several behavioral and hormonal abnormalities often associated with depression. One of the hallmarks of depression consists of alterations in the sleep-wake cycle, particularly in rapid eye movement (REM) sleep. If the WKY rat is indeed an animal model for depression, we hypothesized that it should also show sleep abnormalities relative to the control strain, the Wistar (WIS) rat Under baseline conditions, WKY rats showed a 50% increase in total REM sleep time during the 12 h light phase and an increase in sleep fragmentation during both the light and dark phase. The WKY rats also exhibited lower EEG power densities over the entire frequency range (0.2-25.0 Hz) during REM sleep. After a 6 h sleep deprivation, the REM sleep rebound was more pronounced during the dark but not the light phase in the WKY rats. Since the WKY rat represents a genetic model for depression with altered EEG sleep patterns, this strain may be particularly useful for investigating the relationship between depression and sleep abnormalities.
Previous studies indicate that recurrent forms of depression are associated with greater biological disturbances as compared to single-episode cases. This study examines whether the observed differences in the sleep patterns during recurrent and single-episode depression persist into remission following nonpharmacologic treatment.
Two groups of patients (27 single episode [SE] and 53 recurrent unipolar [RU]) with major depression underwent sleep studies before and after nonpharmacologic treatment. Groups were equated for age, severity, and proportion of men and women. Groups were compared using multivariate analyses of covariance and/or analyses of covariance to examine six sets of sleep measures.
The differences observed between the SE and RU groups during the index episode persisted into early remission. The findings of greater disturbances of sleep continuity, rapid eye movement sleep and diminished slow wave sleep in the RU group supports the hypothesis that recurrent depression is associated with a more severe neurophysiological substrate than clinically comparable SE cases.
Although these observations are consistent with an illness progression model, the possibility that recurrent affective illness is associated with a more virulent, stable phenotype cannot be ruled out. Resolution of this issue requires longitudinal and family studies.
The serotoninergic system is involved in the regulation of sleep and wakefulness, its activity being at maximum during the awake state and minimum during sleep. In particular, the production of rapid eye movement (REM) sleep depends on the decrease of serotoninergic tone in brain stem structures. Thus, serotoninergic compounds which increase this tone (such as antidepressants) induce inhibition of REM sleep. Depression is associated with a functional decrease of serotoninergic neurotransmission and with specific alterations of sleep, notably insomnia. Paradoxically, even though they complain of sleep loss, depressed patients exhibit significant mood improvement after one night of sleep deprivation. This antidepressant effect can be accounted for by the same serotoninergic mechanisms as those described for pharmacological treatments. Indeed, the therapeutic action of antidepressants such as selective serotonin reuptake inhibitors is thought to depend directly on the enhancement of central serotoninergic neurotransmission. Such enhancement is achieved through desensitization of serotoninergic autoreceptors, which results from chronic treatment with these compounds. Sleep deprivation also induces an activation of serotoninergic neurons due to prolonged wakefulness, and leads to similar serotoninergic adaptive processes. The common neurobiological mechanisms resulting from pharmacological antidepressant treatment and sleep deprivation suggest that sleep loss in some insomniac or in depressed patients might be an endogenous compensatory process which would be therapeutical rather than pathological. This proposal should open the way to new strategies in the treatment of depression.
Drug resistance remains a persistent source of morbidity and mortality for patients with bipolar depression. A growing number of clinical studies support the usefulness of chronotherapeutic interventions, such as total sleep deprivation (TSD) and light therapy (LT), in the treatment of nonresistant bipolar depression.
To investigate the clinical usefulness of TSD plus LT in the treatment of drug-resistant bipolar depression, we treated 60 inpatients for 1 week with repeated TSD and LT combined with ongoing antidepressants and lithium salts. All patients had a DSM-IV diagnosis of bipolar I disorder. Drug resistance was rated according to Thase and Rush criteria. The pattern of relapses and recurrences was assessed during a prospective 9-month follow-up. Data were gathered from September 2002 to July 2004.
A 2-way repeated-measures analysis of variance with changes in self-rated perceived mood scores as dependent variable and with time and group (history of drug resistance) as independent factors confirmed significant time-by-group interaction (p = .0339). A logistic regression on rates of achievement of response (50% reduction in Hamilton Rating Scale for Depression ratings) confirmed the significance of observed differences: overall, 70% (23/33) of nonresistant versus 44% (12/27) of drug-resistant patients achieved response (p = .045). A survival time analysis (Cox proportional hazards model) showed that history of drug resistance significantly influenced the pattern of relapses and recurrences, with 57% (13/23) of nonresistant responders and 17% (2/12) of drug-resistant responders being euthymic after 9 months (p = .0212).
The combination of repeated TSD and LT in drug-resistant patients was useful in triggering an acute response. Further clinical research is needed to optimize this treatment option for drug-resistant patients in the long term.
Neurogenesis in the adult hippocampus can be up- or downregulated in response to a variety of physiological and pathological conditions. Among these, dysregulation of hippocampal neurogenesis has been recently implicated in the pathogenesis of depression. In addition, in animal models of depression, a variety of antidepressant treatments reverse that condition by increasing neurogenesis. As one night sleep deprivation is known to improve mood in depressed patients for at least 1 day, we investigated whether a comparable treatment may affect hippocampal neurogenesis in adult rats. Accordingly, rats were sleep-deprived by gentle handling for 12 h during their physiological period of rest, and were injected with bromodeoxyuridine 4 h and 2 h before the end of sleep deprivation. They were then perfused immediately thereafter, or after 15 days and 30 days. We found that 12 h sleep deprivation significantly increased cell proliferation and the total number of surviving cells in the hippocampal dentate gyrus soon after sleep deprivation, as well as 15 days and 30 days later, in comparison to control rats allowed to sleep. No changes were instead found in the subventricular zone of the lateral ventricles, indicating that 12 h sleep deprivation selectively triggers neurogenic signals to the hippocampus. The present data include acute sleep deprivation among the conditions which upregulate hippocampal neurogenesis and raise the possibility that such response could be implicated in the beneficial effects elicited in depressed patients by one night sleep deprivation. Thus, the findings could contribute to the understanding of the intriguing relationship between depression and neurogenesis in the adult brain.
- Dj Taylor
- Kl Lichstein
- Hh Durrence
- Bw Reidel
- Aj Bush
Taylor DJ, Lichstein KL, Durrence HH, Reidel BW, Bush AJ. Epidemiology of Insomnia, Depression, and Anxiety. Sleep
2005;28:1457-64.
Electroencephalographic sleep of younger depressives: comparison with normal
- Dj Kupfer
- Rf Ulrich
- Pa Coble
- Db Jarrett
- Vj Gochocinski
- L Doman
Kupfer DJ, Ulrich RF, Coble PA, Jarrett DB, Gochocinski VJ,
Doman L, et al. Electroencephalographic sleep of younger depressives: comparison with normal. Arch Gen Psychiatry 1985;42:806-10.
Eszopiclone co-administered with fluoxetine for insomnia associated with major depressive disorder (MDD): an analysis of the effects on depression
- V Mccall
- M Fava
- T Wessell
McCall V, Fava M, Wessell T, et al. Eszopiclone co-administered
with fluoxetine for insomnia associated with major depressive disorder (MDD): an analysis of the effects on depression. Sleep
2005;28:A310.
Insomnia as a risk for increased morbidity in depressed elderly subjects treated for depression: the IMPACT cohort
- W Pigeon
- M Hegel
- T Mackenzie
- J M Lyness
- M J Sateia
- M L Perlis
Pigeon W, Hegel M, MacKenzie T, Lyness JM, Sateia MJ, Perlis
ML. Insomnia as a risk for increased morbidity in depressed elderly
subjects treated for depression: the IMPACT cohort. Sleep
2005;28:A307.
États dépressifs et sommeil
- M Ferreri
Ferreri M. États dépressifs et sommeil. J Psy Biol Thérap
1983;10:10-5.