In the clinical picture of depression, along with affective, motor, and autonomic obligate, there are dissominal disorders, which introduces the problem of sleep disturbances into the circle of the most relevant for this disease. The term “dissomic” reflects the diversity of these disorders, including both insomnic and hypersomnic manifestations. The frequency of disturbances in the sleep-wake cycle in depression ranges from 83 to 100%, which is determined by the various methodological possibilities for their assessment; in polysomnographic studies it is always 100%.
This obligatory nature of the sleep-wake cycle disorders in depression is based on general neurochemical processes. A special place in this regard is occupied by serotonin, the mediation disorders of which, on the one hand, play a crucial role in the genesis of depression, and on the other hand, are of great importance in the organization of delta sleep and in the initiation of the REM phase. This also applies to other biogenic amines, in particular, norepinephrine and dopamine, the deficiency of which is important in the development of depression, and also determines the organization of the sleep-wake cycle.
Until now, there are no complete ideas about the characteristic features of sleep disorders in various forms of depression, although their great phenomenological diversity has long been indicated. Changes in sleep during endogenous depression are characterized by a reduction in delta sleep, a shortening of the latent period of PBS, an increase in the density of fast eye movements – BDG (one of the main phenomena that characterize PBS), frequent awakenings. In psychogenic depressions, the prevalence of falling asleep with a compensatory lengthening of morning sleep is indicated in the structure of insomnia, while frequent nightly and final early awakenings prevail in endogenous depression. In patients with depression, a decrease in the depth of sleep, an increase in motor activity and frequent awakenings, a marked reduction in the 4th stage of sleep, against which an increase in the surface (1st and 2nd) stages of the slow sleep phase (FMS) are often noted, are shown. The number of transitions from stage to stage is increasing, which indicates instability in the work of cerebral mechanisms of maintaining the stages of sleep. In addition, a characteristic sign was an increase in the number of awakenings in the last third of the night.
The phenomenon of “alpha-delta sleep” described in patients with depression indicates a significant change in the organization of the deepest stages of PMS. It is a combination of delta waves and a high-amplitude alpha rhythm (lower in frequency by 1-2 oscillations than in the wakeful state) and takes up to 1/5 of the total sleep time. Moreover, the depth of sleep is greater than in the 2nd stage, which is determined by a higher threshold of awakening. It is believed that alpha activity in delta sleep is a reflection of the activity of activating cerebral systems that do not allow dubious systems to fully perform their functions. Violation of the regular distribution of delta activity, as well as a decrease in the amplitude of the delta rhythm and its power, indicate the relationship between the mechanisms of MS and depression. A special relationship between depression and delta sleep is also indicated by the fact that when exiting depression one of the first to recover is delta sleep. The facts obtained later showed, however, that delta sleep disturbances in depression are more characteristic of men and are not specific only to depression. Significant fluctuations in the duration of the 4th stage of sleep associated with age have been established, in particular, its significant reduction during maturity and especially in older people.
In depression, changes and FBS are observed. According to various sources, in patients with depression there is a significant spread in the duration of PBS – from 14 to 31%. The most important indicator reflecting the magnitude of the need for FBS is considered its latent period (LP). The phenomenon of LP reduction in depression has long attracted the attention of researchers. The reduction in the FBS FB was regarded by the authors as a sign of increased activity of the apparatus generating this phase of sleep, and was associated with an increased need for fast sleep. It is shown that the more pronounced depression, the more rapid eye movements are collected in “bundles”, between which there are long periods without any oculomotor activity. However, according to other sources, there is simply an increase in the density of BDG in the first sleep cycles. There are reports that the reduction in RL sleep LP is far from equally characteristic of different types of depression – a short LP is characteristic only for all primary depressions and is absent in secondary ones. At the same time, it is not determined in any way by other sleep parameters and does not depend on the age and effect of drugs. It is possible that these data indicate desynchronization of circadian rhythms in the sleep-wake cycle and their shift to an earlier time of the day. It is also possible that characteristic sleep changes themselves play a role in the pathogenesis of depression. Some authors emphasize the relationship between the nature and severity of dreams with quantitative and qualitative changes in FBS in patients with depression. At the same time, it is quite possible that the decrease in the FBS PF is secondary to the insufficient duration of delta sleep in the first sleep cycle, as mentioned earlier.
With endogenous depressions, the temporary organization of the slow sleep – fast sleep cycle was significantly impaired. Not only the early onset of the first episode of FBS was detected, but also an increase in its duration, as well as a decrease in subcircadian frequency. The duration of the FBS periods is consistently reduced during the night, while maintaining a high frequency of BDG. The latter resembles a similar pattern found in healthy people, with the only difference being that they have a reduction in FBS with maintaining a high frequency of DBD after the 4th or 5th cycle. It is assumed that the shift in the circadian sleep rhythm during endogenous depressions can be either a simple advance of 6-8 hours of normal daily time, or dissociation between real time and sleep frequency, in which the sequence of PMS-FBS cycles remains constant regardless of the time of day.
Sleep disorders are rarely completely normal, even with good clinical improvement. It was shown that even six months after the disappearance of the clinical signs of depression, the sleep structure remains altered. Premorbid sleep inferiority in such patients and a predisposition to sleep disturbances, including hereditary, are not excluded. This is to some extent evidenced by the presence of similar characteristics in individuals with an accentuation of character, prone to hypotensive reactions.
Sleep disorders can be both the main (and sometimes the only) complaint masking depression, and one of its many symptoms. This is especially evident in the so-called latent (masked) depression, because with this form of pathology, sleep disorders can be leading, and sometimes the only manifestations of the disease. It is believed that “a torn dream” or early morning awakening, along with a decrease in awakenings and a decrease in the ability of emotional resonance, can serve as an indication of the presence of depression in the absence of a sad mood.
Patients with depression may have hypersomnic conditions as part of depressive episodes in manic-depressive disorders.
Clinical patterns such as seasonal affective disorders — ATS (seasonal depression), fibromyalgia, and parkinsonism — point to the special relationship between depression and sleep disorders. From the perspective of a depressive radical, they are characterized by a “depression +” situation, and the plus is very significant. All of these clinical models did not describe a decrease in the FBS of PBS and premature early awakening, although depression is undeniable, which can be determined both during clinical analysis and psychological testing. In the treatment of these clinical models, both pharmacological (antidepressants) and nonpharmacological (phototherapy, sleep deprivation) antidepressant methods occupy an important place.
ATS was first described and got its name in the research of N. Rosenthal and his colleagues. Reducing the duration of the photoperiod (the duration of the bright portion of the 24-hour daily cycle) can induce ATS in susceptible patients. Some epidemiological studies have shown that women are 4 times more likely to suffer from ATS than men. According to established criteria, at least 6% of Americans living in New York latitude regularly suffer from ATS; 14% have less severe symptoms and 40% of the population experience some fluctuations in well-being that do not reach the degree of pathological disorder. Mood disorders in ATS are characterized by the annual return of cyclic episodes of dysthymia in the fall and winter, alternating with euthymia or hypomania in late spring and summer. In the fall, increased sensitivity to cold, fatigue, decreased performance and mood, sleep disturbance, the preference for sweet foods, weight gain. Sleep is lengthened by an average of 1.5 hours compared with its duration in the summer, sleepiness in the morning and in the afternoon, poor quality of night sleep disturb. Phototherapy (treatment with bright white light), which exceeds almost all antidepressants in its effectiveness, has become the leading method of treatment for these patients.
Fibromyalgia is a syndrome characterized by the presence of multiple musculoskeletal pain points, depression and insomnia. Moreover, the phenomenon of “alpha-delta-sleep” is determined in the structure of night sleep, along with which, according to our data, an increase in the time of falling asleep, increased motor activity in a dream, and a decrease in the representation of the deep stages of the phase of slow sleep and PBS are detected. Phototherapy (10 sessions in the morning, light intensity of 4,200 lux, exposure time of 30 minutes) reduces the severity of not only pain phenomena, but also depression and sleep disorders. Polysomnographic studies show normalization of sleep structure — an increase in the duration of sleep, FBS, and the activation index of movements. In this case, the LP of the first episode of FBS decreases: before treatment, on average, in the group of 108 minutes and after phototherapy, 77 minutes. The severity of the phenomenon of “alpha delta sleep” is also reduced.
The structure of sleep in patients with Parkinson’s disease also does not have the features characteristic of classical depression. However, all antidepressant efforts are quite effective in this disease: tricyclic antidepressants and antidepressants – serotonin reuptake inhibitors, sleep deprivation, phototherapy. French researchers have identified dopamine-dependent depression, which turned out to be more sensitive to dopaminomimetics than to other antidepressants. The structure of sleep in this case turned out to be similar to that in patients with parkinsonism.
Evaluation of the effectiveness of antidepressants in depression, as a rule, is carried out taking into account the data of polysomnographic studies, i.e. these drugs should increase FBS PF, “delay” awakening at a later time. All drugs used in clinical practice in this group (from amitriptyline to prozac) satisfy these requirements.
Undoubtedly, deprivation (deprivation) of sleep (DS) took an important place in the treatment of depression – the method is all the more effective the more depressive the disorders are. DS helps well mainly with endogenous depression as part of manic-depressive psychosis. There is no doubt that DS is most effective in patients with severe or moderate depression. Peculiarities of responding to DS are associated with individual psychological characteristics, in particular, it is worst experienced by persons who are prone to crowding out undesirable elements from consciousness. DS can be a predictor of the reaction to antidepressants: those responding to DS can be successfully treated with clomipramine with immediate improvement, those whose condition improves on day 2 with maprotiline. Some authors believe that this technique is comparable in effectiveness with electroconvulsive therapy. DS can be an independent method of treating patients with a subsequent transition to antidepressants. Apparently, it should be used in all patients who are resistant to pharmacotherapy to increase the capabilities of the latter.
Thus, violations of the sleep-wake cycle in depression are diverse and include insomnia and hypersomnia. The “cleaner” the depression, the more likely it is to identify sufficiently characteristic changes in the structure of night sleep, the greater the “plus” added to the depressive radical (in the form of motor or pain disorders), the more nonspecific sleep disturbances look. In this regard, some non-pharmacological methods that act on the depressive radical — sleep deprivation and phototherapy, which are quite effective and safe, are of interest. At present, much attention is paid to the study of sleep in depression. The discovery of the commonality of some biochemical mechanisms of depression, sleep disturbances, and circadian rhythms further increases interest in this problem, especially since this opens up the possibility of new integrated approaches to the treatment of sleep disorders in depression.