抑郁症及其亚型的睡眠脑电图研究

目的 探讨抑郁症患者睡眠脑电图的异常改变以及抑郁闰不同亚型之间的差异。方法 采用日本光电ＲＭ－６０００多导生理记录仪,对１８例抑郁症患者和１９名健康人进行睡眠脑电图检查。结果 与对照组比较,抑郁症组出现明显的醒觉时间增多、睡眠总时间减少、晒起时间增加、睡眠效率下降、睡眠维持率下降、第一阶段睡眠百分比增加、快速眼球运动（ＲＥＭ）潜代期缩短和ＲＥＭ密度增加,经统计学处理差异均有显著性（Ｐ〈０．０５）。     

REM sleep latency and morbidity risk of affective disorders in depressive illness

The relationship between rapid eye movements (REM) sleep latency and morbidity risks for affective illness in first-degree relatives of affectively ill probands was investigated in 122 patients suffering from primary major depressive disorder (74 unipolars, 48 bipolars) according to the Research Diagnostic Criteria. Sleep EEG scoring was done blind to the clinical diagnosis of the probands and their relatives, and the evaluation of morbidity risks for affective illness in first-degree relatives was done using Str?mgren's method with age correction. A logistic regression analysis was performed to describe the proportion of affectively ill relatives as a function of variables recorded in 122 probands with primary major depression. Our analysis demonstrates an inverse relationship between REM sleep latency and the risk for depressive disorder in the families of affectively ill probands. These results suggest the possibility that common pathophysiological factors may be involved in the hereditary predisposition to affective illness and in the shortening of REM sleep latency in some depressed patients.     

Electroencephalographic sleep diagnosis of primary depression.

Studies of severely depressed hospitalized patients suggest a shortened rapid eye movement (REM) latency as a specific biological marker for primary affective disease. To assess the validity of these findings, 40 outpatients referred to our Electroencephalographic Sleep Center for evaluation of depressive symptoms were studied. Concurrent with the all night EEG sleep studies, all patients received a brief clinical interview and a battery of self-rating scales. The entire sample was then subdivided into primary and secondary depressives on the basis of follow-up diagnoses. While there were no significant differences between groups on self-ratings of depressive symptoms, the group of primary depressives had significantly shorter REM latencies and higher measures of phasic REM than the secondary depressives. Furthermore, in this patient group, the delineation of primary vs secondary depression was greater than 80% on the basis of only two nights of EEG sleep. Such objective biological measures, if replicated, could provide a method for increasing the accuracy of differential diagnosis among depressed populations in clinical research.     

EEG sleep and affective psychoses: I. Schizoaffective disorders.

The sleep electroencephalogram (EEG) was studied in 41 depressed inpatients. EEG sleep records were compared for two diagnostic subgroups; patients with psychotic depression (n = 29) or with schizoaffective disorders (n = 12). As was true in the previous pilot study, no major EEG sleep variables distinguished the patients with psychotic depression from those with schizoaffective disorders. These data are consistent with the theory that all psychotic depressive states may have certain common psychobiologic features such as shortened rapid eye movement (REM) sleep latency.     

Electroencephalographic sleep in psychotic depression. A valid subtype?

Electroencephalographic (EEG) sleep patterns were examined in 27 psychotic and 79 nonpsychotic subjects with major depression to evaluate the validity of the psychotic-nonpsychotic subtype dichotomy. Sleep in psychotic depression was characterized by increased wakefulness, decreased rapid eye movement (REM) sleep percentage, and decreased REM activity even after controlling for clinical differences in age, severity, and agitation. Psychotic depressive subjects also were more likely to have extremely short sleep-onset REM latencies. In psychotic depression EEG sleep varied as a function of total illness duration. Patients with recent-onset syndromes had profiles characterized by marked initial insomnia, increased stage 1 sleep percentage, and long REM latency; patients with illnesses of longer duration had extremely short REM latencies. Demonstration of selected EEG sleep variables discriminating between psychotic and nonpsychotic depression further supports psychotic depression as a distinct subtype of major affective disorder.     

Mood alterations and sleep

We have reviewed literatures about neurobiological aspect of mood disorders in the light of abnormalities of REM sleep. A shortened REM latency is a consistent finding in depressed patients and may be considered a biological marker for depression. Most depressed patients with shortened REM latency also show non-suppression on dexamethasone-suppression test (DST). The commonly used antidepressant drugs cause a significant reduction in REM sleep. Patients with abnormal DST show a better response to sleep deprivation than those with normal DST. Recent studies indicated that borderline patients, primary dysthymic patients and obsessive-compulsive patients (OCD) have shortened REM latency. Farthermore, patients with OCD have a fairly good response to antidepressant clomipramine. Diagnostic and therapeutic strategies can conceivably be related on the examination of sleep patterns of psychiatric patients.     

Mood Alterations and Sleep

Abstract: We have reviewed literatures about neurobiological aspect of mood disorders in the light of abnormalities of REM sleep. A shortened REM latency is a consistent finding in depressed patients and may be considered a biological marker for depression. Most depressed patients with shortened REM latency also show non-suppression on dexamethasone-suppression test (DST). The commonly used antidepressant drugs cause a significant reduction in REM sleep. Patients with abnormal DST show a better response to sleep deprivation than those with normal DST. Recent studies indicated that borderline patients, primary dysthymic patients and obsessive-compulsive patients (OCD) have shortened REM latency. Farthermore, patients with OCD have a fairly good response to antidepressant clomipramine. Diagnostic and therapeutic strategies can conceivably be related on the examination of sleep patterns of psychiatric patients.     

Sleep is undisturbed in elderly, depressed individuals who have not sought health care

Sleep deficits are commonly found in geriatric depressed patients, particularly shortened rapid eye movements (REM) latency, disturbed sleep continuity, and decreased slow wave sleep (SWS). Here we report the sleep patterns of community volunteers responding to ads about memory loss and depression. The two groups, 24 geriatric-onset major depressive disorder (MDD) subjects with a minimal history of seeking treatment for depression and 24 gender- and age-matched control subjects, significantly differed from each other on only one measure of sleep--sleep latency; the MDD group showed a modest but significant shortening of latency to fall asleep. All other sleep/wake measures, including REM latency, temporal distribution of REM sleep across the night, SWS, and measures of nighttime wakefulness did not differ between groups. This lack of significant sleep disturbance suggests that the sleep deficits reported in many studies of major depression may be related to factors underlying treatment-seeking behaviors, physical health status, severity of the depression, or heterogeneity within the MDD population with some types seeking treatment and others not seeking it, rather than depressive state per se. The data indicate that community-dwelling healthy elderly individuals who have a diagnosed major depression but who have not actively sought health care do not necessarily manifest the sleep disturbances thought to be characteristic of major depressive illness.     

EEG sleep in outpatients with generalized anxiety: A preliminary comparison with depressed outpatients

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.     

Latencies of REM sleep and awakening in major depression: possible indicators of cholinergic activity

REM latency and awakening latency were analyzed in a sample of 26 major depressive inpatients and 8 male controls recorded for two consecutive nights. A significant inverse relationship appeared between REM latency and awakening latency in depressed patients. The relationship was more marked in male than in female patients. No significant correlation between REM latency and awakening latency was observed in male healthy volunteers. The hypothetical cholinergic supersensitivity in major depression is proposed to explain the present relationship. These results suggest that awakening latency might also be taken into account in the evaluation of sleep disturbances in depressive illness.     

无抽搐电休克治疗抑郁症的Quisi研究

目的探讨无抽搐电休克(MECT)疗法对抑郁症患者Quisi的影响。方法对33例抑郁症患者进行MECT治疗前后睡眠脑电记录,监测MECT治疗前后Quisi的变化。结果抑郁症患者经过MECT治疗后,Quisi显示睡眠总时间增加、睡眠潜伏期缩短、觉醒时间减少、眼快动睡眠(REM)时间减少、慢波睡眠增加;而REM潜伏期无明显变化。结论 MECT有改善睡眠的作用,但尚待进一步观察。     

The action of clenbuterol on sleep and symptomatology in depressives

Five female inpatients with major depression (melancholic type, DMS-III-R) were treated with the beta-adrenergic agonist clenbuterol for three weeks, with doses ranging from 100 micrograms to 150 micrograms. Remission of depressive symptomatology during treatment was observed in only one patient. All patients complained of side effects, especially tremor, agitation and restlessness. The sleep EEG showed no consistent effects on sleep parameters, including REM latency and percentage of REM sleep. Thus, the impact of clenbuterol on sleep clearly differs from that of most classical antidepressants. Regarding the lack of therapeutic efficacy, the data are compatible with the hypothesis of a relationship between REM sleep suppression and an antidepressant drug effect. Despite the small sample size, it can be concluded that clenbuterol is not likely to be a promising alternative to proven antidepressants in the treatment of major depression.     

Aspects of short REM latency in affective states: a revisit

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).     

Depression and insomnia: questions of cause and effect

Chronic insomnia is a risk factor for the development of psychiatric disorders, including depression, as well as a prodrome of major depressive episodes, a consequence or complication of depression that often persists beyond the clinical episode, and a prognostic indicator of long-term illness course and treatment response. In addition, sleep is physiologically abnormal in persons at risk for depression; for example, shortened REM sleep latency is present not only during clinical episodes of depression, but also before the clinical episode in subjects at risk for depressive illness. Although insomnia usually disappears as depression is treated, it may persist, indicating heightened vulnerability to depressive relapse or recurrence. Physiological changes in sleep related to depression correlate with the likelihood of response to psychotherapy alone and may also identify which patients are unlikely to do well with psychosocial treatment and, therefore, to need somatic therapy in order to preserve recovery. Electroencephalographic (EEG) sleep changes also correlate with the speed of response and with the brittleness or durability of response (i.eprobability of relapse or recurrence). These observations suggest a close relationship between the regulation of sleep and the regulation of mood. The importance of this relationship is further underscored by recent brain imaging studies of sleep and sleep deprivation in patients with major depression. For example, therapeutic sleep deprivation (TSD) may serve as both a catalyst of rapid antidepressant activity and as a probe of treatment resistance. TSD's effects on brain metabolic rates, especially in limbic areas, may correlate with a therapeutic response to a night of sleep loss and to antidepressant medication. Finally, treating chronic insomnia with newer selective serotonin reuptake inhibitor (SSRI) antidepressant medication may represent an opportunity for preventing complications of insomnia, including depressive illness.     

Sleep in anorexia nervosa, bulimia nervosa and depressive diseases: a polysomnographic comparative study

All-night EEG sleep in 20 anorexics, 10 bulimics, 10 endogenous depressives, and in 10 healthy subjects (all age matched) was compared. In addition, the REM sleep-induction-test was performed in 12 patients with an eating disorder, 7 depressives, and 12 controls by application of the cholinergic agent RS 86. During baseline night, EEG-sleep parameters, especially REM latency, did not differ between the patients and the controls, except for the phasic components of REM sleep (REM density) that were increased in the depressive patients. The frequency of shortened REM latencies, however, was significantly higher in the depressed patients. These observations indicate that in some of the young depressives the disturbance of the REM sleep regulating transmitter system is already present to a similar degree as it is assumed in elderly depressives. After the application of RS 86, REM latency was shortened in all groups under investigation. However, the REM sleep inducing effect of RS 86 was significantly more pronounced in the depressives when compared with both the eating disorder patients and the controls. In the latter two samples, the shortening of REM latency was similar. Furthermore, the eating disorder patients with a concomitant major depression reacted similar to RS 86 as the non-depressed eating disorder patients and the control subjects. Whereas baseline EEG-sleep did not differ significantly among eating disorder patients, young depressives, and healthy subjects, the REM sleep inducing effect of the cholinergic agent RS 86 clearly distinguished between the depressives and both the patients suffering from eating disorders and the controls.(ABSTRACT TRUNCATED AT 250 WORDS)     

The application of EEG sleep for the differential diagnosis of affective disorders.

On the basis of two EEG sleep criteria, REM latency and REM activity, the authors achieved 81% accuracy in distinguishing between 47 patients with primary depression and 48 patients with secondary depression using discriminant analysis. Sleep efficiency, the percentage of delta sleep, and the percentage of REM sleep discriminated between psychotic and nonpsychotic subgroups in the group with primary depression with 75% accuracy. REM activity and intermittent nocturnal awakening accurately discriminated two subtypes of patients with secondary depression at a level of 81%. These results suggest that EEG sleep measurements can yield significant data to aid in differential diagnosis in psychiatry.     

Individual variations in the sleep of depression

Variations in the intensity or severity of affective disorders were evaluated relative to perturbations in nocturnal sleep physiology. Individual variations in polygraphic features of the sleep cycle based upon psychopathologic scale ratings were investigated in two constituencies (Ns = 6) for 8 hr during 1-3 consecutive nights. The constituencies consisted of twelve young adult (18-25 years) nonpsychotic unipolar depressed psychiatric patients with a primary affective illness and an age-matched normal healthy control group (N = 8). The severely versus mildly depressed patient subgroups scored significantly higher on the Hamilton, Beck and Zung psychopathologic rating scales, indicating a larger magnitude of depressive symptomatology. The average value for total time asleep was 6.1 hr in severely versus 7.8 hr among the mildly depressed patients and controls. EEG-sleep of the severely versus mildly depressed patients and controls contained significantly less stages 2 and 3. Although total time asleep was almost identical in the mildly depressed constituency compared with controls, patients accumulated significantly more of stages 2 and 3. Both patient subgroups exhibited a significantly shorter REM latency than controls. REM latency was reduced to a significantly lower level in the severely versus mildly depressed patients. A significant decrease of REM cycle duration occurred in the polygraphic sleep recordings of severely depressed patients compared with the age-matched controls. The shortened REM latencies indicate a disinhibition of neural processes that would normally delay appearance of the initial REM episodes during nocturnal sleep. The present study generally extends and confirms finding on nocturnal EEG-sleep disturbances in depression associated with the severity of affective illness, particularly the disrupted REM cycle and shorter REM latency.     

Sleep and manipulations of the sleep-wake rhythm in depression

OBJECTIVE: Disturbed sleep is typical for most depressed patients and complaints about disordered sleep are the hallmarks of the disorder. Polysomnographic sleep research has demonstrated that besides impaired sleep continuity, sleep in depression is characterized by a reduction of slow wave sleep and a disinhibition of random eye movement (REM) sleep, with a shortening of REM latency, a prolongation of the first REM period and increased REM density. METHOD: Our own experimental work has focused on the reciprocal interaction hypothesis of non-REM and REM sleep regulation as a model to explain the characteristic features of depressed sleep. RESULTS: In agreement with the major tenet of this model, administration of cholinomimetics provoked shortened REM latency in healthy subjects and led to an even stronger REM sleep disinhibition in depressed patients. Manipulations of the sleep-wake cycle, such as sleep deprivation or a phase advance of the sleep period, alleviate depressive symptoms. CONCLUSION: These data indicate a strong bidirectional relationship between sleep, sleep alterations and depression.     

抑郁症和精神分裂症的快眼动睡眠研究

目的探讨抑郁症与精神分裂症的快眼动（ＲＥＭ）睡眠特征。方法用睡眠实验技术对正常受试者、抑郁症和精神分裂症患者各３０例进行多导睡眠图的通夜描录，并结合临床指标，对三组受试者的９项ＲＥＭ睡眠指标进行对照分析。结果抑郁症和精神分裂症有着不同的ＲＥＭ睡眠特征。抑郁症ＲＥＭ睡眠潜伏期（ＲＬ）缩短，ＲＥＭ活动度、强度、密度增高和睡眠次数增多，汉米尔顿抑郁量表分与ＲＬ呈负相关。精神分裂症ＲＥＭ睡眠指标个体间差异大，１０例患者睡眠图的觉醒阶段中发现ＲＥＭ睡眠的插入现象。结论研究抑郁症有异常ＲＥＭ睡眠指标，而ＲＬ则为反映抑郁程度的特殊指标；ＲＥＭ睡眠的插入代表了部分精神分裂症患者的电生理特征     

Sleep electroencephalography in depression and mental disorders with depressive comorbidity

Traditional scoring of sleep EEG in depressed patients shows abnormalities in sleep maintenance, sleep architecture, REM sleep, the distribution of slow wave and REM sleep during the night. Computerized analysis that comprises the period-amplitude analysis procedure and spectral analysis discloses changes in delta activity and distribution of delta activity. However, these methods of analysing EEG sleep are not able to distinguish the various concepts of depression: endogenous and non-endogenous depression, unipolar and bipolar depression, psychotic and non-psychotic depression. Polysomnographical data in patients with recurrent depression show alteration during remission suggesting trait-like abnormalities of sleep in depression illness. Shortened REM latency is not specific in depression. This sleep parameter is defined in many different ways explaining the heterogeneousness of study results and the failure of constituting a biological marker. Many sleep parameters are affected by several factors such as age, gender and severity. Several physiopathological hypotheses have been proposed to explain EEG sleep alterations. They refer either to circadian rhythms such as the two process model of Borbély, the phase advance hypothesis and the circadian amplitude hypothesis, or to neurotransmitter abnormalities such as the cholinergic hypothesis. None of them takes sufficient account of all the sleep abnormalities. Sleep abnormalities have also been described in other psychiatric disorders such as mania, panic and obsessional-compulsive disorders, generalized anxiety, phobias, post-traumatic stress disorder, eating disorders, borderline personality, schizophrenia and dementia. None of them have a particular sleep EEG profile which allows to differentiate between them. A concomitant episode of major depression cannot be uncovered by sleep recordings.