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。     

Electroencephalographic sleep of adolescents with major depression and normal controls

Forty-nine, mostly outpatient (86%), nonbipolar adolescents, aged Tanner stage III to 18 years, with a current diagnosis of major depressive disorder and 40 adolescents without current presence or history of psychiatric disorder were studied polysomnographically for three consecutive nights. Sleep latency was significantly longer in the depressive groups. The nonendogenous depressive patients exhibited significantly more awake time and lower sleep efficiency during the sleep period. No significant group differences were found for first rapid eye movement (REM) period latency, REM density, or any other REM sleep measures. Age correlated significantly with REM latency and delta sleep time, especially among depressive patients. No significant correlations between sleep measures and severity of illness were found. It appears that the classic REM sleep findings associated with the adult depressive syndrome are not present among depressive adolescents, indicating a later ontogeny for these abnormalities.     

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.     

Abnormal rapid eye movement latencies in schizophrenia

Several previous studies have observed short rapid eye movement (REM) latencies in schizophrenic patients without major affective disorder. This study was designed to meet several of the criticisms of those previous studies. Using Research Diagnostic Criteria, we compared the sleep patterns of schizophrenic patients with those of normal controls and patients with major depressive disorder and schizoaffective disorder. All patients were medication free, and REM latency was explicitly defined using both strict and lenient criteria. Chronically ill paranoid or undifferentiated schizophrenics could not be distinguished from patients with major depressive disorder or schizoaffective disorder using any definition of REM latency. These results were not due to longer REM latency in the particular sample of patients with major depressive disorder. They had abnormally low REM latencies; however, the schizophrenic patients showed similar decrements. These data cast serious doubt on the specificity of short REM latency as a biological marker for major depressive disorder.     

Cholinergic REM sleep induction response correlation with endogenous major depressive subtype

We compared central cholinergic responsiveness (using the latency to induction of rapid eye movement sleep after arecoline challenge as a response marker) in 90 subjects: patients with major depressive disorder (MDD) (n = 53), nonaffective psychiatric controls (n = 17), and normal controls (n = 20). MDD patients as a whole showed a supersensitive cholinergic response compared to nonaffective patients and normal subjects. Further analysis indicated a strong association between cholinergic supersensitivity and endogenous subtype of MDD, including a significant correlation with specific endogenous features such as distinct quality of mood, anhedonia, lack of reactivity, and agitation. Unlike rapid eye movement (REM) latency (a more conventional physiological marker), cholinergic sensitivity did not correlate with age or severity of illness but only with the presence of endogenous features. Previously described sleep physiological correlates such as REM latency and REM density of the first REM period also distinguished between endogenous and nonendogenous MDD. There was a statistically significant correlation between REM latency and arecoline REM induction response.     

Electroencephalographic sleep in spousal bereavement and bereavement-related depression of late life.

Although spousal bereavement in late life is common and frequently leads to major depression, the boundary between bereavement without a depressive syndrome and bereavement-related depression has been insufficiently studied from a physiological perspective. Because other forms of depression are associated with physiological changes, including sleep, we have attempted to clarify the relationship of bereavement and bereavement-related depression by investigating electroencephalographic (EEG) sleep in 31 elderly volunteers with recent spousal bereavement, stratified by the presence (n = 15) or the absence (n = 16) of major depression (Research Diagnostic Criteria). Entry into the study was limited to volunteers without a personal history of psychiatric disorder. As hypothesized, bereaved subjects with major depression had significantly lower sleep efficiency, more early morning awakening, shorter rapid eye movement (REM) latency, greater REM sleep percent, and lower rates of delta wave generation in the first nonREM (NREM) period, compared with bereaved subjects without depression. Furthermore, the sleep of bereaved subjects with single-episode major depression resembled that of elderly patients with recurrent unipolar major depression (n = 15) on measures noted above. Sleep in bereavement without depression was similar to that of 15 healthy control subjects (neither bereaved nor depressed). These findings suggest that the current DSM-III-R concept of uncomplicated bereavement is not confirmed, as the sleep patterns of subjects who develop a depressive syndrome in the context of bereavement, many of whom might be considered to have "uncomplicated bereavement" by DSM-III-R standards, are identical to sleep patterns found in major depressive episodes. To our knowledge, this is the first study of EEG sleep in spousal bereavement with and without major depression.     

Internight variability of REM latency in major depression: implications for the use of REM latency as a biological correlate

The internight variability in REM latency in 92 drug-free inpatients with major depressive illness was recorded for 4 consecutive nights and subsequently assessed. Individual coefficients of variation in REM latency [CV = (standard deviation of mean REM latency for 4 recording nights/4-night mean REM latency) X 100] ranged from 5.1 to 121.7, with a mean of 37.0 (SD = 27.3) and a median of 27.4. CV was positively correlated with both age (p less than 0.05) and age at onset of depressive illness (p less than 0.01). Male patients showed more variability in REM latency than female patients (p less than 0.05); likewise, the subgroups of patients who either were incapacitated or had bipolar II illness showed greater variability in REM latency in comparison with the remainder of the sample (p less than 0.05). When the entire patient sample was stratified by CV into three equal subgroups, the subgroup of patients defined by the highest CV presented the longest sleep latency (p less than 0.05) and the shortest REM latency (p less than 0.0001). No other clinical or polysomnographic correlates of REM latency variability were noted nor was REM latency variability related to severity of illness, other subtypes of illness, or clinical response to antidepressant therapy. In selecting REM latency data for assessment of diagnostic sensitivity, the use of the shortest REM latency from at least 3 consecutive nights yielded a higher sensitivity (74%-81%) than did the use of any one individually specified night (50%-56%) or different internight means (49%-52%). The same conclusion applied when patient age was taken into account. These results have implications for standardizing the use of REM latency as a biological correlate in major depression.     

Effects of ECT on sleep and CSF biogenic amines in affective illness

The effects of electroconvulsive therapy (ECT) on sleep and cerebrospinal fluid (CSF) 5-hydroxyindoleacetic acid (5HIAA) and homovanillic acid (HVA) were studied in 11 male patients suffering from major depressive disorders severe enough to require ECT. Total sleep time and sleep efficiency index increased significantly after ECT, while the number of awakenings, the ratio wake/total sleep time, and the time of intermittent awake decreased, indicating that sleep continuity improved after treatment. Sleep architecture was also favorably influenced by ECT as shown by a significant increase in time of stage 2 and rapid eye movement (REM) sleep. REM latency and REM density also normalized after ECT. CSF 5HIAA increased significantly after ECT, but this was not the case for CSF HVA. These results demonstrate a positive effect of ECT on sleep EEG and CSF neurochemical markers for depressive illness.     

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.     

Sleep in depression: the influence of age,gender and diagnostic subtype on baseline sleep and the cholinergic REM induction test with RS 86

Summary One hundred and eight healthy controls and 178 patients with a major depressive disorder according to DSM-III were investigated in the sleep laboratory after a 7-day drug wash-out period. Subsamples of 36 healthy controls and 56 patients additionally took part in the cholinergic rapid eye movement (REM) sleep induction test with RS 86. Data analysis revealed that age exerted powerful influences on sleep in control subjects and depressed patients. Sleep efficiency and amount of slow wave sleep (SWS) decreased with age, whereas the number of awakenings, early morning awakening, and amounts of wake time and stage 1 increased with age. REM latency was negatively correlated with age only in the group of patients with a major depression. Statistical analysis revealed group differences for almost all parameters of sleep continuity with disturbed indices in the depressed group. Differences in SWS were not detected. REM latency and REM density were altered in depression compared to healthy subjects. Sex differences existed for the amounts of stage 1 and SWS. The cholinergic REM induction test resulted in a significantly more pronounced induction of REM sleep in depressed patients compared with healthy controls, provoking sleep onset REM periods as well in those depressed patients showing baseline REM latencies in the normal range. Depressed patients with or without melancholia (according to DSM-III) did not differ from each other, either concerning baseline sleep or with respect to the results of the cholinergic REM induction test. The results stress the importance of age when comparing sleep patterns of healthy controls with those of depressed patients. Furthermore they underline the usefulness of the cholinergic REM induction test for differentiating depressed patients from healthy controls and support the reciprocal interaction model of nonREM-REM regulation and the cholinergic-aminergic imbalance hypothesis of affective disorders.     

抑郁症患者睡眠障碍与血浆增食欲素A的关系

目的 探讨抑郁症患者睡眠障碍与血浆增食欲素A的关系,以期为抑郁症睡眠障碍的干预提供理论基础.方法 67例抑郁症患者行24项汉密尔顿抑郁量表(HAMD-24)及匹兹堡睡眠质量指数量表(Pittsburgh sleep quality index,PSQI)评定,根据睡眠情况分为睡眠障碍组(研究组,n=37)及非睡眠障碍组(阳性对照组,n =30),多导睡眠图检测睡眠情况,放射免疫法检测血浆增食欲素-A水平,并与26例健康体检者进行对比(阴性对照组).结果 与正常对照组及非睡眠障碍组比较,抑郁症睡眠障碍组患者HAMD抑郁量表评分及血浆Orexin-A水平均明显增加(P＜ 0.05,P＜0.01);总睡眠时间减少,睡眠潜伏期长,觉醒次数及时间增多,睡眠效率及维持率明显下降,浅睡(S1期睡眠)增加而深睡(S3、S4期睡眠)减少(P＜0.05,P＜ 0.01);REM潜伏期缩短,REM睡眠时间增多,REM活动度、强度及密度明显增强(P＜0.05,P＜0.01);相关性分析表明,血浆Orexin-A水平与睡眠潜伏期、觉醒时间、觉醒次数均呈正相关(r分别为0.447、0.591、0.670,P＜0.01),与S3％+S4％呈负相关(r=-0.872).结论 睡眠障碍者抑郁程度较非睡眠障碍者更高,血浆Orexin-A水平升高可能是引起抑郁症睡眠障碍的一项重要因素,其机制可能与其促进觉醒有关.     

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.     

Biological heterogeneity of major depressive disorder: indications by sleep EEG and TRH stimulation test findings

A group of 27 patients with definite (n = 20) or probable (n = 7) RDC major depressive disorder underwent 2 sleep EEGs and 1 TRH test while in a drug-free depressive phase. A short mean REM latency (less than 60 min) identified 55.5% of major depressives while added use of blunted TSH responses (delta max. less than 5 microU/ml) increased that percentage by 11%. When patients were subdivided into RDC endogenous and nonendogenous, mean REM latency and global depression scores distinguished the 2 groups, while delta TSH did not. A short mean REM latency identified endogenous depression with 80% specificity and 76% sensitivity. The combination of REM latency and delta TSH reduced the specificity to 60%, and therefore cannot be recommended for differentiating endogenous from nonendogenous depression.     

Polysomnography in patients with post‐traumatic stress disorder

Aims: The purpose of the present study was to investigate sleep structure in post‐traumatic stress disorder (PTSD) patients with and without any psychiatric comorbidities. The relationship between sleep variables and measurements of clinical symptom severity were also investigated. Methods: Sleep patterns of 24 non‐medicated male PTSD patients and 16 age‐ and sex‐matched normal controls were investigated on polysomnography on two consecutive nights. Six PTSD‐only patients and 15 PTSD patients with major depressive disorder (MDD) were also compared to normal controls. Sleep variables were correlated with PTSD symptoms. Results: Compared to the normal controls, the PTSD patients with MDD had difficulty initiating sleep, poor sleep efficiency, decreased total sleep time, decreased slow wave sleep (SWS), and a reduced rapid eye movement (REM) sleep latency. The PTSD patients without any comorbid psychiatric disorders had moderately significant disturbances of sleep continuity, and decreased SWS, but no abnormalities of REM sleep. REM sleep latency was inversely proportional to the severity of startle response. SWS was found to be inversely correlated with the severity of psychogenic amnesia. Conclusions: PTSD patients have disturbance of sleep continuity, and SWS deficit, without the impact of comorbid depression on sleep. The relationship between SWS and the inability to recall an important aspect of trauma may indicate the role of sleep in the consolidation of traumatic memories. The relationship between the severity of the startle response and REM latency may suggest that REM sleep physiology shares common substrates with the symptoms of PTSD.     

Sleep and depression: toward a standardization of the use of the latency of paradoxical sleep as a biological marker of major depression

Among the various disturbances in sleep architecture among major depressive patients, the shortening of REM latency seems the most specific feature. Therefore, several groups have tested the usefulness of this parameter as a "biological marker" of major depression. The divergent results of those studies probably result from the marked differences in the methodology used. In this context, we compared the diagnostic sensitivity of various methodologies for selection of REM latency data among 92 major depressive inpatients recorded for 4 consecutive nights. The selection of individual night values or of mean values yielded very similar diagnostic sensitivity. However, the selection of the shortest REM latency from consecutive nights was associated with a higher diagnostic sensitivity, especially if at least 3 nights were included. After controlling for age, 87% of patients were identified by this methodology (sum of REM latency and age less than 90). Therefore we propose to standardize the methodology for use of REM latency: recording of 3 consecutive nights and selection of the shortest REM latency. If the sum of this value and of patient'age equals 90 or less, the diagnosis of major depression is supported.     

Reduced REM latency predicts response to tricyclic medication in depressed outpatients

Forty-two outpatients with major depressive disorder entered a double-blind, randomized trial of either desipramine or amitriptyline for a minimum of 6 weeks. Pretreatment polysomnographic and clinical measures were used to predict response. Response was defined as a 17-item Hamilton Rating Scale for Depression score less than or equal to 9 at the end of treatment. There was a 61.1% response rate for patients treated with amitriptyline and a 66.7% response rate for patients treated with desipramine. Reduced REM latency (2-night mean less than or equal to 65.0 min) predicted a positive response to these tricyclic antidepressants. REM latency did not differentiate between desipramine or amitriptyline responders. More patients with reduced REM latency (80%) responded to treatment compared with patients with nonreduced REM latency (50%). The 80% response rate in reduced REM latency depressed patients confirms our previous findings in a mixed inpatient and outpatient sample. Contrary to our hypothesis, in this sample, endogenous depression was not associated with a good response to tricyclic medication.     

The role of circadian clock genes in mental disorders

The study of molecular clock mechanisms in psychiatric disorders is gaining significant interest due to data suggesting that a misalignment between the endogenous circadian system and the sleep-wake cycle might contribute to the clinical status of patients suffering from a variety of psychiatric disorders. Sleep disturbances in major depressive disorder (MDD) are characterized by increased sleep latency, poorer sleep efficiency reduced latency to the first rapid eye movement (REM) sleep episode, and early-morning awakening, but there is little data to indicate a role of circadian clock genes in MDD. There is also relatively little information regarding the role of clock genes in anxiety. In contrast, a significant amount of evidence gathered in bipolar disorder (BPD) patients suggests a circadian rhythm disorder, namely an advanced circadian rhythm and state-dependent alterations of REM sleep latency. Most research on the role of clock genes in BPD has focused on polymorphisms of CLOCK, but the lithium target GSK3 may also play a significant role. A circadian phase shift is also theorized to contribute to the pathophysiology of winter seasonal affective disorder (SAD). Certain allelic combinations of NPAS2, PER3, and BMAL1 appear to contribute to the risk of SAD. In chronic schizophrenia, disturbances of sleep including insomnia and reduced sleep efficiency have been observed. Genetic studies have found associations with CLOCK, PER1, PER3, and TIMELESS. Sleep and circadian changes associated with dementia due to Alzheimer's disease suggest a functional change in the circadian master clock, which is supported by postmortem studies of clock gene expression in the brain.     

Frequency analysis of the sleep EEG in depression

Eight patients with major depressive disorder (seven bipolar and one unipolar) and matched controls had sleep studies, on which frequency analysis of the electroencephalogram (EEG) was performed. Total sleep and sleep efficiency were decreased in the patients, but there was no significant difference in rapid eye movement (REM) latency between the two groups. Frequency analysis revealed no group differences in power in the delta band (0.23-2.5 Hz) or the whole EEG spectrum (0.23-25 Hz). These findings suggest that mean REM latencies are not always shorter in major depression. The results are discussed in light of a previous report of decreased delta energy in the sleep EEG of unipolar patients.     

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.