Sleep EEG of patients with obsessive-compulsive disorder

Summary Twenty-two patients suffering from an obsessive and compulsive disorder (OCD) according to DSM-III-R were investigated by polysomnographic sleep EEG recordings under drug-free conditions and compared to age- and sex-matched healthy controls. Sleep efficiency was significantly lower and wake % SPT was significantly increased in the patient group compared to healthy subjects. Sleep architecture did not differ among the two samples. Especially REM sleep measures, in particular, REM latency did not differ among the groups. No positive correlation was found between sleep variables and rating inventories for obsession and compulsions (Y-BOCS), depression (Hamilton) and anxiety (CAS). A secondary depression did not influence sleep EEG variables. The results of this study contradict the assumption that OCD patients show REM sleep and slow wave sleep abnormalities similar to those shown by patients with primary depression.     

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.     

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.     

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）。     

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.     

MAO activity and EEG sleep in primary depression

Platelet monoamine oxidase (MAO) activity and electroencephalographic (EEG) sleep measures were examined in 56 drug-free hospitalized patients with primary depression as defined by the Research Diagnostic Criteria. The group included 35 females and 21 males with a mean age of 42.6 +/- 1.4 years. Platelet MAO and EEG sleep data were compared for the group as a whole and separately for the unipolar, bipolar, male, and female subgroups. No significant relationships could be demonstrated for the entire group or for the unipolar, male, or female subgroups. However, an inverse relationship between MAO activity and REM sleep percent was noted in the bipolar subgroup (p < 0.02). While changes in REM sleep have been relatively firmly established in primary depression, the relationship of MAO to depression and to REM sleep remains unclear.     

Electroencephalographic sleep in secondary depression: a revisit

EEG sleep studies are reported in 23 inpatients with secondary depression compared to a similar number of primary depressives matched for age and severity. No major patterns of EEG sleep abnormalities were found to differentiate between these closely matched samples at baseline or during amitriptyline treatment. Such results indicate that more severely ill secondary depressives manifest the characteristic EEG sleep abnormalities of depression. While these features had been reported previously to be specific for primary depression, earlier studies of psychobiological differences between primary and secondary subtypes may reflect an epiphenomenon of sample differences in age, severity, or percentage of patients with endogenous depression. Implications for further research and clinical practice are discussed.     

Electroencephalographic sleep studies in depressed outpatients treated with interpersonal psychotherapy: II. Longitudinal studies at baseline and recovery.

Electroencephalographic (EEG) sleep studies may help to identify persistent versus episodic biological characteristics of major depressive disorder. This report examines longitudinal EEG sleep studies in depressed patients treated with psychotherapy alone. Nineteen patients were studied during a symptomatic baseline period and again during early remission after treatment with interpersonal psychotherapy (IPT). EEG sleep findings at baseline were not markedly abnormal, but they were similar to those in other published studies of young adult outpatients. No changes were found in visually scored EEG sleep measures between depression and early remission. Automated measures of delta sleep and rapid eye movement (REM) activity showed small state-related changes, with delta activity increasing from baseline to remission, and automated REM measures decreasing. Strong baseline-remission correlations were noted for most sleep measures, including slow wave sleep, phasic REM activity, and automated delta EEG counts; measures of sleep continuity and tonic REM sleep were not strongly correlated. Consistent adaptation effects across nights were observed for sleep continuity and REM measures during each clinical phase. These findings support the hypothesis that most visually scored EEG sleep measures, as well as the sleep adaptation process, are stable through the acute episode of depression, at least into early symptomatic remission. They also suggest that finer-grained automated analyses of delta and REM activity may provide more sensitive tools for examining state-related changes.     

Depression in borderline patients: a prospective EEG sleep study

The relationship between borderline personality disorder and primary major depression was studied prospectively using Schedule for Affective Disorders and Schizophrenia-Lifetime Version (SADS-L) interviews and electroencephalographic (EEG) sleep studies. Ten consecutively admitted borderline patients (a prospective sample), defined by Gunderson's Diagnostic Interview for Borderlines (DIB), underwent EEG sleep studies on two consecutive nights and were compared to previously reported samples of nonborderline depressed patients (defined by Research Diagnostic Criteria; RDC), normal controls, and DIB-defined borderline patients who had been referred "to rule out major depression" (a retrospective sample). EEG sleep data were analyzed visually and by automated techniques. Rapid eye movement (REM) latency values were similar in depressed and both borderline groups but significantly different from controls. Eighty-five percent of REM latency values in RDC major depressives were less than or equal to 65 minutes, compared to similar rates of 75% in the prospective sample of borderline patients and 65% in the retrospective sample, versus 35% for controls (chi 2 = 10.7, p less than 0.005). The REM latency in borderline patients did not vary with the severity of depression as measured by the Hamilton Rating Scale for Depression. In the prospective borderline sample, the major SADS-L diagnoses were chronic intermittent depression (five), current major depression (four) (two unipolar, two bipolar II), and labile personality (one). A convergence of nosologic and EEG sleep data is suggested, and supports the concept of a close relationship between criteria-defined borderline personality disorder and affective illness.     

Electroencephalographic sleep in late-life neuropsychiatric disorders

Late-life depression and dementia of the Alzheimer's type both have profound, although different, effects on electroencephalographic (EEG) sleep patterns. Thus, while depression is associated with REM sleep disinhibition and extreme sleep fragmentation (e.g., sleep onset REM periods and early morning awakenings), Alzheimer's disease is associated with deficits in the production of phasic activity during sleep (e.g., rapid eye movements and K-complexes) and with increased rates of sleep-disordered breathing. These differences have been shown to be reliable in large numbers of patients during the past five years and appear to extend to differences in sleep between depressive pseudodementia and dementia with secondary depression. Preliminary data also suggest that pretreatment sleep onset REM periods may be associated with enhanced vulnerability to recurrent depression. In summary, sleep physiological measures provide useful diagnostic and prognostic indexes in late-life neuropsychiatric disorders.     

Electroencephalographic sleep studies in depressed outpatients treated with interpersonal psychotherapy: I. Baseline studies in responders and nonresponders.

Electroencephalographic (EEG) sleep measures have been examined as predictors of therapeutic response in patients with major depression. Although some studies have reported that EEG sleep measures are predictive of a favorable outcome with medications, two recent studies found no differences in the baseline sleep characteristics of responders and nonresponders to psychotherapy. To clarify this issue, we compared baseline EEG sleep in a group of patients with recurrent depression who responded to interpersonal psychotherapy (n = 19) and a comparable group who did not respond (n = 18). Baseline ratings of depression severity did not differ in the groups, but some differences in baseline sleep were noted. Psychotherapy nonresponders had longer sleep latencies, lower sleep efficiency, and increased automated measures of phasic rapid eye movement (REM) activity. In addition, the two groups had different EEG sleep adaptation patterns for REM latency and phasic REM density measures across the two study nights. These preliminary results suggest that baseline EEG sleep patterns, as well as the pattern of laboratory adaptation, may differ for depressed patients who respond to psychotherapy and those who do not.     

Wake and sleep EEG provide biomarkers in depression

Both wake and sleep electroencephalogram (EEG) provide biomarkers of depression and antidepressive therapy, respectively. For a long time it is known that EEG activity is altered by drugs. Quantitative EEG analysis helps to delineate effects of antidepressants on brain activity. Cordance is an EEG measure with a superior correlation with regional brain perfusion. Prefrontal quantitative EEG cordance appears to be a predictor of the response to antidepressants. Sleep EEG shows characteristic changes in depression as impaired sleep continuity, desinhibition of REM sleep and changes of nonREM sleep. Elevated REM density (a measure for frequency of rapid eye movements) characterizes an endophenotype in family studies of depression. REM-sleep changes including a more distinct REM rebound after sleep deprivation are found in animal models of depression. Most antidepressants suppress REM sleep in depressed patients, normal controls and laboratory animals. REM suppression appears to be a distinct, but not an absolute requirement for antidepressive effects of a compound. Sleep-EEG variables like REM latency or certain clusters of variables were shown to predict the response to the treatment with a certain antidepressant or even the course of the disorder for several years. Some of these predictive sleep-EEG markers of the longterm course of depression appear to be closely related to hypothalamo-pituitary-adrenocortical system activity.     

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.     

REM latency: a psychobiologic marker for primary depressive disease.

Previous investigations have indicated that one of the most consistent EEG sleep findings in depressive patients has been a shortened REM latency. On the basis of these studies, we have concluded that with the exception of drug withdrawal states (such as CNS depressant or amphetamine withdrawal and narcolepsy) shortened REM latency points to a strong affective component in the patient's illness. Short REM latency has also been observed in patients suffering from schizo-affective illness as well as in certain schizophrenic patients who require tricyclic antidepressants in their management. Furthermore, this psychobiologic marker is a persistent, rather than a transient phenomenon, and can be observed over a period of several weeks unless a patient's condition becomes more favorable through clinical intervention. This present report indicates that short REM latency is found in virtually all primary depressive illness and is absent in secondary depression. Thus, REM latency appears to be a dependable, measurable marker for diagnosing primary depression, and we argue that the phenomenon is independent of age, drug effect and changes in other sleep parameters. It is expected that EEG sleep and motor measurements can yield further significant data and improve differential diagnosis in psychiatry, in much the same way that laboratory data support other medical specialities.     

EEG sleep diagnosis of medical disease in depression.

The diagnosis of medical disease in the context of a depressive syndrome which may mimic medical illness has traditionally relied on a combination of exhaustive medical screening and neuropsychological testing. When 10 patients with primary depression were compared to 10 patients whose depression occurred in the context of concurrent medical disease, a single EEG sleep variable, total phasic REM activity (RA), correctly identified 95% of all 20 patients as either primary depressives or medical patients with depression. Conventional psychiatric assessment and neuropsychological testing were significantly less powerful discriminators among this sample.     

抑郁症患者可乐定快速眼运动睡眠抑制试验的对照研究

目的探讨重性抑郁症患者α2-肾上腺能受体功能状况。方法对15例重性抑郁症患者（抑郁症组）和15名正常人（正常对照组）分别进行多导睡眠脑电图检查。在第1个快速眼运动（REM）睡眠周期结束10min内,向所有被试者静脉注射可乐定（剂量按2mg/kg体重计算,并稀释于9ml生理盐水中）,比较两组的睡眠情况。结果可乐定注射前,抑郁症组的REM比例［（26.8±5.6）%］、REM次数［（6.8±1.2）次］及REM时间［（120.6±25.1）min］较正常对照组增加［分别为（19.2±3.3）%、（4.9±0.8）次、（78.8±14.4）min;P<0.05］,REM潜伏期缩短［（64.1±27.0）min,对照组为（96.1±27.0）min］;可乐定注射后,对两组非快速眼运动睡眠几乎无影响,而抑郁症组和对照组的REM比例［分别为（21.3±4.8）%和（13.6±2.7）%］、次数［分别为（5.3±1.2）次和（3.8±0.6）次］、时间［（101.0±24.0）min和（61.0±10.3）min］分别较注射前减少（P<0.05）,抑郁症组第1次和第2次REM间隔时间的差值小于正常对照组（P<0.01）;而两组REM潜伏期注射前后的差异均无显著性。提示抑郁症患者REM睡眠的可乐定反映较正常对照组迟钝。结论重性抑郁症患者可能存在α2-肾上腺能受体功能低下。     

The utility of the REM latency test in psychiatric diagnosis: a study of 81 depressed outpatients

To examine the utility of the REM (rapid eye movement) latency test in identifying outpatient primary depressions, 81 consecutive referrals to a sleep disorders center were evaluated in a phenomenologic, sleep polygraphic, and psychometric study. Modified Feighner (St. Louis) diagnoses were definite primary depression (n = 19), probable primary depression (n = 30), depression chronologically secondary to preexisting psychiatric disorders (n = 19), and nonaffective psychiatric disorder (n = 13). There were 18 nonpsychiatric controls. REM latency less than 70 minutes on 2 consecutive nights detected 62% of primary depressions, discriminating them from the other diagnostic groups with 88% specificity. There were no false positives among controls. These data provided a 90% confidence for the diagnosis of primary depression in this outpatient sample. Requiring 2 consecutive nights of shortened REM latency appears to improve significantly the specificity of a test previously considered to have high sensitivity but relatively low specificity for depressive disorders.     

MHPG excretion and EEG sleep in primary depression

Measures of daily urinary 3-methoxy-4-hydroxyphenylglycol (MHPG) excretion and electroencephalographic (EEG) sleep data were examined in 30 patients hospitalized for depression. This sample (mean age = 35 years) comprised 17 females and 13 males, all of whom were drug-free for 2 weeks and met Research Diagnostic Criteria for primary depressive disorder. Data analyses were conducted on the entire group, as well as the male, female, unipolar, and recurrent subgroups. No significant relationships were observed between total MHPG excretion and rapid eye movement (REM) or non-REM sleep variables. In particular, the absence of an interrelatedness of MHPG and REM sleep fails to confirm earlier findings in a smaller patient sample. These results, therefore, raise new questions about the proposed role of central noradrenergic activity in the mediation of REM sleep in depression.     

Electroencephalographic sleep in mania

Electroencephalographic (EEG) sleep patterns were examined in nine unmedicated patients meeting DSM-III-R criteria for a current manic episode (four men and five women) for two to four consecutive nights. Compared with age- and sex-matched normal control subjects, manic patients exhibited significantly decreased total recording period, decreased time spent asleep, increased time awake in the last two hours of recording, shortened rapid eye movement (REM) latency, increased REM activity, and increased REM density. These results suggest that mania is associated with marked disturbances of sleep continuity and REM measures. Sleep continuity and REM sleep abnormalities of a similar nature and degree have been reported in major depression and psychotic depression. Thus, it is possible that various forms of affective disorders and psychotic disorders have pathophysiologic mechanisms in common.