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.     

Post-traumatic stress disorder and sleep-what a nightmare!

According to DSM IV criteria, sleep disturbances are incorporated in the definition of post-traumatic stress disorder (PTSD). These include the re-experiencing symptoms (nightmares, criteria B) and a hyperarousal state (difficulty initiating and maintaining sleep, criteria D). PTSD patients commonly complain of sleep disturbances. Moreover, insomnia, restless sleep and trauma-related dreams might be the primary complaint of some patients. However, although subjective sleep disturbances are considered characteristic of PTSD, sleep laboratory studies have provided inconsistent evidence of objective sleep disorders. A variety of sleep architectures and sleep patterns has been reported in PTSD. However, only a few studies have controlled for comorbidities. Thus, uncertainty exists to what extent the sustained complaints of sleep disturbances in chronic PTSD are specifically related to the impact of exposure to traumatic stress, or rather are a consequence of comorbid disorders. Specific changes in REM sleep suggest a pathophysiologic role of REM sleep abnormality in PTSD (e.g. anxiety dreams, increased REM density, exaggerated startle response, decreased dream recall and elevated awakening thresholds from REM sleep). However, again, studies have failed to show consistent changes in percentage of REM sleep or in REM latency. There might be a coexistence of pressure to REM along with inhibitory forces of REM that result in high variability of REM parameters across patients. Alternatively, changes in REM sleep might reflect the effect of comorbid psychiatric disorders that results in inconsistent findings between patients. The current review tries to address these issues based on recent studies carried out in this field.     

Effects of comorbid diagnoses on sleep disturbance in PTSD

Objective: Patients with post-traumatic stress disorder (PTSD) are frequently diagnosed with other psychiatric comorbid conditions. This study tested the hypothesis that PTSD patients suffer a greater proportion of sleep problems according to comorbid diagnoses. Method: National Comorbidity Survey (NCS) data from 591 individuals diagnosed with PTSD were analyzed. Revised versions of the Diagnostic Interview Schedule and Composite International Diagnostic Interview were administered to a representative sample of males and females. Groups consisted of patients diagnosed with lifetime PTSD and with current comorbid panic disorder, major depressive disorder, generalized anxiety disorder, and alcohol dependence. Results: Patients diagnosed with PTSD/panic disorder reported a significantly greater proportion of nightmare complaints (96%) and insomnia (100%) compared with the other comorbid groups. Conclusions: A greater proportion of PTSD patients with comorbid panic disorder complain of sleep-related problems than other comorbid groups. This effect appears unique to panic, rather than other general anxiety disorder or depression. Prospective sleep studies are needed to differentiate the role of sleep in PTSD and PD, as well as to examine the role of psychiatric comorbidity in worsening sleep in PTSD patients.     

Sleep findings in young adult patients with posttraumatic stress disorder.

BACKGROUND: Laboratory sleep studies in posttraumatic stress disorder (PTSD) have not provided consistent evidence of sleep disturbance, despite apparent sleep complaints. Most of these studies have investigated middle-aged chronic PTSD subjects with a high prevalence of comorbidities such as substance dependence and/or personality disorder. METHODS: Ten young adult PTSD patients (aged 23.4 +/- 6.1 years) without comorbidities of substance dependence and/or personality disorder underwent 2-night polysomnographic recordings. These sleep measures were compared with those of normal control subjects and were correlated with PTSD symptoms. RESULTS: Posttraumatic stress disorder patients demonstrated significantly poorer sleep, reduced sleep efficiency caused by increased wake time after sleep onset, and increased awakening from rapid eye movement (REM) sleep (REM interruption). We found significant positive correlations between the severity of trauma-related nightmare complaints and the percentage of REM interruption, as well as wake time after sleep onset. CONCLUSIONS: The results indicate that trauma-related nightmares are an important factor resulting in increased REM interruptions and wake time after sleep onset in PTSD.     

Electroencephalographic sleep in panic disorder. A focus on sleep-related panic attacks

Sleep electroencephalograms were studied in 13 patients with panic disorder, six of whom experienced panic from sleep, and seven controls. Sleep was disturbed in the patients, as manifested by increased sleep latency, decreased sleep time, and decreased sleep efficiency. Rapid eye movement (REM) latencies were not reduced in the patient group. All six of the panic awakenings were preceded by non-REM sleep, which could be further characterized as a transition from stage II toward delta sleep. The overall degree of sleep disturbance (ie, sleep latency, sleep efficiency) did not appear to be influenced by the occurrence of sleep panic. There was also an association of increased REM latency with nights of sleep panic.     

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.     

Nocturnal polysomnography in obsessive–compulsive disorder

To determine if sleep abnormalities occur in obsessive–compulsive disorder (OCD), 2 nights of sleep electroencephalographic (EEG) recordings were obtained from 13 medication-free outpatients with OCD and 13 age- and sex-matched normal volunteers. Patients were awake more on night 2 than on night 1, whereas control subjects had less time awake on night 1; no other differences between groups were found on sleep latency, sleep time, minutes of movement, sleep efficiency, rapid eye movement (REM) latency or amount of stage 1, 2, 3, or 4 or REM sleep. Within the patient group, total scores on the Yale–Brown Obsessive–Compulsive Scale were negatively correlated with total sleep time (r=−0.51, P=0.07), sleep efficiency (r=−0.51, P=0.07), and duration of stage 1+2 sleep (r=−0.49, P=0.09) but not with REM time (r=−0.05, P=0.87) or latency (r=−0.26, P=0.39). Previous sleep studies in OCD have had divergent results, especially regarding REM latency; our results suggest that many OCD patients have essentially normal sleep EEG findings.     

Cholinergic REM induction response: separation of anxiety and depression

Five groups of subjects underwent EEG sleep recordings, arecoline rapid eye movement (REM) induction response testing, and Schedule for Affective Disorders and Schizophrenia (SADS) interview. Group I: 20 patients with primary major depressive disorder (MDD) (endogenous) without any coexisting anxiety disorder; Group II: 19 primary MDD (endogenous) patients with secondary panic, GAD, or phobic disorders; Group III: 18 patients with primary anxiety disorder without coexisting MDD; Group IV: 14 patients with primary anxiety plus secondary MDD; Group V: 26 normal controls. Modified Research Diagnostic Criteria (RDC) were used for diagnosis, based on the SADS interview. There was considerable overlap of SADS scaled scores between patient groups, which is consistent with a heterogeneous clinical presentation of depressive and anxiety states. REM latency was significantly shorter in patients with primary MDD (without anxiety) as compared with that in patients with primary anxiety (no MDD) and normals. Arecoline REM induction response time was significantly shorter in both primary affective groups (I and II) as compared with primary anxiety (no MDD) patients and normal controls. REM latency and arecoline REM induction time was not significantly different between the primary anxiety groups (III and IV) and normals. The study highlights the use of biological markers in differentiating between clinical syndromes confounded by mixed or overlapping phenomenology.     

Electroencephalography during sleep of patients with panic disorder

Sleep electroencephalograms (EEGs) of subjects with primary panic disorder were compared to those of normal controls matched for age and sex. Significant differences were found between patients and controls in sleep latency, sleep efficiency, and stage 2 sleep duration. No differences were found between the two groups in REM latency. Because depressed patients are known to have reduced latency to REM sleep, these data add support to the hypothesis that panic disorder and depression are distinct disorders.     

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.     

Sleep in obsessive compulsive disorder

Several lines of evidence suggest that brain serotonergic systems may be disturbed in obsessive compulsive disorder (OCD). The serotonergic system strongly affects sleep and characteristic abnormalities of sleep are documented in depression. This study, therefore, aimed to investigate sleep structure of OCD patients in order to evaluate whether similar changes as in depression are present. Up to now, this issue has been addressed only in few studies with small numbers of patients. Sleep patterns of 62 unmedicated patients with primary OCD and 62 age- and sex-matched healthy controls were investigated by polysomnography. Additionally, the impact of tryptophan depletion on sleep was studied in a subgroup of 12 OCD patients and 12 controls. The OCD patients exhibited moderate, but significant disturbances of sleep continuity measures but no abnormalities of slow wave sleep or REM sleep, except a significant elevation of 1st REM density. Tryptophan depletion induced a worsening of sleep continuity, but no changes of REM sleep or slow wave sleep. Assuming that changes of sleep architecture indicate underlying neurobiological abnormalities, this study indicates that neurobiological disturbances are different in primary OCD as compared with primary depression.     

抑郁症、焦虑症、强迫症患者睡眠脑电图及P300的比较

目的探讨抑郁症、焦虑症、强迫症患者睡眠脑电图的差异及其与事件相关诱发电位P300关系.方法对31例抑郁症、20例焦虑症、20例强迫症患者进行多导睡眠脑电图和P300测定,将3组的多导睡眠脑电图结果与P300各指标进行相关分析.结果 (1)抑郁症、焦虑症、强迫症3组睡眠进程各个指标的差异均无统计学意义;(2)与焦虑症组和强迫症组比较,抑郁症组快速眼动(REM)睡眠的活动量小、强度低、睡眠时间少,睡眠周期数少、睡眠结构中REM睡眠比率均低,而睡眠结构的第1阶段比率高(P<0.01和<0.05);焦虑症组与强迫症组间睡眠脑电图各项指标的差异无统计学意义;(3)各组睡眠脑电图的各项指标与P300存在不同的相关性.结论抑郁症与焦虑症、强迫症睡眠结构比率和REM睡眠的特点不同,关注睡眠特别是REM睡眠的神经机制可能会进一步认识认知功能的改变.     

Sleep in Posttraumatic Stress Disorder

Posttraumatic stress disorder (PTSD) is often associated with sleep disturbances. In this review, we focus on the published literature on subjective and objective findings of sleep in patients with PTSD. Insomnia and nightmares are most commonly reported subjective sleep disturbances. Polysomnographic investigations have frequently reported rapid eye movement (REM) sleep abnormalities in PTSD. However, studies have not been consistent about the type of REM sleep dysfunction in PTSD patients. Antidepressants such as nefazodone, trazodone, fluvoxamine, and imagery rehearsal therapy are found to be beneficial in the treatment of PTSD associated sleep disturbances as well as core symptoms of this anxiety disorder. We propose use of such modalities of treatment in PTSD patients with predominant sleep disturbances. Further studies are required to clarify polysomnographic sleep changes especially role of REM sleep dysregulation and treatment of sleep disturbances in PTSD.     

Actigraphic sleep monitoring in posttraumatic stress disorder (PTSD) patients

Posttraumatic stress disorder (PTSD) patients frequently complain that they suffer from sleep disturbances. To date, the polysomnographic studies that have attempted to study PTSD patients' subjective complaints of sleep difficulties have produced conflicting results. The objective of the present study was to compare PTSD patients' subjective complaints of poor sleep and objective actigraphic recordings of their sleep over a period of several consecutive nights. The results indicate that PTSD patients do not suffer from poorer sleep than a control group, based on actigraphic measures, and that their subjective sleep evaluation is inconsistent with objective sleep measures. These patients fail to correctly estimate their sleep.     

The sleep of non-depressed patients with panic disorder: a comparison with normal controls

Arriaga F, Paiva T, Matos-Pires A, Cavaglia F, Lara E, Bastos L. The sleep of non-depressed patients with panic disorder: a comparison with normal controls. Acta Psychiatr Scand 1996: 93: 191–194. © Munksgaard 1996. All-night sleep EEG recordings were performed in non-depressed patients with panic disorder, agoraphobia, and a group of age- and sex-matched normal controls. Patients were selected according to DSM-IV and all subjects were studied under drug-free conditions. In addition to sleep continuity disturbances, patients with panic disorder have a reduced percentage of slow wave sleep, mainly due to diminished amounts of stage 4. REM sleep characteristics are identical in the two groups. When depressive co-morbidity and non-specific causes of insomnia are excluded, the sleep EEG of panic patients seems to be characterized by modest changes in sleep continuity and sleep architecture. These findings favour the existence of a neurophysiological frontier between anxiety disorders and depressive illness.     

Effects of one night's sleep deprivation on mood and behavior in panic disorder. Patients with panic disorder compared with depressed patients and normal controls

The effects of one night's sleep deprivation on mood and behavior were evaluated in 12 patients with panic disorder, ten depressed patients, and ten controls. In contrast to the improvement in symptoms of anxiety and depression shown by the majority of depressed patients, the response of patients with panic disorder as a group did not differ from that of normal controls, although a subgroup did experience noticeable worsening in their symptoms of anxiety, with 40% experiencing panic attacks on the day following sleep deprivation. Electroencephalographic recordings with nasopharyngeal electrodes on the day following sleep deprivation were normal, further suggesting that patients with panic disorder do not have seizure activity characteristic of temporal lobe epilepsy.     

Clinical and EEG sleep changes in primary dysthymia and generalized anxiety: a comparison with normal controls

All night EEG sleep recordings and clinical assessments of sleep quality were performed in normal controls, patients with generalized anxiety disorder and primary dysthymia. Patients were selected according to DSM-III R. Changes of sleep architecture, namely a reduction of slow wave sleep, are similar in generalized anxiety and dysthymia. Also the two groups do not exhibit the REM sleep disturbances usually observed in affective illness. Duration and continuity measures are unchanged in dysthymics, but anxious patients show some features of insomnia. The analysis of subjective aspects of sleep showed no relevant differences between the two groups of patients. Using a conventional set of EEG sleep parameters, primary dysthymia seems closer to anxiety disorders than to affective illness. However, the reduction of slow wave sleep in dysthymics and anxious patients may have different pathogenic meanings and the analysis of nonconventional sleep parameters may prove useful in this regard.     

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 in lifetime posttraumatic stress disorder: a community-based polysomnographic study

BACKGROUND: Sleep complaints are common in posttraumatic stress disorder (PTSD) and are included in the DSM criteria. Polysomnographic studies conducted on small samples of subjects with specific traumas have yielded conflicting results. We therefore evaluated polysomnographic sleep disturbances in PTSD. METHODS: A representative cohort of young-adult community residents followed-up for 10 years for exposure to trauma and PTSD was used to select a subset for sleep studies for 2 consecutive nights and the intermediate day. Subjects were selected from a large health maintenance organization and are representative of the geographic area except for the extremes of the socioeconomic status range. The subset for the sleep study was selected from the 10-year follow-up of the cohort (n = 913 [91% of the initial sample]). Eligibility criteria included (1) subjects exposed to trauma during the preceding 5 years; (2) others who met PTSD criteria; and (3) a randomly preselected subsample. Of 439 eligible subjects, 292 (66.5%) participated, including 71 with lifetime PTSD. Main outcomes included standard polysomnographic measures of sleep induction, maintenance, staging, and fragmentation; standard measures of apnea/hypopnea and periodic leg movement; and results of the multiple sleep latency test. RESULTS: On standard measures of sleep disturbance, no differences were detected between subjects with PTSD and control subjects, regardless of history of trauma or major depression in the controls. Persons with PTSD had higher rates of brief arousals from rapid eye movement (REM) sleep. Shifts to lighter sleep and wake were specific to REM and were significantly different between REM and non-REM sleep (F(1,278) = 5.92; P =.02). CONCLUSIONS: We found no objective evidence for clinically relevant sleep disturbances in PTSD. An increased number of brief arousals from REM sleep was detected in subjects with PTSD. Sleep complaints in PTSD might represent amplified perceptions of brief arousals from REM sleep.