Abnormal Rapid Eye Movement Latencies in Schizophrenia

Plasma cholinesterase isozymes and REM latency in schizophrenia

Mid-morning Tryptophan Depletion Delays REM Sleep Onset in Healthy Subjects

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

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

Respiratory-related leg movements (RRLMs) may contribute to the cardiovascular risk associated with obstructive sleep apnea (OSA). Selective serotonin reuptake inhibitors (SSRIs), but not bupropion, increase periodic leg movements in sleep. This study examines whether patients with OSA using SSRIs have more RRLMs than those taking bupropion or no antidepressant. Patients with an apnea-hypopnea index (AHI) of at least 10 events/h during a full-night diagnostic study or split-night study, who were taking bupropion (n = 32), an SSRI (n = 31), or no antidepressant (n = 31), were selected from a database of prestudy questionnaires. RRLMs were scored according to World Association of Sleep Medicine 2016 standards. Patients using SSRIs had significantly greater overall RRLM% (defined as the percentage of respiratory events associated with a leg movement, including apneas, hypopneas, and respiratory effort-related arousals), RRLM index, and periodic limb movement index relative to patients using bupropion and control patients. The difference between the RRLM% in the SSRI and bupropion groups was limited to patients undergoing split-night studies, and that of the SSRI and control groups was limited to patients undergoing full-night diagnostic studies. The greater number of RRLMs and PLMs in the SSRI group may contribute to treatment-emergent insomnia often seen with SSRI use. Fragmented sleep and elevated autonomic nervous system activation associated with increased RRLMs in patients with OSA taking SSRIs might also limit the tolerability of antidepressant treatment, as well as increase the risk for cardiovascular disease.

Sleep EEG features of adolescents with major depression

Insomnia complaints are frequent in Parkinson disease (PD), affecting up to 55% of patients. Factors related to insomnia in PD are multifactorial and may be associated with the degenerative process of the disease, comorbidities related to aging, and medication use. The aim of this study is to determine the factors associated with the presence of chronic insomnia in patients with PD. A cross-sectional study was performed involving 63 consecutive patients with PD from an outpatient clinic. Participants underwent clinical interviews with neurologists and a psychiatrist and were assessed with standardized scales (Epworth Sleepiness Scale, Parkinson's Disease Questionnaire, Pittsburgh Sleep Quality Index and, for individuals with a diagnosis of restless legs syndrome(RLS)/Willis-Ekbom disease (WED), the International RLS/WED grading scale) and video-polysomnography. The main factors associated with chronic insomnia in PD were the habit of staying in bed without sleeping, large rapid eye movement (REM) sleep latency, high Pittsburgh Sleep Quality Index scores, and absence of obstructive sleep apnea (OSA). Insomnia in PD is related to specific factors including inadequate sleep habits, REM sleep latency, absence of OSA, and quality of sleep.

Objectives To compare the sleep parameters and certain neurocognitive tasks between patients with unipolar and bipolar depression,and to explore the correlation between sleep pattern and certain cognitive function. Methods Fifteen patients with unipolar depression,thirteen patients with bipolar depression,and fifteen health controls were recruited.Sleep parameters were recorded by polysomnography for three groups respectively.The certain cognitive tasks were finished in patients group. Results Compared with control group,the bipolar patients had longer sleep latency (P=0.004),poorer sleep efficiency (P=0.007),while the unipolar patients had poorer sleep efficiency (P=0.038),less slow wave sleep (P=0.002),more numbers of wake (P=0.019),longer duration of wake after sleep onset (P=0.035),increased proportion of S1 (P=0.028) and S2 sleep (P=0.014),decreased proportion of S3 (P=0.002),and longer REM sleep latency (P=0.019).No significant difference of polysomnographically recorded sleep parameters were found between unipolar and bipolar group.There was no significant correlation between sleep parameters and certain cognitive tasks in bipolar group.In unipolar group,the verbal learning field was related with REM sleep duration (r=0.63,P=0.034),proportion of REM (r=0.69,P=0.020),REM sleep latency (r=-0.74,P=0.009),while the visual memory field was related with proportion of S2 (r=-0.65,P=0.029) and REM sleep latency (r=-0.72,P=0.012). Conclusions The sleep disturbance in the bipolar group may be mild,while in the unipolar group,the disturbance is focused on the sleep continuity and architecture.The relationship of the sleep parameters and certain neurocognitive field may be different between unipolar and bipolar depression. Key words: Bipolar disorder; Polysomnography; Cognition

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

This open study evaluates the effect of agomelatine, a melatonergic receptor agonist and 5-HT2C antagonist antidepressant, on sleep architecture in patients suffering from major depressive disorder. Fifteen outpatients with a baseline HAMD score > or = 20 were treated with 25 mg/d agomelatine for 42 d. Polysomographic studies were performed at baseline, day 7, day 14, and day 42. Sleep efficiency, time awake after sleep onset and the total amount of slow-wave sleep (SWS) increased at week 6. The increase of SWS was predominant during the first sleep cycle. The amount of SWS decreased throughout the first four sleep cycles from day 7 and delta ratio increased from day 14 onwards. No change in rapid eye movement (REM) latency, amount of REM or REM density was observed and agomelatine was well tolerated. In conclusion agomelatine improved sleep continuity and quality. It normalized the distribution of SWS sleep and delta power throughout the night.

Repeated exposure to an anxiogenic stressor (AS) is a known environmental factor for the development of depression, yet the progression of sleep-wake (S-W) changes associated with the onset of AS-induced depression (ASID) is not completely understood. Thus, the aim of this study was to identify these progressive S-W changes by developing ASID in rats, via repeated exposure to an AS, and compare this ASID-associated sleep phenotype with the sleep phenotype of human depression. To achieve this aim, rats were first recorded for a 6 h period of baseline S-W activity without AS. Then, rats were subjected to 5 days of AS [Day 1: inescapable foot-shock; 5 trials of 3 s foot-shocks (1.0 mA) at 3 min intervals; Days 3–5: 15 trials of 5 s foot-shocks at 45 s intervals]. S-W activity was recorded for 6 h immediately after each AS treatment session. Two days later rats were again recorded for 6 h of S-W activity, but with no exposure to the AS (NASD). Compared to the baseline day: Day 1 of AS (ASD-1) increased wakefulness, slow-wave sleep (SWS) latency, and rapid-eye movement (REM) sleep latency, but decreased the total amount of REM sleep; ASD-2 animals remained awake throughout the 6 h S-W recording period; ASD-3, ASD-4, and ASD-5 (ASDs-3–5) decreased wakefulness, SWS latency, and REM sleep latency, but increased the total amount of REM sleep. Interestingly, these results reveal that initial exposure to the AS versus later, repeated exposure to the AS produced opposing S-W changes. On NASD, animals exhibited baseline-like S-W activity, except slightly less REM sleep. These results suggest that repeated AS produces a sleep phenotype that resembles the sleep phenotype of depression in humans, but consistent re-exposure to the AS is required. These results are promising because the methodological simplicity and reversibility of the ASID-associated S-W phenotype could be more advantageous than other animal models for studying the pathophysiological mechanisms that underlie the expression of ASID.

We want to evaluate the effect of sertraline on polysomnogram (PSG) and clinical variables in depression. An 8-week and open-label trial (n = 31) was applied. The primary outcome was mean baseline-to-visit changes in PSG variables. The secondary outcomes were clinical improvement, side-effects, and the subjective sleepiness. Rapid eye movement (REM) latency was prolonged significantly over the course of the study. The arousal index reached the highest level on the 1st day (13.8 _ 7.2). From the 14th day onward, the sleep latency (SL) and wake after sleep onset (WASO) decreased significantly. The percentage of stage 3 sleep increased in this trial. The Hamilton Rating Scale for Depression (HRSD) and Clinical Global Impression (CGI) scores on the 14th, 28th, and 56th days were significantly lower than baseline. Furthermore, a significant correlation was shown between the decreasing score rate of HRSD on the 56th day and the decreasing score rate of REM latency on the 1st day (r = -0.733, P = 0.003). The effectiveness of sertraline positively correlated with the reduction of REM latency. The final clinical improvement could be predicted by the extent of the prolongation of REM latency on the first night.

24-Hour cortisol measures in adolescents with major depression: A controlled study

P-306 – L'allergie aux protéines de lait de vache – à propos de 39 observations

Our objective was to assess the effects of nortriptyline on electroencephalographic sleep and subjective sleep quality in spousally bereaved, depressed elders. Ten elderly volunteers with bereavement-related major depression had electroencephalographic sleep studies while depressed, after remission of depressive symptoms while still taking nortriptyline, and after nortriptyline discontinuation. Changes in sleep measures over time were compared both within bereaved subjects and with age- and sex-matched healthy controls. Remission of depressive symptoms while still on nortriptyline was associated with improvements in sleep quality (P < .002), rapid eye movement (REM) percent (P < .02), REM latency (P < .05), REM density (P < .05), and delta sleep ratio (P < .05). After discontinuation of nortriptyline, REM percent, REM latency, and delta ratio reverted to pretreatment levels, while sleep efficiency and sleep quality continued to show improvement coincident with sustained clinical remission. These data suggest that nortriptyline may be clinically useful in treating the sleep disturbance of elders with bereavement-related depression and that a double-blind, placebo-controlled, randomized clinical trial is warranted.