Long-term melatonin administration does not alter pituitary-gonadal hormone secretion in normal men

The role of melatonin in the regulation of reproduction in humans is still controversial. In the present study the effects of melatonin were examined, 6 mg given orally every day at 1700 h for 1 month in a double-blind, placebo controlled fashion, on the nocturnal secretory profiles of luteinizing hormone (LH), follicle stimulating hormone (FSH), testosterone and inhibin beta in six healthy adult men. Serum concentrations of LH, FSH, testosterone and inhibin beta were determined before and after treatment every 15 min from 1900 to 0700 h over 3 nights in a controlled dark-light environment with simultaneous polysomnographic sleep recordings. The following sleep parameters were determined: total recording time, sleep latency, actual sleep time, sleep efficiency, rapid eye movement (REM) sleep latency and percentages of sleep stages 2, 3/4 and REM. There were no statistically significant differences in all sleep parameters between baseline and placebo or between baseline and melatonin except for longer REM latency and lower percentage REM at baseline than under melatonin treatment. These are explained as reflecting first-night effect at baseline. The mean nocturnal LH, FSH, testosterone and inhibin beta integrated nocturnal secretion values did not change during the treatment period. Likewise, their pulsatile characteristics during melatonin treatment were not different from baseline values. Taken together, these data suggest that long-term melatonin administration does not alter the secretory patterns of reproductive hormones in normal men.     

REM sleep behavior disorder and REM sleep without atonia in patients with progressive supranuclear palsy

STUDY OBJECTIVE: To compare sleep characteristics, rapid eye movement (REM) sleep without atonia, and REM sleep behavior disorder (RBD) in patients with progressive supranuclear palsy (tauopathy), patients with Parkinson's disease (a synucleinopathy), and control subjects. DESIGN: Sleep interview, overnight polysomnography, and Multiple Sleep Latency Tests. PATIENTS: Forty-five age- and sex-matched patients with probable progressive supranuclear palsy, (n=15, aged 68 +/- 8 years, 7 men), patients with Parkinson disease (n=15), and control subjects (n=15). SETTINGS: Tertiary-care academic hospital. INTERVENTION: N/A. RESULTS: Compared to the 2 other groups, patients with progressive supranuclear palsy had a longer duration of wakefulness after sleep onset and twice as much sleep fragmentation and percentage of stage 1 sleep but had similar apnea-hypopnea indexes, periodic leg movements indexes, and mean daytime sleep latencies. REM sleep percentage was as low in patients with progressive supranuclear palsy (8% +/- 6% of total sleep time) as in patients with Parkinson disease (10% +/- 4%), versus 20% +/- 6% in controls (analysis of variance, P < .0001). Interestingly, patients with progressive supranuclear palsy had percentages of REM sleep without atonia (chin muscle activity: 33% +/- 36% of REM sleep) similar to those of patients with Parkinson disease (28% +/- 35%) and dramatically higher than those of controls (0.5% +/- 1%, analysis of variance, P = .008). Four (27%) patients with progressive supranuclear palsy had more than 50% REM sleep without atonia (as did a similar number of patients with Parkinson disease), and 2 of them (13%, vs 20% of patients with Parkinson disease) had clinical RBD. The four patients with progressive supranuclear palsy with excessive daytime sleepiness slept longer at night than the 11 patients with progressive supranuclear palsy who were alert (442 +/- 14 minutes vs 312 +/- 74 minutes, student t tests, P = .004), suggesting a primary nonnarcoleptic hypersomnia. CONCLUSION: REM sleep without atonia and RBD were as frequent in patients with progressive supranuclear palsy as in patients with Parkinson disease. It suggests that the downstream cause of parkinsonism, rather than its primary neuropathology (synucleinopathy vs tauopathy), is a key factor for REM sleep behavior disorder.     

Sleep and nighttime pruritus in children with atopic dermatitis

The number of scratching episodes and average frequency with which they started during each sleep stage as well as the effects of nighttime pruritus on objective sleep parameters in nine children with atopic dermatitis were assessed in the sleep laboratory. Scratching episodes occurred during rapid eye movement (REM) sleep and non-REM (NREM) sleep. The largest average frequency corresponded to stage 1, followed by stage 2, REM sleep, stage 4, and stage 3. Sleep maintenance was markedly altered. Total sleep time decrease was related mainly to smaller amounts of stage 4 NREM sleep. REM sleep percentage of total sleep time was increased as compared with normal children of the same age. Furthermore, in six of nine patients REM sleep latency was found to be decreased.     

A quantitative statistical analysis of the submentalis muscle EMG amplitude during sleep in normal controls and patients with REM sleep behavior disorder

The aim of this study was to evaluate quantitatively the amplitude of the submentalis muscle EMG activity during sleep in controls and in patients with idiopathic REM sleep behavior disorder (RBD) or with RBD and multiple system atrophy (MSA). We recruited 21 patients with idiopathic RBD, 10 with MSA, 10 age-matched and 24 young normal controls. The average amplitude of the rectified submentalis muscle EMG signal was used for the assessment of atonia and a Sleep Atonia Index was developed; moreover, also chin muscle activations were detected and their duration and interval analyzed. The Sleep Atonia Index was able to distinguish clearly REM from NREM sleep in normal controls with values very close to 1 in young normal subjects and only slightly (but significantly) lower in old controls. Idiopathic RBD patients showed a further significant decrease of this index; MSA patients showed the lowest values of REM Sleep Atonia Index, which were very well distinguishable from those of normal controls and of idiopathic RBD patients. The distribution of the duration of chin activations was monomodal in all groups, with idiopathic RBD patients showing the highest levels. This study is a really quantitative attempt to provide practical indices for the objective evaluation of EMG atonia during REM sleep and of EMG activations. Our proposed Sleep Atonia Index can have a practical application in the clinical evaluations of patients and represents an additional useful parameters to be used in conjunction with the other criteria for the diagnosis of this sleep motor disorder.     

Melatonin advances the circadian timing of EEG sleep and directly facilitates sleep without altering its duration in extended sleep opportunities in humans

The rhythm of plasma melatonin originating from the pineal gland and driven by the circadian pacemaker located in the suprachiasmatic nucleus is closely associated with the circadian (approximately 24 h) variation in sleep propensity and sleep spindle activity in humans. We investigated the contribution of melatonin to variation in sleep propensity, structure, duration and EEG activity in a protocol in which sleep was scheduled to begin during the biological day, i.e. when endogenous melatonin concentrations are low. The two 14 day trials were conducted in an environmental scheduling facility. Each trial included two circadian phase assessments, baseline sleep and nine 16 h sleep opportunities (16.00–08.00 h) in near darkness. Eight healthy male volunteers (24.4 ± 4.4 years) without sleep complaints were recruited, and melatonin (1.5 mg) or placebo was administered at the start of the first eight 16 h sleep opportunities. During melatonin treatment, sleep in the first 8 h of the 16 h sleep opportunities was increased by 2 h. Sleep per 16 h was not significantly different and approached asymptotic values of 8.7 h in both conditions. The percentage of rapid eye movement (REM) sleep was not affected by melatonin, but the percentage of stage 2 sleep and sleep spindle activity increased, and the percentage of stage 3 sleep decreased. During the washout night, the melatonin-induced advance in sleep timing persisted, but was smaller than on the preceding treatment night and was consistent with the advance in the endogenous melatonin rhythm. These data demonstrate robust, direct sleep-facilitating and circadian effects of melatonin without concomitant changes in sleep duration, and support the use of melatonin in the treatment of sleep disorders in which the circadian melatonin rhythm is delayed relative to desired sleep time.     

Electroencephalogram and cardiovascular responses to noise during daytime sleep in shiftworkers

Summary Intermittent noise occurring during sleep has been found to induce heart rate, peripheral vasomotor and electroencephalogram (EEG) changes. This study analysed these responses during the daytime and night-time sleep of shiftworkers doing a three shift system, to determine the influence of the inversion of the sleep-wake cycle on the sensitivity to noise. A group of 14 shiftworkers [aged 37 (SD 5) years] underwent an habituation daytime sleep, two experimental daytime sleeps and a night-time sleep. Traffic noises were presented during sleep [truck, 71 dB(A); motorbike, 67 dB(A); and car, 64 dB(A)] at a rate of nine each hour. The EEG measurements of sleep, electrocardiogram and finger pulse amplitude were recorded continuously. The results were expressed by computing the percentage of observed cardiac response (%HRR) and vasoconstrictive response (%FPR), magnitude of heart rate variation (heart rate response; HRR), percentage of reduction of the digital blood flow (finger pulse response, FPR), cardiac cost (CC = % HRR x HRR) and vasomotor cost (VC = % FPR x FPR). The results showed that, compared to night-time sleep, there was change in the structure of daytime sleep, that is an increase in slow wave sleep (SWS), especially stage 4 sleep decrease of stage 2 and rapid eye movement (REM) sleep latencies, and an earlier SWS and REM sleep barycentric point. During daytime sleep the % FPR was significantly smaller in SWS than in stage 2 or REM sleep. Large differences were observed in % HRR, HRR and CC between daytime sleep stages (SWS less than stage 2 less than REM sleep). These differences were not observed during night-time sleep. Moreover, compared to night-time sleep, CC was increased during daytime REM sleep and decreased during daytime SWS. The inversion of the sleep-wake cycle in shiftworkers, did not influence the overall cardiovascular reactivity to noise. This was explained by a compensatory effect due to an increase in this reactivity during daytime REM sleep and its decrease in daytime SWS. The second reason is due to an increase in the percentage of stage 4 sleep during daytime sleep (less disturbed by noise than other sleep stages). This increased percentage of stage 4 sleep was probably a consequence of the partial sleep deprivation occurring after a week working on nightshift.     

REM sleep characteristics in narcolepsy and REM sleep behavior disorder

STUDY OBJECTIVES: To assess the presence of polysomnographic characteristics of REM sleep behavior disorder (RBD) in narcolepsy; and to quantify REM sleep parameters in patients with narcolepsy, in patients with "idiopathic" RBD, and in normal controls. DESIGN: Sleep laboratory study PARTICIPANTS: Sixteen patients with narcolepsy and cataplexy matched for age and sex with 16 patients with "idiopathic" RBD and with 16 normal controls were studied. MEASUREMENTS AND RESULTS: Higher percentages of REM sleep without atonia, phasic electromyographic (EMG) activity, and REM density were found in patients with narcolepsy than normal controls. In contrast, RBD patients had a higher percentage of REM sleep without atonia but a lower REM density than patients with narcolepsy and normal controls. Based on a threshold of 80% for percentage of REM sleep with atonia, 50% of narcoleptics and 87.5% of RBD patients had abnormal REM sleep muscle activity. No significant behavioral manifestation in REM sleep was noted in either narcoleptics or controls. We also found a higher frequency of periodic leg movements during wake (PLMW) and during sleep (PLMS) in narcoleptic patients compared to controls. CONCLUSIONS: The present study demonstrates abnormalities in REM sleep motor regulation with an increased frequency of REM sleep without atonia, phasic EMG events and PLMS in narcoleptic patients when compared to controls. These abnormalities were seen more prominently in patients with RBD than in narcoleptics, with the exception of the PLMS index. We proposed that dysfunctions in hypocretin/dopaminergic system may lead to motor dyscontrol in REM sleep that results in dissociated sleep/wake states.     

A preliminary understanding of mania: roles for melatonin, vasotocin and rapid-eye-movement sleep

Speculation about mania links melatonin, vasotocin and rapid-eye-movement (REM) sleep. Normal REM sleep can have the loss of reality testing and this feature intruding into the wake period could be the cause of the distorted reality present in manic delusions. REM sleep has a role in memory formation. Abnormal levels and/or rhythms of melatonin are thought to be involved in mania. Decreased melatonin production with malfunction of REM sleep is proposed to be a cause of sudden infant death syndrome and Alzheimer's disease, because the loss of the antioxidant function of melatonin allows brain injury to occur.     

Polysomnographic study of nocturnal sleep in idiopathic hypersomnia without long sleep time

We investigated nocturnal sleep abnormalities in 19 patients with idiopathic hypersomnia without long sleep time (IH) in comparison with two age‐ and sex‐ matched control groups of 13 normal subjects (C) and of 17 patients with narcolepsy with cataplexy (NC), the latter considered as the extreme of excessive daytime sleepiness (EDS). Sleep macro‐ and micro‐ (i.e. cyclic alternating pattern, CAP) structure as well as quantitative analysis of EEG, of periodic leg movements during sleep (PLMS), and of muscle tone during REM sleep were compared across groups. IH and NC patients slept more than C subjects, but IH showed the highest levels of sleep fragmentation (e.g. awakenings), associated with a CAP rate higher than NC during lighter sleep stages and lower than C during slow wave sleep respectively, and with the highest relative amount of A3 and the lowest of A1 subtypes. IH showed a delta power in between C and NC groups, whereas muscle tone and PLMS had normal characteristics. A peculiar profile of microstructural sleep abnormalities may contribute to sleep fragmentation and, possibly, EDS in IH.     

注意缺陷多动障碍综合征患儿睡眠结构的初探

目的 探讨注意缺陷多动障碍（ADHD）综合征患儿的睡眠结构，睡眠中痢性放电及睡眠周期性肢体运动（PLMS）的情况；比较ADHD各亚型问睡眠结构的差异。方法 利用多导睡眠监护仪对2005年6月至2006年11月在首都儿科研究所神经科门诊就诊的符合DSM-Ⅳ诊断标准的58例ADHD患儿及30名正常儿童进行整夜睡眠结构监测。结果 ADHD组58例，其中4例睡眠监测未完成，实际完成54例。ADHD组中混合型（ADHD—C）31例（57．4％，31／54），注意缺陷型（ADHD-I）15例（27．8％，15／54），多动／冲动型（ADHD．H）8例（14．8％，8／54）。①与对照组比较，ADHD组快速动眼期（REM）潜伏期短、睡眠潜伏期延长和睡眠效率降低，差异有统计学意义（P〈0．05）；②ADHD-C患儿睡眠Ⅱ期百分比较ADHD-I增加，差异有统计学意义（P〈0．05）；③ADHD组PLMS发生率为37．0％（20／54），对照组PLMS发生率为13．3％（4／30），差异有统计学意义（P〈0．05）；④ADHD组和对照组EEG未见痢性放电。结论 ①ADHD患儿存在REM睡眠结构的改变、入睡困难及睡眠效率降低；②睡眠Ⅱ期百分比的增多可使ADHD-C较ADHD-I有更多和更重的症状；③ADHD患儿睡眠过程中PLMS发生率较对照组显著升高，PLMS也是导致ADHD患儿睡眠质量下降的原因之一。     

Motor dyscontrol in sleep of narcoleptic patients (a lifelong development?)

In our retrospective study 27 narcoleptic patients were divided into two groups: Group A comprised 14 patients (10 male, 4 female) with a history of REM behaviour disorder (RBD) and Group B comprised 13 age- and sex-matched patients (10 male, 3 female) without a history of RBD. Polygraphic and videometry data, medical history, medication, blood chemistry, psychological and neuroradiological data of the two groups of patients were compared. The narcoleptic patients with a history of RBD differed from the narcoleptic control group without history of RBD in that they had: (a) a higher frequency of parasomnias in their history; (b) a higher percentage of stage 1 REM (P < 0.01); (c) a lower number of arousals during REM sleep; (d) fewer sleep stage changes. Compared to the heterogenous RBD patient group of Mahowald and Schenck, the REM behaviour of most of our narcoleptic patients was less violent. Thus it can be speculated that the motor disorder in REM sleep might still be in the process of developing towards a full-blown REM sleep behaviour disorder. In a possible lifelong development of a motor disorder starting in NREM sleep, the onset of narcolepsy might represent the turning point for its intrusion into REM sleep.     

Effect of growth hormone treatment on sleep EEGs in growth hormone-deficient children

Total sleep time, sleep stages 1-4, REM, REM latency, and sleep efficiency were analyzed in seven children with growth hormone deficiency (GHD) before and after growth hormone (GH) therapy. Before GH therapy, GHD children spent 19.5% of their total sleep time in REM sleep, 9.7% in stage 1, 41.0% in stage 2, 10.0% in stage 3, and 19.7% in stage 4. GHD children had more stage 1 and 3 sleep and less REM as compared with age-matched normal children reported by Williams et al. After GH therapy was initiated, six of the seven patients had decreases in the duration of stage 3 sleep, with an average decrease of 21.8 min. The difference between stage 3 sleep before and during GH treatment was significant, with a p value of less than 0.025. When the results were expressed as the percentage of the total sleep period, the difference was also significant, (10.0 +/- 2.0 to 7.5 +/- 3.1%, mean +/- SD; p less than 0.05). No other sleep parameters were significantly affected by GH therapy. The changes observed in stage 3 sleep, non-REM sleep, and the lack of any other changes in sleep before and after GH therapy have not been described before in GH-deficient children. They differ from studies in normal humans and animals which showed that REM sleep increased with administration of growth hormone. These differences suggest that GH deficiency is associated with a specific sleep EEG anomaly that is corrected in part by GH therapy.     

Activity of human hippocampal formation and amygdala neurons during sleep.

Fine wire microelectrodes were implanted for diagnostic purposes in 17 patients suffering from psychomotor epilepsy. Single- and multiunit activity during waking and natural nocturnal slow wave sleep and REM sleep was recorded in the hippocampus (n = 42), hippocampal gyrus (n = 53), and amygdala (n = 32). The firing rates of hippocampal gyrus units usually decreased during slow wave sleep and then increased to levels equal to or above waking during REM. In contrast, the firing rates of hippocampal neurons generally increased during slow wave sleep and fell to very low levels during REM. The amygdala presented a more mixed pattern. Since the projection from the hippocampal gyrus to hippocampus is excitatory, their opposite patterns during sleep suggest that the tonic firing patterns of HC neurons may be mainly the result of subcortical afferents.     

Serum brain‐derived neurotrophic factor (BDNF) in sleep‐disordered patients: relation to sleep stage N3 and rapid eye movement (REM) sleep across diagnostic entities

Experimental and clinical evidence suggests an association between neuroplasticity, brain‐derived neurotrophic factor and sleep. We aimed at testing the hypotheses that brain‐derived neurotrophic factor is associated with specific aspects of sleep architecture or sleep stages in patients with sleep disorders. We included 35 patients with primary insomnia, 31 patients with restless legs syndrome, 17 patients with idiopathic hypersomnia, 10 patients with narcolepsy and 37 healthy controls. Morning serum brain‐derived neurotrophic factor concentrations were measured in patients and controls. In patients, blood sampling was followed by polysomnographic sleep investigation. Low brain‐derived neurotrophic factor levels were associated with a low percentage of sleep stage N3 and rapid eye movement sleep across diagnostic entities. However, there was no difference in brain‐derived neurotrophic factor levels between diagnostic groups. Our data indicate that serum levels of brain‐derived neurotrophic factor, independent of a specific sleep disorder, are related to the proportion of sleep stage N3 and REM sleep. This preliminary observation is in accordance with the assumption that sleep stage N3 is involved in the regulation of neuroplasticity.     

Sleep in human narcolepsy revisited with special reference to prior wakefulness duration.

Sleep of 11 narcoleptic subjects was recorded on baseline and after 16 and 24 hours of prior wakefulness (16 and 24 hours sleep deprivation). Eleven sex- and age-matched control subjects were recorded for comparisons. All recordings in narcoleptic subjects were characterized by frequent sleep onset rapid eye movement (REM) episodes, increased amounts of wake time after sleep onset and low sleep efficiencies. Mean total sleep time (TST) was significantly decreased in narcoleptic subjects after sleep deprivation (SD). Recovery sleep after 24 hours SD showed reduced nonREM (NREM) sleep stage 2 percentage, whereas percentages of stage 4 and slow-wave sleep (SWS = stages 3 + 4) were significantly increased. The values of REM sleep percentage of TST were remarkably constant throughout and did not differ significantly as a function of experimental conditions, indicating a normal REM sleep pressure in narcolepsy. Sleep stage analysis per sleep cycles revealed significant differences between the two groups. Percentages of stage 4 and SWS were increased during the first cycle of recovery sleep in narcoleptic subjects. Stage 2 was decreased during the third cycle, and SWS decreased rapidly from cycle 1 to cycle 2 and slightly increased thereafter. These results indicate that sleep need is increased in narcolepsy, whereas its decrease over the first NREM-REM cycle is accelerated. We hypothesize that this could reflect an alteration of the homeostatic process of sleep regulation in narcolepsy.     

A two‐part,double‐blind,placebo‐controlled trial of exogenous melatonin in REM sleep behaviour disorder

Rapid eye movement (REM) sleep behaviour disorder (RBD) has been suggested to predict the development of neurodegenerative disorders. Patients with RBD are acting out dream behaviour associated with loss of normal muscle atonia of REM sleep. The aim of the present study was to confirm that exogenous melatonin improves RBD. Eight consecutively recruited males (mean age 54 years) with a polysomnographically (PSG) confirmed diagnosis of RBD were included in a two‐part, randomized, double‐blind, placebo‐controlled cross‐over study. Patients received placebo and 3 mg of melatonin daily in a cross‐over design, administered between 22:00 h and 23:00 h over a period of 4 weeks. PSG recordings were performed in all patients at baseline, at the end of Part I of the trial and at the end of Part II of the trial. Compared to baseline, melatonin significantly reduced the number of 30‐s REM sleep epochs without muscle atonia (39% versus 27%; P = 0.012), and led to a significant improvement in clinical global impression (CGI: 6.1 versus 4.6; P = 0.024). Interestingly, the number of REM sleep epochs without muscle atonia remained lower in patients who took placebo during Part II after having received melatonin in Part I (–16% compared to baseline; P = 0.043). In contrast, patients who took placebo during Part I showed improvements in REM sleep muscle atonia only during Part II (i.e. during melatonin treatment). The data suggest that melatonin might be a second useful agent besides clonazepam in the treatment of RBD.     

78例睡眠呼吸暂停综合征患者的睡眠特征及其与夜间低氧血症的关系

目的 :了解SAS患者的睡眠特征及其与夜间低氧血症的关系。方法 :采用PSG对 78例SAS患者和 30例正常对照者进行整夜睡眠监测 ,比较两组间的睡眠特征。并对不同严重程度的夜间低氧血症SAS患者进行睡眠变量比较 ,分析二者的关系。结果 :与正常对照者相比 ,SAS患者夜间睡眠结构紊乱 ,主要为深睡眠减少、浅睡眠相对增加、REM睡眠减少、觉醒增加、睡眠潜伏期缩短、呼吸暂停或低通气次数增加、动脉血氧饱和显著下降 (P <0 .0 5 )。SAS患者夜间最低血氧饱和度与夜间总睡眠时间、睡眠效率、NREM睡眠时间及呼吸紊乱指数呈显著负相关 (r>0 .3,P <0 .0 5 ) ,与觉醒比例呈显著正相关 (r >0 .5 ,P <0 .0 1)。结论 :SAS患者睡眠结构紊乱突出 ,夜间反复发作的低氧血症对睡眠质量产生较大影响。     

Periodic leg movements during sleep and wakefulness in narcolepsy

The objectives of the study were to measure the prevalence of periodic leg movements during NREM and REM sleep (PLMS) and while awake (PLMW) and to assess the impact of PLMS on nocturnal sleep and daytime functioning in patients with narcolepsy. One hundred and sixty-nine patients with narcolepsy and 116 normal controls matched for age and gender were included. Narcoleptics with high and low PLMS indices were compared to assess the impact of PLMS on sleep and Multiple Sleep Latency Test (MSLT) variables. More narcoleptics than controls had a PLMS index greater than 5 per hour of sleep (67% versus 37%) and an index greater than 10 (53% versus 21%). PLMS indices were higher both in NREM and REM sleep in narcoleptic patients, but the between-group difference was greater for REM sleep. A significant increase of PLMS index was also found with aging in both narcoleptic patients and controls. PLMW indices were also significantly higher in narcoleptic patients. Patients with an elevated index of PLMS had a higher percentage of stage 1 sleep, a lower percentage of REM sleep, a lower REM efficiency and a shorter MSLT latency. The present study demonstrates a high frequency of PLMS and PLMW in narcolepsy, an association between the presence of PLMS and measures of REM sleep and daytime functioning disruption. These results suggest that PLMS represent an intrinsic feature of narcolepsy.     

REM sleep behavior disorder in patients with guadeloupean parkinsonism, a tauopathy

STUDY OBJECTIVE: To describe sleep characteristics and rapid eye movement (REM) sleep behavior disorder in patients with Guadeloupean atypical parkinsonism (Gd-PSP), a tauopathy resembling progressive supranuclear palsy that mainly affects the midbrain. It is possibly caused by the ingestion of sour sop (corossol), a tropical fruit containing acetogenins, which are mitochondrial poisons. DESIGN: Sleep interview, motor and cognitive tests, and overnight videopolysomnography. PATIENTS: Thirty-six age-, sex-, disease-duration- and disability-matched patients with Gd-PSP (n = 9), progressive supranuclear palsy (a tauopathy, n = 9), Parkinson disease (a synucleinopathy, n = 9) and controls (n = 9). SETTINGS: Tertiary-care academic hospital. RESULTS: REM sleep behavior disorder was found in 78% patients with Gd-PSP (43% of patients reported having this disorder several years before the onset of parkinsonism), 44% of patients with idiopathic Parkinson disease, 33% of patients with progressive supranuclear palsy, and no controls. The percentage of muscle activity during REM sleep was greater in patients with Gd-PSP than in controls (limb muscle activity, 8.3%+/-8.7% vs 0.1%+/- 0.2%; chin muscle activity, 24.3%+/- 23.7% vs 0.7%+/-2.0%) but similar to that of other patient groups. The latency and percentage of REM sleep were similar in patients with Gd-PSP, patients with Parkinson disease, and controls, whereas patients with progressive supranuclear palsy had delayed and shortened REM sleep. CONCLUSION: Although Gd-PSP is a tauopathy, most patients experience REM sleep behavior disorder. This suggests that the location of neuronal loss or dysfunction in the midbrain, rather than the protein comprising the histologic lesions (synuclein versus tau aggregation), is responsible for suppressing muscle atonia during REM sleep. Subjects with idiopathic REM sleep behavior disorder should avoid eating sour sop.     

卒中后抑郁患者的多项睡眠图研究

目的：探讨多项睡眠图（PSG）各项指标对卒中后抑郁（PSD）患者的诊断价值。方法：卒中后抑郁组（PSD组）和卒中后无抑郁组（对照组）以年龄1：1配对,用PSG仪对两组各59例患者进行整夜睡眠描记并对结果进行分析。结果：睡眠进程：PSD组睡眠潜伏期延长,觉醒时间增多,睡眠总时间减少,睡眠效率下降,睡眠维持率下降,两组比较差异有统计学意义;非快速眼动睡眠（NREM）：PSI）组S1增多,S2减少,但S3＋S4两组比较差异无显著意义;快速眼动睡眠（REM）：PSD组REM潜伏期缩短,REM时间减少,REM周期数减少。结论：PSI）患者存在PSG指标变化,PSG对PSD的诊断和鉴别诊断有临床价值。