Nocturnal Rapid Eye Movement Research Articles

Gulf War veterans exhibit broadband sleep EEG power reductions in regions overlying the frontal lobe

AimsNearly a third of U.S. veterans who deployed in support of the 1990–1991 Persian Gulf War are affected by Gulf War illness (GWI). Here we aimed to characterize whether subjective sleep complaints in GWI veterans are associated with objective sleep EEG disturbances relative to healthy veterans and controls; and whether Gulf War veterans show alterations in neural activity during sleep that differentiate them from healthy subjects. Main methodsWe used high-density EEG (HDEEG) to assess regional patterns of rapid eye movement (REM) sleep and non-REM (NREM) sleep between three groups: Gulf War male veterans with fatigue and GWI, Gulf War male veterans without fatigue or GWI, and control males. The groups were matched relative to age, sex and obstructive sleep apnea. Topographic comparisons of nocturnal NREM and REM sleep were made between groups for all frequency bands. Key findingsTopographic analysis revealed a broadband reduction in EEG power in a circumscribed region overlying the frontal lobe in both groups of Gulf War veterans, regardless of GWI and fatigue. This frontal reduction in neural activity was present, to some extent, across all frequency bands in NREM and REM sleep. SignificanceGiven that our findings were observed in all Gulf War veterans, it appears unlikely that frontal sleep HDEEG power reductions prove wholly responsible for fatigue symptoms. These results provide avenues for research which may someday contribute to improved clinical care of formerly deployed veterans of the Persian Gulf War.

Combining information on nocturnal rapid eye movement sleep latency and atonia to facilitate diagnosis of pediatric narcolepsy type 1.

The diagnosis of narcolepsy type 1 (NT1) at its onset in children and adolescents is often difficult, with substantial diagnostic delay. We aimed to test and validate the effectiveness of rapid eye movement (REM) sleep latency (REML), the REM sleep atonia index (RAI), and their combination for the automatic identification of pediatric patients with NT1 based on the standard scoring of nocturnal polysomnograms. A retrospective cohort of 71 pediatric patients with NT1 and 42 controls was subdivided in test and validation cohorts. A novel index (COM) was developed as a nonlinear function of REML and RAI. The effectiveness of REML, RAI, and COM in identifying patients with NT1 was assessed with receiver operating characteristic (ROC) curves. REML, RAI, and COM significantly identified patients with NT1 both in the test and validation cohorts. Optimal thresholds that maximized identification accuracy were estimated in the test cohort (REML, 49.5 min; RAI, 0.91; COM, 4.57 AU) and validated in the other cohort. COM performed significantly better in identifying patients with NT1 than either REML or RAI, with ROC area under the curve of 94%-100%, sensitivity 85%-96%, and specificity 92%-100%, and with good night-to-night agreement (Cohen's k = 0.69). The analysis of REML, RAI, and particularly their combination in the COM index may help shorten diagnostic delay of NT1 in children and adolescents based on the standard scoring of nocturnal polysomnography.

Sleep–wake stability in narcolepsy patients with normal, low and unmeasurable hypocretin levels

ObjectiveTo compare diurnal and nocturnal electrophysiological data from narcolepsy patients with undetectable (<20 pg/mL), low (20–110 pg/mL) and normal (>110 pg/mL) cerebrospinal fluid (CSF) hypocretin-1 levels. Patients/MethodsA total of 109 narcolepsy patients and 37 controls were studied; all had available CSF hypocretin-1 measurements. The sleep laboratory studies were conducted between 2008 and 2014. The study retrospectively examined measurements of sleep stage transitions in diurnal and nocturnal continuous polysomnography. The percentage distribution of time awake and rapid eye movement (REM) sleep, and the occurrence of sleep onset REM (SOREM) in the nocturnal polysomnography were also measured. ResultsParticipants with undetectable hypocretin-1 levels had significantly higher frequencies of transitions than controls and those with normal hypocretin-1 levels. Participants with low hypocretin-1 levels showed more transitions than controls and, in some cases, also more than those with normal hypocretin-1. Participants with normal hypocretin-1 failed to show any significant difference from the controls, except in the overall diurnal transitions. ConclusionUndetectable hypocretin-1 levels in particular, but also low hypocretin-1 levels, were associated with a less stable phenotype featuring more sleep state transitions and SOREM episodes. In addition, there was a distinction between nocturnal and diurnal REM sleep in hypocretin-deficient participants, expressed as increased diurnal REM sleep, which was not reflected in nocturnal sleep.

Spectral electroencephalography profile of rapid eye movement sleep at sleep onset in narcolepsy type 1.

The sleep-onset rapid eye movement (REM) period (SOREMP), the hallmark of narcolepsy, may be a specific state and not the simple anticipation of REM sleep. We analyzed the electroencephalographic spectral content in untreated patients with narcolepsy type 1 (NT1) during the sleep-onset period (SOP) and during nocturnal REM sleep in two consecutive nocturnal recordings from 31 patients with NT1 (mean age 34 ± 15 years, 18 males) and a single nocturnal recording from 36 controls (mean age 38 ± 13 years, 21 males). The SOP was defined as the first 10 min starting at the beginning of the first epoch of any sleep stage, and further divided into two consecutive 5-min periods (SOP-1 and SOP-2); 1 min of artifact-free quiet wakefulness after lights-off was identified as well as 5 min of REM sleep in the middle of the night and another 5 min during the last REM sleep period. Electroencephalographic spectral analysis was performed using the C3/A2 channel. The SOP-1 and, more strikingly, SOP-2 had significantly less delta and sigma activity in patients with NT1 in the SOREMP condition versus both controls and patients with NT1 without SOREMP. SOP-2 also showed less theta and alpha activity. Conversely, sigma and beta activity were more represented during SOREMP compared with the nocturnal REM period in patients with NT1. The analysis of the SOP supports the concept that SOREMP is a different state compared with both nocturnal REM sleep and non-REM sleep onset.

Sleep characteristics in the quail Coturnix coturnix

As mammals, birds exhibit two sleep phases, slow wave sleep (SWS) and REM (Rapid Eye Movement) sleep characterized by presenting different electrophysiological patterns of brain activity. During SWS a high amplitude slow wave pattern in brain activity is observed. This activity is substituted by a low amplitude fast frequency pattern during REM sleep. Common quail (Coturnix coturnix) is an animal model that has provided information related to different physiological mechanisms present in man. There are reports related to its electrophysiological brain activity, however the sleep characteristics that have been described are not. The objectives of this study is describing the sleep characteristics throughout the nychthemeral cycle of the common quail and consider this bird species as an avian model to analyze the regulatory mechanisms of sleep. Experiments were carried out in implanted exemplars of C. coturnix. Under general anesthesia induced by ether inhalation, stainless steel electrodes were placed to register brain activity from the anterior and posterior areas during 24 continuous hours throughout the sleep–wake cycle. Ocular and motor activities were visually monitored. Quail showed four electrophysiologically and behaviorally different states of vigilance: wakefulness (53.28%), drowsiness (14.27%), slow wave sleep (30.47%) and REM sleep (1.98%). The animals presented 202 REM sleep episodes throughout the nychthemeral cycle. Sleep distribution was polyphasic; however sleep amount was significantly greater during the period corresponding to the night. The number of nocturnal REM sleep episodes was significantly greater than that of diurnal one. ConclusionThe quail C. coturnix shows a polyphasic distribution of sleep; however the amount of this state of vigilance is significantly greater during the nocturnal period.

REM Sleep Phase Preference in the CrepuscularOctodon degusAssessed by Selective REM Sleep Deprivation

To determine rapid eye movement (REM) sleep phase preference in a crepuscular mammal (Octodon degus) by challenging the specific REM sleep homeostatic response during the diurnal and nocturnal anticrepuscular rest phases. We have investigated REM sleep rebound, recovery, and documented REM sleep propensity measures during and after diurnal and nocturnal selective REM sleep deprivations. Nine male wild-captured O. degus prepared for polysomnographic recordings. Animals were recorded during four consecutive baseline and two separate diurnal or nocturnal deprivation days, under a 12:12 light-dark schedule. Three-h selective REM sleep deprivations were performed, starting at midday (zeitgeber time 6) or midnight (zeitgeber time 18). Diurnal and nocturnal REM sleep deprivations provoked equivalent amounts of REM sleep debt, but a consistent REM sleep rebound was found only after nocturnal deprivation. The nocturnal rebound was characterized by a complete recovery of REM sleep associated with an augment in REM/total sleep time ratio and enhancement in REM sleep episode consolidation. Our results support the notion that the circadian system actively promotes REM sleep. We propose that the sleep-wake cycle of O. degus is modulated by a chorus of circadian oscillators with a bimodal crepuscular modulation of arousal and a unimodal promotion of nocturnal REM sleep

Nocturnal Rapid Eye Movement Sleep Latency for Identifying Patients With Narcolepsy/Hypocretin Deficiency

Narcolepsy, a disorder associated with HLA-DQB1*06:02 and caused by hypocretin (orexin) deficiency, is diagnosed using the Multiple Sleep Latency Test (MSLT) following nocturnal polysomnography (NPSG). In many patients, a short rapid eye movement sleep latency (REML) during the NPSG is also observed but not used diagnostically. To determine diagnostic accuracy and clinical utility of nocturnal REML measures in narcolepsy/hypocretin deficiency. Observational study using receiver operating characteristic curves for NPSG REML and MSLT findings (sleep studies performed between May 1976 and September 2011 at university medical centers in the United States, China, Korea, and Europe) to determine optimal diagnostic cutoffs for narcolepsy/hypocretin deficiency compared with different samples: controls, patients with other sleep disorders, patients with other hypersomnias, and patients with narcolepsy with normal hypocretin levels. Increasingly stringent comparisons were made. In a first comparison, 516 age- and sex-matched patients with narcolepsy/hypocretin deficiency were selected from 1749 patients and compared with 516 controls. In a second comparison, 749 successive patients undergoing sleep evaluation for any sleep disorders (low pretest probability for narcolepsy) were compared within groups by final diagnosis of narcolepsy/hypocretin deficiency. In the third comparison, 254 patients with a high pretest probability of having narcolepsy were compared within group by their final diagnosis. Finally, 118 patients with narcolepsy/hypocretin deficiency were compared with 118 age- and sex-matched patients with a diagnosis of narcolepsy but with normal hypocretin levels. Sensitivity and specificity of NPSG REML and MSLT as diagnostic tests for narcolepsy/hypocretin deficiency. This diagnosis was defined as narcolepsy associated with cataplexy plus HLA-DQB1*06:02 positivity (no cerebrospinal fluid hypocretin-1 results available) or narcolepsy with documented low (≤ 110 pg/mL) cerebrospinal fluid hypocretin-1 level. Short REML (≤15 minutes) during NPSG was highly specific (99.2% [95% CI, 98.5%-100.0%] of 516 and 99.6% [95% CI, 99.1%-100.0%] of 735) but not sensitive (50.6% [95% CI, 46.3%-54.9%] of 516 and 35.7% [95% CI, 10.6%-60.8%] of 14) for patients with narcolepsy/hypocretin deficiency vs population-based controls or all patients with sleep disorders undergoing a nocturnal sleep study (area under the curve, 0.799 [95% CI, 0.771-0.826] and 0.704 [95% CI, 0.524-0.907], respectively). In patients with central hypersomnia and thus a high pretest probability for narcolepsy, short REML remained highly specific (95.4% [95% CI, 90.4%-98.3%] of 132) and similarly sensitive (57.4% [95% CI, 48.1%-66.3%] of 122) for narcolepsy/hypocretin deficiency (area under the curve, 0.765 [95% CI, 0.707-0.831]). Positive predictive value in this high pretest probability sample was 92.1% (95% CI, 83.6%-97.0%). Among patients being evaluated for possible narcolepsy, short REML (≤15 minutes) at NPSG had high specificity and positive predictive value and may be considered diagnostic without the use of an MSLT; absence of short REML, however, requires a subsequent MSLT.

Poor sleep quality is associated with late noninvasive ventilation failure in patients with acute hypercapnic respiratory failure*

To determine whether sleep quality helps to predict noninvasive ventilation outcome in patients with acute hypercapnic respiratory failure. Despite an initial clinical improvement, nearly one fourth of patients may fail noninvasive ventilation after several days. Because late intubation is associated with a poor prognosis, it may be useful to identify factors that may predict or explain late noninvasive ventilation failure. We prospectively studied 27 hypercapnic patients in a medical intensive care unit who required noninvasive ventilation for >48 hrs. A 17-hr sleep polysomnography (3 PM-8 AM) was recorded 2 days to 4 days after noninvasive ventilation initiation. Late noninvasive ventilation failure was defined as death, endotracheal intubation, or persistent need for noninvasive ventilation on day 6. An abnormal electroencephalographic pattern that eluded analysis by standard sleep-scoring criteria was noted in seven (50%) of the 14 patients with late noninvasive ventilation failure compared with one (8%) of the 13 patients successfully treated with noninvasive ventilation (p = .03). No clinical or laboratory variables explained the electroencephalographic differences. Patients failing noninvasive ventilation had poorer sleep quality with greater circadian sleep-cycle disruption and less nocturnal rapid eye movement sleep (6 mins [range, 0-12] vs. 26 mins [range, 6-49], p = .03), compared with patients successfully treated with noninvasive ventilation. Noninvasive ventilation failure was associated with delirium during the intensive care unit stay (64% vs. 0%). Late noninvasive ventilation failure in elderly patients with acute hypercapnic respiratory failure was associated with early sleep disturbances including an abnormal electroencephalographic pattern, disruption of the circadian sleep cycle, and decreased rapid eye movement sleep.

Selective enhancement of rapid eye movement sleep by deep brain stimulation of the human pons

Animal studies suggest that rapid eye movement (REM) sleep is governed by the interaction of REM-promoting and REM-inhibiting nuclei in the pontomesencephalic tegmentum. The pedunculopontine nucleus is proposed to be REM promoting. Using polysomnography, we studied sleep in five parkinsonian patients undergoing unilateral pedunculopontine nucleus deep brain stimulation (DBS). We demonstrated a near doubling of nocturnal REM sleep between the DBS "off" and DBS "on" states, without significant changes in other sleep states. This represents the first demonstration that DBS can selectively modulate human sleep, and it supports an important role for the pedunculopontine nucleus region in modulating human REM sleep. Ann Neurol 2009;66:110-114.

Chronic vagus nerve stimulation improves alertness and reduces rapid eye movement sleep in patients affected by refractory epilepsy.

Our study aimed to evaluate the existence and entity of changes in sleep structure following vagus nerve stimulation in patients with refractory epilepsy. A polysomnographic study was performed on the nocturnal sleep of 10 subjects with refractory epilepsy. Subjects were recorded both in baseline conditions and after chronic vagus nerve stimulation. Sleep parameters of the entire night were evaluated. Mean power value of slow-wave activity was computed in the first non-rapid eye movement sleep cycle. A sleep-wake diary evaluated quantity of both nocturnal and daytime sleep, while visual-analog scales assessed quality of sleep and wake. The differences between the 2 conditions underwent parametric and nonparametric statistical evaluation. Vagus nerve stimulation produced a significant reduction in REM sleep (in all subjects with vagus nerve stimulus intensity greater than 1.5 milliampere, but not in the only patient with a stimulus intensity less than 1.5 milliampere), along with an increase in the number of awakenings, percentage of wake after sleep onset, and stage 1 sleep. Data from a sleep-wake questionnaire show a decrease in both nocturnal sleep and daytime naps and an increased daytime alertness, while the quality of wakefulness is globally improved. Spectral analysis shows an enhancement of delta power during non-rapid eye movement sleep. Our data demonstrate major effects of vagus nerve stimulation on both daytime alertness (which is improved) and nocturnal rapid eye movement sleep (which is reduced). These effects could be interpreted as the result of a destabilizing action of vagus nerve stimulation on neural structures regulating sleep-wake and rapid eye movement/non-rapid eye movement sleep cycles. Lower intensity vagus nerve stimulation seems only to improve alertness; higher intensity vagus nerve stimulation seems able to exert an adjunctive rapid eye movement sleep-attenuating effect.

Phasic activities of rapid eye movement sleep in vegetative state patients.

To assess the phasic components of rapid eye movement (REM) sleep in patients in vegetative state and to evaluate the possible relationship of these activities to patient outcome. Sleep disorders unit at a major rehabilitation hospital. Comparative control study. Eleven patients in vegetative state (10 males and 1 female) aged 17-53 years. Continuous 24-hour polysomnographic recording. All the patients had REM sleep periods during the 24-hr recording session. Mean total REM sleep time for the whole session was 66.5 +/- 34.9 min, and for the nocturnal hours only, 37.3 +/- 19.7 min. Comparison with the control group (79.2 +/- 11.5 min) yielded a significant difference only for nocturnal REM sleep time (p<0.0003). The duration of the REM sleep periods was significantly shorter in the patients than the controls for the whole 24-hr session (10.9 +/- 6.0 vs.19.6 +/- 4.9 min, p<0.008), but not for the nocturnal period alone. Compared to controls, the density of rapid eye movements (REMs) (p=0.001), chin twitches (p=0.002), and leg muscle twitches (p=0.023) was significantly lower in the patient group. The density of the sawtooth waves was also lower in the patients, but the difference did not reach significance (p=0.069). Similar results were obtained when the comparison was done only for the nocturnal period. There was no significant difference for any of the REM sleep characteristics or REM sleep phasic activities (24-hr, nocturnal and diurnal periods) between the patients who recovered consciousness and those who did not. The present study shows that patients in vegetative state have a significant reduction in the phasic activities of REM sleep. However, the amount of these activities is unrelated to recovery from the clinical condition. These findings may reflect possible damage to the pedunculopontine tegmentum cholinergic mechanisms in vegetative state.

Sleep onset REM periods during multiple sleep latency tests in patients evaluated for sleep apnea.

Although 2 or more sleep onset rapid eye movement (REM) periods (2omSOREMPs) on a Multiple Sleep Latency Test (MSLT) raise the possibility of narcolepsy, patients with obstructive sleep apnea (OSA) also can have 2omSOREMPs, which may then cause diagnostic uncertainty. To explore what features among OSA patients predict 2omSOREMPs on an MSLT that follows nocturnal polysomnography, we reviewed data from 1,145 consecutively studied patients suspected or confirmed to have OSA rather than narcolepsy. Overall, 4.7% of the subjects had 2omSOREMPs. Variables that were independently predictive of 2omSOREMPs in logistic regression models included male gender (OR = 4.4, 95% CI = 1.9 to 12.7), a 5-min decrease in the MSLT-derived mean sleep latency (OR = 1.9, 95% CI = 1.3 to 2.8), a 90-min decrease in nocturnal latency to REM sleep (OR = 1.6, 95% CI = 1.1 to 2.5), and a 15-unit decrease in minimal recorded oxygen saturation (OR = 1.6, 95% CI = 1.3 to 2.0). We conclude that among patients suspected or confirmed to have OSA, one or more of these four variables-male sex, sleepiness, nocturnal REM sleep latency, and extent of oxygen desaturation-could reflect neurophysiological mechanisms responsible for 2omSOREMPs. Consideration of these variables, and especially gender, may be useful in clinical practice when 2omSOREMPs are found unexpectedly.

Clinical and polysomnographic features in DQB1*0602 positive and negative narcolepsy patients: results from the modafinil clinical trial

Background: Narcolepsy, a neurological disorder characterized by excessive daytime sleepiness and abnormal REM sleep, is known to be tightly associated with the human leukocyte antigen (HLA) DQB1*0602. Methods: In this study, baseline data collected for a large clinical trial involving 504 narcolepsy patients were used to compare clinical and polysomnographic features of narcolepsy patients with and without HLA-DQB1*0602. Comparisons were adjusted for possible confounding factors and linear regression modeling was used to extract the best predictors for DQB1*0602 positivity. Results: As previously reported, cataplexy was the best clinical predictor for DQB1*0602 positivity. At the polysomnographic level, subjects with DQB1*0602 were found to have a significantly more disrupted nocturnal sleep, a much shorter nocturnal rapid eye movement (REM) sleep latency and more multiple sleep latency test abnormalities (increased number of sleep onset REM periods and decreased mean sleep latency). We also found that subjects with DQB1*0602 had a much higher incidence of periodic limb movements during sleep, confirming the notion that this symptom is genuinely associated with the narcolepsy phenotype. Conclusions: These results support the notion that HLA-DQB1*0602-positive narcolepsy patients are more etiologically homogenous than HLA-DQB1*0602-negative narcoleptic patients.

Effects of prolactin on sleep in cyclic rats.

We previously demonstrated that pregnancy-associated sleep enhancement is correlated with the daily surges of prolactin (PRL). However, in spite of a surge of PRL in the proestrous night, a reduction of nocturnal sleep occurs in phase with proestrus. Therefore, to clarify the physiological role of PRL in sleep regulation during the estrous cycle, time-course changes in sleep were analyzed in bromocriptine (CB-154)-treated and/or PRL-supplemented female rats. Sleep patterns characteristic of proestrus-to-estrus were not affected by the CB-154 treatment. In contrast, nocturnal rapid eye movement sleep (REMS) was significantly increased after the PRL supplementation. The CB-154 treatment diminished the REMS-enhancing effect of PRL. Thus, the results suggest that the endogenous PRL is not crucial for the regulation of sleep during the estrous cycle, while exogenous PRL can enhance REMS.

Isolated sleep paralysis elicited by sleep interruption.

We elicited isolated sleep paralysis (ISP) from normal subjects by a nocturnal sleep interruption schedule. On four experimental nights, 16 subjects had their sleep interrupted for 60 minutes by forced awakening at the time when 40 minutes of nonrapid eye movement (NREM) sleep had elapsed from the termination of rapid eye movement (REM) sleep in the first or third sleep cycle. This schedule produced a sleep onset REM period (SOREMP) after the interruption at a high rate of 71.9%. We succeeded in eliciting six episodes of ISP in the sleep interruptions performed (9.4%). All episodes of ISP except one occurred from SOREMP, indicating a close correlation between ISP and SOREMP. We recorded verbal reports about ISP experiences and recorded the polysomnogram (PSG) during ISP. All of the subjects with ISP experienced inability to move and were simultaneously aware of lying in the laboratory. All but one reported auditory/visual hallucinations and unpleasant emotions. PSG recordings during ISP were characterized by a REM/W stage dissociated state, i.e. abundant alpha electroencephalographs and persistence of muscle atonia shown by the tonic electromyogram. Judging from the PSG recordings, ISP differs from other dissociated states such as lucid dreaming, nocturnal panic attacks and REM sleep behavior disorders. We compare some of the sleep variables between ISP and non-ISP nights. We also discuss the similarities and differences between ISP and sleep paralysis in narcolepsy.

Differential effects of scopolamine on nocturnal cortisol secretion, sleep architecture, and REM latency in normal volunteers: Relation to sleep and cortisol abnormalities in depression

Scopolamine (SCOP) (3.0 μ/kg and 6.0 μg/kg) and saline were administered intramuscularly at 11:00 pm to eight normal male volunteers in a randomized design, and the effects on the sleep electroencephalogram (EEG) and nocturnal cortisol secretion (via blood sampling every 15 min) were evaluated. Compared to saline, SCOP produced a significant dose-related delay in rapid eye movement (REM) latency. In contrast, neither dose of SCOP significantly affected nocturnal plasma cortisol concentrations. These results suggest that the central cholinergic system that regulates the onset of REM sleep is more sensitive to dysregulation than the cholinergic system that controls the degree of nocturnal cortisol secretion. If central cholinergic overactivity is responsible for both the REM sleep latency and cortisol abnormalities in depressed patients, then our findings with SCOP might help explain why the incidences of these abnormalities are different.

Modulation of sleep by trimipramine in man

We have studied the acute effect of trimipramine (25, 50 and 75 mg) on nocturnal sleep in 6 young men. Fluoxetine (60 mg) and diazepam (10 mg) were included as controls for the potential changes in sleep measures. Trimipramine reduced awake activity, Stage 1 (drowsy) sleep, and the duration of rapid eye movement (REM) sleep. Non-REM (Stage 2) sleep was increased. Residual effects of trimipramine were present the next morning (9 h after ingestion) with impaired coding ability. The effects of trimipramine on sleep and daytime alertness are consistent with its complex pharmacological profile. Reduced wakefulness and sedation are most likely due to synergism between histamine H1, alpha 1-adrenoceptor, and dopamine receptor antagonism. Anticholinergic activity and possibly blockade of alpha 1-adrenoceptors would disturb the balance of transmitter activities which facilitates the optimal appearance of REM sleep. In this way the effects of trimipramine on nocturnal wakefulness and REM sleep are similar to drugs which inhibit the uptake of noradrenaline.

Sleep in Narcolepsy and Depression Does It All Look Alike?

Depression has been reported to be frequent in narcolepsy and has been considered to be variously a reaction to chronic sleepiness or an endogenous expression of the pathophysiology of narcolepsy. Supporting the latter possibility are reports of similarities between the nocturnal rapid eye movement (REM) sleep of narcoleptics and inpatients with endogenous depression. In a comparison of 25 consecutive narcoleptics and 25 age-matched outpatient primary depressives, significant group differences were found in nocturnal EEG sleep measures of sleep continuity, sleep architecture, and REM sleep. Twenty per cent of the narcoleptic sample met Research Diagnostic Criteria (RDC) for a past history of major or chronic intermittent depression, but 60 per cent did not meet RDC criteria for any present or past psychiatric disorder. These findings mandate a cautious reevaluation of the nature of depressive symptoms in narcolepsy and leave open the question of whether there are common neurobiological control mechanisms in narcolepsy and depression.