[Sleepiness among adolescents: etiology and multiple consequences]. / La somnolence chez les adolescents: étiologie et conséquences multiples.

Over the past century a dramatic decline in sleep duration among adolescents, such as more than one hour of sleep loss per night, has been reported. A debt in sleep duration could lead to sleep deprivation, a major risk factor associated with daytime sleepiness. Sleepiness refers to the inability to maintain an adequate level of alertness during the day which may result in more or less being able to control falling asleep at inappropriate times. This literature review updates on sleepiness regarding its characteristics, etiology and consequences on adolescents. Studies revealed that from 25 % to 78 % of adolescents had reported sleepiness. Its manifestations may include heavy lids, yawns, difficulties to concentrate and emotional irritability. In addition, while it is recommended that adolescents under 18 years-old should sleep from eight to ten hours a night, only 63 % of them actually do so. The etiology of sleep deprivation and sleepiness in this population can be explained by various biological and societal factors. First, the sleep-wake cycle of adolescents shows a biological shift from the beginning of pubertal maturation, described as a perfect storm. It refers to a social jetlag by going to sleep and waking up later and accumulating a sleep debt during weekdays which they try to reimburse during weekends. This phenomenon can be explained by physiological changes such as a slower accumulation of sleep pressure. In addition to this perfect storm, environmental and societal factors contribute to the social jetlag and reduce sleep duration in adolescents. Screen exposure before bedtime can delay sleep and wake onset, which is a risk factor for sleeping debt. Substance use such as caffeine, cigarettes or electronic vaporizer, ADHD or freely available medication, alcohol, cannabis use or drug consumption could further disrupt sleep-wake cycle by stimulating, depressing or otherwise disrupting the central nervous system. Early, before 8:30 am, class start times have been associated with chronic sleep deprivation, higher level of sleepiness and delayed melatonin peak secretion. Adolescents working or doing extracurricular occupations for more than 20hours a week are more at risk for reduced sleep duration and sleepiness. Parental supervision about sleep during the weekdays were associated with more appropriate bedtime. Adolescents from low socio-demographic characteristics and from minority ethnic groups have reported displaying a shorter sleep duration. Finally, sleep disorders of a physiological origin such as narcolepsy, sleep apnea or restless legs syndrome, may explain the sleep deprivation and sleepiness. Sleep deprivation and sleepiness in adolescents have consequences on their health. Cognitive functioning, such as problem solving, attention or memory, as well as school performance, can be compromised by sleep deprivation and sleepiness. At the psychological level, adolescents reporting sleepiness are more prone to display mental health problems: associations were found between sleepiness and subjective perception of depression, anxiety, somatic complaints as well as with antisocial behaviors. Finally, 68 % of 16 year-old adolescents reported they drove a car, and the reported sleepiness could lead to road accidents due to reduced attentional functioning, reaction time and decision-making abilities. In the United-States, from 7 % to 16.5 % of deadly accidents were related to driving while drowsy. Highlighting etiology and problems associated with sleep deprivation and sleepiness in adolescents could guide researchers and clinicians towards the development of possible interventions. Public health measures and knowledge transfer programs regarding modifiable psychosocial and societal factors associated with sleep-wake bioregulation could increase awareness in parents as well as in political and societal decision makers.

Cognitive impairment in obstructive sleep apnea.

Obstructive sleep apnea (OSA) is characterised by repetitive cessation or reduction of airflow due to upper airway obstructions. These respiratory events lead to chronic sleep fragmentation and intermittent hypoxemia. Several studies have shown that OSA is associated with daytime sleepiness and cognitive dysfunctions, characterized by impairments of attention, episodic memory, working memory, and executive functions. This paper reviews the cognitive profile of adults with OSA and discusses the relative role of altered sleep and hypoxemia in the aetiology of these cognitive deficits. Markers of cognitive dysfunctions such as those measured with waking electroencephalography and neuroimaging are also presented. The effects of continuous positive airway pressure (CPAP) on cognitive functioning and the possibility of permanent brain damage associated with OSA are also discussed. Finally, this paper reviews the evidence suggesting that OSA is a risk factor for developing mild cognitive impairment and dementia in the aging population and stresses the importance of its early diagnosis and treatment.

Differential effects of sleep deprivation on sleepwalking: Role of demographic and clinical profiles.

BACKGROUND: Although sleepwalking is one of the most prevalent and potentially injurious of the NREM parasomnias, it is still diagnosed primarily based on the patient's clinical history. Early pilot work suggested that sleep deprivation protocols could help obtain a polysomnographically-based (PSG) diagnosis of sleepwalking, but larger studies remain lacking. METHODS: We compared baseline PSG recordings with those obtained after 25hrs of sleep deprivation in a cohort of 124 consecutively assessed adult sleepwalkers. RESULTS: When compared to baseline recordings, post-sleep deprivation PSG assessments resulted in nearly twice as many somnambulistic episodes being recorded in the laboratory and significantly increased the proportion of patients (from 48 % to 63 %) experiencing at least one lab-based episode. Moreover, while 17 % of patients experienced a sleepwalking event exclusively during recovery sleep, only 2 % of patients did so solely at baseline. Sleep deprivation had similar facilitating effects on patents' somnambulistic events regardless of age of onset and positive versus negative family history for sleepwalking. Younger age and higher home episode frequency both predicted a positive response to sleep deprivation. A separate group of 17 patients with comorbid sleep disorders showed a similar increase in their proportion experiencing at least one episode during recovery sleep. CONCLUSION: The results from this large series of sleepwalkers provide strong support for the use of sleep deprivation in facilitating the occurrence of somnambulistic events in the sleep laboratory.

EEG rhythmic and arrhythmic spectral components and functional connectivity at resting state may predict the development of synucleinopathies in idiopathic REM sleep behavior disorder.

STUDY OBJECTIVES: Idiopathic/isolated REM-sleep behavior disorder (iRBD) often precedes the onset of synucleinopathies. Here, we investigated whether baseline resting-state EEG advanced spectral power and functional connectivity differ between iRBD patients who converted towards a synucleinopathy at follow-up and those who did not. METHODS: Eighty-one participants with iRBD (66.89±6.91 years) underwent a baseline resting-state EEG recording, a neuropsychological assessment and a neurological examination. We estimated EEG power spectral density using standard analyses and derived spectral estimates of rhythmic and arrhythmic components. Global and pairwise EEG functional connectivity analyses were computed using the weighted phase-lag index (wPLI). Pixel-based permutation tests were used to compare groups. RESULTS: After a mean follow-up of 5.01±2.76 years, 34 patients were diagnosed with a synucleinopathy (67.81±7.34 years) and 47 remained disease-free (65.53±7.09 years). Among patients who converted, 22 were diagnosed with Parkinson's disease and 12 with dementia with Lewy bodies. As compared to patients who did not convert, patients who converted exhibited at baseline higher relative theta standard power, steeper slopes of the arrhythmic component and higher theta rhythmic power mostly in occipital regions. Furthermore, patients who converted showed higher beta global wPLI but lower alpha wPLI between left temporal and occipital regions. CONCLUSION: Analyses of resting-state EEG rhythmic and arrhythmic components and functional connectivity suggest an imbalanced excitatory-to-inhibitory activity within large-scale networks, which is associated with later development of a synucleinopathy in iRBD patients.

How does parkinsonism start? Prodromal parkinsonism motor changes in idiopathic REM sleep behaviour disorder.

Parkinsonism, as a gradually progressive disorder, has a prodromal interval during which neurodegeneration has begun but cardinal manifestations have not fully developed. A systematic direct assessment of this interval has never been performed. Since patients with idiopathic REM sleep behaviour disorder are at very high risk of parkinsonism, they provide a unique opportunity to observe directly the development of parkinsonism. Patients with idiopathic REM sleep behaviour disorder in an ongoing cohort study were evaluated annually with several quantitative motor measures, including the Unified Parkinson's Disease Rating Scale, Purdue Pegboard, alternate-tap test and timed up-and-go. Patients who developed parkinsonism were identified from this cohort and matched according to age to normal controls. Their results on motor testing from the preceding years were plotted, and then assessed with regression analysis, to determine when markers first deviated from normal values. Sensitivity and specificity of quantitative motor markers for diagnosing prodromal parkinsonism were assessed. Of 78 patients, 20 developed parkinsonism. On regression analysis, the Unified Parkinson's Disease Rating Scale first intersected normal values at an estimated 4.5 years before diagnosis. Voice and face akinesia intersected earliest (estimated prodromal interval = 9.8 years), followed by rigidity (4.4 years), gait abnormalities (4.4 years) and limb bradykinesia (4.2 years). Quantitative motor tests intersected normal values at longer prodromal intervals than subjective examination (Purdue Pegboard = 8.6 years, alternate-tap = 8.2, timed up-and-go = 6.3). Using Purdue Pegboard and the alternate-tap test, parkinsonism could be detected with 71-82% sensitivity and specificity 3 years before diagnosis, whereas a Unified Parkinson's Disease Rating Scale score >4 identified prodromal parkinsonism with 88% sensitivity and 94% specificity 2 years before diagnosis. Removal of action tremor scores improved sensitivity to 94% and specificity to 97% at 2 years before diagnosis (cut-off >3). Although distinction between conditions was often difficult, prodromal dementia with Lewy bodies appeared to have a slower progression than Parkinson's disease (prodromal interval = 6.0 versus 3.8 years). Using a cut-off of Unified Parkinson's Disease Rating Scale >3 (excluding action tremor), 25% of patients with 'still-idiopathic' REM sleep behaviour disorder demonstrated evidence of possible prodromal parkinsonism. Therefore, using direct assessment of motor examination before parkinsonism in a REM sleep behaviour disorder, we have estimated a prodromal interval of ∼4.5 years on the Unified Parkinson's Disease Rating Scale; other quantitative markers may detect parkinsonism earlier. Simple quantitative motor measures may be capable of reliably detecting parkinsonism, even before a clinical diagnosis can be made by experienced movement disorders neurologists.

Clinical prediction of Parkinson's disease: planning for the age of neuroprotection.

As a chronic progressive disease, Parkinson's disease (PD) has a presymptomatic interval; that is, a period during which the pathological process has begun, but motor signs required for the clinical diagnosis are absent. The ability to identify this preclinical stage may be critical in the development and eventual use of neuroprotective therapy. Recently proposed staging systems of PD have suggested that degeneration may occur initially in areas outside the substantia nigra, suggesting that non-motor manifestations may be markers of presymptomatic PD. Decreased olfaction has recently been demonstrated to predict PD in prospective pathological studies, although the lead time may be relatively short, and the positive predictive value is low. Idiopathic RBD has a very high predictive value, with approximately 50% of affected individuals developing PD or dementia within 10 years. This implies that idiopathic RBD patients are ideal candidates to test potential preclinical markers. However, the specificity of symptom screens for RBD is not established, not all persons with PD develop RBD, and there are only limited ways to predict which RBD patients will develop PD. Other simple screens based upon autonomic symptoms, depression and personality changes, quantitative motor testing and other sleep disorders may also be useful markers, but have not been extensively tested. Other more expensive measures such as detailed autonomic testing, cardiac MIBG-scintigraphy, dopaminergic imaging and transcranial ultrasound may be especially useful in defining disease risk in those identified through primary screening.

Markers of neurodegeneration in idiopathic rapid eye movement sleep behaviour disorder and Parkinson's disease.

Idiopathic rapid eye movement sleep behaviour disorder is an important risk factor in the development of Parkinson's disease. Numerous potential predictive markers of Parkinson's disease may present before motor symptoms emerge, but testing of these markers in rapid eye movement sleep behaviour disorder has been performed only in small studies. There has been no comparison of markers between patients with idiopathic rapid eye movement sleep behaviour disorder and Parkinson's disease, and between men and women. We evaluated an array of potential Parkinson's disease predictive markers in 159 patients; including 68 with idiopathic rapid eye movement sleep behaviour disorder, 36 controls, 34 Parkinson's patients with rapid eye movement sleep behaviour disorder and 21 Parkinson's patients without rapid eye movement sleep behaviour disorder. Compared with controls, patients with idiopathic rapid eye movement sleep behaviour disorder demonstrated substantial olfactory loss (P < 0.001). Olfaction was more impaired in Parkinson's disease than idiopathic rapid eye movement sleep behaviour disorder and did not differ between Parkinson's patients with, or without, rapid eye movement sleep behaviour disorder. Numerous measures of motor function including the Unified Parkinson Disease Rating Scale alternate tap, Purdue Peg Board and Timed 'Up and Go' were impaired in idiopathic rapid eye movement sleep behaviour disorder compared with controls (P < 0.01). All of these motor measures were worse with Parkinson's disease than with idiopathic rapid eye movement sleep behaviour disorder, regardless of rapid eye movement sleep behaviour disorder status. Autonomic symptoms and systolic blood pressure drop were impaired in patients with idiopathic rapid eye movement sleep behaviour disorder compared with controls (P = 0.003). Orthostatic abnormalities in Parkinson's disease were found in the group with rapid eye movement sleep behaviour disorder (P < 0.001). However, Parkinson's patients without rapid eye movement sleep behaviour disorder were not different than controls and had less impairment than those with idiopathic rapid eye movement sleep behaviour disorder (P = 0.004) and Parkinson's patients with rapid eye movement sleep behaviour disorder (P < 0.001). Colour vision was impaired in idiopathic rapid eye movement sleep behaviour disorder compared with controls (P < 0.001). However, only Parkinson's patients with rapid eye movement sleep behaviour disorder had abnormalities significantly different than controls (P < 0.001), and there were significant differences between Parkinson's patients with or without rapid eye movement sleep behaviour disorder (P < 0.04). Idiopathic rapid eye movement sleep behaviour disorder patients had slightly increased harm avoidance scores on personality testing (P = 0.04). Other than slightly better performances among women in the Purdue Peg Board, there was no difference in any measure between men and women, suggesting similar pathogenic processes underlying rapid eye movement sleep behaviour disorder. Patients with idiopathic rapid eye movement sleep behaviour disorder demonstrate abnormalities in numerous potential markers of neurodegenerative disease--these markers are heterogeneous, generally correlate with each other and occur equally in men and women. Although these abnormalities are usually intermediate between control values and Parkinson's patients, autonomic dysfunction and colour vision appear to be more linked to rapid eye movement sleep behaviour disorder status than Parkinson's disease, suggesting a unique pathophysiology of these abnormalities.

REM sleep behaviour disorder in Parkinson's disease is associated with specific motor features.

BACKGROUND: Rapid eye movement (REM) sleep behaviour disorder (RBD) is commonly associated with Parkinson's disease (PD), and recent studies have suggested that RBD in PD is associated with increased cognitive impairment, waking EEG slowing, autonomic impairment and lower quality of life on mental health components. However, it is unclear whether the association of RBD in PD has implications for motor manifestations of the disease. METHODS: The study evaluated 36 patients with PD for the presence of RBD by polysomnography. Patients underwent an extensive evaluation on and off medication by a movement disorders specialist blinded to the polysomnography results. Measures of disease severity, quantitative motor indices, motor subtypes, complications of therapy and response to therapy were assessed and compared using regression analysis that adjusted for disease duration and age. RESULTS: Patients with PD and RBD were less likely to be tremor predominant (14% vs 53%; p<0.02) and had a lower proportion of their Unified Parkinson Disease Rating Scale (UPDRS) score accounted for by tremor (8.2% vs 19.0%; p<0.01). An increased frequency of falls was noted among patients with RBD (38% vs 7%; p = 0.04). Patients with RBD demonstrated a lower amplitude response to their medication (UPDRS improvement 16.2% vs 34.8%; p = 0.049). Markers of overall disease severity, quantitative motor testing and motor complications did not differ between groups. CONCLUSIONS: The presence of altered motor subtypes in PD with RBD suggests that patients with PD and RBD may have a different underlying pattern of neurodegeneration than PD patients without RBD.

Effects of obstructive sleep apnea on cognitive function: a comparison between younger and older OSAS patients.

BACKGROUND AND PURPOSE: Patients with obstructive sleep apnea syndrome (OSAS) present cognitive deficits similar to those observed with aging. The aim of the study was to assess the effects of age on cognitive functions in OSAS patients. It was hypothesized that older OSAS patients will exhibit significant cognitive dysfunction relative to younger OSAS patients and controls. PATIENTS AND METHODS: Younger and older OSAS patients were compared to younger and older control subjects (age cut-off set at 50 yrs). Participants underwent a polysomnographic (PSG) and neuropsychological evaluation. Variables were analyzed by two-way analyses of variance (ANOVAs) with two factors: Group (control and OSAS) and Age (younger and older). Additionally, we evaluated the contribution of attentional deficits to cognitive dysfunction for each subgroup of patients by using Spearman correlation coefficients. RESULTS: No Group-by-Age interaction was found for any neuropsychological variables (p<0.05). However, main Group and Age effects were found. Correlations indicated that attentional deficits contributed importantly to a poorer cognitive performance in younger OSAS patients only (p<0.01). CONCLUSIONS: Our results are in agreement with those of the literature for both OSAS-related and aging-related cognitive deficits but did not demonstrate that age interacts with the effects of the OSAS condition to make those cognitive deficits worse.

Age-at-onset in restless legs syndrome: a clinical and polysomnographic study.

OBJECTIVE: To determine the distribution of age-at-onset in a large cohort of patients with restless legs syndrome (RLS) and to compare clinical and polysomnographic characteristics of patients with early and late age-at-onset of RLS. METHODS: Two hundred and fifty patients with RLS were studied. Information on age-at-onset, etiology, familial history and symptoms severity of RLS was obtained. Age-at-onset density functions were determined from bootstrap methods and kernel density estimators. RESULTS: Age-at-onset showed a significant bimodal distribution with a large peak occurring at 20 years of age and a smaller peak in the mid-40s. Early- and late-onset RLS could be separated with a cut-off at 36 years of age. Distributions of age-at-onset differed as a function of presence/absence of a familial history and etiology of RLS. Age-at-onset clearly differentiated patients with a primary RLS (early onset) from those with secondary RLS. Finally, early-onset RLS was associated with increased RLS severity with higher indices of periodic leg movements in sleep (PLMS) associated with microarousals and periodic leg movements during wakefulness (PLMW). CONCLUSIONS: Early- and late-onset RLS could be distinguished depending on familial history and etiology of RLS. Our data suggest that different pathological processes are involved in these two groups, the early-onset group being highly genetically determined.

The effect of gender on autonomic and respiratory responses during sleep among both young and middle-aged subjects.

BACKGROUND AND OBJECTIVES: Sleep affects the control of circulation and respiratory function. Gender and age are also known to have a profound impact on the neural control of circulation. We investigated whether gender affects sleep-related cardiovascular and respiratory responses and whether these vary according to healthy subjects being young or middle-aged. METHODS: We studied 32 subjects: 8 women and 8 men aged 20-30 years (young), and 8 women and 8 men aged 50-60 years (middle-aged). Young women were under oral contraceptive therapy and middle-aged women were postmenopausal and not receiving hormonal replacement therapy. One-night polysomnography was used to assess RR variability during non-rapid eye movement (NREM) (stage 2) and rapid eye movement (REM) sleep. Low-frequency (LF) and high-frequency (HF) components, in normalized units (LFnu and HFnu) and LF/HF ratio were calculated on five-minute segments selected across the night and averaged for each sleep stage. The respiration frequency in NREM and REM sleep was also measured. Interaction between gender, age and sleep on autonomic and respiration variables was assessed by 2 x 2 x 2 analysis of variance (ANOVA). RESULTS: Compared to men, women had a greater NREM-to-REM increment in LFnu (gender-by-state interaction, p<0.01), a greater decrement in HFnu (interaction, p<0.01) and a greater increment in LF/HF (interaction, p<0.05). Women also showed a more pronounced increase in respiratory frequency during REM sleep compared to men in both groups of age (gender-by-state interaction, F=7.1, p<0.05). No gender-by-age-by-state interaction was observed to affect autonomic and respiration variables. CONCLUSION: NREM-to-REM excitatory cardiac and respiratory responses are more marked among women compared to men, regardless of their hormonal status and whether they are young or middle-aged.

Identification of a sleep bruxism subgroup with a higher risk of pain.

Sleep bruxism research diagnostic criteria (SB-RDC) have been applied since 1996. This study was performed to validate these criteria and to challenge the hypothesis that pain is associated with lower frequencies of orofacial activities. Polygraphic recordings were made of 100 individuals presenting with a clinical diagnosis of sleep bruxism and 43 control individuals. TwoStep Cluster analyses (SPSS) were performed with sleep bruxism variables to reveal groupings among sleep bruxers and control individuals. Participants completed questionnaires during screening, diagnosis, and recording sessions. Cluster analysis identified three subgroups of sleep bruxers. Interestingly, 45 of the 46 sleep bruxers with values below SB-RDC were classified in the low-frequency cluster. These individuals were more likely to complain of pain and fatigue of masticatory muscles than were the higher-frequency sleep bruxers (odds ratios > 3.9, p < 0.01). Sleep bruxers were distributed among three heterogeneous groups. Sleep bruxers with low frequencies of orofacial activities were more at risk of reporting pain.

Long-term treatment with pramipexole in restless legs syndrome.

The aim of the present study was to look at the long-term efficacy and side effects profiles of pramipexole in a large cohort of drug naïve patients with regard to dopaminergic medications. In all, 195 consecutive restless legs syndrome (RLS) patients who were prescribed pramipexole more than 1 year previously, agreed to undergo a telephone interview to assess both the efficacy and side effects of pramipexole. Forty-three patients had discontinued pramipexole: 20 because of side effects, six because of a lack of efficacy, six for both and 11 for other reasons. Patients who continued pramipexole for more than 1 year (n = 152) reported a mean decrease in RLS symptoms severity of 80.9% (SD = 19.6%). At the onset of treatment, the most common side effects were nausea (30%), tiredness (9%), dizziness (8%), headache (4%), insomnia (3%), dry mouth (2%), difficulty to concentrate (1.3%) and sleepiness (0.7%), At 30 months, most patients (n = 124/152; 81.6%) reported an absence of side effects of pramipexole. None of the adverse effects occurred in more than 5% of patients at follow-up. The present study confirms, in a large cohort of unselected patients, that pramipexole is effective and safe in the long-term treatment of RLS.

Parkinson's Disease Genetic Loci in Rapid Eye Movement Sleep Behavior Disorder.

Rapid eye movement (REM) sleep behavior disorder (RBD) is a prodromal condition for Parkinson's disease (PD) and other synucleinopathies, which often occurs many years before the onset of PD. We analyzed 261 RBD patients and 379 controls for nine PD-associated SNPs and examined their effects, first upon on RBD risk and second, on eventual progression to synucleinopathies in a prospective follow-up in a subset of patients. The SCARB2 rs6812193 (OR = 0.67, 95 % CI = 0.51-0.88, p = 0.004) and the MAPT rs12185268 (OR-0.43, 95 % CI-0.26-0.72, p = 0.001) were associated with RBD in different models. Kaplan-Meier survival analysis in a subset of RBD patients (n = 56), demonstrated that homozygous carriers of the USP25 rs2823357 SNP had progressed to synucleinopathies faster than others (log-rank p = 0.003, Breslow p = 0.005, Tarone-Ware p = 0.004). As a proof-of-concept study, these results suggest that RBD may be associated with at least a subset of PD-associated genes, and demonstrate that combining genetic and prodromal clinical data may help identifying individuals that are either more or less susceptible to develop synucleinopathies. More studies are necessary to replicate these results, and identify more genetic factors affecting progression from RBD to synucleinopathies.

Sexual activity and sleep in humans.

Polysomnographic recordings were obtained in 10 subjects (5 men and 5 women) for three conditions: following masturbation with orgasm, following masturbation without orgasm, and after reading neutral material. The analysis of several sleep parameters did not reveal any effect of masturbation on sleep. These results suggest that physiological changes that occur during masturbation, with or without orgasm, have no major effect on sleep organization. Other factors associated with sexual activity and potentially responsible for sleepiness after orgasm are discussed, and further strategies to study the interrelationship of sexual activity and sleep are proposed.

Twenty-four-hour recording in REM-narcoleptics with special reference to nocturnal sleep disruption.

Twenty narcoleptic patients and ten age-matched normals were polygraphically monitored for 58 consecutive hours. All subjects were on regimented sleep (hours between 2230 and 0700). Group A (11 patients and 10 normals) had enforced wakefulness during the day whereas Group B (9 patients) were permitted to sleep (mean = 2 1/2 hr.). On day 2, all subjects were permitted to sleep for 15-min periods every 2 hr. In narcoloptics, sleep recordings demonstrated a reduction of sleep latency, an increase of stage 1, and a decrease in stages 3 and 4 compared to normals, but total REM time and percentage of REM sleep were similar. Groups A and B showed no difference in the incidence of nocturnal awakenings. REM cyclic periodicity was larger in narcoleptics who also demonstrated a REM-sleep fragmentation. This fragmentation became more pronounced as time passed, with several shifts from REM to wakefulness and stage 1. Narcoleptics present REM onset sleep period but also show an inability to remain in REM sleep.

Comparative effects of nefazodone and fluoxetine on sleep in outpatients with major depressive disorder.

BACKGROUND: Sleep disturbances are common in major depressive disorder. In previous open-label trials, nefazodone improved sleep continuity and increased rapid eye movement (REM) sleep, while not affecting stage 3/4 sleep or REM latency: in contrast, fluoxetine suppressed REM sleep. This study compared the objective and subjective effects of nefazodone and fluoxetine on sleep. METHODS: This paper reports combined results of three identical, multisite, randomized, double-blind, 8-week, acute-phase trials comparing nefazodone (n = 64) with fluoxetine (n = 61) in outpatients with nonpsychotic major depressive disorder and insomnia. Sleep electroencephalographic (EEG) recordings were gathered at baseline and weeks 2, 4, and 8. Clinical ratings were obtained at weeks 1-4, 6, and 8. RESULTS: Nefazodone and fluoxetine were equally effective in reducing depressive symptoms; however, nefazodone differentially and progressively increased (while fluoxetine reduced) sleep efficiency and reduced (while fluoxetine increased) the number of awakenings in a linear fashion over the 8-week trial. Fluoxetine, but not nefazodone, prolonged REM latency and suppressed REM sleep. Nefazodone significantly increased total REM sleep time. Clinical evaluations of sleep quality were significantly improved with nefazodone compared with fluoxetine. CONCLUSIONS: Nefazodone and fluoxetine were equally effective antidepressants. Nefazodone was associated with normal objective, and clinician- and patient-rated assessments of sleep when compared with fluoxetine. These differential sleep EEG effects are consistent with the notion that nefazodone and fluoxetine may have somewhat different modes and spectra of action.

Regional spectral analysis of the REM sleep EEG in mild to moderate Alzheimer's disease.

Regional spectral analyses of the EEG during wakefulness and REM sleep was performed in eight patients with mild to moderate Alzheimer's disease and compared to that of healthy age-matched controls. Alzheimer patients presented some EEG slowing in frontal, parieto-occipital and temporal regions in the waking state. However, this EEG slowing was much better revealed in REM sleep, whether expressed by the ratio of slow to fast frequencies or by changes in each of the frequency bands. Moreover, regional differences in EEG slowing, relatively nonexistent in the awake EEG, were a prominent feature of the REM sleep EEG. Importance of cholinergic basal forebrain in the desynchronization of the REM sleep EEG might explain these results because this structure is affected in early Alzheimer's disease.

Dream process in asthmatic subjects with nocturnal attacks.

Polygraphic sleep recordings were made and dream reports collected over 3 consecutive nights for 12 asthmatic subjects with nocturnal attacks and 12 matched normal control subjects. The asthmatic group 1) had more episodes of a vivid impression of dreaming without recollection of dream content ("white dreams") after awakening spontaneously in the morning (nights 1 and 2) and after awakening immediately following REM sleep (night 3), 2) used shorter sentences in dream narrations, and 3) had no dream recall when awakened during nocturnal asthma attacks. The authors suggest that conflictual material emerging during REM or other sleep stages may contribute to the occurrence of nocturnal attacks but is repressed on awakening.

Polysomnographic features of REM sleep behavior disorder: development of a scoring method.

REM sleep behavior disorder (RBD) is characterized by the intermittent absence of REM sleep EMG atonia and the appearance of elaborate motor activity associated with dream mentation. There are no specific diagnostic criteria for RBD based upon polysomnographic findings. We describe a new scoring method and show its sensitivity to treatment with clonazepam. An increased phasic submental EMG density occurs in RBD patients, but REM density is similar to that of controls. Clonazepam selectively decreases REM sleep phasic activity but exerts no effect on REM sleep atonia. Periodic limb movements in sleep (PLMS) occur equally in both REM and NREM sleep in RBD patients, suggesting that normal suppression of PLMS in REM sleep is due to motor inhibition.