Daytime Multiple Sleep Latency Test Research Articles

High stability of EEG spectral power across polysomnography and multiple sleep latency tests in good sleepers and chronic insomniacs

To assess the stability of electroencephalographic (EEG) spectral features across overnight polysomnography (PSG) and daytime multiple sleep latency tests (MSLTs) in chronic insomniacs (CIs) and normal controls (NCs). A total of 20 NCs and 22 CIs underwent standard PSG and MSLTs. Spectral analyses were performed on EEG data from PSG and MSLTs and absolute and relative power in central, frontal and occipital channels were obtained for wake (W) and non-rapid eye movement sleep stage 1 and 2 (N1, N2). Intraclass correlation coefficients (ICCs) were used to assess the stability of EEG spectral power across PSG and MSLTs for W, N1 and N2. The absolute power of all frequency bands except delta exhibited high stability across PSG and MSLTs in both NCs and CIs (ICCs ranged from 0.430 to 0.978). Although delta absolute power was stable in NCs during N1 and N2 stages (ICCs ranged from 0.571 to 0.835), it tended to be less stable in CIs during W and sleep stages (ICCs ranged from 0.042 to 0.807). We also observed lower stability of relative power compared to absolute power though the majority of relative power outcomes maintained high stability in both groups (ICCs in relative power ranged from 0.044 to 0.962). Most EEG spectral bandwidths across PSG and MSLT in W, N1 and N2 show high stability in good sleepers and chronic insomniacs. EEG signals from either an overnight PSG or a daytime MSLT may be useful for reliably exploring EEG spectral features during wakefulness or sleep.

Hypersomnia in anti-glutamic acid decarboxylase 65 (GAD65) associated neurological syndromes: A pilot study.

Despite their detrimental impact on the quality of life in autoimmune encephalitis, sleep disorders have not been investigated in anti-glutamic acid decarboxylase (GAD65) associated neurological syndromes. Six consecutive adult patients diagnosed with anti-GAD65-associated neurological syndromes (four with limbic encephalitis and two with stiff-person syndrome) and 12 healthy controls were enrolled. Participants underwent sleep interviews and sleep studies including night-time video-polysomnography, followed by five daytime multiple sleep latency tests (MSLTs, to assess propensity to fall asleep) and an 18 h bed rest polysomnography (to assess excessive sleep need). Patients reported the need for daily naps and that their cognition and quality of life were altered by sleepiness, but they had normal scores on the Epworth sleepiness scale. Compared with controls, sleep latencies during the MSLT were shorter in the patient group (median 5.8 min, interquartile range [IQR] 4.5, 6.0 vs. 17.7 min, IQR 16.3, 19.7, p = 0.001), and the arousal index was reduced (2.5/h, IQR 2.3, 3.0 vs. 22.3/h, IQR 13.8, 30.0, p = 0.002), although total sleep time was similar between groups (621 min, IQR 464, 651 vs. 542.5 min, IQR 499, 582, p = 0.51). Remarkably, all six patients had MSLT latencies ≤8 min, indicating severe sleepiness. No parasomnia or sleep-disordered breathing was detected. Central hypersomnia is a relevant characteristic of anti-GAD65-associated neurological syndromes.

A multicenter, double-blind, placebo-controlled, randomized, Phase 1b crossover trial comparing two doses of ulotaront with placebo in the treatment of narcolepsy-cataplexy

BackgroundUlotaront (SEP-363856) is a novel agonist at trace amine-associated receptor 1 and serotonin 5-HT1A receptors in clinical development for the treatment of schizophrenia. Previous studies demonstrated ulotaront suppresses rapid eye movement (REM) sleep in both rodents and healthy volunteers. We assessed acute and sustained treatments of ulotaront on REM sleep and symptoms of cataplexy and alertness in subjects with narcolepsy-cataplexy. MethodsIn a multicenter, double-blind, placebo-controlled, randomized, 3-way crossover study, ulotaront was evaluated in 16 adults with narcolepsy-cataplexy. Two oral doses of ulotaront (25 mg and 50 mg) were administered daily for 2 weeks and compared with matching placebo (6-treatment sequence, 3-period, 3-treatment). ResultsAcute treatment with both 25 mg and 50 mg of ulotaront reduced minutes spent in nighttime REM compared to placebo. A sustained 2-week administration of both doses of ulotaront reduced the mean number of short-onset REM periods (SOREMPs) during daytime multiple sleep latency test (MSLT) compared to placebo. Although cataplexy events decreased from the overall mean baseline during the 2-week treatment period, neither dose of ulotaront statistically separated from placebo (p = 0.76, 25 mg; p = 0.82, 50 mg), and no significant improvement in patient and clinician measures of sleepiness from baseline to end of the 2-week treatment period occurred in any treatment group. ConclusionsAcute and sustained treatment with ulotaront reduced nighttime REM duration and daytime SOREMPs, respectively. The effect of ulotaront on suppression of REM did not demonstrate a statistical or clinically meaningful effect in narcolepsy-cataplexy. RegistrationClinicalTrials.gov identifier: NCT05015673.

Effect of Objective Daytime Sleepiness on Heart Rate Variability in Patients With Obstructive Sleep Apnea

Excessive daytime sleepiness (EDS) is associated with cardiovascular events in patients with obstructive sleep apnea (OSA). Our study explored the correlation between objective daytime sleepiness assessed with daytime multiple sleep latency tests (MSLT) and heart rate variability (HRV) in OSA patients. The results may provide insight into possible mechanisms underlying increased risk of cardiovascular events in patients with OSA. A retrospective analysis was conducted with the data of 139 patients with OSA and 35 patients with primary snoring. All subjects underwent polysomnography (PSG) and MSLT at West China Hospital between January 2019 and May 2022. We used mean sleep latency (MSL) to measure the severity of EDS and to categorize OSA patients into three groups, severe EDS, light EDS, and non-EDS, with MSL of less than 5 minutes, 5 to 10 minutes, and greater than 10 minutes as the respective defining criteria for classification. A comparison of sleep structure, clinical characteristics, and HRV parameters was performed in order to evaluate the difference between OSA subgroups with varying levels of objective EDS and the primary snoring group. In addition, we also analyzed the correlation between MSL and HRV parameters. Severe EDS patients had higher values of standard deviation of all N-N intervals (SDNN), total spectral power (TOT), and low-frequency power (LF) as compared to non-EDS patients, which was indicative of sympathetic stimulation ( P<0.05). Additionally, high-frequency power (HF) was also higher in severe EDS patients, which indicated decreased parasympathetic drive. A significantly positive correlation was found between MSL and the values of SDNN, TOT, LF, and HF in OSA patients. OSA patients with objective EDS have elevated sympathetic drive and decreased parasympathetic drive. A positive correlation was found between this change in neural activity and the shortening of MSL.

Elevated beta activity in the nighttime sleep and multiple sleep latency electroencephalograms of chronic insomnia patients.

To examine the 24-h hyperarousal hypothesis of insomnia using electroencephalographic (EEG) spectral analysis of overnight polysomnography (PSG) and daytime multiple sleep latency tests (MSLTs). Standard PSG and MSLT were recorded in 31 chronic insomniacs (CIs) (21 females, mean age 36.19) and in 21 normal controls (NCs) (18 females, mean age 34.76). EEG spectral analyses were conducted and relative power was obtained for each sleep stage during PSG and each session during MSLTs. Subsequently, CIs were subdivided based on sleep efficiency (SE < or ≥ 85%) or mean sleep latency (MSL) of MSLT (< or ≥ 15 min), and beta power was compared among NCs and CIs subgroups. General liner regression analyses of beta power and PSG parameters were conducted. CIs had significantly greater beta power in nighttime W, N1, N2, NREM, and in total overnight and in MSLT sessions compared with NCs. CIs with lower PSG-SE or longer MSLT-MSL showed higher beta power at nighttime. Compared with NCs, increased beta power was limited to CIs with lower PSG-SE or longer MSLT-MSL during MSLT sessions. In all subjects, total daytime beta was positively correlated to total overnight beta and MSL, total overnight beta was negatively related to SE. In CIs, total daytime beta and total overnight beta were positively correlated. Our results support the hypothesis of 24-h cortical hyperarousal in insomnia. We conclude that 24-h cortical hyperarousal is clearly present in insomnia and is greater in insomnia with objective findings.

Ambulatory video-EEG-EMG monitoring and analysis during cataplexy in narcolepsy

Objective To comprehensively analyze the clinical and electroneurophysiological characteristics during the process of cataplexy by dynamic video?EEG?EMG monitoring. Methods Six narcolepsy type 1 patients with typical cataplexy were enrolled and 2 of them were diagnosed as status cataplecticus. All patients underwent polysomnography (PSG) and daytime Multiple Sleep Latency Test (MSLT) to clarify the diagnosis. Cataplexy was triggered by emotional stimulus and recorded under dynamic video-EEG-EMG monitoring. EEG characteristics during cataplexy were further compared and analyzed. Objective To comprehensively analyze the clinical and electroneurophysiological characteristics during the process of cataplexy by dynamic video-EEG-EMG monitoring. Methods Six narcolepsy type 1 patients with typical cataplexy were enrolled and 2 of them were diagnosed as status cataplecticus. All patients underwent polysomnography (PSG) and daytime Multiple Sleep Latency Test (MSLT) to clarify the diagnosis. Cataplexy was triggered by emotional stimulus and recorded under dynamic video-EEG-EMG monitoring. EEG characteristics during cataplexy were further compared and analyzed. Results Fourteen cataplectic attacks in 6 patients were recorded. According to the clinical and video- EMG characteristics, cataplectic attack was divided into 4 stages, including triggering phase (CA1), resisting phase (CA2), atonic phase (CA3) and recovering phase (CA4). EEG frequency and amplitude varied from one stage to another and hypersynchronous paroxysmal theta (HSPT) was observed in early resisting phase (CA2), which was supposed to be a distinctive EEG characteristic during the onset of cataplexy. Conclusions Generalized cataplectic ttack contain 4 stages, which indicate a complicated and dynamic process in clinical and electroneurophysiology. Moreover, it's highly possible that HSPT during resisting phase (CA2) is critical in the mechanism of cataplexy. DOI: 10.3969/j.issn.1672-6731.2017.09.006

Sleepiness in Narcolepsy.

Narcolepsy represents the best understood disorder of excessive daytime sleepiness (EDS). EDS presents in 100% of patients with narcolepsy; it is usually the first and the most disabling symptom, which varies in aspects, such as onset age, severity, and clinical characteristics. Early recognition of this symptom leads to early diagnosis and intervention. A diagnosis of narcolepsy is based on clarifying EDS through history, subjective evaluation using questionnaires, and objective measurement, including nocturnal polysomnography followed by a daytime multiple sleep latency test. The therapeutic goal is to optimize control of EDS through wake-promoting medications and nonpharmacologic treatments.

Abnormal daytime sleepiness in dementia with Lewy bodies compared to Alzheimer's disease using the Multiple Sleep Latency Test.

IntroductionExcessive daytime sleepiness is a commonly reported problem in dementia with Lewy bodies (DLB). We examined the relationship between nighttime sleep continuity and the propensity to fall asleep during the day in clinically probable DLB compared to Alzheimer’s disease (AD) dementia.MethodsA full-night polysomnography was carried out in 61 participants with DLB and 26 with AD dementia. Among this group, 32 participants with DLB and 18 with AD dementia underwent a daytime Multiple Sleep Latency Test (MSLT). Neuropathologic examinations of 20 participants with DLB were carried out.ResultsAlthough nighttime sleep efficiency did not differentiate diagnostic groups, the mean MSLT initial sleep latency was significantly shorter in participants with DLB than in those with AD dementia (mean 6.4 ± 5 minutes vs 11 ± 5 minutes, P <0.01). In the DLB group, 81% fell asleep within 10 minutes compared to 39% of the AD dementia group (P <0.01), and 56% in the DLB group fell asleep within 5 minutes compared to 17% in the AD dementia group (P <0.01). Daytime sleepiness in AD dementia was associated with greater dementia severity, but mean MSLT latency in DLB was not related to dementia severity, sleep efficiency the night before, or to visual hallucinations, fluctuations, parkinsonism or rapid eye movement sleep behavior disorder. These data suggest that abnormal daytime sleepiness is a unique feature of DLB that does not depend on nighttime sleep fragmentation or the presence of the four cardinal DLB features. Of the 20 DLB participants who underwent autopsy, those with transitional Lewy body disease (brainstem and limbic) did not differ from those with added cortical pathology (diffuse Lewy body disease) in dementia severity, DLB core features or sleep variables.ConclusionsDaytime sleepiness is more likely to occur in persons with DLB than in those with AD dementia. Daytime sleepiness in DLB may be attributed to disrupted brainstem and limbic sleep–wake physiology, and further work is needed to better understand the underlying mechanisms.

A three-phase epidemiological study of short and long sleepers in a middle-aged Chinese population: prevalence and characteristics

Epidemiological studies of short and long sleepers have not been conducted previously. We collected socioeconomic, psychological, and polysomnographic characteristics of 6501 parents (3252 men and 3249 women) of 4036 primary school children in Guangzhou city. The study data were collected in three phases. The overall prevalence of short (5 h or less) and long (10 h or more) sleep duration was 0.52 and 0.64%, respectively. Long sleepers had higher Eysenck Personality Questionnaire neuroticism scores [odds ratio (OR)=1.224, 95% confidence interval (CI)=1.047-1.409] and lower education levels (OR=0.740, 95%CI=0.631-0.849) than short sleepers. In the polysomnographic assessment, short, long, and normal sleepers (7-8 h) shared similar durations of Stage 3 sleep (short=25.7±10.7, long=20.3±7.9, and normal=28.0±12.8 min, F=1.402, P=0.181). In daytime multiple sleep latency tests, short sleepers (10/19, 52.6%) were more prone to have a short sleep latency (≤8 min) than long sleepers (2/23, 8.7%). In addition to different sleep durations, neuroticism might also contribute to differences between short and long sleepers in social achievements. Stage 3 sleep might be essential for humans. The short sleep latency (≤8 min) of short sleepers in multiple sleep latency tests should be interpreted cautiously, since it was of the same severity as required for a diagnosis of narcolepsy or idiopathic hypersomnia.

Sleep perception and the multiple sleep latency test in patients with primary insomnia

The purpose of this study was to examine the relationship between overnight sleep perception and the daytime multiple sleep latency test (MSLT) among individuals who were primary insomnia patients (PIPs) or good sleeper controls (GSCs). We collected overnight sleep data via polysomnography (PSG), subjective sleep data via a morning questionnaire (self-evaluated) and MSLT data via four 20-min naps over 8 h. Subjects included 122 PIPs and 48 GSCs. Sleep perception was calculated as subjective sleep time/objective sleep time × 100%. PIPs showed a significant difference (P < 0.001) between sleep time, as determined by PSG (387.8 ± 100 min) and self-report (226.3 ± 160 min), but no difference was obtained for GSCs (440.6 ± 53 versus 435.4 ± 65 min). The means for sleep perception were 56.4 ± 38.8% for the PIPs and 99.3 ± 13.6% for the GSCs (P < 0.001). In the PIPs group, weak but statistically significant negative correlations (r: -0.20 to -0.25) were found for MSLT versus sleep perception and versus self- and PSG-evaluated sleep time. Compared to PIPs with low scores on the MSLT, those with high scores had less sleep perception (%), less self- and PSG-evaluated sleep time and greater sleep misperception time. GSCs did not show significant correlations between MSLT and sleep measures or differences in comparisons between individuals with high and low scores on the MSLT. These results add novel data to the literature by suggesting that 24-h hyperarousal potentially plays a key role in the pathophysiological issues of insomnia.

Increasing histamine neurotransmission in Gilles de la Tourette syndrome

Recently, an autosomal-dominant mutation of the gene coding for histidine decarboxylase, the rate-limiting enzyme in histamine synthesis, was demonstrated in a family with eight members suffering from Gilles de la Tourette syndrome (GTS) [1]. Functional analysis suggested that this mutation acts in a dominant-negative manner, thereby diminishing histaminergic neurotransmission. Accordingly, the authors suggested that raising brain histamine levels may decrease tics. We report on a male patient born in 1988 who developed several motor and vocal tics from age 6 years on but was only diagnosed as GTS at the age of 17 years. In rapid succession, several antipsychotics were tried, e.g., pimozide, risperidone and tetrabenazine, which slightly decreased tics but induced fatigue and sedation. More recently (April 2008), aripiprazole (5, then 10 mg/day) was introduced with moderate effect on tics but less sedation and weight gain. Interestingly, this patient also experienced narcolepsy without cataplexy, characterized by excessive daytime sleepiness and dyssomnia. His total sleep time was 363 min with a sleep efficiency of 72%, and no apnea/ hypopnea or leg movements. During daytime multiple sleep latency tests, he fell asleep within a mean of 5.8 min (abnormal is lower than 8 min) sleep onset latency with three sleep onset in REM sleep periods (abnormal is more than 1) [2]. He carried the HLA DBQ1*0602 genotype. The attempts to reduce daytime sleepiness, first with methylphenidate 10 mg/day, then with modafinil 100 mg/ day both resulted in a immediate massive increase in tics as well as behavioral problems (irritability and aggressivity) at the lowest dosage and led to rapid discontinuation of these treatments. Thus, based on the above-mentioned study, we wondered whether treatment by an inverse agonist of the H3 receptor which raises histaminergic neurotransmission might allow to treat his narcolepsy without increasing or even decreasing his tics. This molecule (BF2.649 or tiprolisant or pitolisant, Bioprojet Ltd, France) [3], promotes wakefulness in a recent proof-of-concept trial in narcolepsy [4]. After having obtained the patient’s consent, as well as an individual temporary use authorization from the French drug agency, a baseline evaluation was conducted in May 2010 with two subsequent visits in August and October after slowly increasing the pitolisant doses from 5 to 40 mg/day, as a single morning intake (Table 1). As can be seen, daytime sleepiness decreased dramatically, whereas tic scores remained constant. The benefit was maintained after 9 months of treatment. We conclude A. Hartmann Y. Worbe Departement de Neurologie, Groupe Hospitalier Pitie-Salpetriere, APHP, Paris, France

Chronic Interferon-Alpha Administration Disrupts Sleep Continuity and Depth in Patients with Hepatitis C: Association with Fatigue, Motor Slowing, and Increased Evening Cortisol

Consequences of chronic exposure to cytokines of the innate immune system on sleep in humans and the association of cytokine-induced sleep alterations with behavior, motor performance, and cortisol secretion are unknown. Thirty-one patients with hepatitis C without pre-existing sleep disorders underwent nighttime polysomnography, daytime multiple sleep latency testing, behavioral assessments, neuropsychological testing, and serial blood sampling at baseline and after ∼12 weeks of either treatment with the innate immune cytokine interferon (IFN)-alpha (n = 19) or no treatment (n = 12). Fatigue and sleepiness were assessed using the Multidimensional Fatigue Inventory and Epworth Sleepiness Scale. Interferon-alpha administration led to significant increases in wake after sleep onset and significant decreases in stage 3/4 sleep and sleep efficiency. Rapid eye movement latency and stage 2 sleep were significantly increased during IFN-alpha treatment. Decreases in stage 3/4 sleep and increases in rapid eye movement latency were associated with increases in fatigue, whereas decreases in sleep efficiency were associated with reduced motor speed. Increased wake after sleep onset was associated with increased evening plasma cortisol. Despite IFN-alpha-induced increases in fatigue, daytime sleepiness did not increase. In fact, IFN-alpha-treated patients exhibited decreased propensity to fall asleep during daytime nap opportunities. Chronic exposure to an innate immune cytokine reduced sleep continuity and depth and induced a sleep pattern consistent with insomnia and hyperarousal. These data suggest that innate immune cytokines may provide a mechanistic link between disorders associated with chronic inflammation, including medical and/or psychiatric illnesses and insomnia, which, in turn, is associated with fatigue, motor slowing, and altered cortisol.

Excessive daytime sleepiness in obstructive sleep apnea patients after home CPAP treatment: A long-term outcome study

Previous studies have been inconclusive about the improvement in excessive daytime sleepiness (EDS) after continuous positive airway pressure (CPAP) treatment. One hundred and thirty-one obstructive sleep apnea patients, who were on regular home CPAP treatment, were investigated with an overnight polysomnography and daytime multiple sleep latency test (MSLT). Their Epworth Sleepiness Scale (ESS) scores and mean sleep latencies (MSL) before and after treatment were compared. With a mean duration of CPAP treatment for 3.4 ± 2.4 years, improvement in both ESS (12.8 to 9.95) and MSLT (7.32 to 8.92 min) were found (P < 0.001). Residual EDS was found in 38.5% (20 out of 52) and 66.2% (51 out of 77) of subjects, measured by ESS (≥14) and MSL (≤8 min), respectively. Higher body mass index was found in those subjects with persistently shortened post-CPAP MSL of ≤8 min. Our findings suggested that EDS was a reversible symptom in some but not all OSAS patients. Whilst residual EDS could partly be accounted for by underlying obesity, the persistence of a shortened MSLT and sleep-onset REM period could be the result of underlying genetic factors and/or scarring effect due to hypoxic related neuronal damages.

Narcolepsy in Southern Chinese patients: clinical characteristics, HLA typing and seasonality of birth

Objective:To report clinical characteristics, human leukocyte antigen (HLA) typing and seasonality of birth of a series of 54 Southern Chinese patients suffering from narcolepsy.Methods:All subjects underwent detailed medical and psychiatric...

Rapid Eye Movement Sleep Disturbances in Huntington Disease

Sleep disorders including insomnia, movements during sleep, and daytime sleepiness are common but poorly studied in Huntington disease (HD). To evaluate the HD sleep-wake phenotype (including abnormal motor activity during sleep) in patients with various HD stages and the length of CAG repeats. Because a mild hypocretin deficiency has been found in the brains of some patients with HD (hereinafter referred to as HD patients), we also tested the HD patients for narcolepsy. Twenty-five HD patients (including 2 premanifest carriers) underwent clinical interview, nighttime video and sleep monitoring, and daytime multiple sleep latency tests. Their results were compared with those of patients with narcolepsy and control patients. The HD patients had frequent insomnia, earlier sleep onset, lower sleep efficiency, increased stage 1 sleep, delayed and shortened rapid eye movement (REM) sleep, and increased periodic leg movements. Three HD patients (12%) had REM sleep behavior disorders. No sleep abnormality correlated with CAG repeat length. Reduced REM sleep duration (but not REM sleep behavior disorders) was present in premanifest carriers and patients with very mild HD and worsened with disease severity. In contrast to narcoleptic patients, HD patients had no cataplexy, hypnagogic hallucinations, or sleep paralysis. Four HD patients had abnormally low (< 8 minutes) daytime sleep latencies, but none had multiple sleep-onset REM periods. The sleep phenotype of HD includes insomnia, advanced sleep phase, periodic leg movements, REM sleep behavior disorders, and reduced REM sleep but not narcolepsy. Reduced REM sleep may precede chorea. Mutant huntingtin may exert an effect on REM sleep and motor control during sleep.

Perception versus polysomnographic assessment of sleep in CFS and non-fatigued control subjects: results from a population-based study

BackgroundComplaints of unrefreshing sleep are a prominent component of chronic fatigue syndrome (CFS); yet, polysomnographic studies have not consistently documented sleep abnormalities in CFS patients. We conducted this study to determine whether alterations in objective sleep characteristics are associated with subjective measures of poor sleep quality in persons with CFS.MethodsWe examined the relationship between perceived sleep quality and polysomnographic measures of nighttime and daytime sleep in 35 people with CFS and 40 non-fatigued control subjects, identified from the general population of Wichita, Kansas and defined by empiric criteria. Perceived sleep quality and daytime sleepiness were assessed using clinical sleep questionnaires. Objective sleep characteristics were assessed by nocturnal polysomnography and daytime multiple sleep latency testing.ResultsParticipants with CFS reported unrefreshing sleep and problems sleeping during the preceding month significantly more often than did non-fatigued controls. Participants with CFS also rated their quality of sleep during the overnight sleep study as significantly worse than did control subjects. Control subjects reported significantly longer sleep onset latency than latency to fall asleep as measured by PSG and MSLT. There were no significant differences in sleep pathology or architecture between subjects with CFS and control subjects.ConclusionPeople with CFS reported sleep problems significantly more often than control subjects. Yet, when measured these parameters and sleep architecture did not differ between the two subject groups. A unique finding requiring further study is that control, but not CFS subjects, significantly over reported sleep latency suggesting CFS subjects may have an increased appreciation of sleep behaviour that may contribute to their perception of sleep problems.

The Familial Risk and HLA Susceptibility among Narcolepsy Patients in Hong Kong Chinese

To explore the familial aggregation and HLA susceptibility of narcolepsy in Hong Kong Chinese by objective sleep measurements and HLA typing. Case control design Twelve narcoleptic probands, 34 first-degree relatives, and 30 healthy controls. N/A. Each subject underwent a standardized nocturnal polysomnogram (PSG), followed by a daytime multiple sleep latency test (MSLT). HLA typing was performed for all subjects. One relative (2.9%) was diagnosed as suffering from narcolepsy with cataplexy. Nearly 30% of the relatives fulfilled the criteria of narcolepsy spectrum disorder (shortened mean sleep latency [MSL] and/or the presence of sleep onset REM periods [SOREMPs]). When using the population data for comparison, the relative risk of narcolepsy in first-degree relatives was 85.3. The odds ratio of narcolepsy spectrum disorder in first-degree relatives was 5.8 (95% CI: 1.2 - 29.3) when compared to healthy controls. There existed 6 multiplex families, in which all 10 relatives with narcolepsy spectrum disorders, including all 3 relatives with multiple SOREMPs, were positive for HLA DQB1*0602. Our study demonstrated a definitive familial aggregation of narcolepsy, narcolepsy spectrum disorders, and possibly cataplexy in Hong Kong Chinese. This familial aggregation supported an inherited basis for narcolepsy spectrum. The tight co-segregation of HLA DQB1*0602 and narcolepsy spectrum disorders might suggest that HLA typing, especially DQB1*0602, at least partly confer the familial risk of narcolepsy. In addition, our study suggested that the subjective questionnaire measurements including Ullanlinna Narcolepsy Scale and Epworth Sleepiness Scale were unable to detect the presence of narcolepsy spectrum disorders among the relatives. A stringent objective measurement-based design for family studies is suggested for future study. Further studies are indicated for the determination of the mode and molecular level of narcolepsy transmission.

Sleep characteristics of persons with chronic fatigue syndrome and non-fatigued controls: results from a population-based study

BackgroundThe etiology and pathophysiology of chronic fatigue syndrome (CFS) remain inchoate. Attempts to elucidate the pathophysiology must consider sleep physiology, as unrefreshing sleep is the most commonly reported of the 8 case-defining symptoms of CFS. Although published studies have consistently reported inefficient sleep and documented a variable occurrence of previously undiagnosed primary sleep disorders, they have not identified characteristic disturbances in sleep architecture or a distinctive pattern of polysomnographic abnormalities associated with CFS.MethodsThis study recruited CFS cases and non-fatigued controls from a population based study of CFS in Wichita, Kansas. Participants spent two nights in the research unit of a local hospital and underwent overnight polysomnographic and daytime multiple sleep latency testing in order to characterize sleep architecture.ResultsApproximately 18% of persons with CFS and 7% of asymptomatic controls were diagnosed with severe primary sleep disorders and were excluded from further analysis. These rates were not significantly different. Persons with CFS had a significantly higher mean frequency of obstructive apnea per hour (p = .003); however, the difference was not clinically meaningful. Other characteristics of sleep architecture did not differ between persons with CFS and controls.ConclusionAlthough disordered breathing during sleep may be associated with CFS, this study generally did not provide evidence that altered sleep architecture is a critical factor in CFS. Future studies should further scrutinize the relationship between subjective sleep quality relative to objective polysomnographic measures.

The Prevalence of Multiple Sleep-Onset REM Periods in a Population-Based Sample

The presence of 2 or more sleep-onset rapid eye movement periods (SOREMPs) on a Multiple Sleep Latency Test (MSLT) has been used as 1 of the criteria for the diagnosis of narcolepsy and is thought to be specific to this disorder. However, previous studies have shown the prevalence of SOREMPS in healthy volunteers and apneic patients to be higher than expected. The present study determined the prevalence of 2 or more SOREMPs in a representative sample of the population from southeast Michigan and investigated potential associations with other sleep-related variables. Cross-sectional laboratory-based analysis. Sleep disorders clinic. Population-based sample. N/A. A population-based sample of 333 subjects was assessed by nocturnal polysomnography and daytime MSLT (5 naps), and an additional 206 subjectively sleepy people were also assessed (total = 539). Sample demographics were comparable to the 2000 census. Epworth Sleepiness Scale scores were also determined. Groups were formed based on a median split of each sleep variable (Epworth Sleepiness Scale, MSLT, total sleep time from nocturnal polysomnography) for comparisons of SOREMPs in each group. The prevalence of 2 or more SOREMPs was 3.9%. Only mean sleep latency on the MSLT was a discriminator for the presence of 2 or more SOREMPs (short latency = 6.3%, long latency = 1.9%, p < .05). Among the subjects who had an MSLT of 5 minutes or less (an indicator of a pathologic level of sleepiness), 9.5% had 2 or more SOREMPS. The overall prevalence of 2 or more SOREMPs in our sample is 3.9%. Interestingly, of the variables assessed (MSLT, Epworth Sleepiness Scale, and total sleep time from nocturnal polysomnography), objective sleepiness, as determined by the MSLT, was the only measure significantly associated with 2 or more SOREMPs. Therefore, subpopulations with excessive sleepiness (eg, shift workers, young adults, patients with apnea) are likely to have a greater prevalence of SOREMPs.

Excessive daytime sleepiness in obstructive sleep apnea: prevalence, severity, and predictors

Objectives: To assess prevalence, severity, and predictive factors of excessive daytime sleepiness (EDS) in obstructive sleep apnea (OSA) in an Asian population. Methods: A retrospective, cross-sectional study of data from patients diagnosed with OSA over a period of three years and having had overnight polysomnography (PSG) followed by daytime multiple sleep latency test (MSLT). Respiratory disturbance index (RDI) was used for diagnosis and assessment of severity. OSA was classified as mild (RDI 5–20), moderate (RDI 20–40), and severe (RDI>40). EDS was objectively assessed using MSLT. According to MSLT, patients were categorized into two groups; EDS (mean sleep latency:MSL<10) and no EDS (MSL>10). PSG, MSLT and demographic data were subjected to univariate and multivariate analyses to ascertain predictive factors of EDS. Results: There were 195 patients comprising 89.4% males and 10.6% females. The severity of OSA was mild in 35.9%, moderate in 27.2%, and severe in 36.9%. EDS was demonstrated in 87.2%. Sleep onset REM periods were detected in the MSLT of 28.2% patients. Univariate analysis demonstrated age, RDI, sleep efficiency, total arousals, arousals with apnea, arousal index, number of desaturations, and severity of snoring as significant predictors of EDS. However, stepwise logistic regression analysis identified only sleep efficiency, total arousals, and severity of snoring as significant predictive factors. Conclusions: OSA causes EDS in the majority of patients. Severe snoring, higher sleep efficiency and increased total arousals in polysomnography seem to predict EDS.