The endogenous circadian temperature period length (tau) in delayed sleep phase disorder compared to good sleepers

The currently assumed aetiology for delayed sleep phase disorder (DSPD) is a delay of the circadian system. Clinicians have sought to use bright light therapy, exogenous melatonin or chronotherapy to correct the disorder. However, these treatments have achieved unreliable outcomes for DSPD patients and, as such, one suggestion has been that the disorder may be caused by a longer than normal circadian rhythm period length (i.e. tau). The present study investigated this premise using a 78‐h ultradian, ultra‐short sleep–wake cycle. This constant bedrest routine was used to simulate a series of 1‐h long ‘days’ by alternating 20‐min sleep opportunities and 40 min of enforced wakefulness. Thirteen participants were recruited for the study including, six people diagnosed with DSPD according to the International Classification of Sleep Disorders—2 [mean age = 22.0, standard deviation (SD) = 3.3] and seven good sleepers (mean age = 23.1, SD = 3.9) with normal sleep timing. The DSPD participants' core temperature rhythm tau (mean = 24 h 54 min, SD = 23 min) was significantly longer (t = ?2.33, P = 0.04, Cohen's d = 1.91) than the good sleepers' (mean 24 h 29 min, SD = 16 min). The temperature rhythm of the DSPD participants delayed more rapidly (i.e. >25 min day^?1) than the good sleepers'. These findings provide an explanation for the difficulty that DSPD patients have in phase advancing to a more conventional sleep time and their frequent relapse following treatment. The outcomes of this study support a vigorous and continued application of chronobiological and behavioural therapies to entrain DSPD patients to their desired earlier sleep times.     

Objective measures of sleep and dim light melatonin onset in adolescents and young adults with delayed sleep phase disorder compared to healthy controls

Delayed sleep phase disorder is characterized by a delay in the timing of the major sleep period relative to conventional norms. The sleep period itself has traditionally been described as normal. Nevertheless, it is possible that sleep regulatory mechanism disturbances associated with the disorder may affect sleep duration and/or architecture. Polysomnographic data that may shed light on the issue are scarce. Hence, the aim of this study was to examine polysomnographic measures of sleep in adolescents and young adults with delayed sleep phase disorder, and to compare findings to that of healthy controls. A second aim was to estimate dim light melatonin onset as a marker of circadian rhythm and to investigate the phase angle relationship (time interval) between dim light melatonin onset and the sleep period. Data from 54 adolescents and young adults were analysed, 35 diagnosed with delayed sleep phase disorder and 19 healthy controls. Results show delayed timing of sleep in participants with delayed sleep phase disorder, but once sleep was initiated no group differences in sleep parameters were observed. Dim light melatonin onset was delayed in participants with delayed sleep phase disorder, but no difference in phase angle was observed between the groups. In conclusion, both sleep and dim light melatonin onset were delayed in participants with delayed sleep phase disorder. The sleep period appeared to occur at the same circadian phase in both groups, and once sleep was initiated no differences in sleep parameters were observed.     

The use of exogenous melatonin in delayed sleep phase disorder: a meta-analysis

Study Objectives:

To perform a meta-analysis of the efficacy and safety of exogenous melatonin in advancing sleep-wake rhythm in patients with delayed sleep phase disorder.

Design:

Meta analysis of papers indexed for PubMed, Embase, and the abstracts of sleep and chronobiologic societies (1990–2009).

Patients:

Individuals with delayed sleep phase disorder.

Interventions:

Administration of melatonin.

Measurements and Results:

A meta-analysis of data of randomized controlled trials involving individuals with delayed sleep phase disorder that were published in English, compared melatonin with placebo, and reported 1 or more of the following: endogenous melatonin onset, clock hour of sleep onset, wake-up time, sleep-onset latency, and total sleep time. The 5 trials including 91 adults and 4 trials including 226 children showed that melatonin treatment advanced mean endogenous melatonin onset by 1.18 hours (95% confidence interval [CI]: 0.89–1.48 h) and clock hour of sleep onset by 0.67 hours (95% CI: 0.45–0.89 h). Melatonin decreased sleep-onset latency by 23.27 minutes (95% CI: 4.83 –41.72 min). The wake-up time and total sleep time did not change significantly.

Conclusions:

Melatonin is effective in advancing sleep-wake rhythm and endogenous melatonin rhythm in delayed sleep phase disorder.

Citation:

van Geijlswijk IM; Korzilius HPLM; Smits MG. The use of exogenous melatonin in delayed sleep phase disorder: a meta-analysis. SLEEP 2010;33(12):1605-1614.     

The alteration of human sleep and circadian rhythms during spaceflight

Numerous anecdotes in the past suggest the concept that sleep disturbances in astronauts occur more frequently during spaceflight than on ground. Such disturbances may be caused in part by exogenous factors, but also an altered physiological state under microgravity may add to reducing sleep quality in a spacecraft. The present investigation aims at a better understanding of possible sleep disturbances under microgravity. For the first time, experiments were conducted in which sleep and circadian regulation could be simultaneously assessed in space. Four astronauts took part in this study aboard the Russian MIR station. Sleep was recorded polygraphically on tape together with body temperature. For a comparison, the same parameters were measured during baseline periods preceding the flights. The circadian phase of body temperature was found to be delayed by about 2 h in space compared with baseline data. A free-run was not observed during the first 30 d in space. Sleep was shorter and more disturbed than on earth. In addition, the structure of sleep was significantly altered. In space, the latency to the first REM episode was shorter, and slow-wave sleep was redistributed from the first to the second sleep cycle. Several mechanisms may be responsible for these alterations in sleep regulation and circadian phase. Most likely, altered circadian zeitgebers on MIR and a deficiency in the process S of Borbély's sleep model cause the observed findings. The change in process S may be related to changes in physical activity as a result of weightlessness.     

Aging young sleep: a test of the phase advance hypothesis of sleep disturbance in the elderly

SUMMARY  With aging, the phase relationship between sleep and body core temperature is altered such that the temperature minimum occurs substantially earlier in the major nocturnal sleep period. The sleep maintenance difficulties that often accompany normal aging are generally assumed to be associated with this age-related change in the phase angle between sleep and temperature. To test this notion, we used timed exposure to bright light to reproduce in healthy young adults a similar phase relationship between temperature and sleep, to determine if such a manipulation would induce the same fragmented nocturnal sleep commonly observed in individuals over 65 years of age. Seven young adults were exposed to morning bright light for 3 consecutive days following a baseline night. Bright light exposure caused a 97 min phase advance of the fitted temperature minimum when compared with baseline. Significant declines in several measures of sleep quality were associated with the phase advance, including wakefulness after initial sleep onset (WASO), sleep efficiency and number of stage changes. Yet, the severity of sleep disturbance exhibited by these subjects did not approach that exhibited by most elderly subjects. The findings suggest that while chronophysiological changes appear to be strongly associated with the tendency to awaken in the early morning, they cannot account entirely for the severity of sleep disturbance frequently observed in older subjects.     

Mental health problems in adolescents with delayed sleep phase: results from a large population‐based study in Norway

The aim of the current study was to compare mental health problems, resilience and family characteristics in adolescents with and without delayed sleep phase (DSP) in a population‐based sample. Data were taken from the youth@hordaland‐survey, a large population‐based study in Hordaland County in Norway conducted in 2012. In all, 9338 adolescents aged 16–19 years (53.5% girls) provided self‐reported data on a wide range of instruments assessing mental health symptoms, including depression, anxiety, obsessive–compulsive behaviours, attention deficit hyperactive disorder (ADHD) symptoms, perfectionism, resilience and sleep. Measures of socioeconomic status were also included. Three hundred and six adolescents (prevalence 3.3%) were classified as having DSP [according to the International Classification of Sleep Disorders‐2 (ICSD‐2)] criteria. Adolescents with DSP reported higher levels of depression, anxiety and ADHD symptoms. Adolescents with DSP also exhibited significantly lower levels of resilience. The Cohen's d effect sizes ranged from small [obsessive–compulsive disorder (OCD): d = 0.15] to moderate (inattention: d = 0.71). In the fully adjusted model, the significant predictors of DSP included inattention [odds ratio (OR): 2.11], lack of personal structure (OR: 2.07), low (OR: 1.85) and high (OR: 1.91) paternal education, parents not living together (OR: 1.81), hyperactivity/inattention (OR: 1.71) and poorer family economy (OR: 1.59). In conclusion, the high symptom load across a range of mental health measures suggests that a broad and thorough clinical approach is warranted when adolescents present with DSP.     

Body temperature,activity and melatonin profiles in adults with attention‐deficit/hyperactivity disorder and delayed sleep: a case–control study

Irregular sleep–wake patterns and delayed sleep times are common in adults with attention‐deficit/hyperactivity disorder, but mechanisms underlying these problems are unknown. The present case–control study examined whether circadian abnormalities underlie these sleep problems in a naturalistic home setting. We included 12 medication‐naïve patients with attention‐deficit/hyperactivity disorder and delayed sleep phase syndrome, and 12 matched healthy controls. We examined associations between sleep/wake rhythm in attention‐deficit/hyperactivity disorder and circadian parameters (i.e. salivary melatonin concentrations, core and skin temperatures, and activity patterns) of the patients and controls during five consecutive days and nights. Daily bedtimes were more variable within patients compared with controls (F = 8.19, P < 0.001), but melatonin profiles were equally stable within individuals. Dim‐light melatonin onset was about 1.5 h later in the patient group (U = 771, Z = ?4.63, P < 0.001). Patients slept about 1 h less on nights before work days compared with controls (F = 11.21, P = 0.002). The interval between dim‐light melatonin onset and sleep onset was on average 1 h longer in patients compared with controls (U = 1117, Z = ?2.62, P = 0.009). This interval was even longer in patients with extremely late chronotype. Melatonin, activity and body temperatures were delayed to comparable degrees in patients. Overall temperatures were lower in patients than controls. Sleep‐onset difficulties correlated with greater distal–proximal temperature gradient (DPG; i.e. colder hands, r² = ?0.32, P = 0.028) in patients. Observed day‐to‐day bedtime variability of individuals with attention‐deficit/hyperactivity disorder and delayed sleep phase syndrome were not reflected in their melatonin profiles. Irregular sleep–wake patterns and delayed sleep in individuals with attention‐deficit/hyperactivity disorder and delayed sleep phase syndrome are associated with delays and dysregulations of the core and skin temperatures.     

Sleep tendency during extended wakefulness: insights into adolescent sleep regulation and behavior

Sleep tendency (latency to sleep onset) was examined during extended waking in prepubertal and mature adolescents to determine whether sleep pressure is lower near bedtime in the latter group. Participants were nine prepubertal (pubertal stage Tanner 1, mean age 11.1 years, SD+/-1.3 years, five males) and 11 pubertally mature adolescents (Tanner 5, 13.9+/-1.2 years, three males). They spent 10 nights at home on an identical fixed 10-h sleep schedule followed by a 36-h constant routine with sleep latency tests at 2-h intervals using standard polysomnography. Saliva was collected to assess dim-light melatonin onset (DLMO) phase. DLMO was earlier in the Tanner 1 (mean clock time=20:33 hours, SD=49 min) than Tanner 5 group (21:29 hours+/-42 min). Sleep latency compared at a 'critical period' spanning 12.5 (20:30 hours clock time) to 18.5 h (02:30 hours) after waking did not differ at 20:30 hours, but was shorter for the Tanner 1 group at 22:30 hours (Tanner 1=9.2+/-6.3 min; Tanner 5=15.7+/-5.8 min), 00:30 hours (Tanner 1=3.6+/-1.7 min; Tanner 5=9.0+/-6.4 min), and 02:30 hours (Tanner 1=2.0+/-1.7 min; Tanner 5=4.3+/-3.2 min; trend). These differences were apparent controlling for circadian phase by partial correlation. Sleep tendency after 14.5, 16.5, and 18.5 h awake was lower in mature versus prepubertal adolescents, supporting our hypothesis that a developmental change of intrinsic sleep-wake regulation may provide physiologically mediated 'permission' for later bedtimes in older adolescents.     

Implementation of napping In industry and the problem of sleep inertia

SUMMARY  It seems reasonable to believe that in specific situations napping at the work place would be possible and used if authorized and encouraged. Very short naps could have very positive long-term effects on biological functions. Training someone to sleep for short periods appears feasible if there is a high motivation to do so. Sleep inertia can be considered as one of the main limiting factors in napping strategy. Sleep inertia depends on different factors such as sleep stage preceding the awakening, temporal placement of the nap, duration of nap and wakefulness preceding it, etc. The effects of sleep inertia might be different depending on the type of task, and a reactivation technique applied immediately after awakening may remove it. Despite the fact that its implementation in industry raises some practical issues, napping can be considered as a possible strategy to increase the vigilance level of night workers.     

Delayed sleep phase syndrome is related to seasonal affective disorder

Background

Both delayed sleep phase syndrome (DSPS) and seasonal affective disorder (SAD) may manifest similar delayed circadian phase problems. However, the relationships and co-morbidity between the two conditions have not been fully studied. The authors examined the comorbidity between DSPS and SAD.

Methods

We recruited a case series of 327 DSPS and 331 controls with normal sleep, roughly matched for age, gender, and ancestry. Both DSPS and controls completed extensive questionnaires about sleep, the morningness-eveningness trait, depression, mania, seasonality of symptoms, etc.

Results

The prevalences of SAD and subsyndromal SAD (S-SAD) were higher in DSPS compared to controls (χ² = 12.65, p = 0.002). DSPS were 3.3 times more likely to report SAD (odds ratio, 3.34; 95% CI, 1.41-7.93) compared to controls as defined by the Seasonal Pattern Assessment Questionnaire (SPAQ). Correspondingly, DSPS showed significantly higher seasonality scores compared to controls in mood, appetite, and energy level subscores and the global seasonality score (t = 3.12, t = 0.002; t = 2.04, p = 0.041; t = 2.64, p = 0.008; and t = 2.15, p = 0.032, respectively). Weight fluctuation during seasons and winter-summer sleep length differences were also significantly higher in DSPS than controls (t = 5.16, p < 0.001 and t = 2.64, p = 0.009, respectively). SAD and S-SAD reported significantly higher eveningness, higher depression self-ratings, and more previous mania symptoms compared to non-seasonal subjects regardless of whether they were DSPS or controls.

Conclusions

These cases suggested that DSPS is partially comorbid with SAD. These data support the hypothesis that DSPS and SAD may share a pathophysiological mechanism causing delayed circadian phase.     

The evening light environment in hospitals can be designed to produce less disruptive effects on the circadian system and improve sleep

Study ObjectivesBlue-depleted lighting reduces the disruptive effects of evening artificial light on the circadian system in laboratory experiments, but this has not yet been shown in naturalistic settings. The aim of the current study was to test the effects of residing in an evening blue-depleted light environment on melatonin levels, sleep, neurocognitive arousal, sleepiness, and potential side effects.MethodsThe study was undertaken in a new psychiatric hospital unit where dynamic light sources were installed. All light sources in all rooms were blue-depleted in one half of the unit between 06:30 pm and 07:00 am (melanopic lux range: 7–21, melanopic equivalent daylight illuminance [M-EDI] range: 6–19, photopic lux range: 55–124), whereas the other had standard lighting (melanopic lux range: 30–70, M-EDI range: 27–63, photopic lux range: 64–136), but was otherwise identical. A total of 12 healthy adults resided for 5 days in each light environment (LE) in a randomized cross-over trial.ResultsMelatonin levels were less suppressed in the blue-depleted LE (15%) compared with the normal LE (45%; p = 0.011). Dim light melatonin onset was phase-advanced more (1:20 h) after residing in the blue-depleted LE than after the normal LE (0:46 h; p = 0.008). Total sleep time was 8.1 min longer (p = 0.032), rapid eye movement sleep 13.9 min longer (p < 0.001), and neurocognitive arousal was lower (p = 0.042) in the blue-depleted LE. There were no significant differences in subjective sleepiness (p = 0.16) or side effects (p = 0.09).ConclusionsIt is possible to create an evening LE that has an impact on the circadian system and sleep without serious side effects. This demonstrates the feasibility and potential benefits of designing buildings or hospital units according to chronobiological principles and provide a basis for studies in both nonclinical and clinical populations.     

Evening administration of melatonin and bright light: Interactions on the EEG during sleep and wakefulness

Both the pineal hormone melatonin and light exposure are considered to play a major role in the circadian regulation of sleep. In a placebo- controlled balanced cross-over design, we investigated the acute effects of exogenous melatonin (5 mg p.o. at 20.40 hours) with or without a 3-h bright light exposure (5000 lux from 21.00 hours–24.00 hours) on subjective sleepiness, internal sleep structure and EEG power density during sleep and wakefulness in healthy young men. The acute effects of melatonin, bright light and their interaction were measured on the first day (treatment day), possible circadian phase shifts were assessed on the post-treatment day. On the treatment day, the evening rise in subjective sleepiness was accelerated after melatonin and protracted during bright light exposure. These effects were also reflected in specific changes of EEG power density in the theta/alpha range during wakefulness. Melatonin shortened and bright light increased sleep latency. REMS latency was reduced after melatonin administration but bright light had no effect. Slow-wave sleep and slow-wave activity during the first non-rapid eye movement (NREMS) episode were suppressed after melatonin administration and rebounded in the second NREMS episode, independent of whether light was co-administered or not. Self rated sleep quality was better after melatonin administration whereas the awakening process was rated as more difficult after bright light. On the post-treatment day after evening bright light, the rise in sleepiness and the onset of sleep were delayed, independent of whether melatonin was co-administered or not. Thus, although acute bright light and melatonin administration affected subjective sleepiness, internal sleep structure and EEG power density during sleep and wakefulness in a additive manner, the phase shifting effect of a single evening bright light exposure could not be blocked by exogenous melatonin     

Sleep propensity and sleep architecture after bright light exposure at three different times of day

SUMMARY  The aim of this work was to study the effects of bright light-induced circadian phase shifts on sleep propensity and sleep architecture while the timing of the sleep/wake cycle is kept constant. Twenty-three normal subjects underwent an 11-day study including: (i) baseline sleep and vigilance evaluation; (ii) baseline evaluation of the circadian temperature rhythm with a 40-h constant routine; (iii) five hours of bright light exposure on each of three days; (iv) post-treatment sleep and vigilance evaluation; (v) post-treatment circadian rhythm evaluation with a second 40-h constant routine. Subjects were divided into three groups: eight subjects were exposed to bright light in the morning ('Morning group'), eight subjects were exposed in the evening ('Evening group'), and seven subjects were exposed in the afternoon ('Afternoon group'). After light exposure, the Morning group showed an advance of 1.23 h in the phase of the temperature rhythm, the Evening group showed a delay of 1.62 h, and the Afternoon group showed a non-significant advance of 0.5 h. In support of expectations, early-night sleep propensity was decreased by evening bright light, was increased in almost all subjects exposed to morning bright light, and was not changed by afternoon bright light exposure. The phase shift created by bright light exposure did not seem to be large enough to have a systematic effect on sleep consolidation or on REM sleep parameters in any of the three groups, suggesting that these variables are less sensitive to alterations in phase of the circadian oscillator than early-night sleep propensity.     

beta(1)-adrenergic antagonists improve sleep and behavioural disturbances in a circadian disorder, Smith-Magenis syndrome

Smith-Magenis syndrome (SMS) is a clinically recognisable contiguous gene syndrome ascribed to interstitial deletions of chromosome 17p11.2. Patients have a phase shift of their circadian rhythm of melatonin with a paradoxical diurnal secretion of the hormone. Serum melatonin levels and day-night behaviour were studied in nine SMS children (aged 4 to 17 years) given acebutolol, a selective β₁-adrenergic antagonist (10 mg/kg early in the morning). Cardiac examination, serum melatonin, motor activity recordings, and sleep diaries were monitored before and after drug administration. The present study shows that a single morning dose of acebutolol suppressed the inappropriate secretion of melatonin in SMS. A significant improvement of inappropriate behaviour with increased concentration, delayed sleep onset, increased hours of sleep, and delayed waking were also noted. These results suggest that β₁-adrenergic antagonists help to manage hyperactivity, enhance cognitive performance, and reduce sleep disorders in SMS.


Keywords: Smith-Magenis syndrome; circadian rhythms; melatonin     

The dim light melatonin onset following fixed and free sleep schedules

The time at which the dim light melatonin onset (DLMO) occurs can be used to ensure the correct timing of light and/or melatonin administration in order to produce desired circadian phase shifts. Sometimes however, measuring the DLMO is not feasible. Here we determined if the DLMO was best estimated from fixed sleep times (based on habitual sleep times) or free (ad libitum) sleep times. Young healthy sleepers on fixed (n=60) or free (n=60) sleep schedules slept at home for 6 days. Sleep times were recorded with sleep logs verified with wrist actigraphy. Half-hourly saliva samples were then collected during a dim light phase assessment and were later assayed to determine the DLMO. We found that the DLMO was more highly correlated with sleep times in the free sleepers than in the fixed sleepers (DLMO versus wake time, r=0.70 and r=0.44, both P<0.05). The regression equation between wake time and the DLMO in the free sleepers predicted the DLMO in an independent sample of free sleepers (n=23) to within 1.5 h of the actual DLMO in 96% of cases. These results indicate that the DLMO can be readily estimated in people whose sleep times are minimally affected by work, class and family commitments. Further work is necessary to determine if the DLMO can be accurately estimated in people with greater work and family responsibilities that affect their sleep times, perhaps by using weekend wake times, and if this method will apply to the elderly and patients with circadian rhythm disorders.     

Sleep in healthy seniors: a diary study of the relation between bedtime and the amount of sleep obtained

The aim of this study was to determine whether naturally occurring inter-individual and intra-individual differences in bedtime selection in the elderly might be lawfully related to the amount of sleep that is obtained. A total of 128 seniors (63f, 65m) aged 70-92 years each provided a week of sleep diary data yielding a total of 896 subject-nights for analysis. From each subject-night the diary was used to derive measures of time in bed (TIB) and total sleep time (TST). These measures were used as dependent variables in mixed-effect linear models (nights nested within subjects) with the independent variable being bedtime for that subject-night, arbitrarily expressed as minutes since 19:00 hours. Although there were strong inter-individual and intra-individual differences, for both genders, bedtime had a statistically significant effect (P < 0.001) on both TIB and TST. We observed that later bedtimes were associated with less time in bed and less time asleep. On average between 7 and 8 min of less TIB and TST were associated with each 10-min delay in bedtime from 19:00 hours. These results are interpreted in terms of increases in sleep being derived from living in a better harmony with an earlier peaking circadian pacemaker characteristic of older age, although other possible mechanisms are also considered (e.g. age-dependent alterations in phase angle and homeostatic sleep need).     

Circadian and sleep/wake dependent aspects of subjective alertness and cognitive performance

Circadian and sleep/wake dependent processes underlying variations in subjective alertness and cognitive performance were assessed in a constant routine protocol and in a protocol in which the sleep/wake cycle was uncoupled from the output of the endogenous circadian pacemaker. In the latter protocol, the contribution of a sleep/wake dependent process and a circadian process to alertness and performance were separated by folding the data at either the period of the sleep/wake cycle or at the period of the endogenous circadian body temperature rhythm. This analysis revealed that prior wakefulness within a range of 0-18 h significantly reduced alertness and performance and that the circadian rhythm of core body temperature paralleled the circadian rhythm of alertness and performance. During the first 16 h of the constant routine protocol, which coincided with the subjects' habitual period of wakefulness, alertness and performance remained at a stable level. The latter finding was explained by assuming that during our usual waking day the circadian system counteracts the detrimental effects of increasing duration of prior wakefulness.     

Interaction of chronic sleep restriction and circadian system in humans

Nocturnal sleep restriction and compensation with daytime naps is common in today’s society. In a between‐participants design, we examined the effects of chronic (10 nights) sleep restriction on 24 h plasma melatonin profiles in humans. Following a baseline period with 8.2 h time in bed (TIB) for sleep, participants were randomized to a control (8.2 h TIB) or sleep‐restriction condition (4.2 h TIB), with and without diurnal naps. Sleep restriction was achieved via delaying bedtime and advancing wake time by 2 h each relative to the baseline sleep period. Participants were maintained in a controlled, time isolated laboratory environment throughout the protocol, with light levels below 40 lx at all times. Twenty‐four hour plasma melatonin profiles were assessed at baseline and at the end of the sleep‐restriction period, with subjects maintained in a constant posture protocol. Compared with the baseline assessment and the 8.2 h TIB control group, a significant phase delay in melatonin onset (1.2 ± 0.9 h) occurred in all sleep‐restriction (4.2 h TIB) groups (P < 0.05). There was no evidence of a phase advance or shortening of the period of melatonin secretion associated with the advanced waking time. These results suggest that nocturnal light and dark exposure may be more potent in effecting circadian phase shifts than exposure to morning light, at least in conditions of controlled, dim lighting in the laboratory.     

Reversal of the sleep/wake cycle disorder of sleeping sickness after trypanosomicide treatment

To determine whether the circadian disruption of the sleep/wake cycle observed in sleeping sickness, human African trypanosomiasis (HAT), can be reversed after trypanosomicide treatment, 10 Congolese patients infected by Trypanosoma brucei gambiense underwent 24-h polysomnographic recordings before treatment with melarsoprol and after each of three weekly treatment sessions. Polysomnography consisted of a continuous recording of the electroencephalogram, electromyogram and electro-oculogram on a Minidix Alvar polygraph. Sleep traces were analysed in 20-sec epochs for wakefulness, REM sleep, and NREM sleep [stages 1, 2, 3, 4; stages 3 and 4 representing slow-wave sleep (SWS)]. As previously described (Buguet et al. 1993), the 24-h distribution of the sleep/wake cycle was disturbed proportionally to the severity of the illness. The overall amounts of each sleep/wake stage did not change after treatment. However, the patterns of occurrence of sleep episodes, REM sleep and SWS phases were determinant in the evaluation of treatment efficacy. The trypanosomicide action of melarsoprol led to a reduction in the number of sleep episodes, except in one patient whose health condition worsened during the third treatment session: sleep onset REM sleep phases (SOREMPs) decreased and the number of SWS episodes during a sleep episode increased. We conclude that in HAT, the reversibility of the sleep/wake cycle alteration and that of sleep structure constitute the basis for an evaluation of the healing process.     

The prevalence of restless sleep disorder among a clinical sample of children and adolescents referred to a sleep centre

Restless sleep disorder (RSD) is a newly described sleep disorder in children characterized by large body movements and repositioning that lasts all night with at least five body movements per hour and a significant impact on daytime behaviours. The authors have previously identified and described the syndrome and compared the sleep parameters and sleep‐related movements to those in children with restless legs syndrome, normal controls and snorers. The current study is a retrospective review of the sleep diagnosis in 300 consecutive children seen and evaluated in a single sleep disorders centre; 252 children underwent polysomnography, as clinically indicated, to identify the proper diagnosis. The current research estimates the prevalence of RSD in a sleep clinical setting to be 7.7% and compares it to the prevalence of other common sleep disorders in the same setting. Another important addition to the literature is the fact that RSD can coexist with other sleep disorders, such as habitual snoring and parasomnia, without confounding the diagnosis.