Sleep in fibromyalgia: review of clinical and polysomnographic data]

Fibromyalgia syndrome is a common chronic pain syndrome that is often associated with sleep disturbances characterized by subjective experience of non-restorative sleep. The complaints of sleep disturbances are correlated with polysomnographic features showing clear abnormalities in the continuity of sleep as well as in the sleep architecture. Sleep-recording abnormalities are characterized by a reduced sleep efficiency with increased number of awakenings, a reduced amount of slow wave sleep and an abnormal alpha wave intrusion in non rapid eye movement, termed alpha-delta sleep. These data were confirmed by spectral analysis of sleep showing an increased EEG power density in the higher frequency band and a reduced EEG power density in the lower frequency bands. Moreover, other microstructural aspects of sleep were modified with high frequency of arousals and alpha-K complex reported, both indicators of fragmented sleep. The fibromyalgia symptoms may relate to a non-restorative sleep disorder associated with the alpha-EEG sleep anomalies. However, alpha-EEG sleep anomaly is non-specific for fibrositis, also seen in normal controls during stage 4 sleep deprivation. Moreover, fibromyalgia patients may also experience primary sleep disorder such as sleep apnea or periodic leg movements. The etiology of this common condition is incompletely understood and the existence of a specific entity of fibromyalgia is still a matter of debate. However, several studies have found abnormal brain metabolism of substances such as serotonin implicated in sleep arousal and pain mechanisms and administration of tricyclic antidepressants and selective serotonin reuptake inhibitors may be useful in fibromyalgia. Pain, poor sleep quality and anxiety may contribute to the clinical picture. Several factors such as psychological, environmental, genetic factor, altered serotonin metabolism and altered sleep physiology are involved in the pathogenesis of fibromyalgia.     

Convergent validity of the Child Behavior Checklist sleep items with validated sleep measures and sleep disorder diagnoses in children and adolescents referred to a sleep disorders center

ObjectiveThe Child Behavior Checklist (CBCL) is a commonly used measure of child and adolescent functioning, and a handful of items from the CBCL are often used to measure sleep functioning. The objective of this study was to examine the convergent, discriminant, and external validity of the individual CBCL sleep items and a CBCL sleep composite with validated measures of sleep functioning and youth adjustment as well as sleep disorder diagnoses.MethodsThe participants were 383 youths (ages 6–18 years; 52.5% male; 80% non-Hispanic White) evaluated in a behavioral sleep medicine clinic. A sleep psychologist diagnosed sleep disorders following a comprehensive evaluation. Parents completed the CBCL in addition to the Children's Sleep Habits Questionnaire (CSHQ) and the Sleep Disorders Inventory for Students (SDIS). Adolescents completed the Adolescent Sleep–Wake Scale (ASWS).ResultsIndividual CBCL sleep items were generally associated with sleep scales on validated sleep measures and with sleep disorder diagnoses. The CBCL sleep composite was associated with total scores on each of the sleep-specific measures, as well as with the CBCL attention, social, internalizing, and externalizing problems scales.ConclusionsAlthough the CBCL is inadequate for thoroughly assessing sleep problems and disorders, sleep items on the CBCL may be useful in epidemiological/archival studies that lack a more comprehensive sleep measure or to clinicians who do not use other validated sleep measures in their typical practice. Individual CBCL sleep items may be optimal when assessing specific facets of sleep functioning whereas the CBCL sleep composite may be optimal when examining overall sleep functioning and external correlates of sleep.     

Manipulating REM sleep in older adults by selective REM sleep deprivation and physiological as well as pharmacological REM sleep augmentation methods

Experimental approaches to manipulate REM sleep within the cognitive neuroscience of sleep are usually based on sleep deprivation paradigms and focus on younger adults. In the present study, a traditional selective REM sleep deprivation paradigm as well as two alternative manipulation paradigms targeting REM sleep augmentation were investigated in healthy older adults. The study sample consisted of 107 participants, male and female, between the ages of 60 and 82 years, who had been randomly assigned to five experimental groups. During the study night, a first group was deprived of REM sleep by selective REM sleep awakenings, while a second group was woken during stage 2 NREM sleep in matched frequency. Physiological REM sleep augmentation was realized by REM sleep rebound after selective REM sleep deprivation, pharmacological REM sleep augmentation by administering an acetylcholinesterase inhibitor in a double-blind, placebo-controlled design. Deprivation and augmentation paradigms manipulated REM sleep significantly, the former affecting more global measures such as REM sleep minutes and percentage, the latter more organizational aspects such as stage shifts to REM sleep, REM latency, REM density (only pharmacological augmentation) and phasic REM sleep duration. According to our findings, selective REM sleep deprivation seems to be an efficient method of REM sleep manipulation in healthy older adults. While physiological rebound-based and pharmacological cholinergic REM sleep augmentation methods both failed to affect global measures of REM sleep, their efficiency in manipulating organizational aspects of REM sleep extends the traditional scope of REM sleep manipulation methods within the cognitive neuroscience of sleep.     

Sleep epilepsy

BACKGROUND: Seizures during sleep have been recognized for centuries, and it is well known that both sleep and lack of sleep can influence the occurrence of ictal and interictal events. Sleep epilepsy refers to the subset of epilepsy in which seizures occur exclusively or predominantly during sleep. Primary generalized, secondarily generalized, and focal partial epilepsy syndromes can all manifest as sleep epilepsy. The spread of polysomnography has increased our ability to accurately diagnose sleep epilepsy and facilitated the discovery of an autosomal dominant sleep epilepsy. REVIEW SUMMARY: This review summarizes the epidemiology of sleep epilepsy and reviews a number of epilepsies that can manifest as sleep epilepsy as well as some nonepileptic sleep disorders from which sleep epilepsy must be differentiated.     

Sleep in attention-deficit/hyperactivity disorder in children and adults: past, present, and future

The understanding that sleep can give rise to, or exacerbate symptoms of attention-deficit/hyperactivity disorder (ADHD), and that good sleep hygiene improves attention and concentration tasks has sparked interest in the investigation of possible etiological relationships between sleep disorders and ADHD. Studies indicate that 30% of children and 60-80% of adults with ADHD have symptoms of sleep disorders such as daytime sleepiness, insomnia, delayed sleep phase syndrome, fractured sleep, restless legs syndrome, and sleep disordered breathing. The range and diversity of findings by different researchers have posed challenges in establishing whether sleep disturbances are intrinsic to ADHD or whether disturbances occur due to co-morbid sleep disorders. As a result, understanding of the nature of the relationship between sleep disturbances/disorders and ADHD remains unclear. In this review, we present a comprehensive and critical account of the research that has been carried out to investigate the association between sleep and ADHD, as well as discuss mechanisms that have been proposed to account for the elusive relationship between sleep disturbances, sleep disorders, and ADHD.     

The role and validity of actigraphy in sleep medicine: an update

Activity-based sleep-wake monitoring or actigraphy has gained a central role as a sleep assessment tool in sleep medicine. It is used for sleep assessment in clinical sleep research, and as a diagnostic tool in sleep medicine. This update indicates that according to most studies, actigraphy has reasonable validity and reliability in normal individuals with relatively good sleep patterns. The validity of actigraphy in special populations or with individuals with poor sleep or with other sleep-related disorders is more questionable. The most problematic validity issue is the low specificity of actigraphy in detecting wakefulness within sleep periods reported with certain devices or samples. Overall, the recent literature adds to previous reports in demonstrating that actigraphy is sensitive in detecting unique sleep patterns associated with specific sleep disorders as well as with other medical or neurobehavioral disorders. Furthermore, actigraphy is sensitive in detecting sleep changes associated with drug treatments and non-pharmacologic interventions. Recent developments include the development of devices specially tailored to detect periodic limb movement in sleep and the introduction of new devices and algorithms. Because of the limitations of actigraphy, it is recommended to use complementary assessment methods (objective and subjective) whenever possible.     

Effects of Yoku-kan-san-ka-chimpi-hange on the sleep of normal healthy adult subjects

Yoku-kan-san-ka-chimpi-hange (YKCH) is a drug used for insomnia in Japanese traditional herbal medicine. The present study evaluated the effects of YKCH on sleep by all-night polysomnography using the double-blind method. Yoku-kan-san-ka-chimpi-hange increased the total sleep time significantly, and tended to cause an increase in sleep efficiency and of stage 2 sleep, as well as a decrease of sleep latency and of stage 3 + 4 sleep. There was no apparent influence on rapid eye movement (REM) sleep. In terms of non-REM sleep, the effects of YKCH exhibit a profile similar to those of benzodiazepines.     

Decreased sleep quality and increased sleep related movements in patients with Tourette's syndrome

OBJECTIVE: Sleep quality and movement patterns across sleep stages in patients with Tourette's syndrome were examined to determine the influence of syndrome severity on sleep quality and the differential effect of sleep stages on tic and non-tic movements. METHODS: Twenty five patients with Tourette's syndrome (mean age 29 (SD 7) years) and 11 control subjects (29 (5) years) were studied by polysomnography and simultaneous split screen video monitoring to record standard sleep variables as well as to evaluate movements to differentiate between tics and regular movements. Severity of Tourette's syndrome during the day was assessed with the Tourette's syndrome severity scale. RESULTS: Sleep was significantly more disturbed in patients with Tourette's syndrome than in controls, with decreased sleep efficiency and slow wave sleep percentage, increased sleep latency, percentage of stage I, percentage of awakeness, number of awakenings, and sleep stage changes and more overall movements during sleep. Severity of Tourette's syndrome during the day correlated significantly and positive with number of awakenings and sleep stage changes and negatively with sleep efficiency. In addition to an increased number of regular movements patients had tics in all sleep stages. Tic frequency as well as frequency of regular movements was significantly higher in REM than in non-REM sleep which was also the case for regular movements of the controls. No disturbance of either REM sleep percentage or REM latency was found. CONCLUSION: Despite normal total sleep time and unaltered REM sleep variables patients with Tourette's syndrome have markedly disturbed sleep. Severity of the syndrome during the day is an important predictor of sleep alteration in patients. The increased rate of tics during REM sleep parallels the overall increased movement activity of patients during REM as well as non-REM sleep. The increased motor activity may be attributable to a state of hyperarousal rather than a disturbed cholinergic system.     

Sleep and sleep-wake manipulations in bipolar depression

In the last 30 years, it has been convincingly demonstrated that sleep in major depression is characterized by disturbances of sleep continuity, a reduction of slow wave sleep, a disinhibition of REM sleep including a shortening of REM latency (i.e. the time between sleep onset and the occurrence of the first REM period) and an increase in REM density. Furthermore, manipulations of the sleep-wake cycle like total or partial sleep deprivation or phase advance of the sleep period have been proven to be effective therapeutic strategies for patients with unipolar depression. The database concerning sleep and sleep-wake manipulations in bipolar disorder in comparison is not yet as extensive. Studies investigating sleep in bipolar depression suggest that during the depressed phase sleep shows the same stigmata as in unipolar depression. During the hypomanic or manic phase, sleep is even more curtailed, though subjectively not experienced as disturbing by the patients. REM sleep disinhibition is present as well. An important issue is the question, whether sleep-wake manipulations can also be applied in patients with bipolar depression. Work by others and our own studies indicate that sleep deprivation and a phase advance of the sleep period can be used to treat bipolar patients during the depressed phase. The risk of a switch into hypomania or mania does not seem to be more pronounced than the risk with typical pharmacological antidepressant treatment. For patients with mania, sleep deprivation is not an adequate treatment--in contrast, treatment strategies aiming at stabilizing a regular sleep-wake schedule are indicated.     

Increased delta power and discrepancies in objective and subjective sleep measurements in borderline personality disorder

BACKGROUND: Previous studies have shown depression-like sleep abnormalities in borderline personality disorder (BPD). However, findings in BPD are not unequivocal for REM dysregulation, as well as for a decrement of slow wave sleep and sleep continuity disturbances. Earlier findings in sleep EEG abnormalities in BPD may have been confounded by concomitant depressive symptoms. METHODS: Twenty unmedicated female BPD patients without current comorbid major depression and 20 sex- and age-matched control subjects entered the study. Conventional polysomnographic parameters and for the first time sleep EEG spectral power analysis was performed on two sleep laboratory nights. Subjective sleep parameters were collected by sleep questionnaires in order to assess the relationship between objective and subjective sleep measurements. RESULTS: BPD patients showed a tendency for shortened REM latency and significantly decreased NonREM sleep (stage 2). Spectral EEG analysis showed increased delta power in total NREM sleep as well as in REM sleep in BPD patients. Subjective ratings documented drastically impaired sleep quality in BPD patients for the two weeks before the study and during the two laboratory nights. CONCLUSION: Not-depressed BPD patients only showed tendencies for depression-like REM sleep abnormalities. Surprisingly, BPD patients displayed higher levels of delta power in the sleep EEG in NREM sleep than healthy control subjects. There was a marked discrepancy between objective and subjective sleep measurements, which indicates an altered perception of sleep in BPD. The underlying psychological and neurobiological mechanisms of these alterations are still unclear and need to be clarified in future studies including interventions on a pharmacological and cognitive-behavioral level.     

Recent developments in the diagnosis and treatment of sleep disorders

The publication of a new nosology of sleep and arousal disorders in 1979 established the need for differential diagnosis of sleep disorders based on polysomnographic evaluations as well as medical history and physical examination. This review of recent developments in diagnosing and treating sleep disorders covers such topics as prevalence, findings related to sleeping pills and insomnia, effects of depression on sleep, and managing the elderly patient with disturbed sleep. The authors caution against misuse of hypnotic drug therapy for treatment of insomnia and encourage physicians to inquire about sleep patterns even when a patient is presenting a seemingly unrelated problem.     

Sleep and pain

Noxious stimuli and painful disorders interfere with sleep, but disturbances in sleep also contribute to the experience of pain.Chronic paroxysmal hemicrania and possibly cluster headaches are related to REM sleep. Whereas headache is associated with snoring and sleep apnea, morning headaches are not specific for any primary sleep disorder. Nevertheless, the management of the sleep disorder ameliorates both morning headache and migraine.Noxious stimuli administered into muscles during slow-wave sleep (SWS) result in decreases in delta and sigma but an increase in alpha and beta EEG frequencies during sleep. Noise stimuli that disrupt SWS result in unrefreshing sleep, diffuse musculoskeletal pain, tenderness, and fatigue in normal healthy subjects. Such symptoms accompany alpha EEG sleep patterns that often occur in patients with fibromyalgia. The alpha EEG patterns include phasic and tonic alpha EEG sleep as well as periodic K alpha EEG sleep or frequent periodic cyclical alternating pattern. Moreover, alpha EEG sleep, as well as sleep-related breathing disorder and periodic limb movement disorder, occur in some patients with fibromyalgia, rheumatoid arthritis and osteoarthritis. Depression and not alpha EEG sleep are features of somatoform pain disorder. Disturbances in sleep, pain behaviour and psychological distress influence return to work in workers who have suffered a soft tissue injury, e.g. low back pain. Patients with irritable bowel disorder have disturbed sleep and have increased REM sleep. In conclusion, there is a reciprocal relationship between sleep quality and pain. The recognition of disturbed or unrefreshing sleep influences the management of painful medical disorders.     

Wakefulness-sleep transition: emerging electroencephalographic similarities with the rapid eye movement phase

The covert-rapid eye movement (REM) sleep hypothesis of dreaming suggests that elements of REM sleep emerge during sleep onset, leading to vivid hypnagogic imagery. We tested the physiological part of this hypothesis by analysing scalp-recorded electroencephalograms of 15 human subjects during wake–sleep transition and subsequent night time sleep. Wake–sleep transition was categorised semi-automatically as alpha activity, alpha dropout and as early Stage 2 sleep. The slow oscillation, the slow and the fast subdivisions of the delta and the theta frequencies respectively, as well as alpha and sigma bands were analysed. The similarity of individual-specific wake–sleep transition periods and the whole night Stage 2 or REM sleep periods was expressed in a composite similarity measure covering the spectral power of all analysed frequency bands and in frequency-specific similarities related to power values in single bands. A significant increase in composite similarity with the whole night REM sleep emerged in the period of alpha dropout and diminished in early Stage 2 sleep. The alpha dropout period was more similar to whole night REM sleep than to whole night Stage 2 sleep. These region-independent effects were mirrored in region-specific manner by frequency bands of the delta-slow theta range. Findings are in accordance with the covert REM sleep hypothesis, with previous electrocorticographic results and with the frequency range of the sawtooth waves in humans.     

Sleep inertia

Sleep inertia is a transitional state of lowered arousal occurring immediately after awakening from sleep and producing a temporary decrement in subsequent performance. Many factors are involved in the characteristics of sleep inertia. The duration of prior sleep can influence the severity of subsequent sleep inertia. Although most studies have focused on sleep inertia after short naps, its effects can be shown after a normal 8-h sleep period. One of the most critical factors is the sleep stage prior to awakening. Abrupt awakening during a slow wave sleep (SWS) episode produces more sleep inertia than awakening in stage 1 or 2, REM sleep being intermediate. Therefore, prior sleep deprivation usually enhances sleep inertia since it increases SWS. There is no direct evidence that sleep inertia exhibits a circadian rhythm. However, it seems that sleep inertia is more intense when awakening occurs near the trough of the core body temperature as compared to its circadian peak. A more controversial issue concerns the time course of sleep inertia. Depending on the studies, it can last from 1 min to 4 h. However, in the absence of major sleep deprivation, the duration of sleep inertia rarely exceeds 30 min. But all these results should be analysed as a function of type of task and dependent variables. Different cognitive functions are probably not sensitive to the same degree to sleep inertia and special attention should be provided to dependent variables as a result of the cognitive processes under review. Finally, sleep disorders represent risk factors which deserve new insight in treatment strategies to counteract the adverse effects of sleep inertia.     

Correlation dimension of the human sleep electroencephalogram

Sleep electroencephalogram (EEG) was analyzed by nonlinear analysis. Polysomnography of a healthy male subject was analyzed and the correlation dimension was calculated. The mean correlation dimensions decreased from stage 'awake' to stages 1, 2 and 3, and increased during rapid eye movement (REM) sleep. These results were also seen at every sleep cycle. During each sleep cycle the correlation dimensions decreased for slow wave sleep, then increased for REM sleep. The mean correlation dimension of the sleep EEG in the second half of the night was significantly higher than those in the first half of the night. A significant change was seen both during REM sleep as well as in sleep stage 2. Nonlinear analysis may be a useful method in the analysis of the entire sleep electroencephalogram.     

Electroencephalographic sleep in panic disorder. A focus on sleep-related panic attacks

Sleep electroencephalograms were studied in 13 patients with panic disorder, six of whom experienced panic from sleep, and seven controls. Sleep was disturbed in the patients, as manifested by increased sleep latency, decreased sleep time, and decreased sleep efficiency. Rapid eye movement (REM) latencies were not reduced in the patient group. All six of the panic awakenings were preceded by non-REM sleep, which could be further characterized as a transition from stage II toward delta sleep. The overall degree of sleep disturbance (ie, sleep latency, sleep efficiency) did not appear to be influenced by the occurrence of sleep panic. There was also an association of increased REM latency with nights of sleep panic.     

Ethanol effect on sleep electroencephalogram by the correlation dimension.

The influence on sleep of alcohol (ethanol) was investigated in nine males using the correlation dimension (CD). Polysomnography (PSG) was recorded on a baseline night (BL-N) and on an ethanol (0.8 g/kg) night (Et-N). The mean correlation dimensions on Et-N, as well as on BL-N, significantly decreased from sleep stage 'awake' to sleep Stages 1, 2 and 3 and increased during rapid eye movement (REM) sleep. The mean correlation dimensions of the sleep EEG during sleep Stage 2 and those for the second sleep cycle on the Et-N were significantly higher than those on the BL-N. The changes in the correlation dimensions between sleep cycles were reduced on Et-N as compared to BL-N.     

Muscarinic supersensitivity: A possible model for the sleep disturbance of primary depression?

The sleep changes induced in normal volunteers following the administration of scopolamine on 3 consecutive mornings resemble many of the abnormalities observed in the sleep of patients with primary depression: increased sleep latency and reduced rapid eye movement (REM) latency, total sleep time, and sleep efficiency. Furthermore, in a multivariate discriminant analysis--previously shown to distinguish the sleep records of depresed patients from those of normal controls and insomniac patients--the records from baseline nights were selected as normal and those after scopolamine as predominately depressed. Those observations suggest to us that muscarinic supersensitivity in normals may function as a pharmacological model for the sleep disturbances of depression.     

Epidemiology of sleep and sleep disorders in The Netherlands

ObjectiveThere is a surging public interest in The Netherlands concerning sleep, sleep disorders and associated health. For a proper perspective, it is necessary to have reliable information on the prevalence of sleep characteristics at the national level. This study set out to assess prevalence rates and key characteristics of sleep and sleep disorders in The Netherlands.MethodsIn 2012, a nationally representative sample of 2089 individuals, aged 18–70 years, responded to a set of 48 questions, including the Holland Sleep Disorders Questionnaire, a validated questionnaire based on the International Classification of Sleep Disorders.ResultsPrevalence rates were: 32.1% for a general sleep disturbance (GSD), 43.2% for insufficient sleep, 8.2 for insomnia, 5.3% for circadian rhythm sleep disorder, 6.1% for parasomnia, 5.9% for hypersomnolence, 12.5% for restless legs disorder and limb movements during sleep, 7.1% for sleep related breathing disorder, and 12.2% for the presence of comorbidity, ie, the presence of two or more concurrent sleep disorders. In addition, sleep onset time as well as sleep duration showed U-shaped relationships with GSD prevalence rates, with respectively the 22:00–24:00 period and seven to 8 h as optimal associates.ConclusionsSleep disorders and insufficient sleep have a high prevalence. As matter of concern, female adolescents reached the highest prevalence rates for most sleep disorders, insufficient sleep and daytime malfunctioning.