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Results for “REM Sleep Behavior Disorder”

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PubMed1999

Factors associated with the development of substance use disorder in depressed adolescents.

OBJECTIVE: To document rates of substance use disorders (SUD) in adolescents with unipolar major depressive disorder and to examine demographic, clinical, and biological factors associated with the development of SUD. METHOD: Twenty-eight adolescents with unipolar major depression and no SUD history and 35 group-matched normal controls who participated in a cross-sectional sleep polysomnography and neuroendocrine study were reassessed clinically 7 years later. RESULTS: The risk for SUD was high in both groups (34.6% in the depressed group and 24.2% in the controls). Depressed adolescents had earlier onset of SUD than controls. Depressed adolescents who developed SUD had more significant psychosocial impairment than depressed adolescents who did not develop SUD. More anxiety traits and elevated cortisol secretion near sleep onset were associated with SUD in depressed teenagers, whereas less emotional responsiveness to exciting stimuli and higher density of eye movements during REM sleep were related to depression without SUD. CONCLUSIONS: Depressed adolescents who have anxiety traits and whose hypothalamic-pituitary-adrenal axis is active when the system is normally quiescent may be at risk for developing SUD. Co-occurrence of depression and SUD is associated with serious psychosocial morbidity. Identification of risk factors for SUD in depressed teenagers may be helpful in developing more effective treatment and prevention programs.

Adolescent↗
PubMed1982

Daytime sleep stage organization in three-month-old infants.

Sleep monitoring at 3 months post term of clinically normal term infants, pre-term infants with no demonstrable pathologic clinical signs, and pre-term and term infants with a history of metabolic disorders show that these infants have EEG sleep stages resembling those seen in adults, as well as the adult pattern of sleep stage organization. The presence of NREM stage organization and stage sequencing suggest that sleep regulatory mechanisms are approaching a level of functional maturity in the human infant at 3 months post term. There is a significant relationship between sleep staging at 3 months post term and mental and motor performance at 12 months post term. In light of this, it is hypothesized that early bioelectric maturation may reflect the development of neural mechanisms which are also the substrate for later cognitive and behavioral functioning. Sleep stage organization at 3 months post term may be utilized as a benchmark of CNS development and for research on the pathophysiology of sleep disorders.

Brain↗
PubMed1996

NREM sleep parasomnias.

The three states of mammalian being--wakefulness, REM sleep, and NREM sleep--are not mutually exclusive and may occur simultaneously, oscillate rapidly, or appear in dissociated or incomplete form to produce primary sleep parasomnias. Dysfunctions of a wide variety of organ systems may take advantage of the sleeping state to declare themselves, resulting in the secondary sleep parasomnias. Contrary to popular opinion, most of these often bizarre and frightening experiences are not the manifestation of underlying psychological or psychiatric conditions. Formal study in an experienced sleep disorders center usually reveals a diagnosable and treatable condition. Various parasomnias may result in injurious or violent behavior. The forensic science implications are beyond the scope of this article but have been reviewed extensively elsewhere. Continued study of unusual sleep-related events undoubtedly will reveal more fascinating conditions, expanding our knowledge of sleep physiology and strengthening the bonds between clinicians and basic science sleep researchers.

Bruxism↗
PubMed2006

Correlates of sleep and pediatric bipolar disorder.

STUDY OBJECTIVE: To determine, based on a large community sample, the prevalence and associated sleep characteristics of children with a bipolar mood disturbance behavioral profile. METHODS: Participants who fit the pediatric bipolar disorder profile as derived from the Child Behavior Checklist were matched to control participants for age, sex, ethnicity, parentally reported attention-deficit/hyperactivity disorder, psychotropic medication usage, and apnea-hypopnea indexes. Paired comparisons were made between the groups to examine differences on polysomnographic data and parentally reported sleep characteristics. RESULTS: Thirteen (approximately 3%) of 438 participants fit the pediatric bipolar disorder profile. These children demonstrated significant sleep-continuity disturbances with poorer sleep efficiency and more awakenings after sleep onset, less rapid eye movement sleep, and longer periods of slow-wave sleep than their matched counterparts during overnight polysomnography. In addition, responses to a parental-report questionnaire about child sleep behavior suggest these children have significant sleep problems, including more difficulty initiating sleep, restless sleep, nightmares, and morning headaches relative to the control group. CONCLUSIONS: Children with a pediatric bipolar disorder profile display consistent quantitative differences in sleep relative to matched controls. Prevalence rates of pediatric bipolar disorder, as assessed by the Child Behavior Checklist, are consistent with those found in the adult bipolar population.

Aggression↗
PubMed1987

[Dangerous snoring. Sleep-apnea syndrome].

Snoring usually is trivial and unimportant, but it can turn into a social or medical problem. Obesity, hypertension and heart disease are more frequent among snorers than among nonsnorers, and especially snorers with hypersomnia during the day are at risk. Hypersomnia in association with snoring usually signifies obstructive sleep apnea. Increased resistance in the upper airways, together with negative inspiratory pharyngeal pressure and muscular hypotonia during deep non-REM and REM sleep, lead to collapse of the pharynx, hypoxia and hypercapnia. Only after arousal from sleep does muscle tone return, pharyngeal obstruction reopen and airflow resume. Since this process can occur 300 or 400 times a night, repetitive alveolar hypoventilation leads to pulmonary-arterial hypertension and cor pulmonale, and the repetitive sympathetic activations can cause systemic hypertension or serious cardiac arrhythmias. The countless arousals deprive the sufferer of deep non-REM and REM sleep and their consequence is sleep fragmentation. The symptoms are excessive daytime sleepiness, intellectual deterioration and personality and behavioral changes. Oronasomaxillofacial, endocrine and neuromuscular anomalies and diseases predispose to sleep apnea, and alcohol or CNS-depressant drugs can favour its occurrence. Diagnosis is made by nighttime oxymetry, and if this is abnormal, by polysomnography. After polysomnography it is possible to distinguish between obstructive and nonobstructive sleep apnea, and the decisions for an adequate treatment can be made.

Airway Resistance↗
PubMedDate not supplied

Search activity in the context of psychosomatic disturbances, of brain monoamines and REM sleep function.

The author discusses a number of controversial aspects of the search activity concept. This concept, based on an analysis of data cited by other researchers and the results of the author's own investigation, performed together with V. V. Arshavsky, postulates that search activity raises the body's resistance to stress and experimentally induced pathology whereas renunciation of search forms a nonspecific predisposition to somatic disturbances (e.g., psychosomatic disease). REM sleep is regarded as a specific form of search activity aimed at compensating for the state of renunciation of search in walking. In this paper the author argues that 1) renunciation of search can be accompanied either by anxiety or by depression, 2) REM sleep deprivation on a "small platform" raises the requirement in REM sleep by producing renunciation of search, 3) during search activity brain catecholamine synthesis is stimulated by catabolism whereas a state of renunciation of search upsets this feedback system. The actuation of the brain mechanisms of search in REM sleep necessitates a certain brain catecholamine level. If the brain catecholamine level is very high during waking behavior due to intensive search activity, the REM sleep requirement is low, REM sleep becoming reduced. After a moderate drop in the brain catecholamine level at the initial stage of renunciation of search the requirement in REM sleep rises and this phase grows longer. But at the late stage of renunciation of search the brain catecholamine level drops extremely, REM sleep shrinking in spite of the great appropriate requirement, and 4) the functional insufficiency of REM sleep invites various forms of pathology.

Animals↗
PubMed2006

Depression and sleep: pathophysiology and treatment.

This review examines the relationship between sleep and depression. Most depressive disorders are characterized by subjective sleep disturbances, and the regulation of sleep is intricately linked to the same mechanisms that are implicated in the pathophysiology of depression. After briefly reviewing the physiology and topography of normal sleep, the disturbances revealed in studies of sleep in depression using polysomnographic recordings and neuroimaging assessments are discussed. Next, treatment implications of the disturbances are reviewed at both clinical and neurobiologic levels. Most antidepressant medications suppress rapid eye movement (REM) sleep, although this effect is neither necessary nor sufficient for clinical efficacy. Effects on patients' difficulties initiating and maintaining sleep are more specific to particular types of antidepressants. Ideally, an effective antidepressant will result in normalization of disturbed sleep in concert with resolution of the depressive syndrome, although few interventions actually restore decreased slow-wave sleep. Antidepressants that block central histamine 1 and serotonin 2 tend to have stronger effects on sleep maintenance, but are also prone to elicit complaints of daytime sedation. Adjunctive treatment with sedative hypnotic medications--primarily potent, shorter-acting benzodiazepine and gamma-aminobutyric acid (GABA A)-selective compounds such as zolpidem--are often used to treat associated insomnia more rapidly. Cognitive behavioral therapy and other nonpharmacologic strategies are also helpful.

Antidepressive Agents↗
PubMed2002

Polysomnographic characterization of pergolide-induced sleep attacks in idiopathic PD.

Both dopamine agonists and levodopa may induce episodes termed "sleep attacks" in patients with PD. These episodes are well detailed behaviorally, but little is known about their neurophysiologic characterization. The authors performed a 24-hour polysomnography (PSG) in a PD patient taking pergolide in combination with levodopa, in which four of these diurnal sleep episodes occurred. PSG findings were followed up after pergolide withdrawal. Sleep episodes shared with narcolepsy both behavioral and EEG findings. However, pergolide partly restored a more physiologic sleep architecture, which was disrupted during therapy with levodopa alone.

Adult↗
PubMed2004

Sleep, sleep disorders and hypocretin (orexin).

Narcolepsy is a disabling neurologic condition affecting 1 in 2000 individuals, characterized by sleepiness, cataplexy, and transitions from wakefulness into rapid-eye-movement sleep. Current treatments include amphetamine-like stimulants and antidepressants. Human narcolepsy is HLA-associated, multigenic, and environmentally influenced. Positional cloning was used to isolate narcolepsy genes in canine families with autosomal recessive narcolepsy transmission. Three mutations in the G-protein-coupled hypocretin (orexin) receptor-2 (Hcrtr-2) gene were identified. In humans, most cases of narcolepsy are not linked to hypocretin (Hcrt) ligand or receptor mutations but are associated with undetectable cerebrospinal fluid Hcrt-1 levels. A single Hcrt gene/narcolepsy mutation was identified in narcoleptic patients. Hcrt-1 is wake-promoting in vivo, and studies in sporadic human narcolepsy indicate a loss of brain Hcrt-1 and Hcrt-2 and a disappearance of Hcrt-1-containing cells in the hypothalamus. Narcolepsy with cataplexy may therefore be due to Hcrt deficiency. The HLA association in humans suggests possible autoimmune activity against hypothalamic Hcrt-containing cells. Hypocretins may also have roles in regulating normal sleep, appetite, neuroendocrine function and energy metabolism, uniquely positioning them as a link between multiple important behaviors. Abnormal Hcrt transmission is also found in neurologic disorders featuring excessive daytime sleepiness and/or hypothalamic abnormalities. Pharmacologic manipulations of Hcrts may have multiple therapeutic applications.

Alleles↗
PubMed1992

The role of a sleep disorder center in evaluating sleep violence.

To review the state-dependent nature of violence and present a clinically useful classification of sleep violence, this article reviews our experience with sleep-related violence, establishing a differential diagnosis, methods of evaluation, and treatment options. The study occurs in a full-service clinical sleep disorders center evaluating approximately 1000 patients annually with an active participation of 16 physicians representing seven specialties. The patients were self-, physician-, or court/social service-referred for evaluation of violent or injurious behaviors associated with the sleep period. Interventions were dependent on the final diagnosis following clinical and (usually) sleep laboratory evaluation. The main outcome measures were self-reported. During routine clinical evaluations at a multidisciplinary sleep disorder center, it has become apparent that violence is often state-dependent, occurring only during the sleep period, resulting from a number of both neurologic and psychiatric conditions (including malingering and Munchausen syndrome by proxy). In such cases, careful clinical and laboratory evaluation usually results in a specific diagnosis, with effective therapeutic recommendations. Violence may be state-dependent. It is clear that violent behaviors may arise from the sleep period, often without conscious awareness on the part of the subject. This has social, forensic, and clinical implications, and may help contribute to the understanding of violence in general.

Health Facilities↗
PubMed1997

[Epileptic syndromes which show continuous spike and wake complexes during slow wave sleep].

INTRODUCTION AND OBJECTIVE: The association of cognitive and/or behavioral disturbances, epileptic seizures and continuous discharges spike-waves during slow sleep in the EEG, has been described in three epileptic syndromes: continuous spike-wave during slow sleep syndrome (CSWS), Landau-Kleffner syndrome (LKS) or acquired epileptic aphasia, and atypical benign partial epilepsy of childhood (ABPE). MATERIAL AND METHODS: We report 13 patients; two of these have been diagnosed of CSWS. four of LKS and seven of ABPE, according to the definition criteria. RESULTS: The main clinical features in each patient are presented here. In all patients, continuous spike-wave discharges were observed for more than > 80% of the total sleep period at some time during the course of the illness. There are many similarities at the age of onset, the occurrence of several types of seizures, the evolution and the electroencephalographic findings in awake state and sleep. CONCLUSIONS: It suggests that the CSWS, LKS and ABPE have probably the same pathophysiology and that they are the severe, moderate and benign forms of a single epileptic syndrome, age-related, with continuous spike waves and various neuropsychological and behavioral disturbances. The neuropsychological manifestations depend probably on the localization of the original epileptic focus.

Age of Onset↗
PubMed2003

Disturbed sleep in children with Tourette syndrome: a polysomnographic study.

OBJECTIVE: To evaluate objective data on sleep quantity/quality and motor activity during night sleep in children with Tourette syndrome (TS). METHOD: Polysomnography of 17 unmedicated TS children (ages: 7;11-15;5, mean: 11;10 years) without comorbid attention-deficit hyperactivity disorder (ADHD) was compared with 16 age-, sex- and IQ-matched healthy controls. Sleep analyses according to the procedure of Rechtschaffen and Kales were supplemented by counting epochs with short arousal-related movements (<or=15 s), thus allowing to calculate correlations between motor activity and sleep parameters. RESULTS: Children with TS demonstrated changes in sleep parameters, including longer sleep period time, longer sleep latency, reduced sleep efficiency, and prolonged wakefulness after sleep onset. Their sleep profiles showed significantly more time awake and less sleep stage II. However, REM sleep variables, slow-wave sleep, and number of sleep stage changes were unaffected. Movement time was similar in both groups, but epochs with short arousal-related movements were increased in TS. Further analyses showed no significant correlations between sleep parameters and nighttime nontic movements, level of psychopathology or tic severity during daytime. Periodic limb movements during sleep (PLMS) were only seen in one TS patient (low PLMS index of 7.8/h). CONCLUSIONS: Children with TS have disturbed sleep quality with increased arousal phenomena, which both may be intrinsic to the disorder and might trigger tics and other behavioral problems during daytime. This indicates the need for sleep evaluation in patients with TS.

Adolescent↗
PubMedDate not supplied

[Validation of an animal model of anhedonia, a major symptom of depression].

One of the two core symptoms of human depression is anhedonia, the loss of interest or pleasure in daily activities. Daily stressful life events are recognized as predisposing factors in the etiology of depression. Rats submitted to a regimen of chronic, mild, unpredictable stress exhibit behavioral deficits consistent with a loss of responsiveness to reward, such as decreased sucrose consumption, decreased ability to associate rewards with a distinctive environment, and decreased sensitivity to rewarding electrical brain stimulation. Normal behavior can be restored by chronic treatment with tricyclics, atypical antidepressants, monoamine oxydase inhibitors and electroshocks, but not by other psychotropic agents such as antipsychotics. In addition, chronically stressed animals exhibit REM sleep abnormalities resembling those observed in depressed patients and recognized as biological markers of depression. These data provide evidence supporting chronic stress-induced anhedonia in rats as an original animal model of human depression combining convergent elements of biological, etiological, symptomatological and therapeutic validity. This realistic simulation of depression may prove useful for a better understanding of pathophysiological mechanisms involved in depressive disorders.

Animals↗
PubMed2003

Comparison of detrended fluctuation analysis and spectral analysis for heart rate variability in sleep and sleep apnea.

Sleep has been regarded as a testing situation for the autonomic nervous system, because its activity is modulated by sleep stages. Sleep-related breathing disorders also influence the autonomic nervous system and can cause heart rate changes known as cyclical variation. We investigated the effect of sleep stages and sleep apnea on autonomic activity by analyzing heart rate variability (HRV). Since spectral analysis is suited for the identification of cyclical variations and detrended fluctuation analysis can analyze the scaling behavior and detect long-range correlations, we compared the results of both complementary techniques in 14 healthy subjects, 33 patients with moderate, and 31 patients with severe sleep apnea. The spectral parameters VLF, LF, HF, and LF/HF confirmed increasing parasympathetic activity from wakefulness and REM over light sleep to deep sleep, which is reduced in patients with sleep apnea. Discriminance analysis was used on a person and sleep stage basis to determine the best method for the separation of sleep stages and sleep apnea severity. Using spectral parameters 69.7% of the apnea severity assignments and 54.6% of the sleep stage assignments were correct, while using scaling analysis these numbers increased to 74.4% and 85.0%, respectively. We conclude that changes in HRV are better quantified by scaling analysis than by spectral analysis.

Adult↗
PubMed2000

Development of the control of breathing: implications for sleep-related breathing disorders in infants.

Abnormal development of the control of breathing has implications for the occurrence and severity of SDB during infancy. Prevention of prenatal insults such as nicotine exposure should be included in public health programs. Infants at risk for SDB or with symptoms of SDB should be investigated for peripheral and central chemoreceptor dysfunction. Peripheral chemoreceptor function can be assessed using either the hyperoxic test or the alternating breath test, and central chemoreceptor function using the rebreathing test. Optimal treatment of SDB in the developing infant is of central importance for preserving normal behavior and neurocognitive development. Oxygen supplementation and/or ventilatory support during sleep prevent uncontrolled episodes of hypoxemia, sleep fragmentation, and REM sleep reduction. Finally, alterations in homeostatic responses during development may have long-term effects on breathing during sleep in childhood and adulthood. In genetically-predisposed subjects, environmental conditions during the period of development of respiratory control mechanisms may add to the intrinsic vulnerability to SDB.

Arcuate Nucleus of Hypothalamus↗
PubMed2005

A double-blind study in healthy volunteers to assess the effects on sleep of pregabalin compared with alprazolam and placebo.

STUDY OBJECTIVES: To assess the effects of pregabalin compared with alprazolam and placebo on aspects of sleep in healthy volunteers. DESIGN: Randomized, double-blind, placebo- and active-controlled, 3-way crossover. SETTING: Single research center. PARTICIPANTS AND INTERVENTIONS: Healthy adult (12 men) volunteers (N=24) received oral pregabalin 150 mg t.i.d., alprazolam 1 mg t.i.d., and placebo t.i.d. for 3 days. MEASUREMENTS AND RESULTS: Objective sleep was measured by an 8-channel polysomnograph; subjective sleep was measured using the Leeds Sleep Evaluation Questionnaire. Compared with placebo, pregabalin significantly increased slow-wave sleep both as a proportion of the total sleep period and the duration of stage 4 sleep. Alprazolam significantly reduced slow-wave sleep. Pregabalin and alprazolam produced modest, but significant, reductions in sleep-onset latency compared with placebo. Rapid eye movement sleep latency after pregabalin was no different than placebo but was significantly shorter than that found with alprazolam. Although there were no differences between the active treatments, both pregabalin and alprazolam reduced rapid eye movement sleep as a proportion of the total sleep period compared with placebo. Pregabalin also significantly reduced the number of awakenings of more than 1 minute in duration. Leeds Sleep Evaluation Questionnaire ratings of the ease of getting to sleep and the perceived quality of sleep were significantly improved following both active treatments, and ratings of behavior following awakening were significantly impaired by both drug treatments. CONCLUSIONS: Pregabalin appears to have an effect on sleep and sleep architecture that distinguishes it from benzodiazepines. Enhancement of slow-wave sleep is intriguing, since reductions in slow-wave sleep have frequently been reported in fibromyalgia and general anxiety disorder.

Adolescent↗
PubMed1996

Hypersomnia following paramedian thalamic stroke: a report of 12 patients.

Paramedian thalamic stroke (PTS) is a cause of organic hypersomnia, which in the absence of systematic sleep-wake studies has been attributed to disruption of ascending activating impulses and considered a "dearoused" state. However, an increasing mount of data suggests a role of the thalamus in sleep regulation and raises the possibility that a sleep disturbance contributes to hypersomnia in PTS. We evaluated 12 patients with magnetic resonance imaging-proven isolated PTS and hypersomnia with 10 to >20 hours of sleep behavior per day. Nocturnal polysomnographic findings paralleled the severity of hypersomnia. All subjects had increased stage 1 NREM sleep, reduced stage 2 NREM sleep, and reduced numbers of sleep spindles. In patients with severe hypersomnia, slow-wave (stages 3-4) NREM sleep was often reduced, but there were no major REM sleep alterations. Daytime sleep behavior was associated mostly with stage 1 sleep by electroencephalogram; there was no correlation between hypersomnia and results of nap tests. We conclude that hypersomnia following PTS is accompanied by deficient arousal during the day and insufficient spindling and slow-wave sleep production at night. These observations support the hypothesis of a dual role of the paramedian thalamus as "final common pathway' for both maintenance of wakefulness and promotion of NREM sleep.

Adolescent↗
PubMed1996

Relationship of ventricular tachycardia to sleep/wakefulness in a model of sudden cardiac death.

Death from some childhood disorders such as sudden infant death syndrome and the congenital long QT syndrome are associated with specific behaviors such as sleep or emotional stress. We studied young German shepherd dogs that die suddenly during presumed sleep. These dogs have inherited ventricular tachycardia (VT) which is most frequent during sinus bradycardia and sinus arrhythmia. We hypothesized that the number of VT complexes (three or more consecutive ectopic complexes) would be greatest during sleep. Moreover, we hypothesized that pauses in the sinus rhythm of greater than 1000 ms would be greatest in the behavior with the most frequent VT. Behavioral states [excited, ambulatory, sitting, lying, rapid eye movement (REM) sleep] were quantified from 24-h video recordings of seven dogs. VT and pauses were quantified for each behavior using simultaneously recorded ECGs. A multivariate model was used to analyze the results. After controlling for time of day, lying, and REM sleep were significantly (p < 0.02) associated with VT, whereas more active behaviors were not. Time of day also independently affected the number of VT complexes. However, behavior and time of day did not account for all of the variability in the number of VT complexes. Pauses were significantly associated with behavior, with the highest number of pauses occurring during lying and REM sleep. However, pauses were not always associated with VT, indicating that a pause was a necessary, but not sufficient, condition for the development of VT. These results suggest that modulation of VT incidence in these animals is multifactorial and that the highest number of VT complexes is associated with the bradycardia that accompanies REM sleep.

Animals↗