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Results for “REM Sleep Behavior Disorder”

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PubMed1993

Heterozygosity at the canarc-1 locus can confer susceptibility for narcolepsy: induction of cataplexy in heterozygous asymptomatic dogs after administration of a combination of drugs acting on monoaminergic and cholinergic systems.

Narcolepsy is a genetically determined disorder of sleep characterized by excessive daytime sleepiness and abnormal manifestations of REM sleep that affects both humans and animals. Although its exact pathophysiologic mechanisms remain undetermined, recent experiments have demonstrated that in both humans and canines, susceptibility genes are linked with immune-related genes. A striking difference, however, is that the genes thought to be involved in the human pathology are autosomal dominant, whereas canine narcolepsy in Dobermans is transmitted as a single autosomal recessive gene with full penetrance (canarc-1). In this study, we have examined the development of narcoleptic symptoms in homozygous narcoleptic, heterozygous, and control Dobermans. Animals were behaviorally observed until 5 months of age and then treated at weekly intervals with cataplexy-inducing compounds that act on cholinergic or monoaminergic systems (alone and in combination). Our data indicate that cataplexy can be induced in 6-month-old asymptomatic heterozygous animals, but not in control canines, with a combination of drugs that act on the monoaminergic and cholinergic systems. This demonstrates that disease susceptibility may be carried by heterozygosity at the canarc-1 locus. Our data further suggest that cataplexy, a model of REM sleep atonia, is centrally regulated by a balance of activity between cholinergic and monoaminergic neurons.

Aging↗
PubMed1984

Distribution of REM latencies and other sleep phenomena in depression as explained by a single ultradian rhythm disturbance.

The McCarley-Hobson model, describing the alternation of NREM and REM sleep in the cat, was applied to human electroencephalographic data. The influence of initial conditions on oscillatory behavior was especially emphasized. It appears that the distribution of REM latency in depression, the abnormal accumulation of REM sleep, the variability of NREM-REM cycle duration, the frequent stage shifts, and frequent awakenings can be explained in this model by means of a decrease in the initial value of a single variable, which may be regarded as representing the strength of REM inhibition. The observation of slow wave sleep deficiency in depression may well be another reflection of this parameter.

Biological Clocks↗
PubMedDate not supplied

The revised monoamine hypothesis: mechanism of antidepressant treatment in the context of behavior.

The temporal restoration of brain monoamines in the synaptic cleft due to MAO inhibition or by blocking catecholamine reuptake is only the first step on the way to recovery from depression. The second and crucial step represents the feedback system, which can provide the continuous restoration of brain monoamines in the context of free search behavior. This feedback system on the one hand helps to overcome depression and on the other hand causes the hyposensitivity of the postsynaptic catecholamine (CA) receptors, due to the increased activity of the brain CA system. According to the search activity concept, REM sleep in the healthy subject, being a part of the same feedback system, restores brain monoamines. The mechanism of REM sleep deprivation in the treatment of depression is discussed in the context of this feedback system.

Animals↗
PubMed1999

Prenatal stress is associated with depression-related electroencephalographic sleep changes in adult male rats: a preliminary report.

1. Prenatal stress in rats has been shown to produce long-term behavioral, neuroendocrine and neurochemical changes. These changes may model aspects of human depressive illness. 2. In this pilot investigation, adult male offspring exposed to stress in utero and non-stressed controls were studied using 24-hour electroencephalographic sleep recordings. 3. Prenatally stressed animals demonstrated reduced latency to the onset of rapid eye movement (REM) sleep, prolongation of the first REM episode, and diminished slow-wave sleep. 4. Although preliminary, the observed changes parallel those seen in studies of human depression. These data further support the face validity of the prenatal stress model as a potential tool for future studies on the pathophysiology of depressive disorder.

Animals↗
PubMed1980

Preliminary trial of the noradrenergic agonist clonidine in psychiatric patients.

The hypotensive drug clonidine, which stimulates central alpha-adrenergic receptors, was administered to psychiatric patients in a preliminary double-blind study. Two schizophrenic patients became more agitated and aggressive during the trial. The drug showed some antidepressant effects in three of five depressed patients. Clonidine withdrawal appeared to potentiate symptoms in a manic patient. Drug treatment reduced blood pressure and rapid eye movement sleep. Interpretation of behavioral effects of clonidine is limited by uncertainty about the balance of its pre- and postsynaptic effects.

Adult↗
PubMed2001

Delta sleep EEG in depressed adolescent females and healthy controls.

BACKGROUND: Quantitative EEG studies have identified a number of sleep abnormalities in adults with major depressive disorders (MDD), including a reduction in the amplitude of delta activity during NREM sleep. To date, these methodologies have not been used in early onset MDD. METHODS: Delta activity during NREM sleep was compared in eight symptomatic but unmedicated adolescent females with MDD and eight age- and gender-matched healthy controls. RESULTS: The depressed group showed significantly lower delta amplitude and power in the first NREM sleep period. By contrast, standard sleep architecture did not differentiate between groups. LIMITATIONS: Given the sample size, this study is best viewed as tentative. In addition, it has yet to be determined whether adolescent males with MDD also show delta sleep abnormalities. Further, failure to find between-group differences in REM latency or other macroarchitectural measures may be due to the small sample size. CONCLUSIONS: The findings of this study underscore the utility of quantitative sleep EEG techniques in early onset MDD. The results of the present study do, however, diverge from reports in adults with MDD, where delta abnormalities are more prevalent in men. Such findings suggest that the maturational time course of sleep EEG disturbances may differ for males and females with depression. Early emergence of delta abnormalities in depression may be of relevance to clinical course of illness.

Adolescent↗
PubMed1977

Neuroticism and dreaming sleep: a case for interactionism in personality research.

The value of a trait approach to sleep and dreaming characteristics is evaluated by reviewing recent research on differential patterns and interactions manifest by high and low neuroticism subjects. Differential patterning of dream content and REM sleep characteristics under positive and negative presleep conditions suggest a qualitative difference in experience and behavior, and a quantitative difference in "importance" attributable to the dreaming sleep process. It is hypothesized that, under "normal" conditions, low neuroticism individuals make more exclusive use of the dreaming period, while under "artificial" conditions, they demonstrate a greater motivation to compensate for restricted REM by intensification of the REM process (shortened REM onset latencies, greater REM rebound, intensified dream experiences). Finally, it is suggested that theories of dreaming sleep should recognize the importance of traits, as well as situational factors to the psychology of dreaming sleep.

Affect↗
PubMed2004

Effect of cognitive behavioural therapy for insomnia on sleep architecture and sleep EEG power spectra in psychophysiological insomnia.

There is now an overwhelming preponderance of evidence that cognitive behavioural therapy for insomnia (CBT-I) is effective, as effective as sedative hypnotics during acute treatment (4-8 weeks), and is more effective in long term (following treatment). Although the efficacy of CBT-I in the treatment of chronic insomnia is well known, however there is little objective data on the effects of CBT-I on sleep architecture and sleep EEG power densities. The present study evaluated, first, subjective change in sleep quality and quantity, and secondly the modifications occurring in polysomnography and EEG power densities during sleep after 8 weeks of CBT-I. Nine free drug patients with psychophysiological insomnia, aged 33-62 years (mean age 47 +/- 9.7 years), seven female and two male participated in the study. Self-report questionnaires were administered 1 week before and 1 week after CBT-I, a sleep diary was completed each day 1 week before CBT-I, during CBT-I and 1 week after CBT-I. Subjects underwent two consecutive polysomnographic nights before and after CBT-I. Spectral analysis was performed the second night following 16 h of controlled wakefulness. After CBT-I, only scales assessing insomnia were significantly decreased, stages 2, REM sleep and SWS durations were significantly increased. Slow wave activity (SWA) was increased and the SWA decay shortened, beta and sigma activity were reduced. In conclusion CBT-I improves both subjective and objective sleep quality of sleep. CBT-I may enhance sleep pressure and improve homeostatic sleep regulation.

Adult↗
PubMed2005

Assessment and treatment of nocturnal panic attacks.

Nocturnal panic (NP), waking from sleep in a state of panic, is a common occurrence among patients with panic disorder, with 44-71% reporting at least one such attack. NP is a non-REM event that is distinct from sleep terrors, sleep apnea, nightmares or dream-induced arousals. This review outlines recent advances in the characterization of NP, as well as current approaches to the assessment and treatment of NP. In contrast to earlier work, more recent studies suggest that patients with NP do not differ from patients without NP on sleep architecture, sleep physiology, self-reported sleep quality and severity of panic disorder. However, more precise measurement of physiological precipitants and features is warranted. Assessment of NP focuses on ruling out other explanations for NP, with differential diagnosis based on interviews, sleep polysomnography and ambulatory recording of sleep. Psychological treatment (cognitive-behavioral therapy) targets misappraisals of anxiety sensations, hyperventilatory response, and conditioned reactions to internal, physical cues. Recent evidence supports the efficacy of this approach, however, controlled studies on pharmacological agents in the treatment of NP are lacking. Research is needed to examine the effects of combined cognitive-behavioral therapy and medications, compared to medication alone in the treatment of NP.

Antidepressive Agents↗
PubMed1980

A review of psychophysiology in early onset psychosis.

Research on psychophysiological functioning in early onset psychosis is reviewed within the context of etiological formulations stressing perceptual and selective attention abnormalities. Electroencephalographic (EEG) measures, including resting EEG level, alpha blocking, average evoked response, and contingent negative variation, have received most attention in the literature; cardiovascular and electrodermal indices have not been so extensively explored in this group of children. While the nature of differential reactivity in early onset psychosis has not been thoroughly investigated, limited evidence suggests that the central behavioral anomalies associated with the condition may result from abnormal neurophysiological reactivity to sensory stimulation. Further studies of the psychophysiological functioning of these children should yield data useful in the clarification of etiology.

Adolescent↗
PubMed2001

Polysomnographic effects of adjuvant ginkgo biloba therapy in patients with major depression medicated with trimipramine.

Sleep disturbance and cognitive impairment are frequent complaints of depressed patients under standard antidepressant medication. Therefore, additional therapies are required which specifically focus on the improvement of these deficits without exerting major side effects. Ginkgo biloba extract (EGb) has been shown to improve cognitive abilities in elderly subjects and in patients with disorders of the dementia spectrum. Animal studies surmise that EGb may reduce CRH activity, which is substantially related to depressive mood and behavior, predominantly cognition and sleep. An open non-randomized pilot study has been conducted to investigate the effects of ginkgo biloba extract (EGb Li 1370) on cognitive performance and sleep regulation in depressed inpatients. 16 patients were treated with a trimipramine (T)-monotherapy (200 mg) for six weeks. In eight of the 16 patients, an adjunct EGb therapy (240 mg/d) was applied for four weeks after a baseline week, the other eight patients remained on trimipramine monotherapy (200 mg) during the entire study. Polysomnography, cognitive psychomotor performance and psychopathology were assessed at baseline, after short-term and long-term adjunct EGb treatment, and after one week of ginkgo discontinuation (at the respective evaluation times in the eight patients on T-monotherapy). This report focuses on the results of EGb on sleep EEG pattern. EGb significantly improved sleep pattern by an increase of sleep efficiency and a reduction of awakenings. In addition, sleep stage 1 and REM-density were reduced, while stage 2 was increased. Non-REM sleep, predominantly slow wave sleep in the first sleep cycle, was significantly enhanced compared to trimipramine monotherapy. Discontinuation of EGb reversed most of these effects. Based on the animal data, these results suggest that EGb may improve sleep continuity and enhance Non-REM sleep due to a weakening of tonic CRH-activity. The compensation of the deficient Non-REM component in depression by the EGb application may provide a new additional treatment strategy, especially in the treatment of the depressive syndrome with sleep disturbance.

Adult↗
PubMed2001

Genetic ablation of orexin neurons in mice results in narcolepsy, hypophagia, and obesity.

Orexins (hypocretins) are a pair of neuropeptides implicated in energy homeostasis and arousal. Recent reports suggest that loss of orexin-containing neurons occurs in human patients with narcolepsy. We generated transgenic mice in which orexin-containing neurons are ablated by orexinergic-specific expression of a truncated Machado-Joseph disease gene product (ataxin-3) with an expanded polyglutamine stretch. These mice showed a phenotype strikingly similar to human narcolepsy, including behavioral arrests, premature entry into rapid eye movement (REM) sleep, poorly consolidated sleep patterns, and a late-onset obesity, despite eating less than nontransgenic littermates. These results provide evidence that orexin-containing neurons play important roles in regulating vigilance states and energy homeostasis. Orexin/ataxin-3 mice provide a valuable model for studying the pathophysiology and treatment of narcolepsy.

Animals↗
PubMed2001

Clinical and polysomnographic characteristics of 34 patients with Kleine-Levin syndrome.

There is only scant information on sleep characteristics and long-term follow-up in patients with Kleine-Levin syndrome (KLS). This study describes the clinical course, results of polysomnography and long-term follow-up in a relatively large group of patients with KLS. During the years 1982-97, we encountered 34 patients (26 males and eight females) with KLS. We were able to obtain the original polysomnographs from 28 males and four females. In 25 patients, data regarding their present state of health were obtained. Fourteen agreed to be present at a detailed interview and examination while 11 gave the information by phone. The mean age at onset was 15.8 +/- 2.8 years and the mean diagnostic delay, 3.8 +/- 4.2 years. The mean duration of a single hypersomnolent attack was 11.5 +/- 6.6 days. The main abnormal findings extracted out of 35 polysomnographs obtained from 32 patients during and/or in-between attacks included: decreased sleep efficiency, and frequent awakenings from sleep stage 2. All 25 patients reported present perfect health, with no evidence of behavioral or endocrine dysfunction. In adolescents with periodic hypersomnia, the diagnosis of KLS should be explored. Sleep recordings during a hypersomnolent period will often show frequent awakenings from sleep stage 2. The long-term prognosis is excellent.

Adult↗
PubMed1991

Neuronal activity in narcolepsy: identification of cataplexy-related cells in the medial medulla.

Narcolepsy is a neurological disorder characterized by sleepiness and episodes of cataplexy. Cataplexy is an abrupt loss of muscle tone, most often triggered by sudden, strong emotions. A subset of cells in the medial medulla of the narcoleptic dog discharged at high rates only in cataplexy and rapid eye movement (REM) sleep. These cells were noncholinergic and were localized to ventromedial and caudal portions of the nucleus magnocellularis. The localization and discharge pattern of these cells indicate that cataplexy results from a triggering in waking of the neurons responsible for the suppression of muscle tone in REM sleep. However, most medullary cells were inactive during cataplexy but were active during REM sleep. These data demonstrate that cataplexy is a distinct behavioral state, differing from other sleep and waking states in its pattern of brainstem neuronal activity.

Animals↗
PubMed1986

Light treatment in depressive illness. Polysomnographic, psychometric and neuroendocrinological findings.

Objective and subjective quality of sleep and awakening as well as circadian rhythms in cortisol, temperature and well-being were investigated in 10 female hospitalized depressed patients diagnosed as major depressive disorders according to RDC criteria before (baseline), during (intervention) and after (recovery) treatment with biologically active or bright light (BL) and were compared with the findings in 10 normals. Polysomnographic evaluation demonstrated in depressed patients an increased sleep latency, decreased total sleep time, attenuated S4 and augmented REM sleep, as well as a shortened REM latency and a statistically significant increased average REM length as compared with normals. BL tended to shorten sleep onset, decrease number of awakenings, increase REM latency and significantly attenuated the average REM length. Subjective sleep quality tended to improve as did the subjective awakening quality after the recovery night. There was, however, a statistically significant improvement of the objectively evaluated quality of awakening and early morning behavior characterized by an improved attention, reaction time and performance in the reaction time task, while concentration and psychomotor activity tended to improve as as well. BL effects were also seen in hormonal secretion patterns: circadian cortisol secretion maxima occurred earlier in depressed patients than in normals before and after BL treatment, while during BL intervention this difference disappeared. Circadian temperature rhythms did not exhibit any significant findings with the exception of an earlier occurring minimum in depressed patients than in normals after treatment. Finally, subjective well-being as rated by means of an analogue scale was significantly worse in depressed patients than normals before but not during and after light treatment. The findings are discussed.

Adult↗
PubMed2000

Parasomnias. Managing bizarre sleep-related behavior disorders.

Sleep can be a troubling experience for persons plagued by nocturnal disorders known as parasomnias. While they are "asleep," such persons may be walking, screaming in terror, rearranging furniture, eating odd food concoctions, or wielding weapons. Or they may be unable to fall asleep because of the unpleasant sensations of restless legs syndrome. Although these disorders are indeed bizarre, effective treatments are available. In this article, Drs Schenck and Mahowald discuss the evaluation and treatment of parasomnias and provide illustrative patient vignettes from their extensive experience at a sleep disorders center.

Aged↗
PubMedDate not supplied

Is alexithymia a disconnection syndrome? A neuropsychological perspective.

Efforts to relate the syndrome of alexithymia to cerebral dysfunction have generally taken the form of comparing the literal, concretistic, nonimaginative and affect-impoverished cognitive and communicative style of alexithymic patients to similar types of behavior seen in individuals with right-hemisphere damage or commissural disconnection. It is argued that the formulation of a neuropsychological typology of psychiatric syndromes like alexithymia has much heuristic merit as long as appropriate theoretical and methodological caution is exercised in drawing inferences about patterns of cerebral organization in nonneurological populations.

Affective Symptoms↗
PubMed2000

Clinical approach to excessive daytime sleepiness.

Subjective sleepiness is defined as "an elemental feeling state" by which the subject, and only him/her knows whether he/she is alert or sleepy. Subjective sleepiness has little been used for the clinical evaluation of sleepiness. Objective sleepiness is defined as a consequence of the homeostatic need for sleep. In the absence of a measurable marker of the fulfillment of the function of sleep, the evaluation of objective sleepiness has to rely on a behavioral approach based on the postulate that the more you need sleep (i.e., the sleepier you are), the more likely you are to fall asleep. However, as for many other fundamental human behaviors (drinking, eating, sexual behavior), it is likely that the sleeping behavior serves other purposes than its primary objective, which distorts the relationship between the observed sleeping behavior and the actual need for sleep. The likelihood to fall asleep can be measured by the speed with which a sleep episode occurs under standardized laboratory conditions (multiple sleep latency test, maintenance of wakefulness test, OSLER test), or by the frequency of unwanted sleep episodes under the more naturalistic conditions of daily life (Epworth Sleepiness Scale). These various approaches have advantages and drawbacks, but none of them can be considered the "gold standard".

Chronic Disease↗