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PubMed1989

Central alpha 1 adrenoceptor subtypes in narcolepsy-cataplexy: a disorder of REM sleep.

The present study suggests the specific involvement within the central nervous system of an alpha 1 adrenoceptor subtype in a behavior, the control of cataplexy, a pathological analogue of rapid eye movement (REM) sleep atonia. Experiments have shown that prazosin, an alpha 1 antagonist, dramatically aggravates canine narcolepsy-cataplexy through a central mechanism, and that [3H]prazosin binding sites are increased in the amygdala of narcoleptic dogs. However, the corresponding Scatchard plots were curvilinear and best fit was obtained with a two-site model, suggesting the existence of two [3H]prazosin binding sites. These two sites (high and low affinity [3H]prazosin binding sites) met the criteria for authentic receptors and were respectively very similar to the alpha 1a and alpha 1b (high and low affinity for WB4101, respectively) subtypes recently described in the rat and rabbit. Our results of in vivo pharmacology and in vitro [3H]prazosin binding in canine narcolepsy now clearly implicate the low affinity [3H]prazosin binding site (alpha 1b) in canine narcolepsy: (1) Prazosin, an alpha 1 antagonist with similar affinity for both subtypes, was much more potent in increasing cataplexy than WB4101, a compound with more affinity for the alpha 1a receptor. (2) Chlorethylclonidine and phenoxybenzamine, two irreversible blockers of the alpha 1 receptors with more affinity for the alpha 1b receptors, aggravate cataplexy for up to two weeks. (3) The alpha 1 receptor upregulation previously reported by our group in the amygdala of narcoleptic dogs was due to a selective increase in the low affinity [3H]prazosin binding sites. A role for noradrenaline in REM sleep regulation has been suspected for many years, but has never been clearly elucidated.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed2003

Parasomnias.

Parasomnias are common in the benign forms such as sleepwalking and sleep talking. The more dramatic forms such as sleep terrors and confusional awakenings occur frequently in childhood, but attenuate in the teen years. REM behavior disorder, seen in the elderly, is an uncommon entity. Generally diagnosis is based upon clinical history with sleep studies reserved for unusual presentation. The focus of treatment is attention to sleep hygiene with medication(s) reserved for more severe and repetitive cases.

Humans↗
PubMed2001

Initial demonstration of the accuracy and utility of an ambulatory, three-dimensional body position monitor with normals, sleepwalkers and restless legs patients.

Objective: To evaluate the accuracy and provide a pilot demonstration of the clinical utility of the BodyTrac, a new, ambulatory device that identifies body position and records and stores this data for a period of over 2 weeks.Background: Diagnosis and treatment evaluation of behavioral sleep-related events (BSREs) that occur with the major parasomnias such as sleepwalking, night terrors and REM behavior disorder have been hampered by the problems inherent in recording relatively rare events which are mostly not recalled by the patients. The number, time of occurrence and pattern of motor behavior for these events has, therefore, never been adequately described. Even the amount of nocturnal walking associated with the restless legs syndrome (RLS) has been hard to specify given the usual problems of night to night variability and in obtaining accurate, subjective reports. The newly developed BodyTrac monitor, by recording body position once every 30 s during a sleep period, provides an enabling technology for evaluating BSREs and may also enhance evaluation of nocturnal waking activities of RLS patients.Design and methods: Three test protocols were completed: an analog-type laboratory test of the BodyTrac's accuracy, an evaluation of seniors with and without sleep disorders, and, finally, evaluation of adult sleepwalkers and RLS patients including a full-night sleep lab assessment. The last two procedures also included monitoring in the home environment.Results and conclusions: The BodyTrac reliably and accurately identified both the wearer's body position (93% agreement with observer) and BSREs (sensitivity=100%, specificity=94-100%.) Patients were able to wear the BodyTrac during sleep in their home environment with minimal discomfort. The pilot data here suggest that some sleep walkers may have many small BSREs in addition to the larger events that are usually the only ones known to occur.

Journal Article↗
PubMed1997

Changes in sleep architecture following chronic mild stress.

Chronic exposure to mild unpredictable stress causes subsensitivity to rewards (anhedonia). These effects are reversible by chronic treatment with antidepressant drugs, and have been proposed as an animal model of depression. In the present study, sleep architecture, particularly the rapid eye movement (REM) component, was mapped in rats following exposure to chronic mild stress. The study used a unique large scale automated sleep system to record and analyze the sleep signals from 32 rats simultaneously. The effects of stress on sleep were maximal following 21 days of stress, at which time the stressed animals demonstrated decreases in active waking and deep sleep, and disruptions of REM sleep. The changes in REM sleep included increases in the duration of and transitions into REM sleep over the sleep part of the sleep-wake cycle, and most importantly, a reduced latency to the onset of the first REM period. These sleep abnormalities, and in particular the decrease in REM latency, are consistent with those reported in endogenous depression. The results provide further support for the validity of the chronic mild stress paradigm as an animal model to study the mechanisms underlying endogenous depression.

Animals↗
PubMed1983

Evidence for REM sleep deprivation as the mechanism of action of antidepressant drugs.

In the treatment of endogenous depression REM sleep deprivation and imipramine have similar efficacy. Across drugs, efficacy of antidepressant activity is directly related to capacity of drugs to produce large and sustained reductions of REM sleep. Endogenous depression unimproved by REM sleep deprivation is unimproved by imipramine. Endogenous depression improvement by REM sleep deprivation and by amitriptyline have the same biological correlate, viz, REM rebound. In animals REM sleep deprivation produces several behavioral changes (e.g., increased motor, sexual, aggressive, pleasure seeking, feeding activities) which are the reverse of behavioral changes of human endogenous depression.

Amitriptyline↗
PubMed1975

A review of REM sleep deprivation.

Studies on the behavioral consequences of rapid eye movement (REM) sleep deprivation in animals and humans are critically reviewed. In animals, converging evidence--some reasonably well controlled--indicates that REM sleep deprivation probably heightens central neural excitability and increased motivational behavior, but has nuclear or inconclusive effects on learning. In humans, evidence indicates that REM sleep deprivation is not dream deprivation and is not harmful to schizophrenic, depressed, or healthy subjects. Controversy continues about whether or not (some) schizophrenic patients respond abnormally to REM sleep deprivation by having no REM rebound. Controlled but unconfirmed work indicates that that endogenous, but not reactive, depressive patients are improved by REM sleep deprivation, a finding consistent with the animal behavioral consequences of the procedure and with the unique REM-depriving properties of efficacious antidepressant drugs.

Adjustment Disorders↗
PubMed1994

Polysomnographic studies of unmedicated depressed men before and after cognitive behavioral therapy.

OBJECTIVE: Differentiation of stable, trait-like characteristics from more episodic or state-dependent disturbances will be helpful in gaining a better understanding of the pathophysiology of depression. However, research in this area has been complicated by artifactual and clinical problems associated with pharmacologic treatment. In this investigation the authors used EEG sleep studies to assess medication-free depressed male patients before and after cognitive behavioral therapy. METHOD: Forty-five male patients with the diagnosis of major depression according to the DSM-III-R criteria and the Research Diagnostic Criteria underwent EEG sleep studies before and after 16 weeks of cognitive behavioral therapy, during which they were free of medication. In addition to the documentation of changes within these patients, the findings were compared with those for 47 healthy subjects, including 15 who were restudied 12-24 months after their baseline assessments. RESULTS: The EEG sleep profiles of the depressed patients showed a significant reduction in REM sleep density after treatment, suggesting "normalization" of an abnormal state-dependent process. By contrast, slow wave sleep and tonic REM measures, including reduced REM latency, were unchanged after treatment. CONCLUSIONS: These findings suggest that early in remission there is disaggregation of irreversible, trait-like correlates of depression (e.g., diminished slow wave sleep and reduced REM latency) from more reversible disturbances (e.g., increased REM density).

Adult↗
PubMed1997

Diagnosing rhythmic movement disorder with video-polysomnography.

We evaluated the utility of accurate clinical and electrophysiologic characterization in the diagnosis of the rhythmic movement disorder. Seven children with an age range of 1-12 years, referred for evaluation of relatively violent nocturnal behaviors, were clinically assessed during split-screen, video-polysomnographic monitoring sessions, as they experienced unusual nocturnus movements. Differential diagnoses included self-injurious waking behaviors, seizures, and parasomnias such as somnambulism (sleepwalking), pavor nocturnus (night terrors), and the rhythmic movement disorder (headbanging, bodyrocking, and legbanging). The character of movements, level of responsiveness, and electrophysiologic stage of sleep was determined during typical spells. In all the subjects experienced 37 periods of headbanging, bodyrocking, and legbanging that were strongly associated with stage 2 non-rapid eye movement sleep and K-complexes. The patients were unresponsive during and amnestic for the events. Because the differential for the rhythmic movement disorder includes a large number of disorders associated with abnormal and at times violent nocturnal movements, diagnosis can be greatly enhanced by documenting suspected nocturnal behaviors with thorough clinical assessment during split-screen, video-polysomnographic analysis.

Attention Deficit Disorder with Hyperactivity↗
PubMed1975

Individual differences in compensatory rebound of REM sleep, with particular reference to their relationship to personality and behavioral characteristics.

In subjecting 14 healthy university students to partial differential rapid eye movement (REM) sleep deprivation (PDRD), the compensatory rebound of REM sleep during the next night was determined, and showed fairly substantial individual differences in the increased percentage of REM sleep time. This rate was approximately the same for the same individual for two sleep recordings. These individual differences had no positive correlation with the decreased rate of REM time in the PDRD nights or with the percentage of REM time in the baseline night. Therefore, the individual differences in the increased percentage of REM time can be presumed to reflect individual differences in need for deprived REM sleep. Next, we looked into the relationship between the individual subject's personality and behavior characteristics, and his increased percentage of REM time. This revealed that the individuals who were extrovertive, active, optimistic, showy, and who had many friends had significantly higher increases in the percentage of REM time than the individuals who were introvertive, neurotic, inactive, nervous, modest, and who had few friends. Also discussed was the neurophysiological and biochemical basis of the central nervous system as the background for the relationship between the personality and behavioral characteristics and the increased percentage of REM sleep time.

Adult↗
PubMed2002

Sleep in posttraumatic stress disorder.

Posttraumatic stress disorder (PTSD) is often associated with sleep disturbances. In this review, we focus on the published literature on subjective and objective findings of sleep in patients with PTSD. Insomnia and nightmares are most commonly reported subjective sleep disturbances. Polysomnographic investigations have frequently reported rapid eye movement (REM) sleep abnormalities in PTSD. However, studies have not been consistent about the type of REM sleep dysfunction in PTSD patients. Antidepressants such as nefazodone, trazodone, fluvoxamine, and imagery rehearsal therapy are found to be beneficial in the treatment of PTSD associated sleep disturbances as well as core symptoms of this anxiety disorder. We propose use of such modalities of treatment in PTSD patients with predominant sleep disturbances. Further studies are required to clarify polysomnographic sleep changes especially role of REM sleep dysregulation and treatment of sleep disturbances in PTSD.

Antidepressive Agents↗
PubMed1992

Cocaine use and withdrawal: the effect on sleep and mood.

Three recreational cocaine users (age, 26.7 years), after one adaptation night, spent 5 days and nights in the laboratory where their EEG, EOG, and submental EMG were recorded during all of their sleep. On the second afternoon and evening of the study, subjects used an estimated 1 to 2 g cocaine intranasally. They all slept between 2:00 A.M. and 9:00 A.M. that night. Blood samples were drawn each evening and morning. Absolute plasma cocaine levels and patterns of elimination were consistent with subjects report of dose and time of administration. Mood ratings were made repeatedly throughout the study. There was suppression of REM sleep during the use of cocaine followed by a rebound which is specific to REM sleep and is not seen in other stages of sleep. REM variables subsided to normal levels on the third recovery night following cocaine use.

Adult↗
PubMed1986

Anorexia and altered serotonin metabolism in a patient with argininosuccinic aciduria.

We studied serotonin metabolism in a metabolically stable 7-year-old girl with argininosuccinic aciduria who had severe anorexia. The CSF concentration of 5-hydroxyindoleacetic acid (HIAA), the metabolite of serotonin, was markedly elevated at 79 ng/ml (normal 33 +/- 11 ng/ml). Altered serotonin metabolism was also reflected in the sleep EEG, which showed decreased REM sleep. Reducing her intake of tryptophan, the precursor of serotonin, from 35 mg/kg/day to 7 mg/kg/day resulted in a decrease in CSF concentration of HIAA to 20 ng/ml and the onset of spontaneous eating for the first time in 4 1/2 years. REM sleep increased from 3% to 9.5% of total sleep time. Two days after increasing tryptophan intake to 25 mg/kg/day, spontaneous feeding stopped, associated with a rise in CSF HIAA to 45 ng/ml. Caloric/carbohydrate intake was found to affect CSF HIAA levels and food intake in an additive manner with tryptophan intake. These observations suggest that altered serotonin metabolism affected feeding behavior in this child, and that this effect could be modified by changing tryptophan or carbohydrate intake.

Amino Acid Metabolism, Inborn Errors↗
PubMed2002

Microinjection of neostigmine into the pontine reticular formation of C57BL/6J mouse enhances rapid eye movement sleep and depresses breathing.

STUDY OBJECTIVES: The cholinergic model of rapid eye movement (REM) sleep has contributed significantly to understanding sleep neurobiology and sleep-dependent respiratory depression. The model has been used extensively in cat and rat, but no previous studies have demonstrated cholinergic REM sleep enhancement in mouse. The present study used microinjection of neostigmine into pontine reticular formation of mouse to test the hypothesis that enhancing pontine cholinergic neurotransmission would cause increased REM sleep and sleep disordered breathing. DESIGN: Mice (n=8) were anesthetized and implanted with electrodes for measuring cortical electroencephalogram (EEG). Stainless steel cannulae were stereotaxically implanted to permit subsequent microinjections of 50 nl neostigmine (0.133 microg; 8.8 mM) or saline into the pontine reticular formation. Following recovery, an intensive within-subjects design was used to obtain measures of sleep/wake states, breathing, and locomotor activity. Inferential statistics were provided by t-tests. A probability value of < 0.05 indicated statistical significance. SETTING: NA. PATIENTS OR PARTICIPANTS: NA. INTERVENTIONS: NA. MEASUREMENTS AND RESULTS: Behavioral observations and manual scoring of polygraphic recordings showed that neostigmine produced a REM sleep-like state. EEG power analysis using Fast Fourier Transformation confirmed that pontine neostigmine caused EEG activation. Plethysmography demonstrated significantly disordered breathing. Compared to waking, pontine microinjection of neostigmine decreased respiratory rate (-64%) and minute ventilation (-75%). Pontine neostigmine significantly increased duration of inspiration (138%) and expiration (140%) above waking levels and decreased inspiratory flow (-69%). Additional studies showed that pontine neostigmine significantly depressed locomotor activity. CONCLUSIONS: This study is the first to demonstrate cholinergic REM sleep enhancement in unanesthetized, intact mouse. The results encourage future studies to characterize similarities and differences in cholinergic REM sleep enhancement in additional inbred strains and in transgenic mice. Such comparisons will help characterize sleep and breathing as intermediate phenotypes that are determined, in part, by the lower level phenotype of pontine cholinergic neurotransmission.

Animals↗