Showing papers on "Non-rapid eye movement sleep published in 1986"

Chronic behavioral disorders of human REM sleep: a new category of parasomnia.

Abstract: Four men, aged 67-72 years, had 4-month to 6-year histories of injuring themselves or their spouses with aggressive behaviors during sleep, often during attempted dream enactment. A 60-year-old woman had disruptive though nonviolent sleep and dream behaviors. Polysomnography did not detect seizures but did document REM sleep pathology with variable loss of chin atonia, extraordinarily increased limb-twitch activity, and increased REM ocular activity and density. A broad range of REM sleep behaviors was recorded on videotape, including stereotypical hand motions, reaching and searching gestures, punches, kicks, and verified dream movements. Stage 3-4 slow wave sleep was elevated for age in all patients. NREM sleep was devoid of harmful behaviors, although three men had periodic myoclonus. There was no associated psychiatric disorder, whereas serious neurologic disorder was closely associated in four cases: olivo-ponto-cerebellar degeneration, Guillain-Barre syndrome, subarachnoid hemorrhage, and an atypical dementia. Two patients had immediate and lasting sleep behavioral suppression induced by clonazepam, and another patient had the same response with desipramine. All instances of drug discontinuation prompted immediate relapse. In four cases there was associated dream hyperactivity, which resolved with behavioral control. These REM sleep neurobehavioral disorders constitute another category of parasomnia, replicate findings from 21 years ago in cats receiving pontine tegmental lesions, and offer additional perspectives on human behavior, neurophysiology, pharmacology, and dream phenomenology.

Control of breathing during sleep

Abstract: The sections in this article are: 1 Sleep-Wakefulness States 1.1 Identification and Organization 1.2 Mechanisms and Functions 2 Central Neuronal Sleep-Respiratory Interactions 3 Respiratory Muscle Function 3.1 General Concepts 3.2 Diaphragm and Intercostal Muscles 3.3 Upper Airway Muscles 4 Ventilation and Gas Exchange 4.1 NREM Sleep 4.2 REM Sleep 5 Pattern of Breathing 5.1 NREM Sleep 5.2 REM Sleep 6 Ventilatory Responses to Respiratory Stimuli 6.1 Response to CO2 6.2 Response to Hypoxia 6.3 Response to Upper Airway Stimulation 6.4 Response to Bronchopulmonary Stimulation 6.5 Response to Chest Wall Stimulation 6.6 Response to Thermal Stimuli 7 Arousal Responses to Respiratory Stimuli 7.1 Arousal Thresholds 7.2 Mechanisms of Arousal 7.3 Physiological Importance

Induction of periodic breathing during sleep causes upper airway obstruction in humans

Abstract: To test the hypothesis that occlusive apneas result from sleep-induced periodic breathing in association with some degree of upper airway compromise, periodic breathing was induced during non-rapid-eye-movement (NREM) sleep by administering hypoxic gas mixtures with and without applied external inspiratory resistance (9 cmH2O X l-1 X s) in five normal male volunteers. In addition to standard polysomnography for sleep staging and respiratory pattern monitoring, esophageal pressure, tidal volume (VT), and airflow were measured via an esophageal catheter and pneumotachograph, respectively, with the latter attached to a tight-fitting face mask, allowing calculation of total pulmonary system resistance (Rp). During stage I/II NREM sleep minimal period breathing was evident in two of the subjects; however, in four subjects during hypoxia and/or relief from hypoxia, with and without added resistance, pronounced periodic breathing developed with waxing and waning of VT, sometimes with apneic phases. Resistive loading without hypoxia did not cause periodicity. At the nadir of periodic changes in VT, Rp was usually at its highest and there was a significant linear relationship between Rp and 1/VT, indicating the development of obstructive hypopneas. In one subject without added resistance and in the same subject and in another during resistive loading, upper airway obstruction at the nadir of the periodic fluctuations in VT was observed. We conclude that periodic breathing resulting in periodic diminution of upper airway muscle activity is associated with increased upper airway resistance that predisposes upper airways to collapse.

Excessive daytime sleepiness and the pathophysiology of narcolepsy-cataplexy: a laboratory perspective.

Abstract: The main disabling symptom of narcolepsy-cataplexy is shown to be the unrelenting excessive daytime sleepiness (EDS) based upon controlled studies of socioeconomic effects and the poor response to treatment. Objective performance deficits mainly involve tests of ability to sustain performance on repetitive boring tasks and are reversible by improved alertness. Physiologically, EDS is seen to represent relatively slow waxing and waning of alertness rather than punctate microsleeps. Evidence is provided for complex cerebral evoked potentials (P300, contingent negative variation) being very sensitive EDS measures comparable to the multiple sleep latency test (MSLT). EDS appears to have qualitatively somewhat different forms mainly reflecting pressure for REM sleep (REM sleepiness) or pressure for NREM sleep (NREM sleepiness), which have different effects on cerebral evoked potentials as well as subjective and objective (MSLT) differences. It is argued that in pathophysiological terms narcolepsy may best be considered a disease of state boundary control.

Hypnotic activity of an imidazo-pyridine (zolpidem).

Abstract: Effects of an imidazo-pyridine (zolpidem: 10, 20 and 30 mg) on overnight sleep and on performance the next day were studied in young adults and in middle aged individuals. The young adults were used particularly as an homogenous group to establish any possible adverse effects of the drug on sleep and on performance the next day, and the middle aged subjects with their less restful sleep were used to study efficacy. In the young adults zolpidem led to a marked increase in slow wave sleep with a reduction in stage 2 sleep. There were no significant changes in REM sleep, though there was a tendency for REM sleep to be delayed. In the middle aged there was a reduction in awake activity and drowsy sleep with an increase in stage 2 sleep. The latency to REM sleep was increased but the duration of REM sleep over the whole night was not reduced. Digit symbol substitution and a complex reaction time task were used to study performance, but there were no residual effects with zolpidem (9 h after ingestion). Zolpidem is likely to prove useful in the management of transient and short-term insomnia in healthy middle aged individuals when impaired performance the next day is to be avoided.

Paroxysmal awakenings from sleep associated with excessive daytime somnolence A form of nocturnal epilepsy

Abstract: We describe 14 hypersomniac patients whose polysomnographic recordings revealed abnormal EEG patterns consisting of paroxysmal epileptic discharges during stages 2 and 3 of NREM sleep, associated with arousals, fragmentation of sleep, and reduction in sleep efficiency, particularly REM sleep. Three patients who received anticonvulsants showed clinical and polysomnographic documented improvement in sleep patterns. These patients probably had a unique form of nocturnal epilepsy-related sleep disorder, manifested by paroxysmal wakenings from sleep.

Effects of H1- and H2-histamine receptor agonists and antagonists on sleep and wakefulness in the rat

Abstract: The H 1-receptor agonist 2-thiazolylethylamine (2-TEA) given by i.c.v. route dose-dependently increased wakefulness (W) and decreased NREM sleep (NRMS) and REM sleep (REMS) in rats prepared for chronic sleep recordings. The H 1-receptor antagonists pyrilamine and diphenhydramine given by i.p. route decreased W and increased NREMS. Pyrilamine prevented the increase of W and decrease of NREMS produced by 2-TEA. However, REMS reduction was not antagonized, what tends to suggest that two different mechanisms could be involved in the 2-TEA-induced effects on NREMS and REMS. Cimetidine which blocks H 2-receptors, when given by i.p. route showed no significant effects on sleep and W. Administration of the H 2-receptor agonist dimaprit and the H 2-receptor antagonists cimetidine, metiamide and ramtidine by i.c.v. route induced the appearance of high voltage spikes at cortical leads, thus leaving inconclusive the matter of their effects on sleep and wakefulness. Our results tend to support the proposal that the H 1-receptor intervenes in sleep-wakefulness regulation. Limitations in the available H 2-receptor agonists and antagonists presently preclude a more detailed analysis of the role of H 2-receptors on sleep and W.

Electroencephalographic Sleep in Psychotic Depression: A Valid Subtype?

Abstract: • Electroencephalographic (EEG) sleep patterns were examined in 27 psychotic and 79 nonpsychotic subjects with major depression to evaluate the validity of the psychoticnonpsychotlc subtype dichotomy. Sleep in psychotic depression was characterized by increased wakefulness, decreased rapid eye movement (REM) sleep percentage, and decreased REM activity even after controlling for clinical differences in age, severity, and agitation. Psychotic depressive subjects also were more likely to have extremely short sleep-onset REM latencies. In psychotic depression EEG sleep varied as a function of total illness duration. Patients with recent-onset syndromes had profiles characterized by marked initial insomnia, Increased stage 1 sleep percentage, and long REM latency; patients with illnesses of longer duration had extremely short REM latencies. Demonstration of selected EEG sleep variables discriminating between psychotic and nonpsychotic depression further supports psychotic depression as a distinct subtype of major affective disorder.

Olivopontocerebellar degeneration, abnormal sleep, and REM sleep without atonia

Abstract: Polygraphic studies during sleep performed in two patients with olivopontocerebellar degeneration (OPCD) revealed an abnormal control of muscle tone. It was demonstrated by bursts of EMG activity during sleep and progressive disappearance of muscle atonia during sleep. Muscle atonia disappeared during rapid eye movement (REM) sleep, permitting movements and expression of feelings probably associated with REM sleep-related oneiric activity. Patients, unaware of their nocturnal sleep disturbance, complained only of the resulting daytime tiredness and sleepiness.

Sleep apnea in narcolepsy.

Abstract: Polysomnographic and multiple sleep latency studies documented recurrent apneic episodes during NREM sleep stages 1 and 2 and REM sleep in 11 of 16 narcoleptic patients. Episodes were predominantly central, but obstructive and mixed events were also observed. Apneas were accompanied by mild to moderate oxygen desaturation.

Benign neonatal sleep myoclonus. Relationship to sleep states.

Abstract: Neonatal sleep myoclonus is a benign syndrome characterized by myoclonic jerks occurring only during sleep and presenting in the first month of life. There are no associations with abnormal development, neurologic deficits, or seizures. The electroencephalogram is normal and has no correlation with the myoclonic jerks. The myoclonus is present in all sleep states although its frequency is state dependent and greatest during quiet sleep. It is not associated with an arousal response as previously thought. Transient serotonin imbalance and genetic factors might play a role in the pathogenesis of this disorder.

A psychophysiological study of insomnia.

Abstract: Ten insomniacs with age- and sex-matched controls had studies of baseline sleep, relation of polygraphically defined sleep to retrospective reports, and arousal thresholds to electronic tones or to a recording of a voice calling out the subject's name. The two groups differed in 10 out of 13 questions about habitual sleep and daytime feelings. In contrast, polygraphic measures of baseline sleep indicated only that insomniacs tended to have slightly less total sleep and had a small but significant increase in early morning awakening time. Unlike the descriptions of habitual sleep, the subjects' retrospective reports of the previous night's sleep differed significantly only for the variable of total sleep time, and there were virtually no differences in the description of their status at a given moment. Auditory arousal thresholds were similar in the two groups, and both went back to sleep and stayed asleep with equal facility. These findings suggest that subjectively poor sleep is not necessarily "light" sleep. For both groups, arousal thresholds differed across the sleep stages, and thresholds to hearing the subject's name were lower than those in response to electronic tones. Although insomniacs had as much polygraphically defined sleep as controls between the forced awakenings of the arousal threshold studies, they perceived their sleep to be only approximately half as long. Insomniacs described themselves as having been awake more frequently than controls in 8 out of 10 forced awakening situations. In one case, insomniacs also overestimated the time between awakenings. In both groups, there was little relationship between reported habitual aspects of sleep and baseline polygraphically defined sleep variables. On questionnaires the following mornings, however, in both groups there was a positive correlation of subjective quality of sleep on the baseline nights with percentage of rapid eye movement sleep, and a negative correlation to various aspects of slow-wave sleep.

A dose-response study of sleep loss and spontaneous sleep termination.

Abstract: Recent concepts of sleep/wake regulation have emphasized circadian influences and largely disregarded homeostatic ones. The present experiment was designed to study sleep loss homeostasis while minimizing confounding circadian influences. Eight male subjects participated in the study. Night sleep was curtailed across four conditions to yield 0, 2, 4, or 8 hrs of sleep. The effects were studied on subsequent day sleep begun at 1100h and spontaneously terminated. Total sleep time (TST), Stage 2 (S2), and Stages 3+4 (SWS) showed very strong dose-dependent increases with increasing loss. REM sleep did not respond. After maximum sleep loss TST and S2 doubled whereas SWS increased fivefold. Sleep did not terminate until the prior loss of SWS had been recovered. The total SWS recovery approximately matched the loss. TST, S2, and REM failed to recover more than limited amounts of the loss. The results show that homeostatic influences on sleep may be much larger than usually acknowledged and that SWS closely, although not perfectly, reflects the “active component’ of sleep homeostasis.

Sleep and posttraumatic rheumatic pain modulation disorder (fibrositis syndrome).

Abstract: The clinical features and sleep physiology of 11 female patients with "fibrositis syndrome" or rheumatic pain modulation disorder (RPMD) were compared with 11 female postaccident pain (PAP) patients who complained of widespread musculoskeletal pain, fatigue, and nonrestorative sleep following a nonphysically injurious motor vehicle or work-related accident. Both groups had similar musculoskeletal pain, fatigue, sleepiness and an alpha (7.5-11 Hz) EEG non-rapid eye movement (NREM) sleep anomaly. A psychophysiologic arousal mechanism during NREM sleep induced by the emotional stress of the accident may mediate the subsequent nonrestorative sleep, musculoskeletal pain, and fatigue symptoms in the posttraumatic pain disorder.

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

Abstract: 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.

Sleep alterations in ischemic stroke.

Abstract: In 19 patients with cerebral infarctions in the middle cerebral artery territory, investigations of sleep using a mobile EEG recording system were performed. Sleep was found to be markedly altered compared to a normal group. Although an increase of time in bed and sleep period time was observed, total sleep time did not rise in a parallel manner, so that a distinct reduction of the sleep efficiency index was found. This increase of quantitative parameters was particularly caused by a higher amount of NREM time, whereas REM sleep was found to be deeply suppressed. Regarding the different NREM sleep stages, stage 0 (time spent awake during the night) and stage 1 had increased, whereas stage 4 was reduced. Inter-hemispheric differences were noticed referring to the sleep period time, which was found to be increased particularly in right-sided infarctions (because of an increase of NREM time) and a reduction of REM sleep in lesions of the right hemisphere (worsening of the REM to NREM ratio). Slow-wave sleep (stage 4), on the contrary, was found to be decreased in infarctions of the left hemisphere. These results support the hypothesis of a REM-inducing and regulating function of the right hemisphere and will lead to a new understanding of sleep-controlling mechanisms.

Aspects of short REM latency in affective states: A revisit

Abstract: Electroencephalographic (EEG) sleep changes in affective disorders have been characterized by sleep continuity, slow wave sleep, and rapid eye movement (REM) abnormalities. The most commonly cited feature, however, has been shortened REM latency. Because the diagnostic and prognostic significance of shortened REM latency has been debated, this issue was reexamined in a group of 186 psychotic and nonpsychotic depressed inpatients and outpatients. The analyses suggest an increased frequency of sleep onset REM periods in psychotic depression and in elderly depressed patients (psychotic or nonpsychotic).