Showing papers on "Slow-wave sleep published in 1996"
TL;DR: The correlated activity of rat hippocampal pyramidal cells during sleep reflects the activity of those cells during earlier spatial exploration and this memory for temporal order of neuronal firing could be produced by an interaction between the temporal integration properties of long-term potentiation and the phase shifting of spike activity with respect to the hippocampal theta rhythm.
Abstract: The correlated activity of rat hippocampal pyramidal cells during sleep reflects the activity of those cells during earlier spatial exploration. Now the patterns of activity during sleep have also been found to reflect the order in which the cells fired during spatial exploration. This relation was reliably stronger for sleep after the behavioral session than before it; thus, the activity during sleep reflects changes produced by experience. This memory for temporal order of neuronal firing could be produced by an interaction between the temporal integration properties of long-term potentiation and the phase shifting of spike activity with respect to the hippocampal theta rhythm.
1,052 citations
TL;DR: It is concluded that frequency and state specific changes occur as a function of age, and that sleep dependent decline in SWA and increase in sleep spindle activity are attenuated with age.
327 citations
TL;DR: 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.
306 citations
TL;DR: The data show that in healthy young women, sleep spindle frequency activity varies in parallel with core body temperature, whereas homeostatic sleep regulatory mechanisms, as indexed by the time course of EEG slow wave activity are not substantially affected by the menstrual cycle.
Abstract: Cyclic changes in hormones, body temperature, and metabolic rate characterize the menstrual cycle. To investigate whether these changes are associated with changes in sleep and the sleep electroencephalogram (EEG), a total of 138 sleep episodes from 9 women with no premenstrual syndrome symptoms were recorded every second night throughout one ovulatory menstrual cycle and analyzed in relation to menstrual phase. Ovulation and menstrual cycle stage were confirmed by measurements of temperature, urinary LH, and midluteal plasma levels of estrogen and progesterone. No significant variation across the menstrual cycle was observed for subjective ratings of sleep quality and mood as well as for objective measures of total sleep time, sleep efficiency, sleep latency, rapid eye movement sleep latency, and slow wave sleep. In nonrapid eye movement sleep, EEG power density in the 14.25-15.0 hertz band, which corresponds to the upper frequency range of the sleep spindles, exhibited a large variation across the menstrual cycle, with a maximum in the luteal phase. The data show that in healthy young women, sleep spindle frequency activity varies in parallel with core body temperature, whereas homeostatic sleep regulatory mechanisms, as indexed by the time course of EEG slow wave activity are not substantially affected by the menstrual cycle.
276 citations
TL;DR: It is concluded that homeostatic mechanisms can largely account for the dynamics of the sleep EEG under conditions of reduced sleep pressure.
Abstract: Increasing sleep pressure is associated with highly predictable changes in the dynamics of the sleep electroencephalogram (EEG). To investigate whether the effects of reduced sleep pressure also can be accounted for by homeostatic mechanisms, nighttime sleep following an evening nap was recorded in healthy young men. In comparison with the baseline night, sleep latency in the postnap night was prolonged, rapid eye movement sleep (REMS) latency was reduced, and EEG power density in non-REMS was decreased in the delta and theta band. The buildup of both EEG slow-wave activity (SWA; power density in the 0.75-to 4.5-Hz range) and spindle frequency activity (SFA; power density in the 12.25-to 15.0-Hz range) in non-REMS episodes was diminished (SWA: episodes 1-3; SFA: episode 1). The typical declining trend of SWA over consecutive non-REM sleep episodes was attenuated. The time course of SWA could be closely simulated with a homeostatic model of sleep regulation, although some discrepancies in level and buildup of SWA were apparent. We conclude that homeostatic mechanisms can largely account for the dynamics of the sleep EEG under conditions of reduced sleep pressure.
224 citations
TL;DR: Meta-analytical techniques used to re-examine the effects of exercise on sleep and examine possible moderators of these effects indicated that acute and chronic exercise increased slow wave sleep and total sleep time but decreased sleep onset latency and REM sleep.
Abstract: Studies attempting to ascertain the effects of acute and chronic exercise on measures of sleep have yielded conflicting results and interpretations. Methodological differences among studies may explain this lack of consensus; however, small sample sizes and subsequently low statistical power may also have contributed. In an attempt to resolve these issues, this review used meta-analytical techniques to: (a) re-examine the effects of exercise on sleep; and (b) examine possible moderators of these effects. Studies meeting the selection criteria were included in the analysis. Analyses of moderating factors were performed for stage 4 sleep and rapid eye movement (REM) sleep. The results indicated that acute and chronic exercise increased slow wave sleep (SWS) and total sleep time but decreased sleep onset latency and REM sleep. Moderating variables influencing the magnitude and direction of these effects were related to characteristics of the individual (e.g. sex, age, fitness level) and the exercise (e.g. time of day exercise was completed, type of exercise, exercise duration). Mechanisms which have been suggested to explain the relationship between exercise and sleep are discussed and directions for further research are provided.
222 citations
TL;DR: It is concluded that hypersomnia following PTS is accompanied by deficient arousal during the day and insufficient spindling and slow‐wave sleep production at night, supporting the hypothesis of a dual role of the paramedian thalamus as “final common pathway” for both maintenance of wakefulness and promotion of NREM sleep.
Abstract: 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.
194 citations
TL;DR: It is concluded that arousal from NREM sleep evokes a pressor response caused by increased peripheral vascular resistance, and increased sympathetic outflow to skeletal muscle may contribute to, but is not required for, this vasoconstriction.
Abstract: The arterial pressure elevations that accompany sleep apneas may be caused by chemoreflex stimulation, negative intrathoracic pressure, and/or arousal. To assess the neurocirculatory effects of arousal alone, we applied graded auditory stimuli during non-rapid-eye-movement (NREM) sleep in eight healthy humans. We measured muscle sympathetic nerve activity (intraneural microelectrodes), electroencephalogram (EEG; C4/A1 and O1/A2), arterial pressure (photoelectric plethysmography), heart rate (electrocardiogram), and stroke volume (impedance cardiography). Auditory stimuli caused abrupt increases in systolic and diastolic pressures (21 +/- 2 and 15 +/- 1 mmHg) and heart rate (11 +/- 2 beats/min). Cardiac output decreased (-10%). Stimuli that produced EEG evidence of arousal evoked one to two large bursts of sympathetic activity (316 +/- 46% of baseline amplitude). Stimuli that did not alter EEG frequency produced smaller but consistent pressor responses even though no sympathetic activation was observed. We conclude that arousal from NREM sleep evokes a pressor response caused by increased peripheral vascular resistance. Increased sympathetic outflow to skeletal muscle may contribute to, but is not required for, this vasoconstriction. The neurocirculatory effects of arousal may augment those caused by asphyxia during episodes of sleep-disordered breathing.
187 citations
TL;DR: The data on REM sleep provide the first biochemically validated and direct evidence that suppression of DRN serotonergic activity increases REM sleep, and furnish a key complement to the laboratory's in vitro data indicating that mesopontine cholinergic neurons, a target ofDRN projections, are inhibited by 5-HT.
Abstract: In vivo microdialysis was used to analyze the role of dorsal raphe nucleus (DRN) neurons in regulating the sleep-waking cycle. Measurements of extracellular serotonin (5-HT) were made in the DRN of freely moving adult cats before and during microdialysis perfusion of 8- hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), a selective 5-HT1A receptor agonist, in artificial CSF. Behavioral state alterations were measured by simultaneous polygraphic recordings. During waking and artificial CSF perfusion of probes histologically localized to the DRN, extracellular 5-HT was 4 fmol/7.5 micro L dialysate sample. With the addition of 8-OH-DPAT (10 microM in artificial CSF) to the perfusate, 5- HT levels in the same state decreased 50%, to 2 fmol/sample (p < 0.01), presumably through 5-HT1A autoreceptor-mediated inhibition of serotonergic neural activity. Concomitantly, this 8-OH-DPAT perfusion produced a short latency, threefold increase in rapid eye movement (REM) sleep, from 10 to 30% of the total recorded time (p < 0.05), whereas waking was not significantly affected. In contrast, and suggesting DRN specificity, 8-OH-DPAT delivery through a probe in the aqueduct did not increase REM sleep but rather tended to increase waking and decrease slow wave sleep. The data on REM sleep provide the first biochemically validated and direct evidence that suppression of DRN serotonergic activity increases REM sleep, and furnish a key complement to our laboratory's in vitro data indicating that mesopontine cholinergic neurons, a target of DRN projections, are inhibited by 5-HT. The 8-OH-DPAT-induced reduction of DRN 5-HT is consistent with the hypothesis that the concomitant REM sleep disinhibition is mediated by DRN serotonergic projections to mesopontine cholinergic neurons, which other data implicate in REM sleep production.
187 citations
TL;DR: The results indicate that short sleepers live under a higher "non-REM sleep pressure" than long sleepers, however, the two groups do not differ with respect to the homeostatic sleep regulatory mechanisms.
Abstract: Homeostatic sleep regulation in habitual short sleepers (sleep episode 9 h, n = 7) was investigated by studying their sleep structure and sleep electroencephalogr...
184 citations
TL;DR: The chronic effects of antidepressant drugs (ADs) on circadian rhythms of behavior, physiology and endocrinology are reviewed and the effects of ADs on the coupling of the central circadian pacemaker to photic and nonphotic zeitgebers are discussed.
TL;DR: Assessing CAP parameters in OSAS patients and investigating the reciprocal interactions between CAP and the cyclic variations in respiratory rate suggest that phase B of CAP offers a vulnerable background for upper airway collapse and for attenuation of biochemical and neural mechanisms in the control of the ventilatory drive.
Abstract: Obstructive sleep apnea syndrome (OSAS) is characterized by multiple interruptions of airflow between periods of arousals. A key feature of OSAS is the 20- to 40-s cyclic pattern of electrophysiologic parameters. The periodicity of the OSAS-related phenomena is reminiscent of the natural electroencephalographic (EEG) arousal rhythm of non-rapid eye movement (NREM) sleep known as the cyclic alternating pattern (CAP). Morphologically, CAP consists of transient arousals (phase A) that periodically interrupt the tonic theta/delta activities of NREM sleep (phase B). Functionally, CAP translates a condition of sustained arousal instability oscillating between a greater arousal level (phase A) and a lesser arousal level (phase B). CAP is also related to the controls of the motor and autonomic mechanisms. On the basis of the information simultaneously derived from EEG activities, muscle tone, and neurovegetative responses, it is possible to distinguish three subtypes of A phases corresponding to different levels of arousal power: A1 (dominated by EEG synchronization and weak activation of polygraphic variables); A2 (mixture of EEG synchronization/desynchronization and intermediate activation of polygraphic variables); and A3 (dominated by EEG desynchronization and strong activation of polygraphic variables). Unlike standard criteria, CAP parameters offer a more suitable perspective for evaluating sleep pathologies in which brief and frequent arousals appear as a prominent feature. The present study aimed at (a) assessing CAP parameters in OSAS patients and (b) investigating the reciprocal interactions between CAP and the cyclic variations in respiratory rate. Twelve obese middle-aged OSAS subjects complaining of daytime sleepiness were polygraphically compared with age-matched and gender-matched volunteers in good health and with no complaints about sleep and wakefulness (controls). In OSAS patients, conventional parameters showed predictable decrements in total sleep time, slow wave sleep, and REM sleep and increases in stage 1 and nocturnal awakenings. Sleep fragmentation was associated with a significant enhancement of CAP and of the A phases with longer and more desynchronized EEG patterns (especially A3). The increase of A3 subtypes permitted scoring and detecting CAP also in REM sleep. The great majority of respiratory pauses (96% in NREM and 80% in REM sleep) were coupled with CAP. All CAP-related respiratory events rose in close temporal connection with a phase B, while effective breathing was always recovered during phase A (especially A2 and A3 subtypes). These data suggest that (a) phase B of CAP offers a vulnerable background for upper airway collapse and for attenuation of biochemical and neural mechanisms in the control of the ventilatory drive and (b) survival in OSAS patients is effected by the enhancement of the strongest components of the natural arousal rhythm at sleep quality's expense.
TL;DR: Abnormal patterns of cerebral metabolism during non-REM sleep in depressed patients confirmed earlier waking findings of decreased relative frontal and abnormal limbic metabolic activity and striatal metabolism in association with posterior cortical increases.
Abstract: Background: Depression is characterized by several sleeprelated abnormalities shortly before and after sleep onset, such as prolonged sleep latency, loss of stage 3-4 sleep, reduced rapid eye movement (REM) latency, increased nocturnal core body temperature, and abnormal hormone secretion patterns. Sleep deprivation is associated with a temporary improvement in depression. We hypothesized that depressed patients may be "overaroused" and that absolute cerebral glucose metabolism would be elevated during the first nocturnal non-REM sleep period in depressed patients compared with normal controls. In addition, since hypofrontality (greater metabolic activity in occipital compared with frontal cortical activity) has been reported in waking positron emission tomographic studies of depressed patients compared with controls, we predicted significant hypofrontality in depressed patients during the first non-REM period. Methods: Positron emission tomography with fludeoxy-glucose F 18 was used to compare 10 unmedicated men with unipolar depression with 12 normal men during the first non-REM sleep period at normal bedtime. Results: Whole-brain absolute metabolic rate during non-REM sleep was significantly elevated (+47%) in patients compared with controls. Mean absolute cerebral glucose metabolic rate was also higher in every area of the brain in patients compared with normal controls. The greatest significant mean increases were in the posterior cingulate and amygdala ( + 44%), hippocampus ( +37% to +43%), occipital and temporal cortex (+33% to +34%), and pons (+33%). Relative metabolic rates in specific neroanatomical areas, however, varied considerably both within the patient group and between patients and controls. Patients showed significant hypofrontality, particularly in the medio-orbital frontal cortex, compared with controls. Patients also showed significant reductions of relative metabolic rate in the anterior cingulate, caudate, and medial thalamus compared with controls. Conclusions: These findings provide further support for the hyperarousal hypothesis of some types of major depressive disorder. Abnormal patterns of cerebral metabolism during non-REM sleep in depressed patients confirmed earlier waking findings of decreased relative frontal and abnormal limbic metabolic activity and striatal metabolism in association with posterior cortical increases.
TL;DR: The results suggest that REM and non-REM sleep evolved as a differentiation of a single, phylogenetically older sleep state, and it is hypothesized that the physiological changes that occur during postnatal sleep development parallel certain aspects of the changes that have occurred during the evolution of sleep–waking states in mammals.
Abstract: Placental and marsupial mammals exist in three states of consciousness: waking, non-REM sleep, and REM sleep. We now report that the echidna Tachyglossus aculeatus, a representative of the earliest branch of mammalian evolution (the monotremes), does not have the pattern of neuronal activity of either of the sleep states seen in nonmonotreme mammals. Echidna sleep was characterized by increased brainstem unit discharge variability, as in REM sleep. However, the discharge rate decreased and the EEG was synchronized, as in non-REM sleep. Our results suggest that REM and non-REM sleep evolved as a differentiation of a single, phylogenetically older sleep state. We hypothesize that the physiological changes that occur during postnatal sleep development parallel certain aspects of the changes that have occurred during the evolution of sleep-waking states in mammals.
TL;DR: Forebrain structures may be functionally briefly disconnected from the brain-stem during this short-lasting stage of paradoxical sleep, which could possibly account for the mental content of a similar sleep period in humans.
TL;DR: The results suggest that control over sleep/wake schedules is an important methodological issue in adolescent sleep studies and are consistent with a larger body of evidence indicating that dysregulation near sleep onset represents a primary psychobiological change in early-onset depression.
TL;DR: It is demonstrated that late-afternoon ethanol intake in middle-aged men disrupts sleep consolidation, affects the sleep stage distribution, and alters the sleep EEG.
Abstract: The effect of a moderate dose of ethanol (0.55 g/kg of body weight), administered 6 hours before scheduled bedtime, on performance, nocturnal sleep, and the sleep electroencephalogram (EEG) was investigated in 10 healthy, middle-aged men (mean age: 61.6 +/- 0.9 years). By the beginning of the sleep episode, breath-ethanol concentrations had declined to zero in all subjects. Compared with the control condition (mineral water), sleep was perceived as more superficial. Sleep efficiency, total sleep time, stage 1, and rapid eye movement (REM) sleep were reduced. In the second half of the sleep episode, wakefulness exhibited a twofold increase. EEG power density in low delta frequencies was enhanced in non-REM sleep (1.25-2.5 Hz) and REM sleep (1.25-1.5 Hz). In slow wave sleep (i.e., stages 3 + 4), power density was increased not only in the low-frequency range (1.25-1.5, 2.25-4.0, 4.75-5.0 Hz) but also within the alpha (8.25-9.0 Hz) and sigma (12.25-13.0 Hz) band. The data demonstrate that late-afternoon ethanol intake in middle-aged men disrupts sleep consolidation, affects the sleep stage distribution, and alters the sleep EEG.
TL;DR: Because the sleep-onset GH pulse is often the major secretory output in adults, age-related decrements in sleep-related GH secretion likely play a major role in the hyposomatotropism of senescence.
TL;DR: The results indicate that the sex difference in nighttime PS is due to the suppression of PS by ovarian hormones during proestrus and, to a less extent, estrus nights, and appears to be independent of circulating ovarian hormones.
TL;DR: It is concluded that neural reflexes, but not mechanical factors, substantially contribute to the acute blood pressure response to an obstructive apneic event and that arousal produces a separate, additional acute hypertensive response.
Abstract: Recent studies suggest that arousal is the dominant factor acutely increasing blood pressure in obstructive sleep apnea and that neither stimulation of chemoreceptors nor mechanical factors associa...
TL;DR: In this paper, the authors investigated changes in GH and cortisol secretion during sleep in 30 male volunteers age 20 to 92 yr. After an adaptation night, each subject spent another night in the sleep laboratory for polygraphic sleep recording and determination of GH and basal cortisol levels every 15 min.
Abstract: Background. One current hypothesis of biological aging proposes that aging results from the deterioration of neuroendocrine functions. Sleep dependent growth hormone (GH) secretion is diminished in elderly people. However, the time course of this decrease from puberty to senescence is still unknown. Cortisol secretion is also related to sleep processes with the 24 hr nadir occurring, like the sleep dependent GH secretory surge, during the first half of nocturnal sleep. Whether age also affects the sleep-associated nadir of cortisol secretion has yet to be clarified. This study investigated changes in GH and cortisol secretion during sleep in 30 male volunteers age 20 to 92 yr. Methods. After an adaptation night, each subject spent another night in the sleep laboratory for polygraphic sleep recording and determination of GH and cortisol levels every 15 min. Results. GH peak values exponentially decreased with age (r = -.80, p < .001), while the cortisol nadir increased linearly as a function of age (r = .79, p < .001). Age-related changes in sleep-dependent secretion of GH and cortisol correlated significantly (r = .47, r = -.55 , respectively; p < .05) with an age-dependent decrease in slow wave sleep. Conclusion. Alterations of GH peak amplitude and basal cortisol secretion are not restricted to senescence. These changes develop gradually during adult life with different time courses. Both changes in GH and cortisol secretion may act together to reduce anabolic functions of sleep in the aged.
TL;DR: The effects of THIP on sleep resemble those reported earlier for the GABAA agonist muscimol and are dissimilar from those induced by benzodiazepine-agonistic modulators of GAB AA receptors, indicating that agonists and agonistic modulator of GabAA receptors affect sleep differentially.
Abstract: To investigate the effects of the selective gamma-aminobutyric acid (GABA)A receptor agonist 4,5,6,7-tetrahydroisoxazolo (5,4-c)pyridin-3-ol (THIP) on sleep, vehicle or 2 or 4 mg kg-1 of THIP were randomly administered i.p. to 8 rats at light onset. EEG and EMG were recorded during the first 6 hours after injection. THIP 4 mg kg-1 transiently evoked bursts of absence epilepsy-like EEG hypersynchronization. It significantly promoted non-rapid eye movement (non-REM) sleep and elevated delta activity within non-REM sleep. This was accompanied by an increase in both the rise rate and maximal level of delta activity within the non-REM sleep episodes. The effects of THIP on sleep resemble those reported earlier for the GABAA agonist muscimol and are dissimilar from those induced by benzodiazepine-agonistic modulators of GABAA receptors. These data indicate that agonists and agonistic modulators of GABAA receptors affect sleep differentially.
TL;DR: It appears that chronic fragmentation of sleep, whether by apneas or acoustic stimuli, leads to cumulative homeostatic pressure for sleep, which may explain a number of phenomenon characteristic of both untreated OSAS patients and experimentally fragmented sleepers.
Abstract: The neurobehavioral deficits of obstructive sleep apnea syndrome (OSAS) are often attributed to the rate of respiratory disturbance or rate of arousals during sleep. However, sleep disordered breathing is also associated with other changes in sleep infrastructure that may account for cumulative waking deficits. This was illustrated in polysomnographic data from 1,521 patients with OSAS where increasing arousal indices were associated with increased duration of stage 1 sleep and concomitant reduction in total sleep time. Similar results have been found in paradigms in which sleep was experimentally fragmented in healthy individuals. It appears that chronic fragmentation of sleep, whether by apneas or acoustic stimuli, leads to cumulative homeostatic pressure for sleep, which may explain a number of phenomenon characteristic of both untreated OSAS patients and experimentally fragmented sleepers: (1) increased arousal threshold, (2) rapid return to sleep after arousal, (3) fewer awakenings over time, (4) increased sleep inertia on awakenings, (5) increased amnesia for arousals, and (6) daytime sleepiness. Elevated homeostatic drive for sleep appears to be a function of both the frequency of arousals within a night and the chronicity of sleep fragmentation across nights, neither of which have been adequately modeled in experimental studies of healthy subjects.
TL;DR: The results indicate that the increased delta activity during NREM apneas may not be caused by arterial hypoxemia, and could be due to either an arousal mechanism, since arousals may be preceded by slow waves in EEG, or to a breakthrough of slow-wave-sleep activity.
Abstract: To study the effect of transient, apnea-induced hypoxemia on electrocortical activity, five patients with severe obstructive sleep apnea syndrome (OSAS) were investigated during nocturnal sleep. Polysomnographic and simultaneous digitized electro encephalographic (EEG) recordings for topographic and compressed spectral array analysis were made. The EEG recordings were timed exactly to respiratory events. During nonrapid eye movement (NREM) apnea, delta band amplitude increased, starting on average 13 seconds after the apnea onset. Average differences were 268% between initial and maximal values and 202% between initial and final values. In contrast, significant increases in delta amplitudes between the onset and end of REM apneas did not occur, although some caused deep oxygen desaturations. Changes in delta activity were not correlated to NREM apnea duration or degree of desaturation. These results indicate that the increased delta activity during NREM apneas may not be caused by arterial hypoxemia. It could instead be due to either an arousal mechanism, since arousals may be preceded by slow waves in EEG, or to a breakthrough of slow-wave-sleep activity. The sleep disturbance in severe OSAS may create such a propensity for slow-wave sleep that stages pass much more rapidly than in normal persons.
TL;DR: It is suggested that the effects of BP 2.94 or carboperamide on sleep and waking could depend on changes in the availability of histamine at the postsynaptic H1 receptor, which would secondarily result in changes of sleep variables.
TL;DR: Trimipramine is an antidepressant with sleep-improving qualities that possibly acts through inhibition of hypothalamic-pituitary-adrenocortical system activity by a yet unknown mechanism.
Abstract: In a 4-week double-blind clinical trial we compared the effects of the tricyclic antidepressants trimipramine and imipramine on the sleep EEG and on nocturnal bormone secretion in 20 male inpatients with major depression. Both treatments produced rapid significant clinical improvement in depression without severe adverse effects. However, the two drugs had markedly different neurobiologic profiles. Trimipramine enhanced rapid eye movement (REM) sleep and slow wave sleep, whereas imipramine suppressed REM sleep and showed no effect on slow wave sleep. Total sleep time and the sleep efficiency index increased under trimipramine but not under imipramine. Nocturnal cortisol secretion decreased with trimipramine but remained unchanged with imipramine. In contrast to imipramine, trimipramine induced an increase in prolactin secretion compatible with its known antagonism at dopamine (D2) receptors. Imipramine induced a decrease in growth hormone secretion during the first half of the night. Neither of the drugs induced significant changes in plasma testosterone concentration. We conclude that trimipramine is an antidepressant with sleep-improving qualities that possibly acts through inhibition of hypothalamic-pituitary-adrenocortical system activity by a yet unknown mechanism.
TL;DR: It is concluded that cholinergic activation of the central amygdaloid nucleus produces a long-term facilitation of REM sleep occurrence.
Abstract: The effect on sleep organization of carbachol microinjected into different amygdaloid nuclei was analysed in 12 cats. Single carbachol doses of 8 micrograms in 0.50 microliter saline were delivered unilaterally or bilaterally into the central, basal, lateral or basolateral amygdaloid nucleus. Carbachol administration into the central nucleus induced a prolonged (5 days) enhancement of both REM sleep and its preceeding slow wave sleep episodes with PGO waves (sommeil phasique a ondes lentes, SPHOL), which was more pronounced following bilateral than unilateral carbachol administration. However, neither SPHOL nor REM sleep changes were produced by administration of carbachol into the other amygdaloid nuclei. We conclude that cholinergic activation of the central amygdaloid nucleus produces a long-term facilitation of REM sleep occurrence.
TL;DR: To the authors' knowledge, this is the first report of the treatment of headbanging with clonazepam, and both patients benefited from this treatment.
Abstract: Headbanging is a rhythmic movement disorder (RMD) along with headrolling, bodyrocking and bodyrolling. The International Classification of Sleep Disorders defines RMD as a group of stereotyped, repetitive movements involving large muscles, usually of the head and neck, that typically occur immediately prior to sleep onset and are sustained into light sleep. The average onset is 9 months, and by 10 years of age the majority of subjects no longer complain of headbanging. If it continues, it is usually associated with mental retardation of autism. Headbanging is said to occur during presleep drowsiness or early non-rapid eye movement sleep. Often there is no need for treatment other than reassurance. Behavior modification has had little success. Benzodiazepines (such as oxazepam and diazepam) and tricyclic antidepressants have been used with variable success. We present two cases of headbanging with polysomnographic findings and treatment. The patients are two healthy adult males. They both experienced significant daytime somnolence and repeatedly wakened their partners. Only one of our patients had recorded head movements during his overnight sleep study. There was evidence of headbanging during stage 1 and stage 2 sleep but also during slow wave sleep. Headbanging was recorded during 14% of the epochs. Both patients responded to treatment with clonazepam (at a dose of 1.0 mg nightly) with decreased frequency and severity of headbanging. Although headbanging is most common in childhood, there may be significant number of cases that persist into adulthood. To our knowledge, this is the first report of the treatment of headbanging with clonazepam. Both patients benefited from this treatment.
TL;DR: Only by appreciating parent-child interactions when it comes to understanding causes of sleeplessness in the young child can the clinician serve a useful role in helping the family to understand and improve a young child's problematic sleep patterns.
TL;DR: Treatment with nasal ventilation is effective in reversing the nocturnal respiratory failure without significant disturbance to life style and it is important to be vigilant for sleep hypoventilation in these patients.
Abstract: Eight ambulant children aged 6-13 years, four with congenital myopathy, two with congenital muscular dystrophy and two with the rigid spine syndrome, presented with recurrent chest infections, morning headaches, shallow breathing at night, or respiratory failure. Polysomnography confirmed the presence of nocturnal hypoxaemia with oxygen saturation on average less than 90% for 49% of sleep and less than 80% for 19% of sleep accompanied with severe hypoventilation. Additionally there was sleep disturbance characterised by an increased number of wake epochs from deep sleep (in comparison to 10 non-hypoxaemic subjects). The severity of sleep hypoxaemia did not correlate with symptoms. Treatment with night time nasal ventilation was started and repeat polysomnography showed normal overnight oxygen saturation and a reduced number of wake epochs during deep sleep. It is important to be vigilant for sleep hypoventilation in these patients and sleep studies should be part of the routine respiratory evaluation. Treatment with nasal ventilation is effective in reversing the nocturnal respiratory failure without significant disturbance to life style.