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PubMed1999

Sleep EEG studies during early and late partial sleep deprivation in premenstrual dysphoric disorder and normal control subjects.

In this study of 23 patients with premenstrual dysphoric disorder (PMDD) and 18 normal comparison (NC) subjects, we examined sleep EEG measures during baseline midfollicular (MF) and late luteal (LL) menstrual cycle phases and after early sleep deprivation (ESD), in which subjects slept from 03.00 to 07.00 h, and late sleep deprivation (LSD), in which subjects slept from 21.00 to 01.00 h. Each sleep deprivation night was followed by a night of recovery sleep (ESD-R, LSD-R) (sleep 22.30-06.30 h) and was administered in the late luteal phase of separate menstrual cycles. During baseline studies, sleep EEG measures differed significantly by menstrual cycle phase, but not group. Both PMDD and NC groups showed longer REM latencies and less REM sleep (minutes and percent) during the luteal compared with the follicular menstrual cycle phase. PMDD subjects, however, did not show sleep architecture changes similar to those of patients with major depressive disorders. Sleep quality was better during recovery nights of sleep in PMDD compared with NC subjects. REM sleep measures changed in association with clinical improvement in responders to sleep deprivation. Both early and late sleep deprivation may help to correct underlying circadian rhythm disturbances during sleep in PMDD, although differential sleep changes during ESD vs. LSD did not correlate with clinical response. Further sleep studies addressing additional circadian variables may serve to elucidate mechanisms mediating the therapeutic effects of sleep deprivation in PMDD.

Affect↗
PubMed2003

Preliminary observations on the effects of sleep time in a sleep restriction paradigm.

OBJECTIVE: To evaluate of the effect of 7 days of sleep restriction--with sleep placed at the beginning of night or early morning hours - on sleep variables, maintenance of wakefulness test, and serum leptin. METHODS: After screening young adults with questionnaires and actigraphy for 1 week, eight young adult males were recruited to participate in a sleep restriction study. The subjects were studied for baseline data for 2.5 days, with 8.5 h per night in bed, and then over 7 days of sleep restriction to 4 h per night with a 22:30 h bedtime for half the group and a 02:15 h bedtime for the other half. At the end of study, after one night of ad libitum sleep, subjects again had 2 days of 8.5 h in bed. Wakefulness was continuously verified and tests, including Maintenance of Wakefulness (MWT), were performed during the scheduled wake time. Blood was drawn six times throughout the 24 h of the 7th day of sleep restriction and after 2 days of the post-restriction schedule. RESULTS: There was individual variability in response to sleep restriction, but independent of group distribution, MWT was significantly affected by sleep restriction, with the early morning sleep group having less decrease in MWT score. Sleep efficiency was also better in this group, which also had shorter sleep latency. Independent of group distribution there was a greater increase in the percentage of slow wave sleep than rapid eye movement sleep, despite a clear internal variability and variability between subjects. Peak serum leptin was significantly decreased with 7 days of sleep restriction for all subjects. CONCLUSION: Sleep restriction to 4 h affected all subjects, but there were individual and group differences in MWT and sleep data. In this group of young adult males (mean age 19 years), there was a better overall adaptation to the early morning sleep, perhaps related to the general tendency in most adolescents to present some phase-delay during late teen-aged years.

Adolescent↗
PubMedDate not supplied

Changes in emotional responses to aversive pictures across periods rich in slow-wave sleep versus rapid eye movement sleep.

OBJECTIVE: Since Freud's "Interpretation of Dreams," sleep has been related to emotional functions, where dreams were assumed to play a cathartic role. In psychophysiological research, this role was attributed mainly to rapid eye movement (REM) sleep. The present study compared processing pictures with negative emotional impact over intervals covering either early sleep dominated by slow-wave sleep (SWS) or late REM sleep-dominated sleep. METHOD: Emotional reactions were assessed by a nonverbal rating procedure along the two emotional dimensions valence (positive vs. negative) and arousal (low vs. high). Two groups of healthy men were tested across 3-hour periods of early and late nocturnal sleep (sleep group) or corresponding intervals filled with wakefulness (wake group). After the intervals, subjects rated new pictures together with old pictures already presented before the interval. Sleep was recorded polysomnographically. RESULTS: As expected, the amount of REM sleep was about three times greater during late than early nocturnal sleep, whereas a reversed distribution was observed for SWS (p<.001). Valence ratings indicated a shift toward enhanced negative ratings after late sleep (p<.05), contrasting with a trend toward more positive ratings after early sleep (p<.10). Arousal habituated slightly to repeated presentation of the same stimuli, but sleep generally enhanced subsequent arousal ratings (p<.05). Effects of sleep did not depend on whether pictures had low or high emotional impact. CONCLUSIONS: Indicating a priming-like enhancement of emotional reactivity after periods rich in REM sleep, results do not confirm a cathartic function of REM sleep or sleep in general.

Adolescent↗
PubMedDate not supplied

Association between nocturnal vagal tone and sleep depth, sleep quality, and fatigue in alcohol dependence.

BACKGROUND: This study examined whether nocturnal vagal tone as indexed by the high-frequency (HF) power component of heart rate variability is related to measures of sleep depth and daytime perceptions of sleep quality, sleepiness, and fatigue in alcohol dependence. METHODS: Abstinent alcohol-dependent patients (n = 14) and comparison control subjects (n = 14) underwent all-night polysomnography along with assessment of heart rate variability during an awake period before sleep and during sleep. Sleep-quality perceptions, along with self-reported sleepiness and levels of energy and fatigue, were obtained in the morning. RESULTS: As compared with control subjects, alcohol-dependent persons showed marked decreases in delta sleep along with impairments of sleep quality and daytime energy. In addition, alcoholics showed a decrease of the HF power component of heart rate variability during the awake period before sleep and during nocturnal sleep as compared with control subjects. HF power during the awake period before sleep correlated with electroencephalographic delta sleep and delta power observed during the subsequent sleep period. HF power during the awake period before sleep also correlated with morning reports of sleep quality, sleepiness, and fatigue. CONCLUSIONS: Alcohol dependence compromises vagal output measured before sleep onset, which correlates with loss of delta sleep and with morning reports of sleep impairments. Testing of interventions that target sympathovagal balance might identify new strategies for partial amelioration of the sleep disturbances and impairments in daytime functioning observed in persons with alcohol dependence.

Adult↗
PubMed1997

Good sleep--its timing and physiological sleep characteristics.

The present study used short sleep episodes to explore the relation between subjective sleep quality, timing and physiological content of sleep. Eight subjects participated in 18 4-h sleep episodes to provide 4, 8, and 12 h of prior time awake before bedtimes at six different times of day in a sleep laboratory insulated from environmental disturbances. The results were analysed by ANOVAs and multiple regression techniques. Subjective sleep quality, calmness of sleep, ease of falling asleep, ability to 'sleep through', number of awakenings, and sleep latency showed a significant pattern of 'better' sleep with increasing prior time awake and with closeness to the circadian minimum (nadir) of rectal temperature (morning hours). 'Ease of awakening' in contrast, 'decreased' with increasing time awake and with closeness to the nadir/ morning hours. Multiple regression analysis showed that subjective sleep quality was predicted by subjective calmness of sleep and ease of falling asleep, among the subjective measures, and by total sleep time (TST) and slow-wave sleep (SWS - stages 3+4) among the physiological sleep measures. The subjective ease of awakening was predicted by slow-wave sleep (negatively) and the circadian maximum of rectal temperature. The results indicate that the duration of wakefulness prior to sleep and the timing of sleep determine its physiological expression, which in turn determines its subjective impression.

Analysis of Variance↗
PubMed2005

Ramelteon (TAK-375), a selective MT1/MT2-receptor agonist, reduces latency to persistent sleep in a model of transient insomnia related to a novel sleep environment.

OBJECTIVE: Evaluate the efficacy of ramelteon, an MT/1MT2-receptor agonist, for the treatment of transient insomnia in healthy adults. DESIGN: Randomized, double-blind, placebo-controlled design using a model of transient insomnia related to sleeping in a novel environment. SETTING: Fourteen sleep research centers. PARTICIPANTS: Healthy adults (N=375; 228 women), aged 35 to 60 years, who had never previously slept in a sleep laboratory and had a reported usual sleep duration of 6.5 to 8.5 hours and usual bedtime between 8:30 PM and midnight. INTERVENTIONS: Single administration of ramelteon (16 or 64 mg) or placebo 30 minutes before bedtime. OUTCOME MEASURES: Primary efficacy measure was latency to persistent sleep. Also evaluated were total sleep time, wake after sleep onset, percentage of each sleep stage, subjective estimates of sleep from postsleep questionnaire, number of awakenings, and subjective number of awakenings. Residual effects were assessed via Digit Symbol Substitution Test and postsleep questionnaire. RESULTS: Participants in ramelteon-treated groups had significantly shorter latency to persistent sleep relative to placebo. They also were associated with significantly longer total sleep time. Wake after sleep onset and time spent in each sleep stage were not significantly different from placebo. The use of ramelteon (16 mg) was associated with a shorter subjective sleep latency compared to placebo. Other subjective measures of sleep did not differ significantly from placebo. Digit Symbol Substitution Test scores did not differ significantly among the 3 groups, but the use of the 64-mg [corrected] dose was associated with subjective reports of impairment in the morning. CONCLUSIONS: Ramelteon significantly improved latency to persistent sleep and total sleep time in this model of transient insomnia in healthy adults. No dose-related differences in latency to persistent sleep were observed, and both doses were well tolerated.

Adult↗
PubMedDate not supplied

Depression predicts self-reported sleep quality in patients with obstructive sleep apnea.

OBJECTIVE: Depression is a common problem in patients with obstructive sleep apnea. The objective of this study was to examine whether depression is independently associated with lower self-reported sleep quality in patients with obstructive sleep apnea (OSA), after controlling for polysomnographic measures of sleep. METHODS: The sample comprised 135 patients who had been referred to a university teaching hospital's multidisciplinary sleep medicine center for polysomnographic evaluation of OSA. The median age of the subjects was 45 (mean age, 46 years) 55% were female, 69% were white, 31% were black, and their mean body mass index was 37.9 +/- 11.2 kg/m2. Self-reported sleep quality during the past 2 weeks was assessed by the insomnia severity index. Polygraphic measures of sleep quality included the respiratory disturbance index, sleep onset latency, arousals for no apparent reason, sleep efficiency, and periodic leg movements associated with arousal. Depressive symptoms were assessed by the Beck Depression Inventory. RESULTS: None of the polygraphic measures of sleep quality was related to self-reported sleep quality or depression. Oxygen desaturation was correlated with self-reported sleep quality (r = 0.21, p =.02). Depression correlated with self-reported sleep quality (r = 0.55, p <.0001). In a multiple regression analysis, depression remained a significant predictor of self-reported sleep quality after controlling for all of the polysomnographic measures of sleep quality (F = 9.65, partial r2 = 0.28 p =.0001). CONCLUSION: Depression is a better predictor of self-reported sleep quality than are polysomnographic measures of sleep in patients with OSA.

Adolescent↗
PubMedDate not supplied

EEG slow waves and sleep spindles: windows on the sleeping brain.

Slow waves and sleep spindles are prominent features of the EEG in non-REM sleep and some of the neurophysiological mechanisms underlying their genesis have been elucidated. In humans, slow-wave activity in non-REM sleep increases and EEG activity in the frequency range of sleep spindles decreases when wakefulness prior to sleep is varied from 2 to 40 h. The opposite changes are observed in the course of sleep, even when sleep is scheduled out of phase with the circadian rhythm of sleep propensity. Within non-REM sleep episodes the association between slow waves and sleep spindles is bi-phasic: both activities are correlated positively at the beginning and end of non-REM sleep episodes whereas in the middle part of non-REM sleep episodes high values of slow-wave activity coincide with low levels of spindle activity. An extension of wakefulness enhances the rise rate of slow-wave and spindle activity at the onset of sleep. Since macroscopic slow waves and sleep spindles both are dependent on hyperpolarization and synchronization of neurons in thalamo-cortical and cortical circuits, the sleep deprivation induced changes in these EEG activities may be related to reduced activating input to thalamo-cortical and cortical neurons, local facilitation of their hyperpolarization or facilitation of their synchronization. The precise regulation of slow-wave and spindle activity as a function of the duration and intensity of prior sleep and wakefulness demonstrates that these EEG oscillations are accurate indicators of non-REM-sleep homeostasis and suggests that they are fundamental to the sleeping brain.

Animals↗
PubMed1997

Melatonin and the circadian regulation of sleep initiation, consolidation, structure, and the sleep EEG.

The endogenous circadian rhythm of melatonin, driven by the suprachiasmatic nucleus, exhibits a close association with the endogenous circadian component of the sleep propensity rhythm and the endogenous circadian component of the variation in electroencephalogram (EEG) oscillations such as sleep spindles and slow waves. This association is maintained even when the sleep-wake cycle is desynchronized from the endogenous circadian rhythm of melatonin. Administration of melatonin during the day increases daytime sleep propensity as indexed by both the latency to sleep onset and sleep consolidation. The EEG during daytime sleep after melatonin administration exhibits characteristics reminiscent of the nocturnal sleep EEG, that is, increased sleep spindle activity and reduced slow-wave sleep and slow-wave activity, as detected by quantitative EEG analysis. Administration of higher doses of melatonin (5 mg or more) prior to nocturnal sleep results in an increase in rapid eye movement (REM) sleep. These data demonstrate that melatonin exerts effects on the main characteristics of human sleep, that is, latency to sleep onset, sleep consolidation, slow waves, sleep spindles, and REM sleep. There is a need for further studies using physiological doses and delivery systems that generate physiological plasma melatonin profiles to firmly establish the role of the endogenous circadian rhythm of melatonin in the circadian regulation of sleep.

Animals↗
PubMed1994

Effect of sleep deprivation on responses to airway obstruction in the sleeping dog.

The effect of sleep deprivation on sleep architecture and respiratory responses to repetitive airway obstruction during sleep was investigated in four chronically instrumented tracheostomized dogs during 12-h nocturnal experiments. A 24-h period of prior sleep deprivation increased (P < 0.05) the rate at which airway obstruction could be induced from 20 +/- 3 (SE) to 37 +/- 10 times/h compared with non-sleep-deprived dogs. During non-rapid-eye-movement sleep the duration of obstruction, minimum arterial hemoglobin saturation, and peak negative inspiratory effort at arousal were 20.5 +/- 1.0 s, 91.7 +/- 0.5%, and 28.4 +/- 1.8 mmHg, respectively, in non-sleep-deprived dogs. Sleep deprivation increased (P < 0.01) the duration of obstruction to 28.0 +/- 0.9 s, worsened (P < 0.05) the minimal arterial hemoglobin desaturation to 85.4 + 3.1%, and increased (P < 0.025) the peak negative inspiratory effort at arousal to 36.1 +/- 1.6 mmHg. Sleep deprivation also caused increases (P < 0.025) in total sleep time, rapid-eye-movement (REM) sleep time, and percentage of time in REM sleep in a 2-h recovery period without airway obstruction at the end of the study. We conclude that airway obstruction in the sleeping dog can reproduce the disturbances in sleep architecture and respiration that occur in obstructive sleep apnea and that prior sleep deprivation will increase apnea severity, degree of somnolence, and REM sleep rebound independent of change in upper airway collapsibility.

Airway Obstruction↗
PubMed1994

Effects of sleep deprivation and sleep fragmentation on upper airway collapsibility in normal subjects.

Sleep deprivation can induce or worsen nocturnal respiratory disturbances. In patients with sleep apnea hypopnea, sleep abnormalities consist of repetitive episodes of arousals and awakenings that lead to sleep fragmentation. Because the propensity for upper airway collapse is increased in these patients, we wondered if sleep fragmentation could increase upper airway collapsibility and contribute to the pathogenesis of this disease. In eight normal subjects, upper airway collapsibility was assessed during sleep by progressively decreasing the pressure in a nasal mask while recording airflow, mask, and esophageal pressures. The critical pressure was determined by the relationship between breath-by-breath values of maximal inspiratory airflow of each flow-limited inspiratory cycle and the corresponding mask pressure. Critical pressure was measured twice in each subject: after one night of total sleep deprivation and after one night of sleep fragmentation using auditory stimuli. The two measures were done in random order 1 wk apart. A polysomnographic recording was obtained the night after each measurement of critical pressure. Sleep architecture was identical after sleep deprivation and fragmentation. Sleep-related breathing abnormalities were more frequent after sleep fragmentation than after sleep deprivation. Critical pressure was -17.1 +/- 6.8 cm H2O (mean +/- SEM) after sleep deprivation, and -12.3 +/- 6.3 cm H2O after sleep fragmentation (p < 0.05), corresponding to an earlier closing of the upper airway. We conclude that sleep fragmentation leads to a higher upper airway collapsibility than does sleep deprivation.

Adult↗
PubMed1999

Effects of sleep and sleep deprivation on catecholamine and interleukin-2 levels in humans: clinical implications.

The objective of this study was to evaluate the effects of nocturnal sleep, partial night sleep deprivation, and sleep stages on catecholamine and interleukin-2 (IL-2) levels in humans. Circulating levels of catecholamines and IL-2 were sampled every 30 min during 2 nights: undisturbed, baseline sleep and partial sleep deprivation-late night (PSD-L; awake from 0300-0600 h) in 17 healthy male volunteers. Sleep was monitored somnopolygraphically. Sleep onset was associated with a significant (P < 0.05) decline of circulating concentrations of norepinephrine and epinephrine, with a nocturnal nadir that occurred 1 h after nocturnal sleep. On the PSD-L night, levels of norepinephrine and epinephrine significantly (P < 0.05) increased in association with nocturnal awakening. During stage 3-4 sleep, levels of norepinephrine, but not epinephrine, were significantly lower (P < 0.05) compared to average levels during the awake period, stages 1-2 sleep, and rapid eye movement sleep. Nocturnal levels of circulating IL-2 did not change with sleep onset or in relation to PSD-L or the various sleep stages. We conclude that sleep onset is associated with changes in levels of circulating catecholamines. Loss of sleep and disordered sleep with decreases in slow wave sleep may serve to elevate nocturnal catecholamine levels and contribute to cardiovascular disease.

Adult↗
PubMed1989

[Effects of noise on sleep. Part 2. A case report of the effects of three levels of stationary sound on sleep parameters].

The effect of steady noise on sleep was examined experimentally for 24 nights by sleep polygraphy of a twenty-eight-year-old man. The parameters used for sleep polygraphy were sleep stage, sleep latency, frequency of sleep stage shift per hour, average sleep depth, the gradient and intercept of a regression line of sleep depth against time, and subjective sleep. The sleep stage was judged and estimated based on the criteria of Rechtschaffen & Kales by the authors' original system using a microcomputer. For the calculation of sleep depth at a given time, stages W (waking), 1, REM, 2, 3 and 4 were weighted to be 0, 1, 1.5, 2, 3 and 4, respectively. Sleep parameters were compared between the data of non-noise and noise-exposed nights. The noise exposure was overnight stationary pink noise of 40, 50 and 60 dB (A). General findings were a decreased REM stage, an increased stage 2, and deepened average sleep depth of the 60 dB (A)-night sleep compared with the control and 40 dB(A) exposure nights. When the control nights were excluded and parameters were compared between the three levels of stationary noise exposure, stage 2, the intercept of the regression line, and average sleep depth were increased almost in proportion to the increased noise exposure. In contrast, sleep latency, frequencies of sleep stage shift, stages W, 1, 3, MT, and REM, as well as the gradient of the regression line were decreased with increased noise exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2002

NREM sleep EEG frequency spectral correlates of sleep complaints in primary insomnia subtypes.

STUDY OBJECTIVES: To determine whether the frequency spectrum of the sleep EEG is a physiologic correlate of 1) the degree to which individuals with persistent primary insomnia (PPI) underestimate their sleep time compared with the traditionally scored polysomnogram (PSG) and 2) the sleep complaints in PPI subjects who have relatively long traditionally scored PSG sleep times and relatively greater underestimation of sleep time. DESIGN: We compared EEG frequency spectra from REM and NREM sleep in PPI subjects subtyped as subjective insomnia sufferers (those with relatively long total sleep time and relative underestimation of sleep time compared with PSG), and objective insomnia sufferers (those with relatively short PSG total sleep time) with EEG frequency spectra in normals. We also studied the correlation between these indices and the degree of underestimation of sleep. Further, we determined the degree to which sleep EEG indexes related to sleep complaints. SETTING: Duke University Medical Center Sleep Laboratory. PARTICIPANTS: Normal (N=20), subjective insomnia (N=12), and objective insomnia (N=18) subjects. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Lower delta and greater alpha, sigma, and beta NREM EEG activity were found in the patients with subjective insomnia but not those with objective insomnia, compared with the normal subjects. These results were robust to changes in the subtyping criteria. No effects were found for REM spectral indexes. Less delta non- REM EEG activity predicted greater deviation between subjective and PSG estimates of sleep time across all subjects. For the subjective insomnia subjects, diminished low-frequency and elevated higher frequency non- REM EEG activity was associated with their sleep complaints. CONCLUSIONS: NREM EEG frequency spectral indexes appear to be physiologic correlates of sleep complaints in patients with subjective insomnia and may reflect heightened arousal during sleep.

Adult↗
PubMed1992

Update on disorders of sleep and the sleep--wake cycle.

Wakefulness and sleep are antagonistic states competing for the domain of brain activity. Non-REM sleep and REM sleep are different states of being, sustained by activity in brainstem nuclei, hypothalamus, basal forebrain, and thalamus. Such complex phenomenology is subject to many alterations grouped in the new International Classification of Sleep Disorders. The insomnias are the result of interacting psychosocial, psychophysiologic, neurodevelopmental, and medical factors. Proper perspective of each factor provides the clinical strategies to approach medically the symptom-complex of insomnia. The most common cause of daytime hypersomnia is chronic sleep deprivation. Obstructive sleep apnea responds to nasal CPAP, but the failure rate approaches 30%. In intolerant patients BiPAP and surgical remedies should be considered. Motor and behavioral abnormalities of sleep may be linked to REM sleep as in the REM sleep behavior disorder. Paroxysmal nocturnal dystonia and nocturnal wanderings may be associated with epilepsy. Intrusions of one state of being (wakefulness, non-REM sleep, and REM sleep) into another result in mixed, poorly defined, or only partially developed states. Dissociation of states may be responsible for confusional arousals, hallucinations, and cateplexy. Senile degeneration of the suprachiasmatic nuclei may underlie the circadian rhythm changes in old age and the "sundown" syndrome in demented patients. Misalignment of the hypothalamic pacemaker causes dysregulation of sleep-related physiologic and behavioral variables. Exposure to bright light retrains the pacemaker in night-shift workers, transmeridian travelers, and in patients with seasonal affective syndrome. Benzodiazepine compounds are very effective hypnotics, but should be used sparingly in the elderly to avoid falls, memory lapses, and aggravation of a preexisting sleep apnea syndrome. Sleep laboratory evaluations are indicated in patients with hypersomnia, suspected sleep apnea syndrome, motor-behavioral disorders of sleep, and in many individuals complaining of insomnia.

Age Factors↗
PubMed1994

The meaning of good sleep: a longitudinal study of polysomnography and subjective sleep quality.

The present study sought to investigate the meaning of subjectively good sleep, using a longitudinal and intraindividual design. Eight subjects slept in an isolation unit according to an irregular schedule of 6 h sleeps and 1 h naps, designed to give normal amounts of time in bed (1/3 of total), but variable sleep quality. Eight sleeps and eight naps were used for longitudinal simple and multiple regression analyses with standard polysomnographical sleep variables as predictors and subjective sleep quality as dependent variables. The results showed that subjective sleep quality (and related variables) was closely related to sleep efficiency, but not sleep stages. At least 87% efficiency was required for ratings of 'rather good' sleep. In addition, sleep quality ratings improved with closeness (of the awakening) to the circadian acrophase (17.00-21.00 hours) of the rectal temperature rhythm. The subjective ease of awakening differed from most other other variables in that it was related to low sleep efficiency. Objective and subjective homologues of sleep length and sleep latency showed high mean intraindividual correlations (r = 0.55 and 0.64, respectively). It was concluded that objective measures of sleep continuity were closely reflected in perceived sleep quality and that sleep quality essentially means sleep continuity.

Journal Article↗
PubMed2001

Sleep and sleep electroencephalogram in depressed patients treated with phenelzine.

BACKGROUND: The beneficial effect of antidepressant interventions has been proposed to depend on suppression of rapid eye movement (REM) sleep or inhibition of electroencephalographic (EEG) slow-wave activity (SWA) in non-REM sleep. Use of the monoamine oxidase inhibitor phenelzine sulfate can eliminate REM sleep. We studied the relation between REM sleep suppression and antidepressant response and the effect of phenelzine therapy on sleep EEG power spectra. METHODS: Open-labeled prescriptions of 30 to 90 mg of phenelzine were given to 11 patients with major depressive disorder (6 men and 5 women; mean age, 41.4 years); all were physically healthy. Mood, dream recall, sleep, sleep EEG, and ocular and muscular activity during sleep were studied before treatment and during the third and fifth weeks of pharmacotherapy. RESULTS: Six patients remitted from depression, 2 responded partially, and 3 showed no antidepressant response. Independent from clinical response, REM sleep was dramatically suppressed. On average, only 4.9 minutes of REM sleep was observed in treatment week 5, and it was completely absent in 6 patients. This effect was compensated for by increased stage 2 sleep. In non-REM sleep, EEG power was higher than at baseline between 16.25 and 25 Hz. Slow-wave activity (power within 0.75-4.5 Hz) and the exponential decline of SWA during sleep were not affected. CONCLUSIONS: Antidepressant response to phenelzine treatment does not depend on elimination of REM sleep or inhibition of SWA in non-REM sleep. In depressed patients, REM sleep is regulated independently from non-REM sleep and can be manipulated without altering the dynamics of SWA.

Adult↗
PubMed2004

Recurrence quantification analysis of sleep electoencephalogram in sleep apnea syndrome in humans.

The aim of this study is to elucidate whether the results of recurrence quantification analysis (RQA) of sleep EEGs in sleep apnea syndrome are valuable for analyzing sleep EEGs in sleep apnea syndrome. We investigated the ability of RQA to discriminate sleep stages and to characterize the different behaviors of sleep EEGs in sleep apnea syndrome. RQA was applied to EEG signals during sleep stages 1, 2, slow wave sleep (SWS), REM and the stage 'awake.' The sleep EEG signals were obtained from the MIT-BIH polysomnographic database. To examine the differences in the RQA measures for all sleep stages, one-way analysis of variance (ANOVA) and post hoc analysis were performed. From the results, all sleep stages could be distinctly discriminated by means of the RQA measure of %RATIO. We observed that stage 1 and REM had fewer recurrences, and that stage 2 was more autocorrelated than the other stages. The different dynamic behaviors of wakefulness and sleep EEG were also observed. Of significant interest was the observation that RQA was able to distinguish stage 1 from REM. In conclusion, we suggest that the information obtained from RQA of sleep EEGs in sleep apnea syndrome is valuable for its analysis, and that RQA constitutes a useful tool for analyzing sleep EEGs in subjects with sleep apnea syndrome.

Computing Methodologies↗