Nighttime plasma cortisol secretion and EEG sleep—Are they associated?

Since the initial rise in plasma cortisol during sleep usually occurs near the second period of rapid eye movement (REM) sleep, a more precise association between the initial cortisol rise and electroencephalographic (EEG) sleep was examined in 22 normal control subjects. Our results indicate that the length of the total non-REM sleep period between the first and second REM period including awake time was significantly correlated to the cortisol rise time. However, the timing of the initial cortisol rise was not significantly related to the overall plasma cortisol levels during the night. But the second non-REM sleep period (minus awake time) is inversely related to overall cortisol levels during the night.     

Neuropeptide Y (NPY) shortens sleep latency but does not suppress ACTH and cortisol in depressed patients and normal controls

Preclinical and clinical studies suggest that neuropeptide Y (NPY) exerts functional corticotropin-releasing hormone (CRH) antagonistic effects. NPY activity appears to be blunted in depression. Recently, we have found in young normal male controls after repetitive administration of NPY a shortened sleep latency and a decrease of time awake and, in the second half of the night, EEG delta-power; cortisol and ACTH levels were blunted. Since during depression there is an overactivity of CRH, we tested the capacity of NPY to affect sleep endocrine activity in patients with depression compared with controls. After one night of adaptation we administered hourly IV injections of placebo (PL) during the second night and of 50 microg NPY during the third night between 22:00 and 01:00 h. Throughout the night ACTH, cortisol and prolactin levels were measured, simultaneously the sleep electroencephalogram (EEG) was recorded. Depressed patients as well as healthy controls exhibited significant shortening of sleep onset latency (SOL) (mean+/-SD; controls: 41.9+/-48.2 min PL vs 22.1+/-17.3 min NPY; patients: 31.8+/-19.8 min PL vs 24.7+/-20.1 min NPY; P<0.06) and REM latency (controls: 79.3+/-27.5 min PL vs 69.0+/-19.4 min NPY; patients: 79.8+/-45.5 min PL vs 52.4+/-51.2 min NPY; P<0.05). Both patients and controls showed a trend to an increase of prolactin during the night. In contrast to our recent observation in young normal subjects time awake, ACTH and cortisol remained unchanged in patients and controls in response to NPY. Whereas also an adaptation effect may contribute to the shortening of SOL, this change and the prolactin elevation are in line with a CRH antagonistic and GABA(A) agonistic/benzodiazepine-like effect of NPY. The lack of effects on time awake and HPA hormones may be explained by the higher CRH activity due to age and depression in the investigated samples in comparison to our recent study in young subjects.     

Successful separation of depressed, normal, and insomniac subjects by EEG sleep data.

Data from all-night EEG sleep studies were used to distinguish normal subjects, primary depressed patients, and primary insomniac patients. In part 1, we compared 41 normal subjects, 56 depressed patients, and 18 insomniacs. In a univariate comparison with normal subjects, depressed patients showed less total sleep, longer sleep latency, more early morning awake time, more intermittent awake time, less delta sleep, less sleep efficiency, and shorter rapid eye movement (REM) latencies; compared with insomniacs, depressed patients showed greater early morning awake time, shorter REM latency, greater REM index, and greater REM density. Using multivariate discriminant analysis, 82% of the sample were correctly classified by diagnosis: 100% of the normal subjects, 72% of the depressed patients, and 77% of the insomniacs. Eight variables contributed to the multivariate separation of depressed individuals from insomniacs and normals: total sleep time, total recording period, sleep efficiency, sleep latency, early morning awake time, awake time, REM time and REM%. When the discriminant functions were applied to a second group of 18 primary depressed patients, 82% were correctly classified as depressed. These results suggest that primary depressed patients and primary insomniac patients may show relatively characteristic patterns of sleep abnormality.     

Nocturnal polysomnography in obsessive–compulsive disorder

To determine if sleep abnormalities occur in obsessive–compulsive disorder (OCD), 2 nights of sleep electroencephalographic (EEG) recordings were obtained from 13 medication-free outpatients with OCD and 13 age- and sex-matched normal volunteers. Patients were awake more on night 2 than on night 1, whereas control subjects had less time awake on night 1; no other differences between groups were found on sleep latency, sleep time, minutes of movement, sleep efficiency, rapid eye movement (REM) latency or amount of stage 1, 2, 3, or 4 or REM sleep. Within the patient group, total scores on the Yale–Brown Obsessive–Compulsive Scale were negatively correlated with total sleep time (r=−0.51, P=0.07), sleep efficiency (r=−0.51, P=0.07), and duration of stage 1+2 sleep (r=−0.49, P=0.09) but not with REM time (r=−0.05, P=0.87) or latency (r=−0.26, P=0.39). Previous sleep studies in OCD have had divergent results, especially regarding REM latency; our results suggest that many OCD patients have essentially normal sleep EEG findings.     

REM sleep in depression is influenced by ethnicity

The influence of ethnicity on the manifestation of EEG sleep changes in depression was studied in 95 patients (21 African-Americans [AA], 17 Asians [AS], 37 Caucasians [C] and 20 Hispanics [H]) with unipolar major depression. Subjects were studied twice for 2 consecutive nights. On the second night of each 2-night session, placebo or scopolamine (1.5 microg/kg, IM, at 23.00 h) was administered. On the baseline (placebo) night, sleep architecture, sleep continuity and rapid eye movement (REM) sleep variables were generally comparable among the groups. However, REM sleep was less in AA and AS subjects than in C and H subjects. Furthermore, the distribution of REM sleep over the course of the night in AA and AS subjects differed significantly from that in the C and H groups. Although scopolamine significantly affected sleep continuity and REM sleep measures, no significant differential effects of scopolamine were observed. Because many antidepressants suppress REM sleep, the differences in baseline REM sleep observed might be related to the greater sensitivity of some ethnic-minority depressed patients to pharmacotherapy.     

EEG sleep in young depressives: first and second night effects

The sleep electroencephalogram (EEG) of young, drug-free, recurrently depressed outpatients was analyzed for 2 nights and was compared to age-matched controls using a variety of standard and computerized measures of sleep activity. On the first night, young depressives showed significantly greater difficulty in falling asleep and decreased sleep efficiency. Sleep architecture differences between the young depressives and controls were highlighted by increased percentages of Stage 2 sleep and major decreases in Stages 3 and 4 (delta wave) sleep among the depressives, as indicated by either period analyses or spectral analysis. The greatest differences in delta wave activity during night 1 were found in the first two (non-rapid eye movement (NREM) periods as measured by period analysis (NREM period 1, p less than 0.04; NREM period 2, p less than 0.001--average delta wave count) or by spectral analysis for the first 100 min of sleep (0.5-2.0 Hz). In contrast to the NREM sleep findings, various REM variables, including REM latency did not significantly distinguish the two subject groups for either night 1 or 2. Stepwise discriminant analysis demonstrated that night 1 sleep latency and delta wave counts during the second NREM period correctly classified 100% of all 16 individuals studied. The only differences between the young depressed patients and controls that remained on night 2 were significant reductions in slow-wave sleep as quantified by the computerized methods. Taken together, these findings suggest that the EEG response of young outpatients to the first night's stay in a sleep laboratory may be a useful tool for the diagnosis of depression in this age group. In addition, the use of computerized methods in this study point to an underlying deficit in delta sleep waveforms as being a prominent feature of the sleep of young depressed subjects.     

Human sleep EEG analysis using the correlation dimension.

Sleep electroencephalograms (EEG) were analyzed by non-linear analysis. Polysomnography (PSG) of nine healthy male subjects was analyzed and the correlation dimension (D2) was calculated. The D2 characterizes the dynamics of the sleep EEG, estimates the degrees of freedom, and describes the complexity of the signal. The mean D2 decreased from the awake stage to stages 1, 2, 3 and 4 increased during rapid eye movement (REM) sleep. The D2 during each REM sleep stage were high and those during each slow wave sleep stage were low, respectively, for each sleep cycle. The mean D2 of the sleep EEG in the second half of the night was significantly higher than those in the first half of the night. Significant changes were also observed during sleep stage 2, but were not seen during REM sleep and sleep stages 3 and 4. The D2 may be a useful method in the analysis of the entire sleep EEG.     

Sleep Alterations After Acute Administration of Carbamazepine in Cats

Little is known about the effects of carbamazepine (CBZ) on sleep despite the relationship between sleep and epilepsy and the common clinical use of CBZ. As part of a larger study on sleep and interictal activity in kindled cats, we performed sleep recordings in 11 normal cats before and after acute administration of CBZ. Epidural screws (frontooccipital) and depth electrodes (amygdala and hippocampus) were implanted bilaterally for EEG recording. Supraorbital screws and neck intramuscular electrodes were inserted for EOG and EMG. Ten days after electrode implantation, recordings were made of animals for 2 consecutive nights to assess baseline sleep patterns. Before the third night, cats received a single oral dose of 100 mg CBZ. After washout, a second similar drug administration was given before the fourth night. Recordings were scored for wakefulness, stage I and II of NREM sleep, REM sleep, number of stage shifts, awakenings, and REM onsets. The administration of CBZ produced a significant decrease in duration and percentage of REM sleep (p less than 0.001) and an increase in stage I NREM (p less than 0.05). Total sleep time was increased (p less than 0.05); awakenings were shorter (p less than 0.01), and stage I episodes were longer (p less than 0.01).     

Oral Mg(2+) supplementation reverses age-related neuroendocrine and sleep EEG changes in humans

The process of normal aging is accompanied by changes in sleep-related endocrine activity. During aging, an increase in cortisol at its nadir and a decrease in renin and aldosterone concentration occur. In aged subjects, more time is spent awake and slow-wave sleep is reduced: there is a loss of sleep spindles and accordingly a loss of power in the sigma frequency range. Previous studies could show a close association between sleep architecture, especially slow-wave sleep, and activity in the glutamatergic and GABAergic system. Furthermore, recent studies could show that the natural N-methyl-D-aspartate (NMDA) antagonist and GABA(A) agonist Mg(2+) seems to play a key role in the regulation of sleep and endocrine systems such as the HPA system and renin-angiotensin-aldosterone system (RAAS). Therefore, we examined the effect of Mg(2+) in 12 elderly subjects (age range 60-80 years) on the sleep electroencephalogram (EEG) and nocturnal hormone secretion. A placebo-controlled, randomised cross-over design with two treatment intervals of 20 days duration separated by 2 weeks washout was used. Mg(2+) was administered as effervescent tablets in a creeping dose of 10 mmol and 20 mmol each for 3 days followed by 30 mmol for 14 days. At the end of each interval, a sleep EEG was recorded from 11 p.m. to 7 a.m. after one accommodation night. Blood samples were taken every 30 min between 8 p.m. and 10 p.m. and every 20 min between 10 p.m. and 7 a.m. to estimate ACTH, cortisol, renin and aldosterone plasma concentrations, and every hour for arginine-vasopressin (AVP) and angiotensin 11 (ATII) plasma concentrations. Mg(2+) led to a significant increase in slow wave sleep (16.5 +/- 20.4 min vs. 10.1 +/- 15.4 min, < or =0.05), delta power (47128.7 microV(2) +21417.7 microV(2) vs. 37862.1 microV(2) +/- 23241.7 microV(2), p < or =0.05) and sigma power (1923.0 microV(2) + 1111.3 microV(2) vs. 1541.0 microV(2) + 1134.5 microV(2), p< or =0.05 ). Renin increased (3.7 +/- 2.3 ng/ml x min vs. 2.3 +/- 1.0 ng/ml x min, p < 0.05) during the total night and aldosterone (3.6 +/- 4.7 ng/ml x min vs. 1.1 +/- 0.9 ng/ml x min, p < 0.05) in the second half of the night, whereas cortisol (8.3 +/- 2.4 pg/ml x min vs. 11.8 +/- 3.8 pg/ml x min, p < 0.01) decreased significantly and AVP by trend in the first part of the night. ACTH and ATII were not altered. Our results suggest that Mg(2+) partially reverses sleep EEG and nocturnal neuroendocrine changes occurring during aging. The similarities of the effect of Mg(2+) and that of the related electrolyte Li+ furthermore supports the possible efficacy of Mg(2+) as a mood stabilizer.     

Intraindividual long-term stability of sleep electroencephalography in school-aged children

ObjectiveTo examine the long-term stability of sleep duration, sleep continuity, and sleep architecture assessed via unattended home sleep electroencephalography (EEG) during middle childhood.MethodsA total of 69 healthy children (18 girls and 51 boys) aged 8.2 years (standard deviation = 1.3 years) at T1 underwent unattended home sleep EEG on two nights separated by 18.5 months (standard deviation = 3.9 months). Of the children, 34 (49.3%) children were born prematurely (<32 gestational weeks; mean birth weight = 1367 g) and 35 (50.7%) children were born at term (mean birth weight = 3275 g).ResultsWe found moderate to substantial stability (all p <0.001) for total sleep time (TST; intraclass correlation coefficient [ICC] = 0.65), slow wave sleep (SWS; min, %: ICC = 0.49), and stage 2 sleep (min; ICC = 0.47), and found fair stability (all p <0.013) for sleep efficiency (ICC = 0.28), nocturnal awakenings (ICC = 0.33), stage 2 sleep (%; ICC = 0.32), and rapid eye movement (REM) sleep (min: ICC = 0.33; %: ICC = 0.27). Prematurity status was not associated with stability of sleep EEG indices over time.ConclusionsLong-term follow-up of one night of unattended home sleep EEG during middle childhood reveals that TST, stage 2 sleep, and SWS are relatively stable, trait-like characteristics. This applies less strongly for sleep efficiency, nocturnal awakenings, and REM sleep. Stage 1 sleep and REM latency showed no stability.     

Alpha-helical CRH exerts CRH agonistic effects on sleep-endocrine activity in humans

CRH is known to enhance wakefulness and to reduce SWS. In addition, some but not all, studies suggest that CRH promotes REM sleep. Alpha-helical CRH exerts CRH-antagonistic effects in various studies. We studied its effect on sleep EEG and nocturnal secretion of ACTH, cortisol, GH (n = 7) in young normal male subjects. After administering the substance cortisol and ACTH levels were enhanced during the total night compared to placebo. We found an increase of the time spent awake for the first half. ACTH (2nd half of the night) and cortisol (total night and 1st half of the night) increased. The results of the present study correspond to a mixture of agonistic and antagonistic effects of alpha-helical CRH.     

Narcolepsy and sudden onset of REM periods after nocturnal awakenings

The objective of this study was to evaluate polysomnographic data, and especially the sudden onset of REM periods that occur after spontaneous awakenings during the night as characteristics of narcolepsy. We evaluated 148 consecutive patients with excessive daytime somnolence, except for those with sleep apnea. After clinical evaluation, all-night polysomnographic recording and multiple sleep latency test, 55 were diagnosed as narcoleptics and 93 were grouped as non-narcoleptics. The mean age of narcoleptics was 42.9 +/- 14.4 years old and the non-narcoleptics were 40.3 +/- 13.5 years old. Polysomnographic variables were compared between both samples using unpaired t test. Non-significant differences were found for: sex; total time in bed; total sleep time; time in stages 3, 4 and REM; number of arousals (less than 30 sec); number of body movements; REM density. The following significant differences were found: number of sleep onset REM periods during the night was higher for narcoleptics (p less than 0.001); total sleep time was lower for narcoleptics (p = 0.02); sleep latency was shorter for narcoleptics (p less than 0.001); REM latency to stage 1 was shorter for narcoleptics (p less than 0.001); time in stage 1 was higher for narcoleptics (p less than 0.001); time in stage 2 was lower for narcoleptics (p less than 0.001); number of full awakenings (greater than 30 sec) was higher for narcoleptics (p less than 0.001); number of awakenings longer than 5 minutes was higher for narcoleptics (p = 0.002). In conclusion, there were marked differences in the sleep architecture between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Changes in EEG power density during sleep laboratory adaptation in depressed inpatients.

BACKGROUND: The aim of the present study was to evaluate the first-night effect in depressed inpatients, using standard sleep measures as well as all-night spectral analysis of the sleep electroencephalogram (EEG). METHODS: Eighteen drug-free, depressed inpatients were studied for 3 consecutive nights in the hospital sleep laboratory. RESULTS: Visual sleep scoring results showed a slight but measurable first-night effect, characterized by a reduction of rapid eye movement (REM) sleep amount and increased wakefulness. Sleep EEG spectral analysis showed significantly reduced delta (p <.01) and theta (p <.05) power density in non-REM (NREM) sleep of the first night compared with that of the second and third nights. These differences were limited to the early part of the sleep period, a time during the night that is particularly vulnerable to the effects of depressive disorder. In contrast to the NREM sleep findings, spectral REM variables studied did not significantly vary across the three nights. CONCLUSIONS: The results obtained suggest that first-night data should not be simply discarded but could be used in subsequent analyses and could be considered useful in the evaluation of the sleep of depressed patients.     

Comparison of Sleep Characteristics of Subjects in Their 70's with Those in Their 80's

Abstract: This study was undertaken to examine the effect of aging on sleep. All-night sleep polygrams of 15 subjects in their 70's and 11 subjects in their 80's were recorded for three consecutive nights. The increase in stage wakefulness (SW) and the decrease in stage 2 (S2) were significant in the subjects in their 80's in comparison with those in their 70's (p < 0.05, P < 0.01, respectively). After the age of 70, slow wave sleep decreased in the earlier part of the night and REM sleep shifted to the earlier part of the night. These facts support the hypothesis that slow wave sleep and REM sleep compete with each other.     

Should we use oral magnesium supplementation to improve sleep in the elderly?: Article reviewed: K. Held,I.A. Antonijevic,H. Künzel,M. Uhr,T.C. Wetter,I.C. Golly,A. Steiger,H. Murck,Oral MG2+ supplementation reverses age-related neuroendocrine and sleep EEG changes in humans,Pharmacopsychiatry, 35 (2002), 135–143

Objectives: Magnesium (Mg) has been recognized as potentially affecting sleep and sleep-related neuroendocrine function and shown in prior work by these authors to alter EEG sleep characteristics. This study aims to determine if oral Mg supplement also improves sleep and related neuroendocrines, particularly in the elderly (age 60–80).Study design: Double-blinded, randomized, placebo-controlled crossover study.Study population: Healthy elderly subjects, age 60–80 (average 68.1, standard deviation 5.7), six women and six men.Methods: Two 20-day treatment periods, separated by 2 weeks, involved either a placebo or Mg administered as effervescent tablets given in a fixed escalation of the 10 mmol dose, first only in the morning for 3 days, then in the morning and noon for 3 days, and finally three times a day for the remaining 14 days of the treatment period. At the end of each treatment period a polysomnogram (PSG) was obtained for two nights, the first for accommodation without any actual recording and the second for the study data. Sleep was recorded from 11 p.m. to 7 a.m. the next day. An indwelling intravenous cannula was used to obtain repeated blood samples every 30 min from 8 to 10 p.m. and every 20 min from 10 p.m. to 7 a.m. for analyses of adrenocorticotropic hormone (ACTH), cortisol, renin and aldosterone. Arginine-vasopressin (AVP) and angiotensin II (ATII) were measured from the blood samples taken every hour. The blood analyses of ACTH, cortisol, renin and aldosterone were evaluated using standard area under the curve calculated separately for samples from the first (11:00 p.m.–2:20 a.m.) and the second (2:20–7:00 a.m.) parts of the night.Results: The analyses of the PSG for Mg compared to the placebo treatment condition showed significantly more slow-wave sleep (averages±standard deviations: 16.5±20.4 vs. 10.1±15.4 min.), but no significant change in total sleep time or amount of wake time during the night. The spectral analyses of the sleep EEG during the Mg treatment showed greater power in the delta and sigma frequency ranges (differences in both of about 0.5 standard deviations) but no significant differences in the theta, alpha and beta ranges. The analyses of the nocturnal hormones for the Mg compared to the placebo treatment found significantly lower Cortisol and higher renin for the first part of the night and significantly higher renin and aldosterone for the second part of the night. Aldosterone was also higher for the Mg condition in the first part of the night, but the difference was not statistically significant ( f=2.8, n=9 — blood analyses data were lost on three subjects).Serum analyses of Mg levels failed to show any significant difference between the treatment conditions. Adverse effects associated with the Mg treatment included soft stools for all subjects and slight edema in the extremities for one subject.Conclusions: The authors note that aging produces decreases in slow-wave sleep and in delta and sigma (spindle frequency) spectral power and that these three measures are improved with Mg treatment in their sample of older adults. Similarly, aging is associated with increased nocturnal cortisol release and with decreased activity of the renin–angiotensin–aldosterone system. The latter is shown by decreased plasma renin not associated with high blood pressure as well as reduced aldosterone concentration. The Mg treatment reversed the aging effect on both of these measures.The authors note that the increase in aldosterone might account for the slow-wave sleep increase and for the changes in cortisol, both of which have been shown to occur with experimentally induced increases in aldosterone. It is noted, however, that the increase in aldosterone was only marginally significant for the first part of the night. The authors also suggest that the differences observed could have resulted from the Mg effects on both the glutamatergic and GABAergic systems. They further argue that the changes with aging partly reversed by Mg treatment match those for depression, and the Mg treatment might thus serve as a mood stabilizer.     

Differential effects of a dual orexin receptor antagonist (SB-649868) and zolpidem on sleep initiation and consolidation, SWS, REM sleep, and EEG power spectra in a model of situational insomnia

Orexins have a role in sleep regulation, and orexin receptor antagonists are under development for the treatment of insomnia. We conducted a randomised, double-blind, placebo-controlled, four-period crossover study to investigate the effect of single doses of the dual orexin receptor antagonist SB-649868 (10 or 30 mg) and a positive control zolpidem (10 mg), an allosteric modulator of GABA(A) receptors. Objective and subjective sleep parameters and next-day performance were assessed in 51 healthy male volunteers in a traffic noise model of situational insomnia. Compared with placebo, SB-649868 10 and 30 mg increased total sleep time (TST) by 17 and 31 min (p<0.001), whereas after zolpidem TST was increased by 11.0 min (p=0.012). Wake after sleep onset was reduced significantly by 14.7 min for the SB-6489698 30 mg dose (p<0.001). Latency to persistent sleep was significantly reduced after both doses of SB-6489698 (p=0.003), but not after zolpidem. Slow wave sleep (SWS) and electroencephalogram (EEG) power spectra in non-REM sleep were not affected by either dose of SB-640868, whereas SWS (p< 0.001) and low delta activity (<=1.0 Hz) were increased, and 2.25-11.0 Hz activity decreased after zolpidem. REM sleep duration was increased after SB-649868 30 mg (p=0.002) and reduced after zolpidem (p=0.049). Latency to REM sleep was reduced by 20.1 (p=0.034) and 34.0 min (p<0.001) after 10 and 30 mg of SB-649868. Sleep-onset REM episodes were observed. SB-649868 was well tolerated. This dual orexin receptor antagonist exerts hypnotic activity, with effects on sleep structure and the EEG that are different from those of zolpidem.     

Spontaneous sleep interruptions during extended nights. Relationships with NREM and REM sleep phases and effects on REM sleep regulation.

OBJECTIVES: There is no agreement in the literature as to whether sleep interruption causes rapid eye movement (REM) pressure to increase, and if so, whether this increase is expressed as shortened REM latency, increased REM density, or increased duration of REM sleep. The purpose of the present study was to examine the effect of different durations of spontaneous sleep interruptions on the regulation of REM sleep that occurs after return to sleep. METHODS: The occurrence of spontaneous periods of wakefulness and their effects on subsequent REM sleep periods were analysed in a total sample of 1189 sleep interruptions which occurred across 364 extended nights in 13 normal subjects. RESULTS: Compared with sleep interruptions that last less than 10 min, sleep interruptions that last longer than 10 min occur preferentially out of REM sleep. In both the short and long types of sleep interruptions, the duration of REM periods that ended in wakefulness were shorter than the duration of those that were not interrupted by wakefulness. REM densities of the REM periods that terminated in periods of wakefulness were higher than those of uninterrupted REM periods. The proportion of episodes of wakefulness following REM sleep that were long-lasting progressively increased over the course of the extended night period. The sleep episodes that followed the periods of wakefulness were characterised by a short REM latency. REM duration was increased in episodes that followed long sleep interruptions compared to those that followed short sleep interruptions. REM density did not appear to change significantly in the episodes that followed sleep interruption. CONCLUSIONS: REM sleep mechanisms appear to be the main force controlling sleep after a spontaneous sleep interruption, presumably because during the second half of the night, where more sleep interruptions occur, the pressure for non-rapid eye movement sleep is reduced and the circadian rhythm in REM sleep propensity reaches its peak. Processes promoting REM sleep at the end of the night are consistent with the Pittendrigh and Daan dual oscillator model of the circadian pacemaker.     

Inverse coupling between ultradian oscillations in delta wave activity and heart rate variability during sleep.

OBJECTIVE: We investigate the relationship between changes in heart rate variability and electroencephalographic (EEG) activity during sleep. METHOD: Nine male subjects with regular non-rapid-eye movement-rapid-eye movement (NREM-REM) sleep cycles were included in the study. They underwent EEG and cardiac recordings during one experimental night. Heart rate variability was determined over 5-min periods by the ratio of low frequency to low frequency plus high frequency power [LF/(LF+HF)] calculated using spectral analysis of R-R intervals. EEG spectra were analyzed using a fast Fourier transform algorithm. RESULTS: We found an ultradian 80-120 min rhythm in the LF/(LF+HF) ratio, with high levels during rapid eye movement (REM) sleep and low levels during slow wave sleep (SWS). During sleep stage 2 there was a progressive decrease in the transition from REM sleep to SWS, and an abrupt increase from SWS to REM sleep. These oscillations were significantly coupled in a 'mirror-image' to the overnight oscillations in delta wave activity, which reflect sleep deepening and lightening. Cardiac changes preceded EEG changes by about 5 min. CONCLUSIONS: These findings demonstrate the existence of an inverse coupling between oscillations in delta wave activity and heart rate variability. They indicate a non-uniformity in sleep stage 2 that underlies ultradian sleep regulation.     

Quantitative EEG amplitude across REM sleep periods in depression: preliminary report

OBJECTIVE: To determine if there are significant differences in the temporal organization of rapid eye movement (REM) sleep microarchitecture between healthy controls and outpatients with major depressive disorder (MDD). METHODS: Forty age-matched subjects, 20 men and 20 women, half with MDD, were selected from an archive of sleep electroencephalography (EEG) data collected under identical conditions. Each participant spent 2 consecutive nights in the Sleep Study Unit of the University of Texas Southwestern Medical Center at Dallas, the first of which served as adaptation. The average amplitude in each of 5 conventional EEG frequency bands was computed for each REM period across the second night. Data were then coded for group and sex. RESULTS: Aside from REM latency, none of the key sleep macroarchitectural variables differentiated MDD patients from controls. REM latency was longest in men with MDD. Sleep microarchitecture, however, did show a number of between-group differences. In general, slower frequencies declined across REM periods, with a significant REM period effect for delta, theta and alpha amplitude. Group x sex interactions were also obtained for theta and alpha. Beta activity showed a unique temporal profile in each group, supported by a significant REM period x group x sex interaction. In addition, the temporal change in theta amplitude across REM periods was most striking in women with MDD. CONCLUSIONS: This study suggests that, like during non-REM sleep, EEG amplitude shows a systematic temporal change over successive REM sleep periods and also shows elements that are both disease- and sex-dependent.     

Sleep staging and respiratory events in refractory epilepsy patients: Is there a first night effect?

Purpose: We performed this analysis of possible first night effects (FNEs) on sleep and respiratory parameters in order to evaluate the need for two serial night polysomnograms (PSGs) to diagnose obstructive sleep apnea (OSA) in epilepsy patients. Methods: As part of a pilot multicenter clinical trial investigating the effects of treating sleep apnea in epilepsy, two nights of PSG recording were performed for 40 patients with refractory epilepsy and OSA symptoms. Sleep architecture was examined in detail, along with respiratory parameters including apnea/hypopnea index (AHI) and minimum oxygen saturation. Analysis included two‐tailed t‐tests, Wilcox sign rank analysis, and Bland Altman measures of agreement. Results: Total sleep time differed between the two nights (night 1,363.8 min + 59.4 vs. 386.3 min + 68.6, p = 0.05). Rapid eye movement (REM) sleep and percentage of REM sleep were increased during night two (night 1: 12.3% + 5.9 vs. night 2: 15.5% + 6.2, p = 0.007), and the total minutes of slow‐wave sleep (SWS) were increased (night 1: 35.6 + 60.7 vs. night 2: 46.4 + 68.1, p = 0.01). No other sleep or respiratory variables differed between the two nights. Given an AHI inclusion criterion of five apneas per hour, the first PSG identified all but one patient with OSA. Discussion: Respiratory parameters showed little variability between the first and second nights. Sleep architecture was mildly different between the first and second PSG night. Performing two consecutive baseline PSGs to diagnose OSA may not be routinely necessary in this population.