Search PubMed⌕ Search

Biomedical subjects

D G Beersma

Publications and source records attributed to D G Beersma.

At least 37 records · Page 2Linked to original sources
PubMed1995

Light therapy for seasonal affective disorder. The effects of timing.

BACKGROUND: Sixty-eight patients with seasonal affective disorder participated in a 10,000-lux light treatment study in which two questions were addressed: do response rates differ when the light is applied at different times of the day and does short-term rank ordering of morning and evening light influence response rates? METHOD: Three groups of patients received a 4-day light treatment: (I) in the morning (8.00-8.30 a.m., n = 14), (II) in the afternoon (1.00-1.30 p.m., n = 15) or (III) in the evening (8.00-8.30 p.m., n = 12). Two additional groups of patients received two days of morning light treatment followed by two days of evening light (IV, n = 13) or vice versa (V, n = 14). RESULTS: Response rates for groups I, II and III were 69, 57 and 80% respectively, with no significant differences between them. Response rates for groups IV and V were 67 and 50% respectively; this difference was not significant and these percentages did not differ significantly from those of groups I and III. CONCLUSIONS: The results indicate that the timing of light treatment is not critical and that short-term rank ordering of morning and evening light does not influence therapeutic outcome.

Adult↗
PubMed1994

A longitudinal study of diurnal mood variation in depression; characteristics and significance.

The course of 39 depressed in-patients' daily mood was recorded by means of frequent self-ratings during their entire stay (in total 3718 days). The frequency of diurnal variations largely varies between subjects without clear dichotomy in 'diurnal' and 'non-diurnal' subjects and the occurrence of diurnal variations is rather irregular. Mood variability measures rather than average daily mood improvement correlate with the response to sleep deprivation. These observations do not support theories of chronobiological rhythm disturbances in depression. It is argued that depressed subjects largely vary in susceptibility to stimuli. Signals generated by the biological clock or by processes related to the sleep-wake cycle are considered examples of such stimuli.

Adult↗
PubMed1993

Changes in sleep polygraphic variables and clinical state in depressed patients during treatment with citalopram.

Drug-induced improvement of depression may be mediated by changes in sleep physiology. The aim of this study was to relate changes in sleep polygraphic variables to clinical state during treatment with citalopram, a highly specific serotonin uptake inhibitor. Sixteen patients took part. The study was single-blind and uncontrolled. A 1-week wash-out period was followed by 1 week of placebo administration, a medication period of 5 weeks, and a 1-week placebo period. For the entire group a significant decrease of rapid eye movement sleep (REMS) and a significant lengthening of REMS latency were observed initially as well as at the end of treatment. No changes in sleep continuity were found, but non-REMS stage 2 (percentage) was significantly increased. On the basis of clinical change, as expressed by the scores of the Hamilton Rating Scale for Depression, at the end of the citalopram treatment the patient group was split in two halves: eight less and eight more improved patients. The groups did not differ with respect to any sleep polygraphic variable.

Adult↗
PubMed1993

Morning and evening light treatment of seasonal affective disorder: response, relapse and prediction.

Patients with seasonal affective disorder were randomly assigned to treatment with light in the morning (9.00-12.00 a.m.; n = 16; ML) or evening (6.00-9.00 p.m.; n = 11; EL). An intensive 24-day assessment procedure revealed the same response rates: 57% for ML, 50% for EL. During the rest of the winter season a relatively low relapse rate of 54% was found. No differences between ML and EL were found in the time course of depressed mood or fatigue. A significant negative correlation was found between diurnal variation during baseline and therapeutic response: the larger the diurnal variation the less the response, indicating a potential negative predictive value for this symptom. There were no significant correlations between baseline fatigue or hypersomnia and response.

Adult↗
PubMed1992

Can non-REM sleep be depressogenic?

Sleep and mood are clearly interrelated in major depression, as shown by the antidepressive effects of various experiments, such as total sleep deprivation, partial sleep deprivation, REM sleep deprivation, and temporal shifts of the sleep period. The prevailing hypotheses explaining these effects concern the antidepressant potency of the suppression of either REM sleep or non-REM sleep. This issue is discussed in the light of present knowledge of the kinetics of non-REM sleep intensity, REM sleep production, and their interaction. Recent findings have led us to suggest that the suppression of non-REM sleep intensity is the common pathway in the set of experimental data on the antidepressant effects of sleep manipulations.

Antidepressive Agents, Tricyclic↗
PubMed1991

Effect of clomipramine on sleep and EEG power spectra in the diurnal rodent Eutamias sibiricus.

Sleep was recorded in the diurnal rodent Eutamias sibiricus, chronically implanted with EEG and EMG electrodes. The tricyclic antidepressant drug clomipramine suppressed the duration of REM sleep and EEG power density in the frequencies between 1.5 and 13.5 Hz in nonREM sleep. During the administration of clomipramine, 24 h of sleep deprivation by forced locomotion significantly reduced the duration of waking and increased the duration of nonREM sleep. During the first 2 h of recovery sleep, EEG power density of the frequencies between 2.5 and 6 Hz was enhanced. These effects of sleep deprivation were to a large extent similar to those of sleep deprivation under drug free conditions. It is concluded that clomipramine affects the EEG in nonREM sleep but does not interfere substantially with nonREM sleep regulatory processes, which are activated by sleep deprivation.

Animals↗
PubMed1991

Can winter depression be prevented by light treatment?

The administration of light at the development of the first signs of a winter depression appears to prevent it from developing into a full-blown depression. No patient from a group of 10 treated in this way developed any signs of depression during the rest of the winter season, while five of seven patients from a control group became depressed and needed treatment during the winter season.

Adult↗
PubMed1990

REM sleep deprivation during 5 hours leads to an immediate REM sleep rebound and to suppression of non-REM sleep intensity.

Nine healthy male subjects were deprived of REM sleep during the first 5 h after sleep onset. Afterwards recovery sleep was undisturbed. During the deprivation period the non-REM EEG power spectrum was reduced when compared to baseline for the frequencies up to 7 Hz, despite the fact that non-REM sleep was not experimentally disturbed. During the recovery interval a significant rebound of REM sleep was observed, which was only accompanied by a very slight increase of power in the lower non-REM EEG frequencies. In order to control for intermittent wakefulness, the same subjects were subjected to non-REM sleep interruption during the first 5 h after sleep onset 2 weeks later. Again subsequent recovery sleep was undisturbed. The interventions resulted in a similar amount of wakefulness in both conditions. During the intervention period, the non-REM EEG power spectrum was only marginally reduced in the delta frequency range. REM sleep duration was only slightly reduced. During the recovery interval, however, a substantial increase in EEG power in the delta frequency range was noted, without notable changes in REM time. It is concluded that an increased pressure for REM sleep results in longer REM episodes and a reduced intensity of non-REM sleep.

Adult↗
PubMed1990

Sleep deprivation in bright and dim light: antidepressant effects on major depressive disorder.

Twenty-three patients with a major depressive disorder were deprived of a night's sleep twice weekly, one week staying up in the dimly lit living room of the ward (less than 60 lux), and one week in a brightly lit room (greater than 2000 lux). Immediate, but transient beneficial effects of sleep deprivation were observed primarily in eight patients (the 'responders'). The immediate effects did not differ greatly for the two conditions, indicating that exposure to light at night is an implausible explanation for the antidepressant effects of total sleep deprivation. There was some evidence that the bright light condition led to a more prolonged improvement of the responders.

Combined Modality Therapy↗
PubMed1990

Relations between depressed mood and vocal parameters before, during and after sleep deprivation: a circadian rhythm study.

The mechanism underlying improvement after total sleep deprivation (TSD) was studied in 14 major depressed patients. The suggestions that (1) circadian processes and/or (2) dimensions of arousal may play a role in the response to TSD were investigated. Diurnal variation of depressed mood and of mood- and arousal-related vocal parameters was studied in relation to the effect of TSD on depressed mood and vocal parameters. During 3 baseline days, during TSD and 2 days after TSD vocal parameters and depressed mood were assessed 6 and 3 times daily respectively. The mean fundamental frequency (frequency of vocal fold vibration, F0) (presumably reflecting aspects of arousal) as well as the range of the F0 (proposed to reflect sadness) showed a clear circadian pattern with a peak at about 4.00 p.m. TSD affected the circadian organization of the mean F0 and advanced the peak of the curve. After one night of subsequent sleep this effect disappeared. In addition, improvement after TSD coincided with an increase of the mean F0. The diurnal variation of mood before TSD predicted the mood response to TSD, whereas diurnal variation of vocal parameters did not. Moreover, circadian changes in vocal parameters were not related to changes in depressed mood. These findings suggest that the diurnal variations in mood and vocal parameters are regulated by different mechanisms. Data support the presumption that circadian as well as arousal processes are involved in the mood response to TSD. Circadian changes in vocal parameters due to TSD are not likely to reflect changes in the biological clock.

Adult↗
PubMed1990

Electroencephalogram power density and slow wave sleep as a function of prior waking and circadian phase.

Human sleep electroencephalograms, recorded in four experiments, were subjected to spectral analysis. Waking prior to sleep varied from 12 to 36 h and sleep was initiated at different circadian phases. Power density of delta and theta frequencies in rapid-eye-movement (REM) sleep and non-REM (NREM) sleep increased monotonically as a function of prior waking. The increase of power density in the theta frequencies contrasts with the reported decrease of theta activity as detected by period-amplitude analysis. Slow wave activity (power density, 0.25-4.0 Hz) in NREM sleep during the first 3 h of sleep did not deviate significantly from the homeostatic process S of the two-process model of sleep regulation. In contrast, visually scored slow wave sleep, stages 3 and 4, deviated from this prediction at some circadian phases. It is concluded that, in accordance with the two-process model of sleep regulation, slow wave activity in NREM sleep depends on prior waking and is not significantly influenced by circadian phase.

Adult↗
PubMed1989

Effects of seganserin, a 5-HT2 antagonist, and temazepam on human sleep stages and EEG power spectra.

The effects of seganserin, a specific 5HT2 antagonist, on human sleep were assessed in two experiments and compared to the effects of temazepam and sleep deprivation. During daytime recovery sleep after sleep deprivation, seganserin did not significantly enhance visually scored slow wave sleep (SWS, stages 3 + 4) or the EEG power density in the delta frequencies. Under these conditions temazepam reduced the power density in the delta and theta frequencies. During nighttime sleep after a nap in the evening, seganserin caused an increase in SWS, a reduction in intermittent wakefulness, and an enhancement of the power density in the delta and theta frequencies during non-rapid eye movement (NREM) sleep. Temazepam induced a reduction in the power density in the delta and theta frequencies. It is concluded that the 5HT2 antagonist, seganserin, can induce SWS. However, since the spectral results showed that the changes in the sleep EEG were not identical to those induced by sleep deprivation it seems premature to conclude that 5HT2 receptors are primarily involved in NREM sleep regulation.

Adult↗