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Biomedical subjects

R H Van den Hoofdakker

Publications and source records attributed to R H Van den Hoofdakker.

At least 19 recordsLinked to original sources
PubMed1999

Sleep deprivation in depression: what do we know, where do we go?

Manipulations of the sleep-wake cycle, whether of duration (total or partial sleep deprivation [SD]) or timing (partial SD, phase advance), have profound and rapid effects on depressed mood in 60% of all diagnostic subgroups of affective disorders. Relapse after recovery sleep is less when patients are receiving medication; it may be prevented by co-administration of lithium, pindolol, serotonergic antidepressants, bright light, or a subsequent phase advance procedure. Diurnal and day-to-day mood variability predict both short-term response to SD and long-term response to antidepressant drug treatment. These mood patterns can be understood in terms of a "two-process model of mood regulation" based on the model well established for sleep regulation: the interaction of circadian and homeostatic processes. The therapeutic effect of SD is postulated to be linked to changes in disturbed circadian- and sleep-wake-dependent phase relationships and concomitant increase of slow-wave-sleep pressure; additionally, SD-induced sleepiness may counteract the hyperarousal state in depression. This model has the advantage of providing a comprehensive theoretical framework and stringent protocols ("constant routine," "forced desynchrony") to dissect out specific disturbances. Many aspects tie in with current serotonergic receptor hypotheses of SD action. A treatment inducing euthymia in severely depressed patients within hours is an important therapeutic option that has come of age for clinical use.

Antidepressive Agents↗
PubMed1998

Testing the hypothesis of a circadian phase disturbance underlying depressive mood in nonseasonal depression.

In a crossover design, 8 nonseasonal depressed subjects, selected on the presence of diurnal mood variations, and 8 sex- and age-matched controls were exposed to dim light (< 10 lux) in the evening (18:00-21:00 h) and bright light (2500 lux) in the morning (ML, 6:00-9:00 h), to dim light in the morning and bright light in the evening (EL), or to dim light both in the evening and in the morning (DL) during 3 consecutive days in each of these conditions. There were no initial phase differences between depressed and healthy subjects in the timing of dim light melatonin onset, sleep termination, and body temperature. The phase shifts after EL and ML in both healthy and depressed subjects were as expected on the basis of a human phase response curve. On average, there was no therapeutic effect of the light exposure in the depressed patients. Two patients improved, but these effects do not seem to be related to shifts in the circadian system.

Adult↗
PubMed1997

Endogenous and exogenous components in the circadian variation of core body temperature in humans.

Core body temperature is predominantly modulated by endogenous and exogenous components. In the present study we tested whether these two components can be reliably assessed in a protocol which lasts for only 120 h. In this so-called forced desynchrony protocol, 12 healthy male subjects (age 23.7 +/- 1.4 y) were subjected one by one to an artificial light/dark cycle of 20 h (10 lux vs. darkness). Core body temperature was measured continuously. The temperature data were analysed by an iterative method based on the assumption that the endogenous and exogenous components contribute to body temperature in an additive way. The results show that the average temperature curve is an almost perfect addition of the two components. The endogenous component differs from a sinusoid, and the relative contributions of the endogenous and exogenous components to the raw temperature curves differ substantially between the subjects. The average amount of unexplained variance in the individual data was 17%. Averaging of the body temperature curves over subjects reduced the unexplained variance to only 2%. This reduction in unexplained variance upon averaging over subjects must be due to the fact that most of the variance is either differently dependent on circadian phase for the various subjects or not dependent on circadian phase at all. The circadian pacemaker component revealed an average value of tau of 24.30 +/- 0.36 h, which is consistent with recent findings in the literature. We conclude that a short forced desynchrony protocol is sufficient for the distinction between the masking and pacemaker components of core body temperature. The same protocol can be used to study the influence of these components on all kinds of other physiological and psychological signals.

Adult↗
PubMed1996

Nonverbal attunement between depressed patients and an interviewer predicts subsequent improvement.

Depressed patients' support-seeking behaviour and the responses to this behaviour by others (support-giving) are presumed to play a causal role in depression. In interactions between normals, attuning nonverbal behaviour (i.e., equalizing levels of specific behavioural activities) is important for satisfaction of the participants with the interaction. We investigated the attunement of nonverbal support-seeking and support-giving of 31 depressed patients and 1 interviewers during a 20-min admission interview. We defined attunement as the absolute difference between patients' and interviewers' nonverbal behaviour. It was found that the more attunement increased over the interview, the more favourable the subsequent course of depression was. The findings emphasize the potential role of interpersonal processes in depression.

Adult↗
PubMed1996

Long-term changes in open field behaviour following a single social defeat in rats can be reversed by sleep deprivation.

The long-term consequences of a single social defeat on open field behaviour in rats were studied, with special emphasis on the time course of stress-induced changes. Animals were subjected to social defeat by placing them into the territory of an aggressive male conspecific for 1 h. After the defeat session experimental animals were returned to their home cage and their own room, receiving no further cues from the resident. Other animals serving as controls were placed in a clean and empty cage for 1 h. Five-minute open field tests were performed on days 1, 2, 7, 14, and 28 after defeat, with independent groups of rats. Locomotion of the animals was recorded and analyzed with an automated video system. Social defeat resulted in a strong subsequent reduction in open field activity, which lasted till at least 7 days after the conflict. Differences in total travelled distance were no longer significant 2 weeks after the conflict. The latency for moving to the outer ring of the open field arena after the start of the test was still significantly longer 4 weeks after defeat. The stress-induced reduction in open field locomotion could be reversed by 12-h sleep deprivation during the resting phase, an intervention known to have antidepressant effects in humans. Possible relevance of the present findings with respect to human affective disorders is discussed.

Affect↗
PubMed1995

Changes in EEG power density of non-REM sleep in depressed patients during treatment with trazodone.

Recently, it was hypothesized that acute or cumulative suppression of non-REM sleep intensity might be related to the therapeutic effects of antidepressants. This intensity has been proposed to be expressed in the EEG power density in non-REM sleep. In the present study, the relationship was examined between the changes of EEG power density in non-REM sleep and the changes in clinical state in 8 depressed patients during treatment with trazodone. 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. To minimize systematic influences of sleep duration and non-REM-REM sleep alterations, EEG power was measured over the longest common amount of non-REM sleep stages 2-4 (168.5 min), accumulated from sleep onset onwards. During trazodone treatment, the 13- and 14-Hz bins showed a significant reduction in EEG power. No clear-cut change, however, was observed in the EEG power of the delta frequency range (1-4 Hz) which is considered to be the principle manifestation of non-REM sleep intensity. Furthermore, no overall significant relationship between EEG power suppression and clinical improvement could be demonstrated.

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

A longitudinal study of interaction patterns of a psychiatrist and severely depressed patients based on observed behaviour: an ethological approach of interpersonal theories of depression.

Observed behaviour of a psychiatrist interacting with severely depressed patients during an interview was related to the course of depression during hospitalization. The behavioural structure of such interaction could be described by 6 factors for the patients and 7 factors for the psychiatrist. The study focuses on the psychiatrist's behaviour. The severity of depression and the level of the behaviour factors were assessed just after admission (drug-free) and 10 weeks later. Patients were divided a posteriori into non-improved patients (N = 13) and improved patients (N = 18). The psychiatrist displayed low levels of 'active-listening' (intensive body touching and other hand movements during listening) and showed a tendency to more 'encouragement' by use of remarks such as hm, yes, and head-nodding) in his interaction with patients who did not improve. These factors did not change over time, suggesting that they may play a role in the maintenance of depression. They are supposed to express involvement, and probably indicate psychiatrist's giving support to the support-seeking patients. At the same time the psychiatrist exhibited an aversive response to the non-improved patients, by showing higher frequencies of looking away during his encouragement. The results provide support for interactional theories on depression and illustrate the possible value of an ethological approach in the study of interactional processes.

Adult↗
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↗
PubMed1990

Total and partial sleep deprivation in clomipramine-treated endogenous depressives.

Improvement in depression after total sleep deprivation (TSD) is, as a rule, followed by relapse after subsequent ad libitum sleep. This study is addressed to the question of how nocturnal partial sleep following TSD affects this relapse. Thirty endogenously depressed patients participated in the study. During the night after TSD, subjects were allowed sleep during one of three periods, i.e., unlimited sleep (11:00 p.m.-8:00 a.m.), early partial sleep (11:00 p.m.-3:00 a.m.), or late partial sleep (4:00 a.m.-8:00 a.m.). The hypothesis that partial sleep deprivation on the night following TSD prevents relapse has to be rejected. Relapse was inversely related to a drop in minimum rectal temperature during the night with unlimited or partial sleep, compared with minimum rectal temperature on the previous night.

Body Temperature Regulation↗
PubMed1990

Effects of total sleep deprivation on urinary cortisol, self-rated arousal, and mood in depressed patients.

The possibility that the clinical response to total sleep deprivation (TSD) is mediated by dimensions of arousal was investigated in a group of 16 depressed patients. Self-reports of activation, stress, and mood were assessed 3 days before, during, and 2 days after TSD. Urinary cortisol excretion and responses to the dexamethasone suppression test (DST) were also measured. TSD increased cortisol excretion in depressed patients and advanced the time of the maximal excretion of cortisol. No such changes have been reported for normal subjects. Neither the increased excretion nor the time shift was related to the mood response to TSD. The DST results were also unrelated to this response. Indications that the mood response to TSD may be mediated by dimensions of arousal are the significant relationships between this response and the responses of subjective stress and activation to TSD. The TSD-induced cortisol increase was not related to the subjective arousal response to TSD. The increased cortisol excretion itself could be predicted by the averaged baseline levels of subjective stress: the lower the stress levels before TSD, the larger the cortisol response to TSD.

Adult↗
PubMed1988

Body core temperature and depression during total sleep deprivation in depressives.

Endogenously depressed patients were subjected to a total sleep deprivation (TSD) schedule of sleep-TSD-sleep-TSD. They were simultaneously treated with the antidepressant drug clomipramine. Self- and observer-rated depression was measured daily. Continuously measured rectal temperature (RT) data were available for the second TSD. It was found that a higher nocturnal minimum RT during this TSD was associated with a positive clinical response.

Body Temperature Regulation↗
PubMed1988

Prediction of clinical change by ethological methods.

The aim of this paper is to show that ethology may contribute to the search for early indicators of clinical changes in depression. Three studies are presented. One study deals with the prediction of treatment outcome over 10 weeks and the other two with the prediction of the acute clinical response to total sleep deprivation (TSD). In each study a number of behaviours were observed, as displayed during a baseline psychiatric interview by the patients as well as the psychiatrist. In this report, the predictive potency of directly observed behaviours is compared to the predictive value of global clinical measures of psychomotor activation. The behaviours of the patients were interpreted as "relational" and "nonrelational" behaviours. The relational behaviours (i.e., variation in looking, yes-nodding, gesturing) occurred less, the nonrelational behaviours (i.e., intensive body touching, head movements) occurred more in responders than in nonresponders to 10 weeks of treatment. Also in the TSD studies body touching was positively related to improvement. Global clinical assessment of psychomotor activation could not be related to outcome. The advantages of the observational methods are discussed.

Behavior↗
PubMed1988

On the contribution of sleep wake physiology to the explanation and the treatment of depression.

Physiological exploration has disclosed profound disturbances in the regulation of sleep in depression. The finding that depression can be relieved or intensified by manipulation of sleep has inspired the investigation of the possible pathogenetic significance of these dysregulations. Three hypotheses play a leading role in this context: the "phase-advance", the "S-deficiency" and the "acetylcholine-monoamine imbalance" hypothesis. They explain the therapeutic effects of a variety of sleep wake manipulations as consequences of the normalization of depressogenic sleep regulation disturbances. The issue discussed in this paper is whether these claims are valid. To what extent can the hypotheses explain the existing sleep physiological disturbance in depression as well as the results of therapeutic interventions in sleep? The empirical data provide firm evidence for the importance of particularly the timing of sleep in relation to the course of depression, both in respect to the spontaneous and the experimentally induced fluctuations of the clinical state. Without considerable extensions none of the hypotheses provide an adequate explanation of these facts.

Acetylcholine↗
PubMed1987

Quantitative analysis of the effects of slow wave sleep deprivation during the first 3 h of sleep on subsequent EEG power density.

The relation between EEG power density during slow wave sleep (SWS) deprivation and power density during subsequent sleep was investigated. Nine young male adults slept in the laboratory for 3 consecutive nights. Spectral analysis of the EEG on the 2nd (baseline) night revealed an exponential decline in mean EEG power density (0.25-15.0 Hz) over successive nonrapid eye movement--rapid eye movement sleep cycles. During the first 3 h of the 3rd night the subjects were deprived of SWS by means of acoustic stimuli, which did not induce wakefulness. During SWS deprivation an attenuation of EEG power densities was observed in the delta frequencies, as well as in the theta band. In the hours of sleep following SWS deprivation both the power densities in the frequency range from 1 to 7 Hz and the amount of SWS were enhanced, relative to the same period of the baseline night. Both the amount of EEG energy accumulating subsequent to SWS deprivation and its time course could be predicted accurately from the EEG energy deficit caused by SWS deprivation. The data show that the level of integral EEG power density during a certain period after sleep onset depends on the amount of EEG energy accumulated during the preceding sleep rather than on the time elapsed since sleep onset. In terms of the two-process model of sleep regulation (Borbély 1982; Daan et al. 1984) this finding indicates that EEG power density reflects the rate of decay of the regulating variable, S, rather than S itself, as was originally postulated.

Acoustic Stimulation↗
PubMed1987

Response to total sleep deprivation and clomipramine in endogenous depression.

In 44 endogenously depressed patients, response to total sleep deprivation (TSD) was investigated as a function of several biographical and clinical variables. All patients were subjected to a schedule of sleep-TSD-sleep-TSD. Antidepressant drug treatment (clomipramine) was started on the day before the first TSD. Sex, age, educational status, number of previous hospitalizations and duration of the current depressive episode were not related to the response to either the first or the second TSD. Likewise, no significant differences were found in the responses of unipolar and bipolar patients. In contrast, diurnal variation appeared to be positively correlated with response to TSD. Depressives with psychotic features reacted more favourably than non-psychotic depressives.

Adult↗