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Biomedical subjects

M Kerkhofs

Publications and source records attributed to M Kerkhofs.

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

Acute, subchronic and withdrawal sleep EEG changes during treatment with paroxetine and amitriptyline: a double-blind randomized trial in major depression.

Paroxetine (30 mg), a selective serotonin (5-HT) reuptake inhibitor, was compared in a double-blind trial to amitriptyline (150 mg) in a sample of 40 inpatients aged 18-65 years who fulfilled Research Diagnostic Criteria for major depression. Patients were studied after a placebo drug washout period of 10 days and after an active 4-week treatment period. Sleep EEG recordings were performed before and at the end of the study as well as during acute treatment (first 2 days) and following withdrawal of active medication. Paroxetine shows an antidepressant effect similar to amitriptyline with a different side-effect profile typical of 5-HT reuptake inhibition. Paroxetine and amitriptyline decreased the amount of REM sleep, a well-known effect of classical antidepressants. Paroxetine also shared with other 5-HT reuptake inhibitors an alerting effect on sleep that was not shown to be detrimental on subjective sleep quality.

Adolescent↗
PubMed1994

The 24-hour profiles of cortisol, prolactin, and growth hormone secretion in mania.

OBJECTIVE: To characterize sleep and the 24-hour profiles of cortisol, prolactin (PRL), and growth hormone (GH) secretion in mania. METHODS: Blood was sampled at 15-minute intervals, and sleep was polygraphically recorded in eight unmedicated male patients with pure mania and the results compared with those from a group of 14 healthy age-matched controls. The circadian, sleep-related, and pulsatile hormonal variations were quantitatively characterized using specifically designed computer algorithms. RESULTS: The manic state was associated with alterations of corticotropic activity and circadian rhythmicity partially overlapping those previously observed in acute endogenous depression, consisting of an elevation of nocturnal cortisol levels and an early timing of the nadir of the circadian variation. Sleep onset was delayed and the sleep period was reduced. A trend for short rapid eye movement latencies was apparent in the adult patients. Both the amount and the temporal organization of PRL and GH secretion were normal. CONCLUSION: The manic state seems to be characterized by similar but less severe neuroendocrine and circadian abnormalities, compared with major depression.

Acute Disease↗
PubMed1994

TSH response to TRH and EEG sleep in non-bipolar major depression: a multivariate approach.

The TSH response to TRH and selected sleep EEG variables were studied in a homogeneous sample of 280 non-bipolar major depressed inpatients (95 males and 185 females). The TSH response to TRH was blunted in 28% of the sample. delta max TSH was correlated negatively with age, Hamilton rating scale, Newcastle scale, percentage of wake, and positively with basal TSH, percentage of stage II, slow wave sleep, REM sleep and REM latency. delta max TSH was also lower in male patients and in patients suffering from an endogenous or a psychotic subtype of major depression. Basal TSH was only correlated negatively with the Newcastle score. In view of intercorrelations between all these variables, and because of the confounding effect of age, gender and severity on both the TSH response to TRH and sleep EEG variables, a multiple regression analysis was performed and demonstrated that basal TSH and gender were the two variables with the highest contribution to the delta max TSH variance, followed by age and the presence of psychotic symptoms. When controlling strictly for these significant effects, correlation with the severity or with the endogenous character of depression, and with sleep EEG parameters disappeared.

Adult↗
PubMed1993

Twin study of the 24-h cortisol profile: evidence for genetic control of the human circadian clock.

To determine whether genetic factors control the expression of human circadian rhythmicity, we analyzed the 24-h profile of plasma cortisol in 11 monozygotic and 10 dizygotic pairs of normal male twins. Blood was sampled every 15 min, and sleep was monitored. Circadian rhythmicity was characterized by measures of amplitude, phase, and overall waveshape. Pulsatility was quantified by pulse frequency, pulse amplitude, and relative contribution of pulsatile vs. circadian variations. Data were analyzed by a procedure specifically developed for twin studies. Genetic control was demonstrated for the timing of the nocturnal nadir and for the proportion of overall temporal variability associated with pulsatility. Environmental effects were detected for the 24-h mean and the timing of the morning acrophase. The timing of the cortisol nadir is a robust marker of human circadian phase and is dependent, under entrained conditions, on the length of the endogenous period. Animal studies have shown that the endogenous period and the pattern of entrainment to exogenous 24-h periodicities are genetically controlled. Our results indicate that, despite the increased impact of social inputs, genetic factors also control human circadian rhythmicity.

Adolescent↗
PubMed1993

Sleep-promoting effects of growth hormone-releasing hormone in normal men.

Growth hormone-releasing hormone (GHRH) promotes rapid-eye-movement (REM) and non-REM sleep in animals, but there is little direct evidence for a hypnogenic action of GHRH in humans. In the present study, the possible somnogenic effects of intravenous bolus injections of a dose of GHRH eliciting physiological elevations of GH secretion in healthy young men were investigated. GHRH (0.3 micrograms/kg body wt) was given in early sleep [i.e., 1st slow-wave (SW) period], late sleep (i.e., 3rd REM period), and early sleep after sleep deprivation until 0400 h (i.e., 1st SW period). In the absence of sleep deprivation, injection of GHRH in early sleep did not modify SW sleep but increased REM sleep. GHRH administration in the third REM period was followed by a marked decrease of wake and an almost 10-fold increase in SW sleep. When GHRH was administered during the first SW period after sleep deprivation until 0400 h, the duration of wake decreased. Thus GHRH has sleep-promoting effects in young adults, particularly when given at a time of decreased sleep propensity.

Adult↗
PubMed1992

Sleep polygraphic variables in anorexia nervosa and depression: a comparative study in adolescents.

Sleep EEG variables were compared in an adolescent population consisting of 11 anorectic girls, 11 young depressed patients and 11 healthy volunteers matched for age and sex. Anorectic patients differed from depressed patients in a greater number and a higher length of awakenings. In comparison with controls, anorectic patients showed less sleep efficiency, a higher length of awakenings and less REM sleep. When anorectic patients were divided in restricting and bulimic subtypes, the bulimic anorectics showed an increase in stage 3 of sleep. These results do not support a direct association between eating disorders and affective disorders. Sleep EEG variables were not significantly correlated to the Body Mass Index.

Adolescent↗
PubMed1992

Biological and clinical features of recurrent brief depression: a comparison with major depressed and healthy subjects.

Recurrent brief depression (RBD) has recently been proposed as a new subtype of affective disorder characterized by episodes of major depression which last less than two weeks. The aim of this study was to further evaluate the validity of this putative subtype by means of clinical and biological data. DST, TSH response to TRH and sleep EEG variables were compared in 25 RBD patients sex- and age-matched to 25 major depressed (MD) and 25 healthy subjects. Family history, age at onset, and psychiatric comorbidity did not discriminate RBD from MD. Recurrent unipolar depression was found to be more prevalent in MD. Although less severely depressed during the biological tests, patients with RBD did not significantly differ from those with MDD on basis of DST non-suppression, blunted TSH response and shortening of REM latency. Compared to controls, a greater sleep onset latency was observed both in RBD and MD and a lower total sleep time in MD patients only. These results suggest that RBD could be viewed as a subtype of affective disorder sharing many characteristics with MDD.

Adult↗
PubMed1992

A quantitative estimation of growth hormone secretion in normal man: reproducibility and relation to sleep and time of day.

Recent reports, based on measurements of plasma GH levels, have challenged the concept that GH secretion is dependent on sleep and not modulated by circadian rythmicity. Because plasma levels reflect not only the secretory process, but also the effects of distribution and degradation, temporal limits of active secretion and, consequently, synchrony with other physiological events cannot be accurately estimated from circulating concentrations. The present study was undertaken to examine the roles of sleep and time of day in modulating pulsatile GH secretion, using a mathematical procedure (deconvolution) allowing secretory rates to be estimated from peripheral levels. Eight young nonobese healthy men participated each in six separate 16-h studies involving either normal or delayed sleep. Plasma GH levels were measured at 15-min intervals, and GH secretory rates were calculated by deconvolution. Each individual study was preceded by one night of habituation, and sleep was polygraphically recorded in all studies. Repeated measurements of plasma insulin-like growth factor-I (IGF-I) were performed in all subjects. Deconvolution revealed the existence of approximately 20% more GH pulses than detected in the plasma profiles. Large peaks of plasma GH concentrations often reflected the occurrence of a succession of secretory pulses. The total amount of GH secreted varied 10-fold across individual studies, but the within-subject variability (32%) was less than half the across-subject variability (65%). IGF-I levels were also more reproducible for a given subject than across subjects (11% vs. 36% variability) and did not correlate with the amount of GH secreted. During normal waking hours, the GH secretory rate was similar in the evening and the morning. This secretory rate was doubled during wakefulness at times of habitual sleep and tripled during sleep, even when sleep was delayed until 0400 h. A pulse starting within 30 min after sleep onset was present in all profiles with normal sleep and in 13 of 16 profiles with delayed sleep. The amount of GH secreted in response to sleep onset was tightly correlated with the level of secretion during wakefulness (r = 0.92). Almost 70% (57 of 83) of the pulses occurring during sleep were associated with slow wave (SW) stages. The amount of GH secreted in SW-associated pulses was correlated with the amount of SW occurring during the pulse, even when sleep-onset pulses were not considered. We conclude that in normal adult men, the amount of GH secretion and the levels of IGF-I are more reproducible within than across individuals.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1992

Sleep, awakenings, and insulin-like growth factor-I modulate the growth hormone (GH) secretory response to GH-releasing hormone.

To delineate possible factors influencing the magnitude of the GH response to GH-releasing hormone (GHRH), eight young healthy men participated in seven 16-h studies involving saline infusions or injections of 0.3 micrograms/kg GHRH at various times of day and stages of sleep. GH responses were quantified by deconvolution, a procedure allowing for secretory rates to be estimated from peripheral levels. While the plasma responses were monophasic, deconvolution revealed that the secretory response to GHRH generally included several distinct bursts in rapid succession. The intersubject variability of GH responses was very wide, but for a given subject, the response was quite reproducible (mean +/- SEM coefficient of variation, 21 +/- 3%). When GHRH was given during the waking period, the magnitude of the response was directly related to the amount of spontaneous GH secretion, negatively correlated with circulating levels of insulin-like growth factor-I (IGF-I) and was not influenced by time of day. When GHRH was given during slow wave sleep, the magnitude of the response was enhanced. When GHRH was given during rapid eye movement sleep, the response was similar to that observed during wake. Awakenings during sleep consistently inhibited the secretory response to GHRH, and resumption of sleep was associated with a reappearance of the secretory process. Thus, in normal men of similar age and body weight, the GH response to GHRH is dependent on the sleep or wake condition, circulating levels of IGF-I, and, possibly, genetic and lifestyle factors.

Adult↗
PubMed1992

Does non-invasive ambulatory blood pressure monitoring disturb sleep?

OBJECTIVE: To assess the effects of non-invasive ambulatory blood pressure monitoring upon sleep in healthy men. METHODS: Spontaneous variations in the quality of sleep were assessed by taking polygraph recordings in 44 healthy men aged 17-69 years. Subjects were allowed one night to become accustomed to the laboratory environment, and then their sleep was recorded for 4 consecutive nights. On day 4 blood pressure was measured every 10 min for 24 h. RESULTS: The blood pressure recording procedure caused a small but significant decrease in the amount of slow-wave sleep and an increase in the duration of nocturnal awakenings. As a result, sleep efficiency was decreased. The number of nocturnal awakenings was not affected by the blood pressure measurements. The effects of ambulatory blood pressure monitoring were qualitatively similar in young and older volunteers. CONCLUSION: Non-invasive ambulatory blood pressure monitoring induces modest sleep disturbances which are unlikely to artifactually distort the physiological 24-h blood pressure profile.

Adult↗
PubMed1991

Circadian and sleep-related endocrine rhythms in schizophrenia.

Plasma levels of prolactin, growth hormone, corticotropin, and cortisol were measured at 15-minute intervals for 24 hours in nine unmedicated male schizophrenic patients and in nine age-matched normal male subjects. Each study was preceded by 3 days of habituation to the laboratory environment. Sleep was polygraphically recorded. The circadian and pulsatile variations present in each hormonal profile were quantitatively characterized with the use of computer algorithms specifically designed for analyses of hormonal fluctuations. The major abnormality of neuroendocrine release that was observed in the schizophrenic patients was an almost threefold enhancement of the sleep-related increase in the prolactin level, associated with an intensified frequency of nocturnal prolactin pulses. This increased stimulatory effect of sleep on prolactin secretion was evident immediately after sleep onset. The normal inhibition of cortisol secretion during early sleep was absent in schizophrenic patients. The major sleep abnormalities were a prolonged sleep latency and a reduction in total rapid eye movement stage sleep. During wakefulness, prolactin and cortisol levels were normal. The 24-hour profile of growth hormone was unaltered in schizophrenic patients, and a sleep-onset growth hormone pulse was observed in all patients. No abnormalities were noted in the levels or temporal organization of corticotropin secretion. Both the amplitude and the timing of the cortisol rhythm were normal. We conclude that, in schizophrenic men, pituitary-adrenal function and circadian time-keeping are normal but prolactin secretion is hyperresponsive to the physiologic stimulus of sleep onset. Schizophrenia thus appears to be characterized by a subset of neuroendocrine disturbances distinct from that observed in major endogenous depression.

Adrenocorticotropic Hormone↗
PubMed1991

Genetic determinants of EEG sleep: a study in twins living apart.

In order to investigate the genetic components of sleep and, in particular, of REM sleep, we performed 3 consecutive all-night EEG recordings in 26 pairs of normal male twins living apart (11 monozygotic and 15 dizygotic). Our results indicate that in man non-genetic rather than genetic influences substantially determine variance in stage REM, in contrast to stages 2, 4 and to delta sleep. In this sample of male twins, waking measures also showed a significant genetic component.

Adult↗
PubMed1991

Twenty-four-hour patterns of sleep in depression.

Alterations of nocturnal sleep have been widely described in affective disorders. However, little is known about putative daytime sleep and to what extent daytime sleep could interfere with nocturnal sleep. The goal of this study was to investigate 24-hr sleep patterns in 12 depressed patients hospitalized for a major depressive disorder and in 10 control subjects studied under the same experimental conditions. Patients and controls were free to sleep whenever they chose, and sleep recordings were performed using the Oxford Medilog System during 60 hr. Daytime sleep episodes were detected in 50% of the patients and in 60% of the controls. Patients took naps at various times of the day, whereas controls napped in the early afternoon, during the well-known "postlunch dip". Thus daytime sleep prevalence was similar in both groups; however, the biphasic distribution of sleep observed in controls disappeared in the patients. Napping did not affect subsequent nocturnal sleep in either group.

Adult↗
PubMed1991

Neuroendocrine rhythms and sleep in aging men.

To delineate the physiological effects of aging on basal levels and temporal patterns of neuroendocrine secretions, the 24-h profiles of cortisol, thyroid-stimulating hormone (TSH), melatonin, prolactin, and growth hormone (GH) levels were simultaneously obtained at frequent intervals in eight healthy, active elderly men, age 67-84 yr and in eight young male adults, age 20-27 yr. The study was preceded by an extended period of habituation to laboratory conditions, and sleep was polygraphically recorded. Mean cortisol levels in the elderly were normal, but the amplitude of the circadian rhythm was reduced. Circulating levels of daytime and nighttime levels of both TSH and GH were greatly diminished in old age. In contrast, prolactin and melatonin concentrations were decreased during the nighttime only. The circadian rises of cortisol, TSH, and melatonin occurred 1-1.5 h earlier in elderly subjects, and the distribution of rapid-eye-movement stages during sleep was similarly advanced, suggesting that circadian timekeeping is modified during normal senescence. Despite perturbations of sleep, sleep-related release of GH and prolactin occurred in all elderly men. Age-related decreases in hormonal levels were associated with a decrease in the amplitude, but not the frequency, of secretory pulses. These findings demonstrate that the normal process of aging involves alterations in the central mechanisms controlling the temporal organization of endocrine release in addition to a reduction of secretory outputs.

Adult↗
PubMed1991

Sleep electroencephalography in depressive illness. A collaborative study by the World Health Organization.

Eight WHO research centres from Europe, North America and Asia took part in a WHO study aimed at assessing the reliability and consistency of sleep-EEG abnormalities in major depression. Each centre was asked to include in the study ten depressed patients aged 20-65 years meeting the Research Diagnostic Criteria for a major depressive disorder, and to match them by age and gender with ten controls. There were 67 patients and 66 controls included in the study. Compared with controls, depressed patients showed sleep-continuity disturbances such as increase in sleep-onset latency, and decrease in total sleep time and in sleep efficiency. Stages 2 and 3, as percentages of total sleep time, were reduced in depressed patients, REM latency was shortened and REM density increased. These findings confirm the presence of specific sleep-EEG abnormalities in major depression.

Adult↗
PubMed1990

Fluoxetine in major depression: efficacy, safety and effects on sleep polygraphic variables.

Fluoxetine (60 mg), a selective inhibitor of the reuptake of 5-HT, was compared in a double-blind trial to amitriptyline (150 mg) in a sample of 34 patients fitting the Research Diagnostic Criteria for a major depressive disorder. Patients were studied after a drug washout period of 10 days and an active treatment period of 42 days. Sleep polygraphic recordings were performed before and at the end of the study. As indicated by the significant decrease in the Hamilton Depression scale and the Montgomery Asberg Depression scale, fluoxetine showed similar antidepressant effects to amitriptyline with significantly fewer adverse effects. Fluoxetine and amitriptyline decreased the amount of REM sleep, a well known effect of classical antidepressants. Fluoxetine showed some specific effects on sleep continuity (potentially dose related) as indicated by the significant increase in the number of awakenings and in stage shifts, without interfering with the therapeutic response.

Adolescent↗
PubMed1989

The 24-hour profile of plasma prolactin in men with major endogenous depressive illness.

Plasma prolactin (PRL) levels were measured at 15-minute intervals for 24 hours in 18 men suffering from major endogenous depressive illness and in 7 age-matched healthy men. Eleven of the 18 depressed patients were restudied during clinical remission following either electroconvulsive therapy or treatment with amitriptyline hydrochloride. During the acute phase of the illness, the unipolar depressed patients had fragmented patterns of PRL secretion with an early timing of the nocturnal secretory phase of PRL, which started, on the average, 2 hours earlier than in healthy subjects. Moreover, the amplitude of the circadian variation of PRL was reduced in these patients, with subnormal PRL levels occurring during the midsleep period. This latter abnormality was also observed in bipolar patients, who had otherwise normal PRL profiles. These lower midsleep PRL concentrations were associated with a significant increase in the amount of time spent awake during the same period. Antidepressant treatment did not consistently correct the abnormalities in the patterns of PRL release observed during the acute phase of the illness. These results indicate that early timing of nocturnal PRL secretion and damping of the nighttime PRL elevation may be found in men with endogenous depressive disorders. In contrast to disturbances of the corticotropic and somatotropic axes, these abnormalities of PRL secretion may still be present during clinical remission following antidepressant treatment.

Adult↗