Biomedical subjects

Ulrich Voderholzer

Publications and source records attributed to Ulrich Voderholzer.

28 records · Page 2Linked to original sources

PubMed2003

Are there gender differences in objective and subjective sleep measures? A study of insomniacs and healthy controls.

It is well known that insomnia is more frequent in women than in men throughout all age groups. In this respect insomnia resembles other psychiatric disorders that occur more frequently in women such as anxiety and depressive disorders. Since insomnia is frequently a symptom of anxiety and depression, it remains an open question whether the comorbidity with psychiatric disorders fully explains the gender differences in the prevalence of insomnia or whether gender influences sleep independently from psychiatric conditions. We analyzed sleep measures of patients diagnosed with a primary insomnia (n=86) and of an age- and sex-matched healthy control group (n=86) by polysomnography; additionally, subjective rating scales were available for 70 patients and 54 controls matched for mean age and sex ratio. Surprisingly, none of the sleep continuity measures (sleep duration, sleep efficiency, arousal index, and wake%), nor slow wave or REM sleep % showed significant gender differences in both insomniacs and healthy controls. Also, subjective estimates of sleep quality were comparable in both sexes. As expected, insomniacs strongly differed from the control group in all subjective measures of sleep. Polysomnography showed significantly reduced sleep duration and efficiency, increased arousal index, and slightly, but significantly, less REM sleep in the insomniacs as compared to the healthy controls. These studies indicate that gender seems to have, if any, relatively little influence on sleep per se. We hypothesize that the clear gender differences in the prevalence of insomnia are caused predominantly by gender differences in the prevalence of anxiety and depression. Primary insomnia may be, at least in a part of the cases, a subclinical or subthreshold form of anxiety or depression.

Adolescent↗

PubMed2003

Primary insomnia: a risk factor to develop depression?

BACKGROUND: Chronic insomnia afflicts approximately 5-10% of the adult population in Western industrialized countries. Insomnia may be secondary, i.e. triggered and/or maintained by psychiatric/organic illnesses, the intake of prescribed/illicit drugs or alcohol, or by a combination of these factors. Insomnia can also occur as primary insomnia, caused by a psychophysiological hyperarousal process. In the present review a literature search was undertaken to identify longitudinal epidemiological studies which investigate the question whether primary insomnia at baseline predicts the development of depression at follow-up measurements. METHODS: MEDLINE search for the medical subject headings insomnia and depression; identification of longitudinal epidemiological studies with at least two measurement points 1 year apart measuring insomnia and depression and indicating explicit criteria for both disorders. RESULTS: Eight relevant epidemiological studies were identified. Almost unambiguously insomnia at baseline significantly predicted an increased depression risk at follow-up 1-3 years later. CONCLUSION: As insomniac symptoms alone seem to be of predictive value for the development of depression in the succeeding years, it would be worthwhile to investigate if early adequate treatment is able to prevent psychiatric sequelae of primary insomnia.

Adult↗

PubMed2002

Nocturnal cortisol and melatonin secretion in primary insomnia.

The present study investigated evening and nocturnal serum cortisol and melatonin concentrations in patients with primary insomnia to test if this clinical condition is accompanied by an increase of cortisol secretion and a simultaneous decrease of nocturnal melatonin production. Ten drug-free patients (4 males, 6 females) with primary insomnia (mean age+/-S.D.: 39.2+/-9.1 years) and 10 age- and gender-matched healthy controls participated in the study. All subjects spent three consecutive nights in the sleep laboratory with polysomnography. Measurement of cortisol and melatonin (from 19:00 h to 09:00 h) was performed prior to and during the last laboratory night. Contrary to expectation, cortisol secretion did not differ between healthy controls and insomniac patients. On the other hand, nocturnal melatonin production was significantly diminished in insomniac patients. Polysomnographically determined sleep patterns, in contrast to subjective ratings of sleep, demonstrated only minor alterations of sleep in the insomniac group. The lack of increased cortisol secretion in the patients with primary insomnia indicates that results from studies on the biological consequences of experimental sleep loss in healthy subjects cannot be applied to primary insomnia in general, especially if there are only minor objective sleep alterations. In spite of the negligible objective sleep disturbances in the present sample, nocturnal melatonin production was reduced, which tentatively suggests a role for this hormone in primary insomniacs. The pathophysiological significance of this finding is, however, still a matter of debate.

Adaptation, Physiological↗

PubMed2002

The tryptophan depletion test: impact on sleep in primary insomnia - a pilot study.

The application of the tryptophan depletion test is based on the assumption that the decrease of plasma or serum tryptophan concentration following the ingestion of a tryptophan-free amino acid drink reflects a central nervous effect on serotonin metabolism. In the present study the impact of tryptophan depletion on polysomnographically recorded sleep in patients with primary insomnia was studied. Fifteen patients with primary insomnia slept for four nights in the sleep laboratory. Prior to the fourth night the tryptophan depletion test was applied. Sleep EEG variables served as outcome parameters. Patients with primary insomnia, compared to baseline values showed a highly significant decrease of serum tryptophan concentrations after the amino acid drink. Concerning sleep parameters, stage 1 (% sleep period time=SPT) was increased, whereas stage 2 (% SPT) was decreased. Indices of phasic activity of rapid eye movement (REM) sleep (REM density) were increased after the tryptophan depletion compared to baseline. The results suggest a negative impact of tryptophan depletion on sleep continuity and a stimulating effect on phasic measures of REM sleep in patients with primary insomnia.

Adult↗

PubMed2002

Periodic limb movements during sleep in alcohol dependent patients.

Complaints of sleep disturbances are common among alcohol dependent patients during subacute abstinence. Recovered patients may show persistent sleep abnormalities for months or even years. In the present study we studied the issue whether periodic limb movements in sleep and disturbances of nocturnal respiration are more frequent in alcohol dependent patients than healthy subjects and may be of predictive value for sustained abstinence vs. relapse after withdrawal. Forty alcohol dependent patients spent three nights in the sleep laboratory at three time points: 2 to 3 weeks after withdrawal (T0) and at follow-up investigations 6 (T1) and 12 (T2) months after discharge from the hospital. Measurements of PLMS-arousal index and nocturnal respiration were performed during the first laboratory night of each measurement point. Alcohol dependent patients displayed a significantly enhanced PLMS-arousal index at T0 compared to age- and gender-matched healthy subjects, whereas no alterations of nocturnal respiration were found.The PLMS-arousal index at T0 was significantly elevated in patients who relapsed during the next 6 months compared to abstinent patients. In a discriminant function analysis the PLMS-arousal index classified 55 % of the patients correctly with respect to outcome after 6 months. It correctly predicted 80 % of abstainers and 44 % of the patients who relapsed. According to neurobiological models of the generation of PLMS and the etiopathology of alcohol dependence a genetically determined vulnerability of the dopaminergic system is discussed as a factor underlying an increased risk of relapse in a subgroup of alcohol dependent patients.

Adult↗

PubMed2002

Fluoxetine and sleep EEG: effects of a single dose, subchronic treatment, and discontinuation in healthy subjects.

The goals of the current study were to evaluate whether a single dose of fluoxetine causes qualitatively different changes in sleep architecture and NREM sleep EEG than subchronic administration in healthy subjects and to determine degree and duration of such changes after the single dose and after discontinuation from subchronic administration. Our hypothesis was that subchronic intake should cause changes qualitatively different from the single dose and that such changes could be sufficiently long-lived to suggest the possibility of a dosing in intervals of several days. Ten healthy volunteers first took one single 60-mg dose of fluoxetine and a week later started to take a 40-mg dose every morning for three weeks. Sleep laboratory nights included two nights before and four nights after the single dose and every second night for two weeks after discontinuation from subchronic administration. The single dose caused only a slight increase in drug plasma concentrations but relatively clear changes in sleep structure. After discontinuation from subchronic administration, sleep quality indices normalized quickly (within 2-4 days), whereas REM latency and spectral power effects correlated with total SSRI plasma concentration and normalized more slowly, corresponding to the drug plasma half-life of about 10 days. The REM fraction of the sleep period showed a rebound, whereas the delta sleep ratio did not correlate with drug plasma levels and yet remained increased after the medication interval. Thus, the only qualitative difference seen between acute and subchronic medication was the initial sleep disturbance. REM latency and especially the delta sleep ratio remained increased for several days after discontinuation from subchronic administration, indicating the possibility of a less-than-daily maintenance medication after an initial daily interval. Finally, the pattern of change observed for the delta sleep ratio indicates that it may be due to secondary, adaptive effects possibly linked to the antidepressant effect of fluoxetine in depressed patients.

Adult↗

PubMed2002

Effects of the neuropeptide substance P on sleep, mood, and neuroendocrine measures in healthy young men.

The neuropeptide substance P (SP) has been supposed to be involved in the etiopathology of affective disorders, mainly because of the finding of increased levels of SP in the cerebrospinal fluid of depressed patients and the preliminary evidence of antidepressant effects of SP-receptor antagonists in depressed patients. We investigated whether SP may induce changes of sleep, mood and neuroendocrine measures that are similar to those in depressed patients. In a double-blind, randomized cross-over design, 12 healthy young men were investigated in two blocks of three consecutive nights, in which SP or NaCl was intravenously infused during the third night. Polysomnographic recordings were obtained during all nights and blood samples were drawn every 30 min during the third night. Infusion of SP caused a significant worsening of the mood of the subjects, led to an increase of REM latency and time awake during the SP-infusion intervals, caused increased stage 1 sleep in the first part of the night, and led to increased cortisol and thyroid stimulating hormone levels and a trend for decreased growth hormone levels. These effects can be interpreted as evidence for a central arousing effect of SP. Further studies should focus on the effects of substance P in patients with depressive or other psychiatric disorders.

Adult↗

PubMed2002

Transient total sleep loss in cerebral Whipple's disease: a longitudinal study.

A case with transient, almost complete sleep loss caused by cerebral manifestation of Whipple's disease (WD) is presented. Cerebral WD is rare and in most cases occurs after gastrointestinal infection. In our case, a progressive and finally almost complete sleep loss was the initial and predominant symptom. Polysomnographic studies in several consecutive nights and over 24 h showed a total abolition of the sleep-wake cycle with nocturnal sleep duration of less than 15 min. Endocrine tests revealed hypothalamic dysfunction with flattening of circadian rhythmicity of cortisol, TSH, growth hormone and melatonin. Cerebrospinal fluid (CSF) hypocretin was reduced. [18F]Deoxyglucose positron emission tomography (FDG-PET) revealed hypermetabolic areas in cortical and subcortical areas including the brainstem, which might explain sleep pathology and vertical gaze palsy. In the course of treatment with antibiotics and additional carbamazepine for 1 year, insomnia slowly and gradually improved. Endocrine investigations at 1-year follow-up showed persistent flattening of circadian rhythmicity. The FDG-PET indicated normalized metabolism in distinct regions of the brain stem which paralleled restoration of sleep length. The extent of sleep disruption in this case of organic insomnia was similar to cases of familial fatal insomnia, but was at least partially reversible with treatment.

Adult↗

PubMed2002

Sleep and sleep-wake manipulations in bipolar depression.

In the last 30 years, it has been convincingly demonstrated that sleep in major depression is characterized by disturbances of sleep continuity, a reduction of slow wave sleep, a disinhibition of REM sleep including a shortening of REM latency (i.e. the time between sleep onset and the occurrence of the first REM period) and an increase in REM density. Furthermore, manipulations of the sleep-wake cycle like total or partial sleep deprivation or phase advance of the sleep period have been proven to be effective therapeutic strategies for patients with unipolar depression. The database concerning sleep and sleep-wake manipulations in bipolar disorder in comparison is not yet as extensive. Studies investigating sleep in bipolar depression suggest that during the depressed phase sleep shows the same stigmata as in unipolar depression. During the hypomanic or manic phase, sleep is even more curtailed, though subjectively not experienced as disturbing by the patients. REM sleep disinhibition is present as well. An important issue is the question, whether sleep-wake manipulations can also be applied in patients with bipolar depression. Work by others and our own studies indicate that sleep deprivation and a phase advance of the sleep period can be used to treat bipolar patients during the depressed phase. The risk of a switch into hypomania or mania does not seem to be more pronounced than the risk with typical pharmacological antidepressant treatment. For patients with mania, sleep deprivation is not an adequate treatment--in contrast, treatment strategies aiming at stabilizing a regular sleep-wake schedule are indicated.

Animals↗

PubMed2002

Neurobiological findings before and during successful lithium therapy of a patient with 48-hour rapid-cycling bipolar disorder.

48-hour rapid cycling is a very rare form of bipolar disorder, characterized by regular periodic changes of mood from one day to the other. We report on a patient who suffered from a 48-hour rapid cycling without a history of bipolar disorder before the abrupt onset of his rapid mood cycles. We present polysomnographic and neuroendocrine findings and the clinical course based on daily self-ratings of mood. Treatment with lithium carbonate effectively reduced the amplitude of the mood cycles. With plasma levels between 0.8 and 1.0 mmol, almost complete remission occurred. An overview on previous reports on the therapeutic effect of mood stabilizers in this rare form of bipolar disorder is presented.

Adult↗