[Obsessive-compulsive disorders].
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Diagnosis, Differential↗
Biomedical subjects
U Voderholzer
Publications and source records attributed to U Voderholzer.
Impact of experimentally induced serotonin deficiency by tryptophan depletion on saliva cortisol concentrations.
BACKGROUND: Tryptophan depletion (TD) has been shown to induce a transient mood-lowering effect in psychiatric patients and susceptible healthy subjects. We investigated the effects of TD on cortisol secretion in psychiatric patients and healthy subjects based on the hypothesis that the potential mood-lowering effects may be associated with increased activity of the hypothalamic-pituitary-adrenal axis, thus leading to a rise of cortisol secretion. METHODS: After TD at 18.00 h, salivary cortisol was sampled in the evening and on the following morning. The first study was a randomized, placebo-controlled, crossover study in healthy subjects. Two further open trials in patients with obsessive-compulsive disorder (OCD) and primary insomnia compared the effects of TD on cortisol with baseline conditions. RESULTS: In healthy subjects, TD significantly diminished cortisol the next morning compared with placebo. In OCD patients and primary insomniacs, cortisol the morning after TD was lowered compared with baseline. Evening cortisol was not affected by TD in any of the groups. CONCLUSIONS: Contrary to expectation, TD led to a comparable decrease of morning cortisol in all groups investigated. However, these findings are consistent with former studies analyzing the impact of antiserotonergic drugs on cortisol secretion. The results underline that the antiserotonergic effects caused by TD may influence cortisol secretion.
Adult↗
[Algorithms for diagnosis and therapy of sleep disorders in general practice].
Complaints of insomnia, i.e. problems to fall asleep or maintain asleep and/or non-restorative sleep are very common in general practice. This article presents the clinical algorithm non-restorative sleep which was devised by the German Society for Sleep Research and Sleep Medicine. This algorithm presents a guideline for the diagnosis and the treatment of insomnia.
Age Factors↗
[Non-restorative sleep and insomnia. Diagnostic and therapeutic options for psychiatry and psychotherapy].
Over the last few years, a shift in paradigm has taken place in the diagnosis and therapy of insomnia. Traditionally, treatment focused on improving night sleep, i.e. shortening sleep latency and prolonging total sleep time. Modern approaches aim at improving or restoring the recuperative value of sleep and ensuring daytime functioning on a social, psychological and professional level. Based on the guidelines "Non-restorative Sleep" of the German Society of Sleep Research and Sleep Medicine, this article presents a clinical algorithm for the diagnosis and therapy of non-restorative sleep with predominant insomnia. The term "non-restorative sleep" permits us to view the restorative value of sleep and the resulting daytime functioning of the individual afflicted with insomnia as the focus for the diagnosis of and therapy for insomnia. This algorithm is suitable for the clinical practice of outpatient psychiatric and psychotherapeutic services as well as for psychiatric inpatients. The main features for psychiatrists and psychotherapists in the diagnosis and therapy of non-restorative sleep are underlying psychiatric-psychological factors or secondary psychiatric sequelae of chronic primary insomnias. For primary, organic and psychiatric insomnias, a broad spectrum of psychopharmacological and cognitive behavioral methods can be applied either alone or in combination.
Algorithms↗
Is the antidepressive effect of sleep deprivation stabilized by a three day phase advance of the sleep period? A pilot study.
Sleep deprivation (SD) induces a rapid amelioration of mood in about 60 % of depressed patients. After the next night of sleep, however, most patients experience a relapse. Previous studies demonstrated that a six day sleep-phase advance protocol prevents relapses in about 60 % of patients who responded positively to SD. We investigated whether also a three day phase advance of the sleep period might be able to maintain the antidepressant effects of SD. Twenty-eight medicated depressed inpatients, who had a significant improvement after a SD in one night were recruited for this study. The phase advance protocol began on the first day after SD with a bed time from 5:00 p. m. to 12:00 p. m. on the first, from 7:00 p. m. to 2:00 a. m. on the second and 9:00 p. m. to 4:00 a. m. on the third day after SD. Three patients dropped out because of protocol violations. Only ten of the remaining 25 SD responders had a relapse during the three days of phase advance treatment or during the two days after it. Two of the relapsers improved again until day 6, i. e. 68 % showed an improvement of at least 30 % six days after the beginning of the treatment. This study indicates that even a three day phase advance protocol may help to prevent relapses after successful SD.
Circadian Rhythm↗
Trimipramine in primary insomnia: results of a polysomnographic double-blind controlled study.
In recent years, sedating antidepressants have been increasingly used to treat primary insomnia. Up to now, only one open pilot study with trimipramine and one double-blind placebo-controlled study with doxepin have provided scientific support for this approach in treating primary insomnia. In order to test the hypothesis that sedating antidepressants are useful in the treatment of primary insomnia, the effect of trimipramine on objectively and subjectively measured parameters of sleep was investigated in a double-blind placebo- and lormetazepam-controlled study in a sample of 55 patients with primary insomnia attending outpatient sleep-disorder clinics. Trimipramine was selected since it has shown positive effects on sleep continuity with a lack of REM sleep suppression in studies on depressed patients and in one pilot study on patients with primary insomnia. Trimipramine at an average dose of 100 mg over a period of 4 weeks significantly enhanced sleep efficiency, but not total sleep time (which had been the primary target variable) compared to placebo as measured by polysomnography. Changes in objective sleep parameters were paralleled by changes in subjective sleep parameters. Trimipramine did not suppress REM sleep. Lormetazepam decreased wake time and sleep stage 3 and increased REM sleep compared to placebo. After switching trimipramine to placebo, sleep parameters returned to baseline. There was no evidence of any rebound effect from trimipramine. Side effects from trimipramine were only marginal. This first double-blind placebo-controlled study with trimipramine suggests its efficacy in the treatment of primary insomnia. However, due to the large intra- and interindividual variance in the parameters of interest before and during treatment a larger sample size would have been necessary to strengthen the validity of our findings.
Adult↗
[Restless legs syndrome. Guidelines for diagnosis and therapy].
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Dopamine Agents↗
[Sleep disorders. Differential diagnosis and therapy in general practice].
Sleep Disorders are one of the most common complaints of patients seen by general practitioners. Prevalences vary considerably--depending on the kind of research and the definition of sleep disorders--between 4 and 40%. In 2000 the first grand nationwide survey was carried out in primary care settings [1]. 12.3% of the 17,928 questioned stated sleep disorders as the main reason for their consultation, the prevalence of all kinds of sleep disorders being 29%. Like seen in other studies sleep complaints increased with age and predominated significantly in women. In one-third of the sample the differential diagnosis was primary or non-organic insomnia [1] while treatment was mainly conducted by the general practitioner. In two-thirds of the patients sleep disorders existed for more than 12 months while 41%--by their own account--took sleep agents at least once a week. This article gives an overview of the causes and treatment of sleep disorders, particularly therapy of non-organic insomnia.
Central Nervous System Agents↗
[Neurobiological findings in a patient with 48-hour rapid cycling bipolar affective disorder. A case report].
Forty-eight-hour rapid cycling is a rare subclass of affective disorders and entails a regular periodic change of moods. The following case study describes the symptoms, therapy, and outcome of a patient suffering from daily switching between mania and depression along with neurobiological findings correlated to the affective cycles. We found alternating reduction and prolongation of sleep duration during manic and depressive days as well as differences in the amount of REM sleep. Cortisol secretion was regularly increased during depressive days. Regarding thyroid-stimulating hormone (TSH) secretion, the circadian rhythm was absent on depressive days. However, the glucose metabolic rate as measured by positron emission tomography (PET) did not differ on manic and depressive days. The patient reached almost complete remission under treatment with lithium.
Bipolar Disorder↗
A double-blind, randomized and placebo-controlled study on the polysomnographic withdrawal effects of zopiclone, zolpidem and triazolam in healthy subjects.
Rebound effects after withdrawal from hypnotics are believed to trigger their chronic use and to enhance the risk of tolerance and dependence. It was the purpose of this study to investigate the acute polysomnographic withdrawal effects after a 4 week treatment with standard doses of the non-benzodiazepine hypnotics zopiclone and zolpidem compared with triazolam and placebo. Healthy male subjects between 22 and 35 years of age participated in a parallel study design. They received either zopiclone 7.5 mg (n=11), zolpidem 10 mg (n=11), triazolam 0.25 mg (n=10) or placebo (n=7) over 4 weeks in randomized and double-blind order. Sleep EEG was registered during 2 nights before treatment under placebo, on days 1, 27 and 28 of treatment and on days 29,30,41 and 42 under placebo. Total sleep time and sleep efficiency were lower in the 1st night after discontinuation of triazolam (p < 0.05, t-test). After withdrawal from zopiclone or zolpidem slight but not significant rebound effects concerning sleep continuity were observed. Self-rating scales showed minimal rebound insomnia after discontinuation of all three hypnotics. In the placebo group no changes of sleep parameters were observed. Assuming that rebound insomnia is part of a withdrawal reaction, this study indicates that the risks of tolerance and dependency are low when administering zopiclone or zolpidem at the recommended doses.
Adult↗
Long-term effectiveness of a short-term cognitive-behavioral group treatment for primary insomnia.
The long-term effectiveness of a short-term cognitive-behavioral therapy was evaluated. The structured group treatment consisted of six weekly sessions and included progressive muscle relaxation, cognitive relaxation, modified stimulus control with bedtime restriction, thought stopping and cognitive restructuring. Twenty patients with chronic primary insomnia took part in the study. All patients were referred by physicians for diagnosis and therapy of insomnia. During a waiting period of six weeks prior to treatment, patients did not experience any change of their sleep parameters. After therapy, patients improved their total sleep time and sleep efficiency and reduced their sleep latency and negative sleep-related cognitions. Furthermore, depression scores decreased. Most of the treatment effects were significant at the end of the treatment and remained stable over the long-term follow-up, which was evaluated after a mean of almost three years (35 +/- 6.7 months). The subjective estimated total sleep time improved from 298 +/- 109 min prior to therapy to 351 +/- 54 min at the end of treatment, to 376 +/- 75 min at the 3-month follow-up, to 379 +/- 58 min at the 12-month follow-up and to 381 +/- 92 min. at the long-term follow-up.
Adult↗
Antidepressive response to sleep deprivation in unipolar depression is not associated with dopamine D3 receptor genotype.
The psychostimulant theory of antidepressive sleep deprivation (SD) proposes a contribution of dopamine D3 receptors (DRD3) in the limbic system to the antidepressant effects of SD. Neuroendocrinological studies suggest a positive correlation of clinical response to SD and cortisol secretion. We hypothesized that the clinical response to SD and amount of cortisol secretion upon SD is associated with the 1-1 genotype of the Bal1 polymorphism of DRD3 on exon 1. In this study, aiming at evaluating the feasibility of screening large patient samples, 52 inpatients (19 males/33 females) with unipolar depression and a score of 18 or more on the 21-item Hamilton Depression Rating Scale were treated with 1 night of total SD. We found that 31% of our patients responded to SD. There was no association between response to SD and the genotype of the DRD3 Bal1 polymorphism (p < 0.879). There was also no association between increase in cortisol secretion after SD and DRD3 genotypes (p < 1.000) in a subgroup of patients. Statistical power analysis ruled out a major effect of the DRD3 Bal1 polymorphism on clinical response to SD. These results suggest that the DRD3 Bal1 polymorphism is not a promising lead to be followed up in larger patient samples.
Adult↗
Doxepin in the treatment of primary insomnia: a placebo-controlled, double-blind, polysomnographic study.
BACKGROUND: Over recent years, the use of antidepressants for the symptomatic treatment of insomnia has grown substantially, but controlled studies are still lacking. Our study is the first investigation to prove objective efficacy and tolerability of low doses of a sedating antidepressant in a randomized, double-blind, and placebo-controlled manner in patients with primary insomnia. METHOD: Forty-seven drug-free patients meeting DSM-IV criteria for primary insomnia (mean +/- SD duration of complaints = 11.2+/-9.7 years) received either 25-50 mg of the tricyclic antidepressant doxepin or placebo for 4 weeks followed by 2 weeks of placebo withdrawal. Sleep was measured by polysomnography at baseline and the first night of application, at 4 weeks of treatment and the first to third night of withdrawal, and after 2 weeks of withdrawal. RESULTS: In the doxepin-treated patients who completed the study (N = 20, 47.6+/-11.3), medication significantly increased sleep efficiency after acute (night 1, p < or = .001) and subchronic (night 28, p < or = .05) intake compared with the patients who received placebo (N = 20, 47.4+/-16.8 years of age). Latency to sleep onset was not affected since the patients had normal baseline sleep latencies. Investigators found doxepin to cause significantly (p < or = .05) better global improvement at the first day of treatment. Patients rated sleep quality (p < or = .001) and working ability (p < or = .005) to be significantly improved by doxepin during the whole treatment period. Overall rebound in sleep parameters was not observed, but patients with severe rebound insomnia were significantly more frequent in the doxepin group (night 29, p < .01, night 30, p < or = .01; night 31, p < or = .05). No significant group differences in side effects were found, but 2 doxepin-treated patients dropped out of the study due to specific side effects (increased liver enzymes, leukopenia, and thrombopenia). CONCLUSION: The results support the effectiveness of low doses of doxepin to improve sleep and working ability in chronic primary insomniacs, although subjective effects were light to moderate, and in some patients, rebound insomnia and specific side effects have to be considered.
Antidepressive Agents, Tricyclic↗
Sleep deprivation and growth-hormone secretion.
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Adult↗
Comparison between eye movement latency and REM sleep parameters in major depression.
Alterations of sleep can be observed polysomnographically in approximately 90 percent of depressed patients. Most of the registered sleep abnormalities in depression also occur in other psychiatric disorders. Only some types of REM sleep alterations-- short REM latency, increase of REM density and shortening of mean latency of eye movements--were reported as more specific for affective disorders. In the present study polysomnograms of 21 medication free patients with major depressive disorder (assessed with a structured interview for DSM-III-R and Hamilton Scale) and 21 healthy controls were analysed. REM latency (LREM), REM density (RD), latencies of eye movements (LEM) and mean latency of eye movements (M-LEM) were calculated for both groups. Depressed patients (compared with healthy controls) showed increased RD (38.2% vs. 28.2%, p < 0.0001), shortened M-LEM (35.7 s vs. 48.3 s, p < 0.04) and shortening of LEM in the 1st (28.9 s vs. 48.9 s, p < 0.007) and 4th (27.0 s vs. 59.1 s, p < 0.043) REM sleep periods. LREM was not shortened significantly in depressives (78.5 min vs. 91.3 min, ns). In healthy subjects a negative correlation between M-LEM and RD was found (rho = -0.47, p < 0.03). Since in the current study depressed patients differed from healthy controls, especially concerning phasic activity during REM sleep, presented data support the essential role of REM density for the assessment of sleep in depression. As a quick and easy manner to compute measurement, M-LEM is suggested as additional parameter for the assessment of phasic activity during REM sleep.
Adult↗
The tryptophan depletion test. Impact on sleep in healthy subjects and patients with obsessive-compulsive disorder.
UNLABELLED: The tryptophan depletion test is a research tool to study the functional consequences of decreasing the brain serotonin metabolism. Since serotonin is involved in sleep regulation and assumed to be of high importance in the etiology of psychiatric disorders, the acute polysomnographic effects of tryptophan depletion were studied in healthy subjects and patients with obsessive compulsive disorder (OCD). According to the reciprocal interaction model of non-REM and REM-sleep regulation we expected that tryptophan depletion in healthy controls should provoke alterations of sleep similar to depression, whereas we assumed that these effects would be more pronounced in patients with OCD. METHODS: 12 healthy subjects with a mean age of 34 years and 12 patients suffering from OCD with a mean age of 30 years had 4 polysomnographic investigations. After 1 adaption and 1 baseline night subjects received a low protein diet on day 3 and 4 until midday. On day 4 at 18.00 h subjects ingested an aminoacid mixture devoid of tryptophan. This procedure resulted in a decrease of 85% in healthy subjects and 80% in OCD patients at 22.00 h. RESULTS: The tryptophan depletion led to more pronounced disturbances of sleep continuity in OCD patients than in healthy subjects in terms of an increase of wake time and a decrease of total sleep time. In both groups a decrease of sleep stage 2 could be observed. Healthy subjects showed significant alterations of phasic REM parameters as REM density and total number of rapid eye movements, what was not the case for OCD patients. CONCLUSIONS: Our results indicate the important role of the serotonergic system for sleep maintainance and the phasic aspects of REM sleep. Furthermore our data demonstrate that the tryptophan depletion test is a useful tool to evaluate the hypothesis of a serotonergic involvement in sleep regulation and the etiology of psychiatric disorders.
Adult↗
How to preserve the antidepressive effect of sleep deprivation: A comparison of sleep phase advance and sleep phase delay.
Total sleep deprivation (TSD) leads to an immediate amelioration of depressed mood in approximately 70 % of patients with the melancholic subtype of depression. The clinical utility of this procedure is limited, as the improvement usually subsides after the next night of sleep. In the present study, 40 depressed inpatients, being free of psychoactive medication for at least 7 days and who had responded to a TSD were then distributed (according to a matched-pair design) to a sleep phase advance (SPA = time in bed scheduled from 1700-2400 hrs) or a sleep phase delay (SPD = time in bed from 0200-0700 hrs) with a succeeding shift back (for one hour in the SPA group per day) respectively shift forward (for 30 minutes in the SPD group per day), until the initial sleep phase (2300-0600 hrs) was reached after seven days again. Based on previous observations it was hypothesized that a phase advance of the sleep period should prevent responders to TSD from relapsing. Whereas 75% of the TSD responders were stabilized by the phase advanced condition and did not relapse over a period of seven days, only 40% of the patients in the phase delayed condition did not relapse. Polysomnography during the course of the study gave no evidence that the unusual sleep schedules caused prolonged sleep deprivation. Abnormalities of REM sleep persisted both in the clinical responders and non-responders after the sleep wake manipulation. It is concluded that the clinical effectiveness of TSD can be significantly improved by combining TSD with a following phase advance of the sleep period.
Adult↗