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Biomedical subjects

U Voderholzer

Publications and source records attributed to U Voderholzer.

At least 37 records · Page 2Linked to original sources
PubMed1999

Independent sleep EEG slow-wave and spindle band dynamics associated with 4 weeks of continuous application of short-half-life hypnotics in healthy subjects.

OBJECTIVES: Habituation and adverse withdrawal reactions after prolonged medication with benzodiazepine (BZ) hypnotics are believed to play a role in dose escalation and the development of dependence. METHODS: In the current sleep EEG study in 43 healthy male subjects, the known property of BZ- and similar hypnotics to change the NREM sleep EEG spectrum is utilized for a detailed quantitative analysis across 4 weeks of continuous medication and a subsequent two-week withdrawal period. The BZ hypnotic triazolam and the non-BZ hypnotics zopiclone and zolpidem, differing in pharmacological properties and reported adverse effects, were examined in parallel to a placebo group. RESULTS: Reliably occurring spectral effects in the sleep stage 2 EEG were found in the 3 frequency bands 0.8-5 Hz, 5-10 Hz and 10-15 Hz. All 3 hypnotics showed the typical 'benzodiazepine signature', a 10-15 Hz increase and lower-frequency (<10 Hz) suppression relative to the preceding drug-free night. However, these effects developed differently across the first medication night, across the 4 medication weeks and after withdrawal: While the 5-10 Hz effect covaried with the blood presence of the drugs as estimated from the known plasma half-lifes, showed habituation and a rebound after withdrawal, the 10-15 Hz power increased across medication days and showed no rebound. Effects in the 0.8-5 Hz band in the first medication night correlated with the decrease of sleep efficiency at later withdrawal for triazolam and zolpidem.

Adult↗
PubMed1998

Magnesium therapy for periodic leg movements-related insomnia and restless legs syndrome: an open pilot study.

Periodic limb movements during sleep (PLMS), with or without symptoms of a restless legs syndrome (RLS), may cause sleep disturbances. The pharmacologic treatments of choice are dopaminergic drugs. Their use, however, may be limited due to tolerance development or rebound phenomena. Anecdotal observations have shown that oral magnesium therapy may ameliorate symptoms in patients with moderate RLS. We report on an open clinical and polysomnographic study in 10 patients (mean age 57 +/- 9 years; 6 men, 4 women) suffering from insomnia related to PLMS (n = 4) or mild-to-moderate RLS (n = 6). Magnesium was administered orally at a dose of 12.4 mmol in the evening over a period of 4-6 weeks. Following magnesium treatment, PLMS associated with arousals (PLMS-A) decreased significantly (17 +/- 7 vs 7 +/- 7 events per hour of total sleep time, p < 0.05). PLMS without arousal were also moderately reduced (PLMS per hour of total sleep time 33 +/- 16 vs 21 +/- 23, p = 0.07). Sleep efficiency improved from 75 +/- 12% to 85 +/- 8% (p < 0.01). In the group of patients estimating their sleep and/or symptoms of RLS as improved after therapy (n = 7), the effects of magnesium on PLMS and PLMS-A were even more pronounced. Our study indicates that magnesium treatment may be a useful alternative therapy in patients with mild or moderate RLS-or PLMS-related insomnia. Further investigations regarding the role of magnesium in the pathophysiology of RLS and placebo-controlled studies need to be performed.

Aged↗
PubMed1998

Impact of experimentally induced serotonin deficiency by tryptophan depletion on sleep EEG in healthy subjects.

The tryptophan depletion test is a research strategy to investigate the functional consequences of decreasing the brain serotonin metabolism. Because serotonin is involved in sleep regulation and the regulation of affective states, we studied the acute polysomnographic effects of tryptophan depletion and expected to induce similar changes of sleep EEG as observed in depressed patients. A total of 12 healthy subjects (mean age 34 +/- 3 years) had eight polysomnograms, divided in two blocks of 4 consecutive nights. After one adaptation and 1 baseline night, subjects received a low-protein diet on day 3 and 4 until midday. On day 4 at 18.00 h, they drank an amino acid mixture either devoid of tryptophan or containing 2.3 g of tryptophan (placebo control) in randomized and double-blind order, resulting in an 85% decrease (tryptophan depletion) and a 144% increase (placebo control) of serum tryptophan at 22.00 h. After tryptophan depletion but not placebo, significant effects on sleep EEG were observed in terms of decreased non-rapid eye movement (non-REM) stage 2, increase of wake %, and of rapid eye movement (REM) density compared with baseline. REM latency was not altered, however the first and second REM period interval were significantly shorter after tryptophan depletion. This study underlines the impact of the serotonergic system on sleep maintenance and on REM sleep.

Adult↗
PubMed1998

A 19-h spontaneous sleep period in idiopathic central nervous system hypersomnia.

Reports of prolonged sleep periods in idiopathic central nervous system hypersomnia, as shown by ad libitum sleep recordings, are rare. A patient with idiopathic hypersomnia with extremely long sleep periods and sleep drunkenness after awakening is described. Polysomnographic recordings showed a spontaneous sleep period of 19.4 h and a normal Multiple Sleep Latency Test. These polysomnographic findings are clearly abnormal but essentially different form those of narcolepsy. Unlike narcolepsy, 'idiopathic hypersomnia' does not seem to be a distinct clinical entity but a category for different heterogenous subtypes.

Adolescent↗
PubMed1998

Sleep and the cholinergic rem sleep induction test in patients with primary alcoholism.

Sleep disturbances of alcoholics while actively drinking and at the beginning of, and during, abstinence were frequently reported. Recently, Gillin et al. (1994) showed that a high "REM sleep pressure" at the time of admission to a 1-month inpatient alcohol treatment program predicted the relapse in nondepressed patients with primary alcoholism at 3 months following hospital discharge. We investigated 24 patients with primary alcoholism after 2-3 weeks abstinence in the sleep laboratory; in 15 of these patients the cholinergic REM sleep induction test (CRIT) with 10 mg galanthamine was performed additionally. In comparison with an age- and sex-matched healthy control group, patients had a heightened "REM sleep pressure" including shortened REM latency and increased REM density. A decrease of serotonergic neurotransmission is proposed as being the neurochemical mechanism to explain the results in alcoholic subjects. Follow-up investigations will clarify whether the sleep abnormalities in alcoholism are state- or trait-markers and whether they are suitable to predict the relapse risk.

Adult↗
PubMed1997

Circadian profiles of melatonin in melancholic depressed patients and healthy subjects in relation to cortisol secretion and sleep.

Circadian secretion of melatonin was measured in melancholic depressed patients (n = 9) and age- and sex-matched healthy control patients (n = 9). The mean age of the depressed patients was 29 years, i.e. younger than in most earlier studies, and a drug-free interval of 3 weeks preceded the investigations. Melatonin secretion was similar in depressed patients and healthy subjects with no significant differences at any of the time points, thus not confirming earlier studies in which depressed patients were found to have lower melatonin levels than control patients. The discrepancy between our result and earlier studies may be explained by different patient characteristics such as age, duration of illness, previous treatment, and alcohol intake. It is conceivable that a diminution of nocturnal melatonin secretion in depressed patients might only occur during the long-term course of the depressive illness and/or its pharmacological treatment.

Adult↗
PubMed1997

Periodic limb movements during sleep are a frequent finding in patients with Gilles de la Tourette's syndrome.

Gilles de la Tourette's syndrome (GTS) and restless legs syndrome (RLS) are two different neurological disorders with common features such as involuntary movements. In both disorders a disturbance of the dopaminergic system has been considered among other possible mechanisms. Since periodic leg movements (PLMS) during sleep are the predominant objective finding in RLS, the aim of this study was to investigate sleep parameters in GTS patients with particular emphasis on PLMS. Seven drug-free patients with GTS and seven age- and sex-matched healthy controls were studied polysomnographically, including superficial electromyogram (EMG) leads on all four extremities. A high number of PLMS were found in five of seven, and periodic arm movements in four of seven GTS patients. Total sleep time was significantly lower (P < 0.05) in the GTS patients than in the controls, which confirms earlier findings. The presence of PLMS in GTS might point towards evidence for a pathophysiological relationship between GTS and RLS, which, however, is not supported by the different responses to pharmacological treatments.

Adolescent↗
PubMed1997

Sleep deprivation combined with consecutive sleep phase advance as a fast-acting therapy in depression: an open pilot trial in medicated and unmedicated patients.

OBJECTIVE: The authors' goal was to test the hypothesis that the antidepressant effect of total sleep deprivation can be maintained by initially avoiding sleep during a supposedly "critical" time period in the early morning. METHOD: They studied 33 inpatients with major depression, melancholic type, all of whom responded positively to total sleep deprivation. Twelve of the patients were men and 21 were women; their mean age was 46.7 years (SD = 13.7). After total sleep deprivation, the patients started a sleep schedule from 5:00 p.m. to 12:00 midnight, which then was shifted back by 1 hour each day until a sleep time of 11:00 p.m. to 6:00 a.m. was reached. RESULTS: Twenty (61%) of the 33 patients who responded to total sleep deprivation with an improved state of mood maintained this improvement during sleep phase advance therapy. Drug-free and medicated patients did not differ from each other. CONCLUSIONS: The rapid amelioration of mood observed with total sleep deprivation can be preserved with a succeeding phase shift of the sleep period.

Antidepressive Agents↗
PubMed1996

Advanced vs. normal sleep timing: effects on depressed mood after response to sleep deprivation in patients with a major depressive disorder.

Total sleep deprivation (TSD) exerts beneficial but only transient effects on mood in patients with a major depressive disorder (MDD). Though approximately 50 to 70% of depressed patients improve after sleep deprivation, the majority relapse after recovery sleep, some even after a short nap. One theoretical model postulates a critical period in the early morning hours where sleep is likely to induce a relapse, and nap studies indicate that sleep may be particularly 'depressogenic' at this time of day. A second model attributes the relapse to the release of non-REM sleep. We therefore compared the impact of an advanced sleep period (17:00-24:00 h) to a normal sleep period (23:00-06:00 h) on mood in patients who had responded to sleep deprivation. Less relapses into depression occurred after advanced sleep. Polysomnographic data showed that, as expected, normal sleep was characterized by a more pronounced improvement of sleep continuity and increased slow-wave sleep. The normal sleep group showed a stronger decrease in REM sleep density than the advanced sleep group compared with baseline. These data add to a growing body of evidence that the timing of sleep following successful sleep deprivation may be crucial for a stabilization of its antidepressant effect. Thus, avoidance of sleep during a "critical period' for more than a single night is necessary to provide a longer-lasting treatment modality.

Adult↗
PubMed1995

[Case report: treatment of a patient with sleep phase advance disorder with phototherapy].

We report on a patient with a moderate form of a sleep-phase advance syndrome. As a biological correlate we found an early temperature and cortisol minimum before midnight, respectively. Light therapy during the evening hours (2500 Lux) given over 17 months induced a complete remission of the symptoms. The good treatment outcome could be maintained after the end of daily light therapy by only sporadic application.

Adult↗
PubMed1994

Lateralization of the Bereitschaftspotential to the left hemisphere in patients with major depression.

Fourteen patients with major depression and 18 healthy subjects performed a Bereitschaftspotential (BP) paradigm, which required them to clench the right fist at self-paced intervals. The BP was calculated as the integrated negative amplitude from BP onset to movement onset. The latter was defined by recording the electromyogram (EMG) from the right forearm. To evaluate lateralization, the integrated BPs at C3, C4, P3, and P4 were analyzed. In depressives, a significant asymmetry of the BP to the left was found, whereas in normals the BP was nearly symmetrically distributed around the midline. Three patients were retested when clinically improved. At that time the asymmetry to the left hemisphere had nearly vanished. This asymmetry to the left hemisphere is interpreted as a cortical deactivation of the right cerebral hemisphere and seems to be a state marker of depression.

Adolescent↗
PubMed1994

Tourette's syndrome associated with restless legs syndrome and akathisia in a family.

A family with coincidence of a restless leg syndrome (RLS) in the mother and a Gilles de la Tourette syndrome (GTS) in the son who also shows increased vulnerability to neuroleptic induced akathisia (NIA) is presented. Since these diseases show parallels from a genetic, pathogenetic and clinical point of view, the familiar coincidence is discussed under these aspects with respect to suggested disturbances of the dopamine and the opiate systems in RLS, GTS, and NIA.

Adolescent↗
PubMed1993

Profiles of spontaneous 24-hour and stimulated growth hormone secretion in male patients with endogenous depression.

Abnormalities of both the spontaneous and the stimulated release of growth hormone (GH) have been described in patients with endogenous depression. In this study, six unmedicated male patients with endogenous depression (ICD 296.1/3) were compared with six age-matched healthy men. Levels of GH were determined at 15-minute intervals over 26 hours. A combined releasing hormone test was performed during the last 2 hours of blood sampling. The 24-hour profile of GH secretion was significantly lower in the depressed patients than in the healthy control subjects due to a significantly diminished sleep-related GH secretion. GH stimulation following releasing hormones was lower in the depressed patients than in healthy subjects. Hypersecretion of GH before the stimulation test might therefore not explain the blunted GH response to stimulation that has been observed in depressive patients.

Adult↗
PubMed1993

Dependency of growth hormone (GH) stimulation following releasing hormones on the spontaneous 24-hour GH secretion in healthy male and female subjects.

The purpose of this investigation was to evaluate whether in healthy subjects the GH response following stimulation with releasing hormones is dependent on the spontaneous GH secretion within 24 hr prior to the stimulation test. In 18 male and 9 female healthy subjects (21-59 years) GH was measured every 15 min over 26 hr. Twenty-four hours after the beginning of blood sampling, a GH stimulation test was performed by using a combined releasing hormone test. Sleep was recorded in three consecutive nights. A positive correlation was found between the AUCs of the 24-hr GH secretion and the AUCs of GH stimulation, which could not be explained by an age effect only. This study demonstrates that subjects with comparatively high amounts of GH secreted within 24 hr also show good GH secretory responses when immediately after the 24-hr sampling period a stimulation test is undertaken. Therefore, a low GH response to stimulation cannot be explained by feedback effects of high GH amounts secreted during the 24 hr before the test or by empty pituitary GH storages.

Adult↗