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Horst Gann

Publications and source records attributed to Horst Gann.

9 recordsLinked to original sources

Sleep electroencephalographic spectral power after withdrawal from alcohol in alcohol-dependent patients.

BACKGROUND: Dysfunctional hyperarousal is suspected to be a neurophysiological determinant of relapse in abstinent alcohol-dependent patients. In the present study, we used spectral power analysis of the sleep electroencephalographic (EEG) to quantify brain activity during sleep in patients during subacute withdrawal as well as in control subjects. Our hypothesis was that the subgroup of patients who relapsed within the 3 months to follow-up would exhibit-increased dysfunctional arousal manifested by higher-frequency (beta) EEG power during sleep. METHODS: Twenty-six alcohol-dependent in-patients were examined with polysomnography over 2 nights 2 to 3 weeks after withdrawal. At the 3-month clinical follow-up assessment, 12 of them had relapsed and 14 abstained. The control group consisted of 23 healthy subjects similar to the patients with alcohol dependence in age and gender distribution. Spectral sleep EEG analysis was performed on both nights (adaptation and baseline) of all subjects. Logarithmic artifact-controlled spectral band power of sleep stage 2 and rapid eye movement (REM) sleep was analyzed for Group, Gender, and Age effects using multiple analyses of covariance. Three groups were compared with the Group factor: relapsers, abstainers, and controls. RESULTS: Generally, both Group and Age effects were significant for the second, baseline night for the visually scored sleep parameters, while spectral EEG parameters showed significant differences in the adaptation night. In the adaptation night, a significant enhancement in the beta2 band (24-32 Hz) was seen in REM sleep in relapsers relative to both abstainers and controls. CONCLUSIONS: The beta2 increase could be interpreted as a sign of dysfunctional arousal during REM sleep "unmasked" by the additional stressor of sleep environment adaptation. Its determinants are likely to be both premorbid and drinking history related.

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Effects of alcohol on polysomnographically recorded sleep in healthy subjects.

BACKGROUND: After studying the sleep of alcohol-dependent patients at the beginning and over the course of abstinence in earlier studies, our interest in the current study focused on the direct effect of 2 doses of alcohol [0.03 and 0.1% blood alcohol level (BAL)] on healthy sleep. This is the first polysomnographic study testing the impact of 2 doses of alcohol ingestion (thus reflecting "normal" social drinking and alcohol abuse) in a single-blind randomized design in healthy volunteers. The study evaluated a short-term acute drinking period for 3 and 2 days of withdrawal from alcohol not only for polysomnographic variables but also for subjective estimates of sleep quality. METHODS: In a crossover design with a 1-week interval, healthy subjects received alcohol to raise their blood alcohol to either 0.03 or 0.1% BAL at bedtime for 3 consecutive nights after an alcohol-free baseline night. Objective (polysomnography) and subjective sleep (questionnaires) was recorded each night. During the following 2 days, alcohol was discontinued with simultaneous measurements of sleep to gauge withdrawal effects. RESULTS: At a dose of alcohol leading to BAL of 0.03%, no clear effects could be detected. Following an evening BAL of 0.1%, a hypnotic-like effect (shortened sleep latency, reduced number of wake periods, decreased stage 1 sleep) occurred primarily during the first half of the night with signs of rebound effects being already present during the second half of the night (increased stage 1 sleep). At this dose, alcohol significantly increased slow-wave sleep (SWS) in the first half of the night and reduced REM density in the beginning of the night. After discontinuation of the higher alcohol dose, REM sleep amount increased. No significant withdrawal or rebound effects could be observed for parameters of sleep continuity during the 2 nights after discontinuation from alcohol at a BAL of 0.1%. CONCLUSIONS: Owing to the small sample size, the results of this study need to be interpreted with caution. Short-term moderate alcohol consumption (BAL 0.03%) did not significantly alter objective or subjective parameters of sleep. Higher doses of alcohol resulting in a BAL level of 0.10% immediately before going to bed mainly influenced sleep in the first half of the night, resembling the effects of a short-acting hypnotic drug, including a suppression of phasic aspects of REM sleep (REM density). Interestingly, analysis of the latter part of these nights indicated the immediate presence of withdrawal effects (increased light sleep). No statistically significant effects on sleep parameters were observable during the 2 nights of withdrawal from alcohol at the higher BAL. Interpreted carefully, our data indicate that negative effects on sleep occur already with short-term use of alcohol at doses of BAL of 0.10%, despite hypnotic-like effects during the first hours of sleep, especially during the latter part of the night.

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The effects of clomethiazole on polysomnographically recorded sleep in healthy subjects.

Clomethiazole is widely used in European countries to treat alcohol withdrawal symptoms including delirium tremens. The current study aimed to explore the effects of clomethiazole on the sleep of healthy volunteers. We postulated both a hypnotic and a REM suppressive effect as well as the occurrence of a rebound phenomenon following three days of treatment with clomethiazole. The study group was composed of five men and five women. The probands were examined in the sleep laboratory throughout a course of seven nights. The first night was considered as the adaptation night and the second as the baseline night. Prior to nights 3 to 5, probands took 384 mg clomethiazole at 22 hours. The 6th and 7th nights served to record potential effects of medication discontinuation. The current study confirms the indication in the scientific literature with regard to hypnotic and REM-suppressive effects of clomethiazole, as well as a rebound phenomenon following discontinuation of the medication. The effect of clomethiazole on the sleep EEG was most obvious in the first half of the night. The analysis of the polysomnogram in terms of each half of the night gave no indication of a rebound phenomenon during the second half. The REM sleep-suppressing component of clomethiazole is of great interest in connection with its use in treating delirium tremens. The rebound phenomenon in healthy controls after only three days of medication at a relatively low dosage of clomethiazole underscores the need to administer it in doses individually tailored to the extent of the alcohol withdrawal syndrome in the individual patient.

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Polysomnographic comparison between patients with primary alcohol dependency during subacute withdrawal and patients with a major depression.

Complex neurobiological models based on animal research have been formulated in an attempt to explain the cyclic pattern of nonREM and REM sleep. The "reciprocal interaction model" of nonREM and REM sleep regulation, which has been updated to incorporate new evidence is still the most convincing. Therefore it is reasonable to apply this model also to REM sleep abnormalities such as shortened REM latency and increased REM density, observed in patients with depression and alcohol dependency. In a retrospective analysis baseline data from 40 subjects with primary alcohol dependency are compared with a group of 40 patients diagnosed with major depression (diagnoses according to DSM-III-R) and healthy subjects. All alcohol dependent patients were examined in the sleep laboratory during subacute withdrawal at least 7 days off medication and after at least 14 days of abstinence. The patients with major depression (at least 7 days off psychoactive medication) and the healthy subjects had been examined previously by polysomnography during the last few years in the context of various studies and were assembled from our database to match the group of alcohol dependent patients with respect to age and sex. Alcohol dependent patients exhibited similar disturbances in sleep continuity and REM sleep as depressed patients in comparison to healthy controls while parameters of sleep architecture were even more strongly disturbed in alcohol dependence. While enhanced sensitivity of cholinergic receptors is the most likely explanation for the increase in "REM pressure" in depressives, this appears not to apply to alcoholics, who rather exhibit a decreased response to cholinergic stimulation. Thus, according to the reciprocal interaction model of nonREM- and REM sleep regulation and in contrast to the interpretation of the findings in depressed patients, an impaired aminergic rather than an increased cholinergic neurotransmission might be responsible for the increased REM sleep pressure in alcohol dependent patients. Alternatively or in addition the REM anomalies in alcoholic patients could also be due to adaptive regulatory processes during chronic alcohol consumption that lead to downregulation of GABA(A)- and upregulation of NMDA-receptors or their intracellular signalling and become apparent with alcohol withdrawal. Such adaptive counterregulation might also explain the alterations in slow wave sleep found in alcoholics that are even more pronounced in these patients than in patients with major depression.

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Magnesium treatment of primary alcohol-dependent patients during subacute withdrawal: an open pilot study with polysomnography.

BACKGROUND: Sleep electroencephalogram alterations and insomnia complaints persist after alcohol withdrawal in dependent patients and are considered strong predictors of relapse. Although disturbances of magnesium household due to alcohol consumption are well known, the relationship of magnesium metabolism and sleep disturbances has not been investigated in this patient group. We conducted an open pilot study to evaluate the effects of magnesium treatment on the sleep of primary alcohol-dependent patients during subacute withdrawal. METHODS: Patients were treated with 30 mmol magnesium daily over 4 weeks. Eleven of the 14 included patients were evaluated. Patients were free of any kind of psychotropic medication or other substances known to influence sleep. Polysomnographic recordings with monitoring of periodic leg movements in sleep (PLMS) were performed for two consecutive nights 2 weeks after acute withdrawal (baseline) and 4 weeks later at the end of the treatment period. After the baseline polysomnography, patients were investigated by the magnesium loading test to verify magnesium depletion. RESULTS: We found a significant decrease of sleep onset latency from 40.6 to 21.7 min (p = 0.03) and a significant improvement of subjective sleep quality, as assessed by the Pittsburgh Sleep Quality Index, from 8.1 to 5.8 (p = 0.05) during magnesium treatment. Changes in PLMS indices revealed two subgroups of patients: one with an increase of PLMS from 30.7 to 39.4 per hour of sleep (n = 4) and the other one with a decrease of PLMS from 8.9 to 2.1 per hour of sleep (p = 0.04). Patients with PLMS decreases seemed to have a more favorable prognosis: total sleep time, gamma-glutamyltransferase, carbohydrate-deficient transferrin, and Beck Depression Inventory scores improved significantly during treatment in this group. The magnesium loading test revealed a magnesium deficiency in only one patient, five patients showed normal retention values, and the remaining five patients had an increased magnesium excretion, indicating a possible continued renal magnesium loss during abstinence. CONCLUSIONS: The results of this study should be interpreted with caution, because no control group with placebo was investigated. Both subjective and, partly, objective parameters of sleep improved during the 4-week study period. Further research is needed to clarify the relationship of magnesium metabolism and sleep alterations.

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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.

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Assessing cerebral dysfunction with probe-evoked potentials in a CNV task -- a study in alcoholics.

OBJECTIVES: Contrary to event-related potential (ERP) components N1, N2 and P3, slow ERPs have rarely been used in assessing cerebral dysfunction in mental disorders. Focussing on slow waves (SWs) and on patients with mild cerebral dysfunction, we recorded ERPs in alcoholics using a dual task design. METHODS: ERPs to auditory probes presented either 1s before the warning or 1s before the imperative stimulus of a visual contingent negative variation (CNV) paradigm were recorded from 33 scalp electrodes in 27 alcoholics following detoxification and 12 healthy controls. Independent component analysis (ICA) was used to separate potentially overlapping spatial components. RESULTS: In alcoholics compared to controls, probe ERPs showed increased N2, decreased P3 and increased negative SWs of two types appearing pre- and post-P3, respectively. Both negative SWs significantly correlated with neuropsychological indices reflecting verbal intelligence and memory functions. The increase in probe-evoked N1 and P3 potentials during CNV, putatively associated with enhanced cortical excitability, significantly correlated with clinical features of protracted alcohol withdrawal syndrome in alcoholics. CONCLUSIONS: Our experimental approach revealed two types of negative SWs which strongly correlated with neuropsychological deficits of mildly impaired patients. It is suggested that our methods might enhance diagnostic efficiency of ERPs. An electrophysiological measure of protracted alcohol withdrawal might be useful for managing central nervous system dysfunction in alcoholics.

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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.

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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.

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