[Identification and treatment of personality disorders in the physician's office].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to F Hohagen.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Obsessive-compulsive disorders are characterized by recurrent and persistent obsessive thoughts that are experienced as obtrusive and inappropriate, and (often stereotypic and repetitive) compulsive actions. Their lifetime prevalence is estimated to be 1-2%. Men and women are affected by such disorders in about equal numbers. The most common comorbidities are depression and anxiety. The etiology is considered to encompass both psychological and neurobiological aspects. The most effective therapeutic approach is cognitive behavioral therapy with exposure and response prevention as the central element, which leads to a lasting improvement in symptoms in some 60-80% of the patients. If a depressive disorder is also present, or if obsessive thoughts are predominant, a combination of cognitive behavioral therapy and pharmacological treatment with (selective) serotonin reuptake inhibitors has proven effective.
OBJECTIVE: The study investigated whether impaired decision-making as measured by the Gambling Task and Sensation Seeking, on one hand, and nicotine-dependence and readiness to change, on the other hand, show mutual influences in cigarette smokers. METHODS: Cigarette smokers were classified as dependent or non-dependent smokers. Assessment included stages of change (RCQ), decisional balance (DBS), Sensation Seeking Scale Form-V (SSS-V), and performance on the Gambling Task (GT). RESULTS: With the exception of a significant higher score in the SSS-V subscale Experience Seeking in dependent smokers, correlations between nicotine-dependence and cognitive features were not significant. The directions of the non-significant differences were not consistent. No significant relationship was found between the SSS-V and the GT, on one hand, and the readiness to change smoking behaviour, on the other hand. CONCLUSIONS: The results of the present study suggest that impaired performance on the GT and high scores in Sensation Seeking do not play an important role in nicotine-dependence and readiness to change smoking behaviour or vice versa.
Explore the source record for details and available documents.
BACKGROUND: A new observer depression scale which is based on the descriptive operationalized classification principles of ICD-10 is introduced. The AMDP Depression Scale (AMDP-DS), a 22-item clinician-rated inventory, provides the opportunity of dimensional as well as categorical depression severity assessment. METHODS: A sample of 50 patients with depressive symptoms were assessed with the AMDP-DS by two raters in a joint rater session. A number of widely used depression scales were applied separately by an independent rater. The ICD-10 symptom checklist was used for categorical assessment of depressive disorders. RESULTS: The inter-rater reliability for the total score of the AMDP-DS was excellent (Intraclass coefficient: 0.97). There were high correlations with the sum scores of the other scales under study. The correlations between the ICD-10 symptom-checklist and the AMDP-DS ranged from 0.75 to 0.89 for the total sample and 0.44 to 0.51 for patients with acute depressive episode. LIMITATIONS: The results are limited by the method of a joint rater setting and the relatively small subsample of patients with depressive episode. CONCLUSIONS: The AMDP-DS satisfies the requirements of psychometric criteria with a sufficient degree. A new depression scale designed to cover dimensional as well as categorical aspects has successfully been developed.
BACKGROUND: In schizophrenia, affective disorders, and obsessive-compulsive disorder (OCD) dysfunction of frontal neuronal circuits has been suggested. Such impairments imply corresponding oculomotor deficits. METHOD: Eye movement response to foveofugal and foveopetal step-ramp stimuli was recorded within the same study design in patients with schizophrenia (N= 16), affective disorder (N= 15), and OCD (N= 18) and compared with controls (N=23) using infra-red reflection oculography. RESULTS: In the foveofugal task steady-state velocity was lower in all patient groups compared with controls. Post-saccadic eye velocity was also decreased in patients with schizophrenia and affective disorder. In the foveopetal stimulus steady-state velocity was reduced in schizophrenic patients, only. Changes of saccadic latencies or position errors were not found in any of the patient groups. Also, pursuit latency was unchanged and initial eye acceleration was not decreased. CONCLUSIONS: Unaltered saccadic parameters indicate intact motion perception in cortical visual area V5. Therefore, the observed deficit of pursuit maintenance implies a dysfunction of frontal networks in all patient groups including the pursuit region of the frontal eye field (FEF). In patients with schizophrenia and affective disorder reduced post-saccadic pursuit initiation may indicate an impaired interaction between the pursuit and the saccadic system.
Explore the source record for details and available documents.
INTRODUCTION: The present study was designed to assess if the routine application of clomethiazole to ameliorate withdrawal symptoms in chronic alcohol dependent patients perpetuates sleep disturbances. METHODS: Twenty inpatients with alcohol dependence according to DSM-IV criteria received clomethiazole or placebo in a double-blind, randomized design upon admission. 11 patients were randomized to the clomethiazole group and 9 patients to the placebo group. During the first 5 days of treatment the patients received either clomethiazole (1st day: 3 x 384 mg, 2nd day: 4 x 384 mg, 3rd day: 3 x 384 mg, 4th day: 2 x 384 mg and 5th day: 1 x 384 mg) or placebo capsules at constant intervals. The patients spent two consecutive nights in the sleep laboratory at each of three assessment times: the first time at the beginning of abstinence (night 1 and 2, T0), the second time 6 days later (i. e. after 5 days of treatment and one day of discontinuation of clomethiazole or placebo: nights 6 and 7, T1) and the third time after 13 days (nights 13 and 14, T2). The first night at each of the three assessment times was an adaptation night. RESULTS: During the first two weeks of abstinence, the analysis of variance demonstrated a significant variation of Rapid Eye Movement (REM) sleep variables in the clomethiazole group. The placebo group showed no such variation. Clomethiazole evidently had a pronounced REM sleep suppressing effect, whereas the discontinuation of clomethiazole led to a REM sleep rebound. Furthermore, analysis of sleep continuity and sleep architecture variables showed that the clomethiazole group had significantly disturbed sleep at T1 in comparison to the placebo group. Simultaneous statistical testing with alcohol intake as covariate reduced the test power so that contrasts between the groups became nonsignificant. CONCLUSIONS: The REM sleep results are in line with earlier findings that REM sleep disinhibition in primary alcohol dependency is partly due to a REM sleep rebound after withdrawal from medication. Differences in the polysomnographic variables of sleep continuitiy and sleep architecture at T0 and T1 found between the clomethiazole and the placebo patients correspond to rebound insomnia following discontinuation of clomethiazole. Our findings indicate that drugs enforcing GABAergic neurotransmission may perpetuate the neuroadaptative effects caused by chronic alcohol consumption.
Obsessive-compulsive disorder (OCD) is characterized by obsessions, compulsions, or both, which cause significant personal distress or social dysfunction. OCD is a common psychiatric illness with a prevalence of 1-2%. Because most people have regular contact with primary health care services, the patient with OCD is likely to see their general practitioner even though psychological problems may not be the main reason for consultation. Early recognition of the disorder facilitates early intervention. This reduces distress, disability and burden of illness. Pharmacological treatment with serotonin reuptake inhibitors (SRI) and cognitive-behavioral therapy have both been proven to be effective and are evidence based.
Effective medications, as well as other effective options, are available for the treatment of insomnia. Since many patients do not inform their family doctors that they have sleep-related problems, the physician should himself question his patients on this point, with the aim of initiating specific treatment early enough to prevent such a condition becoming chronic.
Reduced 5-HT1A-receptor responsiveness has been reported in patients with panic disorder(PD) and/or agoraphobia (PDA). Although many of these patients are regular smokers, it has not been examined whether psychological or neurobiological effects induced by the selective 5-HT1A-receptor agonist, ipsapirone, are affected by the smoking status of the patients. In order to clarify this question neuroendocrine challenges with oral doses of ipsapirone (0.3 mg/kg) and placebo were performed in 39 patients with PDA, and results were compared between patients who smoked (>10 cigarettes per day, n = 17) and patients who had been non-smokers for at least two years (n = 22). Patients who were smokers (but did not smoke during the challenge procedure) had significantly reduced baseline concentrations of cortisol and a significantly lower body temperature. In comparison to placebo, administration of ipsapirone was associated with significant increases of various psychological symptoms and plasma cortisol concentrations. The subgroup of PD patients who were smokers showed significantly higher cortisol responses to ipsapirone than non-smokers. In conclusion, smoking status has to be taken into account when assessing the responsiveness of 5-HT1A receptors in patients with psychiatric disorders. The prevention of smoking during challenge sessions might not be the ideal approach in heavy smokers, since sudden abstinence from smoking is likely to affect neurobiological and possibly psychological responses to ipsapirone.
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.
BACKGROUND: The present study investigated polysomnographically assessed sleep parameters in alcohol-dependent patients after withdrawal and in healthy control subjects during baseline and after a cholinergic stimulation paradigm. The aim of the study was to test whether sleep parameters, especially rapid eye movement (REM) sleep variables, may serve as predictors for relapse in alcohol-dependent patients. METHODS: Forty patients diagnosed with alcohol dependence were admitted to a specialized ward for alcohol withdrawal and were investigated by polysomnography at three time points: 2-3 weeks after withdrawal (T0) and at follow-up investigations 6 (T1) and 12 (T2) months after discharge from the hospital. A subgroup of patients (n = 17) was studied at T0 after challenge with galanthamine, a reversible cholinesterase inhibitor (cholinergic REM induction test, CRIT). Patients were compared with two control groups: a) 30 healthy control subjects (matched for age- and gender-distribution) for comparison at baseline conditions; and b) 17 age- and gender-matched control subjects for comparison with the CRIT. RESULTS: At baseline the patients showed significant disturbances of sleep continuity and sleep architecture (decreased slow-wave sleep, SWS) and exhibited an increase of "REM sleep pressure" (a combined index of REM latency, REM density, and REM sleep percent). Galanthamine provoked significant alterations of sleep continuity, sleep architecture (reduced SWS), and increased most of the components of REM pressure, taking patients and control subjects together. Apart from SWS %SPT (sleep period time) no significant drug-group interactions occurred. Patients who remained abstinent (n = 11) for at least 6 months at follow-up exhibited significantly less abnormalities of REM sleep at T0 compared to the group of patients that relapsed at 6 months follow-up. CONCLUSIONS: It is concluded that increased REM sleep pressure after alcohol withdrawal is a robust predictor of vulnerability to relapse. Thus, a subgroup of alcoholic patients appears to exhibit distinct neurobiological abnormalities assessable by polysomnography that are related to an increased vulnerability for alcoholism and early relapse.
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.
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.
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.
Explore the source record for details and available documents.