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Thorsten Kienast

Publications and source records attributed to Thorsten Kienast.

8 recordsLinked to original sources
PubMed2006

Treatment of alcohol withdrawal syndrome with a combination of tiapride/carbamazepine: results of a pooled analysis in 540 patients.

This was a retrospective study to examine the efficacy, practicability and medical safety of a combination of tiapride and unretarded (fast acting formula) carbamazepine in the treatment of alcohol withdrawal syndrome. In five hospitals using this combination for treatment of alcohol withdrawal, 540 patients who had been treated with this combination were identified. An intensive evaluation of patients files and charts was performed. Details of alcohol history and comorbid disorders were extracted from patient files. Severity of alcohol withdrawal had been assessed using the CIWA-A-Score. Gender differences and differences between patients in their first and at least second withdrawal were computed by means of variance analyses (GLM). At baseline (day 1) mean dosage given was 796 for tiapride and 543 mg for carbamazepine. A pooled analysis of the results showed that, in general, medication was well tolerated. Withdrawal symptomatology as indicated by CIWA-A scores clearly decreased over time. Although a significant number of patients had a history of alcohol withdrawal delirium (103) and epileptic seizures (151), few patients suffered from them during treatment (8 and 5, respectively). Only 24 (4.4%) patients dropped out because of lack of efficacy or change of medication, 15 (2.8%) because of side effects. No case of malignant neuroleptic syndrome was recorded. Data analysis showed gender differences and differences between patients in their first and at least second withdrawal for side effects, complications, and in some CIWA-A-scores. In general, severe complications of withdrawal syndrome were more frequent in men compared to women and in patients with repeated inpatient treatment. In line with previous research, the results from this study give further evidence that a combination of the anticonvulsant carbamazepine and tiapride is an effective and safe treatment for alcohol withdrawal treatment.

Adult↗
PubMed2006

Dysfunction of ventral striatal reward prediction in schizophrenic patients treated with typical, not atypical, neuroleptics.

RATIONALE: Clinical studies in patients with schizophrenia suggest that atypical neuroleptics are more effective than typical neuroleptics in reducing negative symptoms including apathy and anhedonia. Dysfunction of the dopaminergic reward system may contribute to negative symptoms in schizophrenia. OBJECTIVE: We used functional magnetic resonance imaging to assess the blood oxygen level dependency response in the ventral striatum of medicated schizophrenics and healthy control subjects during reward anticipation. METHODS: Twenty schizophrenics [ten medicated with typical (e.g., haloperidol) and ten with atypical (e.g., olanzapine and risperidone) neuroleptics] and ten age-matched healthy volunteers participated in an incentive monetary delay task in which visual cues predicted that a rapid response to a subsequent target stimulus would result either in monetary gain or no consequence. RESULTS: Healthy volunteers and schizophrenics treated with atypical neuroleptics showed ventral striatal activation in response to reward-indicating cues, but schizophrenics treated with typical neuroleptics did not. In patients treated with typical neuroleptics, decrease in activation of the left ventral striatum was correlated with the severity of negative symptoms. CONCLUSIONS: Failure to activate the ventral striatum during reward anticipation was previously associated with the severity of negative symptoms in schizophrenia and was also found in schizophrenics treated with typical neuroleptics in this study. Significant blunting of ventral striatal activation was not observed in patients treated with atypical neuroleptics, which may reflect the improved efficacy of these drugs in treating negative symptoms.

Adult↗
PubMed2006

Persistent dysfunctional frontal lobe activation in former smokers.

OBJECTIVE: Chronic smoking and nicotine exposure are accompanied by impaired cognitive task performance, modulated cerebral activity in brain imaging studies, and neuritic damage in experimental animals. The profile of the described dysfunctions matches frontal lobe circuits which also play a role in reward processing and reinforcement behavior. However, it is largely unknown if cerebral dysfunctions are reversible or persist during long term abstinence. MATERIALS AND METHODS: Cortical activation during auditory target processing (oddball task, P300 component) was recorded with 32-channel EEG in 247 healthy subjects consisting of 84 smokers, 53 former smokers (mean time of abstinence 11.9 years), and 110 never smokers. RESULTS: Both current smokers and former smokers exhibited significantly diminished P300 amplitudes (Cz, Pz) relative to never smokers. Neuroelectric source analysis (low resolution brain electromagnetic tomography) revealed a hypoactivation of the anterior cingulate, orbitofrontal, and prefrontal cortex in smokers compared to never smokers. A similar profile of hypoactivation was observed in former smokers. CONCLUSION: For the first time, evidence is provided that dysfunctional activation of frontal lobe networks in smokers is also present in long term abstainers.

Adult↗
PubMed2006

Net influx of plasma 6-[18F]fluoro-L-DOPA (FDOPA) to the ventral striatum correlates with prefrontal processing of affective stimuli.

Dopaminergic neurotransmission in the ventral and dorsal striatum interact with central processing of rewarding and reward-indicating stimuli, and may affect frontocortical-striatal-thalamic circuits regulating goal-directed behaviour. Thirteen healthy male volunteers were investigated with multimodal imaging, using the radioligand 6-[(18)F]fluoro-l-DOPA (FDOPA) for positron emission tomography (PET) measurements of dopamine synthesis capacity, and also functional magnetic resonance imaging (fMRI) in a cognitive activation paradigm. We calculated the correlation between FDOPA net blood-brain influx (; ml/g/min) in the ventral and associative dorsal striatum and BOLD signal changes elicited by standardized affectively positive, negative and neutral visual stimuli. The magnitude of in the ventral striatum was positively correlated with BOLD signal increases in the left anterior cingulate cortex and right insular operculum elicited by positive vs. neutral stimuli, but not negative vs. neutral stimuli. In the dorsal striatum, the magnitude of was positively correlated with processing of positive and negative stimuli in the left dorsolateral prefrontal cortex. These findings suggest that dopamine synthesis capacity in the ventral striatum correlates with the attentional processing of rewarding positive stimuli in the anterior cingulate cortex of healthy subjects. Dopaminergic neurotransmission in the associative dorsal striatum has been associated previously with habit learning. The observed correlation between dopamine synthesis capacity in the dorsal striatum and BOLD signal changes in the dorsolateral prefrontal cortex suggests dopaminergic modulation of processing of emotional stimuli in brain areas associated with motor planning and executive behaviour control.

Adult↗
PubMed2006

Smoking and structural brain deficits: a volumetric MR investigation.

Growing evidence from animal studies indicates brain-damaging properties of nicotine exposure. Investigations in humans found a wide range of functional cerebral effects of nicotine and cigarette smoking, but studies focusing on brain damage are sparse. In 22 smokers and 23 never-smokers possible differences of the cerebral structures were investigated using magnetic resonance imaging and voxel-based morphometry. Significantly smaller grey matter volume and lower grey matter density (P = 0.05, corrected) were observed in the frontal regions (anterior cingulate, prefrontal and orbitofrontal cortex), the occipital lobe and the temporal lobe including parahippocampal gyrus, in smokers than in never-smokers. Group differences of either grey matter volume or grey matter density were also found in the thalamus, cerebellum and substantia nigra, among other regions. Smokers did not show greater volumes than never-smokers in any cerebral region. Magnitude of lifetime exposure to tobacco smoke (pack-years) was inversely correlated with volume of frontal and temporal lobes and cerebellum (P = 0.001, uncorrected). The data indicate structural deficits of several cortical and subcortical regions in smokers relative to never-smokers. The topographic profile of the group differences show some similarities to brain networks known to mediate drug reinforcement, attention and working memory processing. The present findings may explain in part the frequently reported cognitive dysfunctions in chronic cigarette consumers.

Adult↗
PubMed2006

Serotonergic dysfunction: brain imaging and behavioral correlates.

Identification of gene-environment and gene-gene interactions has become increasingly important in understanding psychiatric disorders. Dysfunction of central serotonergic neurotransmission has been implicated in alcoholism, depression, and anxiety. We review the literature on nonhuman primates that assesses the interaction between the genetic constitution of the regulatory region ofthe serotonin transporter (5-HTT) and environmental factors. Prospective studies in nonhuman primates that underwent social stress found a reduction of theserotonin turnover rate among carriers of one or two short alleles in a functional polymorphism of the 5-HTT promoter. In these primates, brain imaging studies showed a relative increase in the availability of raphe serotonin transporters. A low serotonin turnover rate and a high availability of serotonin transporters were associated with reduced response to excessive alcohol intake, anxiety, and impulsive aggression. Animal experiments point to a relationship between serotonergic dysfunction, negative mood states, and excessive alcohol intake, which may in part be mediated by reduced alcohol-induced sedation.

Aggression↗
PubMed2005

Therapy and supportive care of alcoholics: guidelines for practitioners.

BACKGROUND/AIMS: Alcoholism is a widespread disorder in our societies. However, only a small percentage of alcoholics appear in specific psychotherapeutic treatment programs. The vast majority are seen by general practitioners or experts of other medical specialties where they are treated intensively for their alcohol-induced comorbidities. But the reason for these comorbidities, alcoholism itself, is rarely treated. This article provides a guideline for specialists and non-specialists on how to treat these patients correctly in nonspecific treatment programs and how to increase motivation to stay abstinent. Moreover, the concept can be quickly and easily integrated into the daily routine of any therapeutic team. METHODS: Literature on the therapeutic methods of brief interventions, motivational interviewing as well as pharmacological relapse prevention was reviewed in PubMed for the years 1991-2005. RESULTS/CONCLUSION: The burden of disease of alcoholism and alcohol abuse as primary disorders is highly evident but often underestimated even by therapists of various medical disciplines. Systematic studies of the brief intervention method, motivational interviewing and also pharmacological treatment with acamprosate have shown that these are potent methods that are easily used to increase the duration of abstinence and patients' motivation to take part in further specific treatment.

Alcohol-Related Disorders↗