Publications by authors named "Lenzinger E"

The present linkage study is a follow-up within the chromosome 3q29 region in schizophrenia and bipolar affective disorder families, based on our recently published genome scan, resulting in evidence for linkage of both disorders to this region (marker D3S1265: NPL [non parametric lod] score Z(all)=3.74, P=0.003).

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Serotonergic pathways have been related to altered personality patterns in seasonal affective disorder (SAD). The short allele (s) of a polymorphism in the serotonin transporter promoter gene (5-HTTLPR) has been associated with neuroticism and anxiety-related personality traits in healthy volunteers. We investigated personality and 5-HTTLPR in female SAD patients using the Temperament and Character Inventory (TCI).

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Aims: To evaluate the impact of mood, affect, and personality on predicting relapse in detoxified alcohol-dependent patients to uncontrolled drinking during a 1-year treatment study.

Methods: A total of 521 patients with a DSM-III-R diagnosis of alcohol dependence, excluding those with major depressive disorder, took part in a European multicentre study (11 centres in the United Kingdom, Irish Republic, Switzerland, and Austria). Depressive symptoms were assessed using the Hamilton Depression Scale, whereas symptoms of anxiety were measured using the 'STAI-X2' of the self-rating scale State-Trait Anxiety Inventory and personality traits were measured by the Tridimensional Personality Questionnaire.

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Background: Despite the widely accepted view that schizophrenia and bipolar disorder represent independent illnesses and modes of inheritance, some data in the literature suggest that the diseases may share some genetic susceptibility. The objective of our analyses was to search for vulnerability loci for the two disorders.

Methods: A genomewide map of 388 microsatellite DNA markers was genotyped in five schizophrenia and three bipolar disorder Austrian families.

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Background: Both seasonal affective disorder/winter type (SAD) and premenstrual dysphoric disorder (PMDD) are cyclical disorders characterized by so-called atypical depressive symptoms. In the present study we compared the point prevalence rates of PMDD between a sample of premenopausal female patients suffering from SAD and healthy female controls.

Methods: Forty-six female patients with SAD and 46 healthy controls were included in our study.

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Objective: Schizophrenia is a relatively common, often chronic and debilitating mental illness. Evidence from various studies has clearly demonstrated that genetic factors contribute substantially to the etiology. The goal of this study was to identify chromosomal regions likely to contain schizophrenia susceptibility genes.

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Alterations in dopamine neurotransmission have been hypothesized to play a role in the etiology of schizophrenia. We considered the dopamine D3 receptor gene on chromosome 3 as a candidate gene for an association analysis. We compared PCR-based genotype markers for healthy controls (n=120) and patients (n=95) with schizophrenia and schizophrenia spectrum disorders as diagnosed by consensus according to DSM-III-R.

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There is some evidence that the neurotransmitter serotonin (5-hydroxytryptamine; 5-HT) may be involved in the pathogenesis of seasonal affective disorder (SAD). Short-term tryptophan (TRP) depletion was carried out in 18 drug-free remitted patients who met DSM-IV criteria for SAD. Behavioral effects were measured with the Hamilton Depression Rating Scale (HDRS) both 24 h before and 24 h after TRP depletion.

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Personality traits have been found as strong predictors for treatment response in different psychiatric disorders. We administered the Tridimensional Personality Questionnaire, which measures the three personality dimensions: novelty seeking, harm avoidance (HA), and reward dependence, as introduced by Cloninger in a multicenter study (11 centers in the United Kingdom, Eire, Switzerland, and Austria) with detoxified alcohol-dependent patients (n = 521). The objective of this study was to evaluate a possible predictive value of these three dimensions on relapse over 1 -year follow up.

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In an open study design, 50 opioid-dependent subjects (DSM-IV: 304. 0) were investigated in a gradual detoxification treatment with buprenorphine. The study was performed at the drug addiction outpatient clinic of the Department of General Psychiatry at the University of Vienna.

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In the present study, the occurrence of tardive dyskinesia (TD) in chronic schizophrenia patients was investigated in relation to pharmacogenetic polymorphisms. It is known that the metabolism of important neuroleptic drugs is influenced by polymorphisms of the CYP2D6 gene, which encodes the cytochrome P450 enzyme debrisoquine/spartein hydroxylase. Forty-five patients meeting the DSM IV criteria for schizophrenia, chronic course, were recruited.

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As part of the European Multicentre Association Study of Schizophrenia (EMASS), we studied polymorphisms in the dopamine DRD2 and DRD3 receptor genes. The EMASS collaboration was established to create a large, statistically powerful sample of schizophrenic patients and controls from different European centres. Previous studies have suggested associations between schizophrenia and the Ser311Cys polymorphism in exon 7 of the dopamine DRD2 receptor gene [Arinami et al.

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Even though premenstrual symptoms had been already described by Hippocrates, premenstrual dysphoric disorder (PMDD) was first mentioned as a special psychiatric diagnosis in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) in 1994. In DSM-III-R-Appendix A is was called late luteal phase dysphoric disorder (LLPDD), Appendix A. Before this diagnosis was established based on operationalized criteria, the term premenstrual syndrome (PMS) was used for patients with severe premenstrual mood disturbances and physical symptoms.

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Pulver et al. [1994a] reported modest linkage evidence for a dominantly (D) inherited "schizophrenia gene" in the vicinity of IL2RB on chromosome 22q12, and Coon et al. [1994] adduced moderate evidence under a recessive (R) model.

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Anticholinergic drugs such as biperiden are used for the treatment of extrapyramidal side effects (EPS) induced by neuroleptics such as haloperidol. The effects of biperiden and haloperidol plasma levels on EPS were studied in 29 chronically ill schizophrenics. The results show relationships between biperiden dose and biperiden plasma levels (BPL), and between BPL and haloperidol plasma levels (HPL).

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Recent studies have suggested that expanded CAG/CTG repeats contribute to the genetic aetiology of schizophrenia and bipolar disorder. However, the nature of this contribution is uncertain and difficult to predict from other known trinucleotide repeat diseases that display much simpler patterns of inheritance. We have sought to replicate and extend earlier findings using Repeat Expansion Detection in an enlarged sample of 152 patients with schizophrenia, 143 patients with bipolar disorder, and 160 controls.

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A blunted thyrotropin (TSH) response is a predictor of a good response to antidepressant drug treatment in depressives and neuroleptic treatment in paraphrenic patients (Larger et al 1986). The aim of the following study was to elucidate possible relationships between different endocrine systems and to shed light on the pathogenetic hypotheses of TSH-blunting. In order to evaluate especially hypothalamic activity in severe depression we were interested in the vasopressin system as another hormonal system underlying hypothalamic control.

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A major problem in the treatment of opiate-dependent patients arises due to illicit drug abuse capted with drug dependence and pregnancy. Drug abuse during pregnancy involves a high risk for the mother as well as for the unborn child. Twenty-three pregnant, opiate-dependent women, were enrolled in a 19-month study of the outpatient clinic for drug addiction.

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Alterations in dopamine neurotransmission and disturbed norepinephrine activity have been implicated in the pathogenesis of schizophrenia. We considered the dopamine-beta-hydroxylase (DBH) gene located on the long arm of chromosome 9 (9q34.3) as a candidate gene for schizophrenia.

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We analysed gender-concordance rates among 29 prospectively sampled schizophrenic probands and their 39 affected and 71 unaffected siblings. We did not find any unusual concordance rates. We found no same-gender concordance particularly in siblings affected by schizophrenia and related disorders.

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We examined the birth distribution of 2,450 schizophrenic and 682 schizoaffective patients first admitted between 1971 and 1992 to the University Hospital for Psychiatry in Vienna. Our data showed an excess of schizophrenic births in the first quarter of the year and a deficit in the third quarter compared with expectation from census data. The quarterly distribution of schizophrenic births seemed to be different from the one of of schizoaffective patients.

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In March 1993 the gene IT 15 was identified on chromosome 4p and it was demonstrated that it contained an unstable (CAG)n trinucleotide repeat that is elongated in patients with Huntington's chorea (HC). Persons with more than 37 (CAG)n repeats tend to have a higher risk of developing the disease. Testing the (CAG)n repeats in Austrian HC patients with PCR techniques shows correspondence between the clinical diagnosis of HC and genotypes [more than 42 (CAG)n repeats].

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