Thorax deformity, joint hypermobility, and anxiety disorders.

OBJECTIVE: To evaluate the association between thorax deformities, panic disorder, and joint hypermobility METHODS: The study includes 52 males diagnosed with thorax deformity, and 40 healthy male controls without thorax deformity, in Tatvan Bitlis and Isparta, Turkey. The study was carried out from 2004 to 2006. The teleradiographic and thoracic lateral images of the subjects were evaluated to obtain the Beighton scores; subjects' psychiatric conditions were evaluated using the Structured Clinical Interview for DSM-IV Axis I Disorders (SCID-1), and the Hamilton Anxiety Scale (HAM-A) was applied in order to determine the anxiety levels. Both the subjects and controls were compared in sociodemographic, anxiety levels, and joint mobility levels. In addition, males with joint hypermobility and thorax deformity were compared to the group with thorax deformity without joint hypermobility. RESULTS: A significant difference in HAM-A scores was found between the groups with thorax deformity and without. In addition, 21 subjects with thorax deformity met the joint hypermobility criteria in the group with thorax deformity, and 7 subjects without thorax deformity met the joint hypermobility criteria in the group without thorax deformity, according to Beighton scoring. The Beighton scores of the subjects with thorax deformity were significantly different from those of the group without deformity. Additionally, anxiety scores of the males with thorax deformity and joint hypermobility were found higher than males with thorax deformity without joint hypermobility. CONCLUSION: Anxiety disorders, particularly panic disorder, have a significantly higher distribution in male subjects with thorax deformity compared to the healthy control group. In addition, the anxiety level of males with thorax deformity and joint hypermobility is higher than males with thorax deformity without joint hypermobility.

Is quality of life associated with cognitive impairment in schizophrenia?

BACKGROUND: The subjectively assessed quality of life of schizophrenia patients is mostly lower than healthy subjects, and cognitive impairment is an integral feature of schizophrenia. The aims of the present study were to compare the quality of life and neurocognitive functioning between the patients with schizophrenia and the healthy subjects, and to examine the relationships between quality of life and neurocognitive functions among the patients with schizophrenia. METHODS: Thirty-eight patients with schizophrenia (15 women and 23 men) and 31 healthy individuals (18 women and 13 men) were included in the study. All participants were administered World Health Organization Quality of Life-Brief Form (WHOQOL-BREF) to assess their quality of life, and Digit Span Test (DST) and Controlled Oral Word Association Test (COWAT) for cognitive functions. RESULTS: The patients with schizophrenia demonstrated lower scores in physical (F=25.6, p=0.0001), psychological (F=15.85, p=0.0001) and social (F=37.7, p=0.0001) domains compared to control group. The patients with schizophrenia showed significantly lower scores on COWAT compared to healthy subjects (F=4.22, p=0.04). The social domain scores of WHOQOL correlated to DST total scores (r=0.45, p=0.007), DST forwards scores (r=0.54, p=0.001) and COWAT total scores (r=0.40, p=0.04) in patients with schizophrenia but not in the control group. The patients with lower level of cognitive functioning had lower scores on social domain of WHOQOL-BREF (z=-2.01, p=0.04). CONCLUSION: Our results confirm that the cognitive deficits in executive function and working memory appear to have direct impact on the patients' perceived quality of life especially in social domain which can either be a cause or a consequence of social isolation of patients with schizophrenia.

[Neurobiological consequences of early life stressors]. / Erken yasam stresörlerinin nörobiyolojik sonuçlari.

This article reviews the neurobiological effects of psychosocial stress. In the first part, the results of childhood traumas, neurobiological models which explain the effects of psychosocial stress and animal studies on this subject are introduced. In a number of studies, an increase in the adulthood prevalence of depression, anxiety disorders and other psychiatric disorders was shown in children who were exposed to early life stress. Pre-clinical and clinical studies have shown that early life stressors cause endocrine, autonomous and behavioral stress responses as a result of permanent sensitivity in corticotropin releasing factor and other neurotransmitter systems in the central nervous system. As a result of this sensitivity, repeating stressors may play an important role in the pathogenesis of depression, anxiety disorders and psychophysiologic disorders. In contrast with the numerous studies investigating the long term effects of early life stressors on the brain, there are very few studies investigating the acute effects of these stressors. In spite of these limitations, it is known that psychosocial stressors may cause different neurobiological results in adults and children. After reviewing the relationship between psychosocial stressors and the neurobiology of affective disorders, it is explained how psychosocial stresses cause sensitivities in the central nervous system and how these sensitivities cause illness. These interactions have implications for treatment in the light of the explained mechanisms. In the last part of the article, new treatment strategies developed for correcting the effects of stress on the central nervous system are introduced.

Treatment-induced manic switch in the course of unipolar depression can predict bipolarity: cluster analysis based evidence.

BACKGROUND: Antidepressants are known to induce manic switch in patients with depression. Treatment-induced mania is not considered as bipolar disorder in DSM IV. The aim of this study was to assess whether clinical characteristics of patients with unipolar depression with a history of treatment-induced mania were similar to those of patients with bipolar disorder. METHOD: The study included 217 consecutive patients with DSM-IV mood disorders, diagnosed as: bipolar disorder type I (BP-I, n = 58) or type II (BP-II, n = 18) whose first episodes were depression, recurrent (unipolar) major depressive disorder with a history of antidepressant treatment-induced mania (switchers = sUD; n = 61) and without such an event (rUD; n = 80). First, the groups were compared with regard to clinical features and course specifiers using variance and chi-square analysis. Variables that differed significantly between the four groups were included in two-step cluster analysis to explore naturally occurring subgroups in all diagnoses. Subsequently, the relationship between the naturally occurring clusters and pre-defined DSM-IV diagnoses were investigated. RESULTS: Two-step cluster analysis revealed two different naturally occurring groups. Higher severity of depressive episodes, with higher rate of melancholic features, higher number of hospitalization and suicide attempts were represented in one cluster where switchers (77%), bipolar I (94.8%) and II (83.3%) patients clustered together. CONCLUSION: The findings of this study confirm that treatment-induced mania is a clinical phenomenon that belongs within the bipolar spectrum rather than a coincidental treatment complication, and that it should be placed under "bipolar disorders" in future classification systems. LIMITATIONS: The study includes the limitations of any naturalistic retrospective study.