Clinical Neuroscience

[The relevance of traumatic life events in schizophrenia spectrum disorders]

KOCSIS-BOGÁR Krisztina1, PERCZEL FORINTOS Dóra1

SEPTEMBER 30, 2014

Clinical Neuroscience - 2014;67(09-10)

[The central goal of this manuscript was to review literature about the interconnections of traumatic life events and symptoms of schizophrenia spectrum of the last 15 years. First of all, the stress-diathesis model and the traumagenic neurodevelopmental model are shortly presented. Psychological effects of traumas and specific psychotic symptoms in connection with traumatic events are discussed. The course of the disease in patients affected by previous traumas and possible mediating factors are also addressed. Studies of both clinical and community samples are cited. It was also our aim to review literature about the neurobiological and neurocognitive processes in people affected by schizophrenia and/or traumatic life events. The role of prefrontal and medial temporal regions are explored with a special emphasis on contextual memory and hippocampal functioning. Finally, the possible effects of exploring traumatic life events on the treatment of schizophrenia are discussed.]

AFFILIATIONS

  1. Semmelweis University, Department of Clinical Psychology, Budapest

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[White matter lesions are defining characteristics of multiple sclerosis (MS), whereas grey matter involvement is a less recognised attribute. Recent investigations using dedicated imaging approaches have made it possible to depict cortical lesions. Additionally, grey matter atrophy may be estimated using various methods. Several studies have suggested that grey matter atrophy closely correlates to clinical disability. In this review we have collected information on grey matter atrophy in MS and the effect of disease modifying therapies upon brain atrophy.]

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[Multiple sclerosis (MS) is a complex trait disorder defined by several genes and their interactions with environmental factors. A comprehensive exploration of the susceptibility variants had not been feasible until recently when new developments in biotechnology and bioinformatics made possible sequencing of the whole human genome, cataloguing of nucleotide variants and alignments of these variants in haplotypes. Earlier observations from epidemiological, candidate gene and linkage studies provided ample evidence to support a complex genetic determination of MS. New biotechnology and bioinformatics resources have been recently applied to further successful explorations of the disease. These efforts were paralleled by more careful and reliable ascertainments of disease phenotypes, collaborations among specialized centers to generate sufficient sample size and involvement of clinician-scientists capable of working both on the clinical and scientific study sides. Data obtained from the whole genome association studies (GWAS) elevated our understanding of MS genetics to a new level by identifying an extensive list of genetic determinants. Pathway analyses of MS-associated variants provided evidence to support the immune etiology of the disease. Future research will likely explore how environmental factors interact with the genome, and contribute to the abnormal immune activation and inflammation. This review summarizes the outcomes of MS genetic explorations including those of recent GWAS, and highlights practical consequences of genetic and genomic studies by pointing out as to how the derived data facilitate further elucidation of MS pathogenesis. A better understanding of disease processes is necessary for future advancements in therapeutics and the development of disease prevention strategies.]

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[Background and purpose - In the central nervous tissue, two types of transsection-resulted axonal degeneration are generally accepted: “watery” and “dark”. The present paper deals with the assumption that the mechanism of this kind of “dark” axonal degeneration has a relationship with that of the “dark” neuronal degeneration. Methods - A minute stab wound is inflicted in the parietal cortex of the rat brain. From 1 h to 3 months postinjury, the resulted ultrastructural events in two distant regions of the corticospinal tract (internal capsule and C3 region of the corticospinal tract) are studied. Results - As a novel finding, the first morphological process of “dark” axonal degeneration was found to consists in a striking reduction of the distances between neighboring neurofilaments, which were readily distinguishable and apparently undamaged. This pattern (compacted ultrastructure) persisted for hours. By day 1 postinjury, the compacted axoplasmic elements aggregated into a homogenous and dense (“dark”) mass in which hardly any ultrastructural elements could be distinguished. Surrounded by apparently normal or mildly abnormal myelin sheat, this mass underwent a non-isotropic shrinkage during the next three months. Morphological signs of phagocytosis were insignificant. Conclusion - The ultrastructural events during the first day post-injury suggest a non-enzymatic mechanism as an alternative to the prevailing molecular-biological mechanism.]

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