23
views
0
recommends
+1 Recommend
1 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Revisiting the Basic Symptom Concept: Toward Translating Risk Symptoms for Psychosis into Neurobiological Targets

      review-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          In its initial formulation, the concept of basic symptoms (BSs) integrated findings on the early symptomatic course of schizophrenia and first in vivo evidence of accompanying brain aberrations. It argued that the subtle subclinical disturbances in mental processes described as BSs were the most direct self-experienced expression of the underlying neurobiological aberrations of the disease. Other characteristic symptoms of psychosis (e.g., delusions and hallucinations) were conceptualized as secondary phenomena, resulting from dysfunctional beliefs and suboptimal coping styles with emerging BSs and/or concomitant stressors. While BSs can occur in many mental disorders, in particular affective disorders, a subset of perceptive and cognitive BSs appear to be specific to psychosis and are currently employed in two alternative risk criteria. However, despite their clinical recognition in the early detection of psychosis, neurobiological research on the aetiopathology of psychosis with neuroimaging methods has only just begun to consider the neural correlate of BSs. This perspective paper reviews the emerging evidence of an association between BSs and aberrant brain activation, connectivity patterns, and metabolism, and outlines promising routes for the use of BSs in aetiopathological research on psychosis.

          Related collections

          Most cited references80

          • Record: found
          • Abstract: found
          • Article: found

          Biological Insights From 108 Schizophrenia-Associated Genetic Loci

          Summary Schizophrenia is a highly heritable disorder. Genetic risk is conferred by a large number of alleles, including common alleles of small effect that might be detected by genome-wide association studies. Here, we report a multi-stage schizophrenia genome-wide association study of up to 36,989 cases and 113,075 controls. We identify 128 independent associations spanning 108 conservatively defined loci that meet genome-wide significance, 83 of which have not been previously reported. Associations were enriched among genes expressed in brain providing biological plausibility for the findings. Many findings have the potential to provide entirely novel insights into aetiology, but associations at DRD2 and multiple genes involved in glutamatergic neurotransmission highlight molecules of known and potential therapeutic relevance to schizophrenia, and are consistent with leading pathophysiological hypotheses. Independent of genes expressed in brain, associations were enriched among genes expressed in tissues that play important roles in immunity, providing support for the hypothesized link between the immune system and schizophrenia.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Cortical inhibitory neurons and schizophrenia.

            Impairments in certain cognitive functions, such as working memory, are core features of schizophrenia. Convergent findings indicate that a deficiency in signalling through the TrkB neurotrophin receptor leads to reduced GABA (gamma-aminobutyric acid) synthesis in the parvalbumin-containing subpopulation of inhibitory GABA neurons in the dorsolateral prefrontal cortex of individuals with schizophrenia. Despite both pre- and postsynaptic compensatory responses, the resulting alteration in perisomatic inhibition of pyramidal neurons contributes to a diminished capacity for the gamma-frequency synchronized neuronal activity that is required for working memory function. These findings reveal specific targets for therapeutic interventions to improve cognitive function in individuals with schizophrenia.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Why do many psychiatric disorders emerge during adolescence?

              The peak age of onset for many psychiatric disorders is adolescence, a time of remarkable physical and behavioural changes. The processes in the brain that underlie these behavioural changes have been the subject of recent investigations. What do we know about the maturation of the human brain during adolescence? Do structural changes in the cerebral cortex reflect synaptic pruning? Are increases in white-matter volume driven by myelination? Is the adolescent brain more or less sensitive to reward? Finding answers to these questions might enable us to further our understanding of mental health during adolescence.
                Bookmark

                Author and article information

                Contributors
                URI : http://frontiersin.org/people/u/268898
                URI : http://frontiersin.org/people/u/11211
                URI : http://frontiersin.org/people/u/165349
                URI : http://frontiersin.org/people/u/12988
                URI : http://frontiersin.org/people/u/299168
                URI : http://frontiersin.org/people/u/103566
                URI : http://frontiersin.org/people/u/88537
                URI : http://frontiersin.org/people/u/76159
                Journal
                Front Psychiatry
                Front Psychiatry
                Front. Psychiatry
                Frontiers in Psychiatry
                Frontiers Media S.A.
                1664-0640
                28 January 2016
                2016
                : 7
                : 9
                Affiliations
                [1] 1University Hospital of Child and Adolescent Psychiatry and Psychotherapy, University of Bern , Bern, Switzerland
                [2] 2Developmental Clinical Psychology Research Unit, Faculty of Psychology and Educational Sciences, University of Geneva , Geneva, Switzerland
                [3] 3Research Department of Clinical, Educational and Health Psychology, University College London , London, UK
                [4] 4Department of Psychiatry, Psychotherapy and Psychosomatics, University Hospital of Psychiatry , Zurich, Switzerland
                [5] 5School of Psychology, University of Birmingham , Birmingham, UK
                [6] 6Norwegian Centre for Mental Disorders Research (NORMENT), Faculty of Medicine, University of Oslo , Oslo, Norway
                [7] 7Department of Psychiatry and Psychotherapy, University of Cologne , Cologne, Germany
                [8] 8Institute of Neuroscience and Psychology, University of Glasgow , Glasgow, UK
                Author notes

                Edited by: Stefan Borgwardt, University of Basel, Switzerland

                Reviewed by: Drozdstoy Stoyanov Stoyanov, Medical University of Plovdiv, Bulgaria; Christina Andreou, University Psychiatric Clinics Basel, Switzerland

                *Correspondence: Frauke Schultze-Lutter, frauke.schultze-lutter@ 123456kjp.unibe.ch

                Specialty section: This article was submitted to Neuroimaging and Stimulation, a section of the journal Frontiers in Psychiatry

                Article
                10.3389/fpsyt.2016.00009
                4729935
                26858660
                4da8111a-91f3-457b-b111-b232c0e76f57
                Copyright © 2016 Schultze-Lutter, Debbané, Theodoridou, Wood, Raballo, Michel, Schmidt, Kindler, Ruhrmann and Uhlhaas.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 03 December 2015
                : 14 January 2016
                Page count
                Figures: 0, Tables: 2, Equations: 0, References: 74, Pages: 15, Words: 10581
                Categories
                Psychiatry
                Perspective

                Clinical Psychology & Psychiatry
                basic symptoms,neurobiology,psychosis,clinical high risk,aetiopathology

                Comments

                Comment on this article