title: The contribution of early traumatic events to schizophrenia in some patients: a traumagenic neurodevelopmental model.
abstract: The current diathesis-stress model of schizophrenia proposes that a genetic deficit creates a predisposing vulnerability in the form of oversenstivity to stress. This model positions all psychosocial events on the stress side of the diathesis-stress equation. As an example of hypotheses that emerge when consideration is given to repositioning adverse life events as potential contributors to the diathesis, this article examines one possible explanation for the high prevalence of child abuse found in adults diagnosed schizophrenic. A traumagenic neurodevelopmental (TN) model of schizophrenia is presented, documenting the similarities between the effects of traumatic events on the developing brain and the biological abnormalities found in persons diagnosed with schizophrenia, including overreactivity of the hypothalamic-pituitary-adrenal (HPA) axis; dopamine, norepinephrine, and serotonin abnormalities; and structural changes to the brain such as hippocampal damage, cerebral atrophy, ventricular enlargement, and reversed cerebral asymmetry. The TN model offers potential explanations for other findings in schizophrenia research beyond oversensitivity to stress, including cognitive impairment, pathways to positive and negative symptoms, and the relationship between psychotic and dissociative symptomatology. It is recommended that clinicians and researchers explore the presence of early adverse life events in adults with psychotic symptoms in order to ensure comprehensive formulations and appropriate treatment plans, and to further investigate the hypotheses generated by the TN model.
authors.affiliation: Psychology Department, University of Auckland, Private Bag 92019, Auckland 1, New Zealand. j.read@auckland.ac.nz
authors.forename: J
authors.initials: J
authors.lastname: Read
authors.forename: B D
authors.initials: BD
authors.lastname: Perry
authors.forename: A
authors.initials: A
authors.lastname: Moskowitz
authors.forename: J
authors.initials: J
authors.lastname: Connolly
mesh_terms: D000328:Adult; D000367:Age Factors; D001921:Brain / Q000378:metabolism; D002648:Child; D002649:Child Abuse / Q000523:psychology; D004298:Dopamine / Q000378:metabolism; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000378:metabolism / Q000503:physiopathology*; D009638:Norepinephrine / Q000378:metabolism; D010913:Pituitary-Adrenal System / Q000378:metabolism / Q000503:physiopathology*; D012559:Schizophrenia / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology*; D012701:Serotonin / Q000378:metabolism; D013313:Stress Disorders, Post-Traumatic / Q000523:psychology*
chemical_list: D012701:Serotonin; D004298:Dopamine; D009638:Norepinephrine