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Could Stress Cause Psychosis in Individuals Vulnerable to Schizophrenia?

Published online by Cambridge University Press:  07 November 2014

Cheryl Corcoran ,
Lilianne Mujica-Parodi ,
Scott Yale ,
David Leitman  and
Dolores Malaspina
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Abstract

It has long been considered that psychosocial stress plays a role in the expression of symptoms in schizophrenia (SZ), as it interacts with latent neural vulnerability that stems from genetic liability and early environmental insult. Advances in the understanding of the neurobiology of the stress cascade in both animal and human studies lead to a plausible model by which this interaction may occur: through neurotoxic effects on the hippocampus that may involve synaptic remodeling. Of late, the neurodevelopmental model of SZ etiology has been favored. But an elaboration of this schema that credits the impact of postnatal events and considers a role for neurodegenerative changes may be more plausible, given the evidence for gene-environment interaction in SZ expression and progressive structural changes observed with magnetic resonance imaging. Furthermore, new insights into nongliotic neurotoxic effects such as apoptosis, failure of neurogenesis, and changes in circuitry lead to an expansion of the time frame in which environmental effects may mediate expression of SZ symptoms.

Type
Feature Article
Information
CNS Spectrums , Volume 7 , Issue 1 , January 2002 , pp. 33 - 42
Copyright
Copyright © Cambridge University Press 2002

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