Can childhood trauma explain the brain volume changes in first episode psychosis? Schiz Bull.Nov.2012


The role of abusive experiences in childhood is increasingly being studied and recognised as a major factor contributing to adult mental disorders.Childhood trauma can influence the developmental processes in the brain mainly via the HPA axis  (Traumogenic neuro developmental model of psychosis ). It has been  shown that HPA axis abnormalities are more in individuals with schizophrenia who were abused as children than those were not (Braehler 2005). Some studies also suggest that child hood trauma cause brain changes that are specific irrespective of the psychiatric diagnosis. Hippocampal volume reduction is the main finding in this regard.

A meta-analysis ( Karl A,2006) has confirmed that a diagnosis of PTSD is associated with decreased hippocampal and left amygdalar volumes, while also revealing a similar influence of trauma in the absence of PTSD. In a Borderline Personality Disorder sample, volume differences between controls and those with BPD were only found when the BPD group also had a history of childhood abuse. (Brambilla P,2004). Smaller hippocampal volumes have been observed in adult women with major depressive disorder with a history of childhood abuse (Vythilingam M,2002).

It is also argued  that the brain changes observed in first episode psychosis could be due to child hood trauma. Trauma exposure during a critical period might affect the brain systems (eg HPA axis: emotional regulatory system) in such a way that the person fails to differentiate threatening from non threatening stimuli.  Amygdalar volume studies lack consensus to support this argument. Previous brain volume/structural studies have in authors own words “neither reported nor controlled for a history of childhood trauma, opting instead to high light possible etiological explanations that are vague or reflect biological reductionism”.

A sub sample of Northern Ireland longitudinal  First-Episode Psychosis (NIFEPS) study is used to examine the association between childhood trauma and brain morphology. Authors claim that this study represents the first investigation of childhood trauma and brain morphology in psychosis.

90 patients from the above larger study  form the cohort in this investigation. 30% were lost to follow- up. Of the remaining 41 (19 males [46%] and 22 females [54%]) declined to participate, leaving a final sample of 21 individuals who had a mixture of diagnosis: ICD-10 schizophrenia (n = 10), bipolar disorder/mania (n = 3), psychotic depression (n = 2), and ‘‘other psychotic diagnoses’’ (n = 6).Traumatic experiences and impact were measured using, Traumatic Experiences Checklist,  Post-Traumatic Diagnostic Scale and  Troubles Related Experiences Questionnaire.


1.76% reported experiencing ‘‘childhood trauma’’ ie, trauma occurring prior to 18 years.

2. The experience of childhood trauma was not significantly associated with any gross volumetric regions.

3.Regression models indicated reductions in Hippocampus/amygdala complex ,  left hippocampal volume and amygdala volume were significant.  The model for total hippocampus volume approached, but did not achieve, significance.

Authors consider the possibility that specific neurocognitive deficits and neuroanatomical abnormalities observed in  psychosis may at least in part be a consequence of childhood trauma.

Limitations: 1. Small sample size 2. mixed diagnostic group 3. retrospective design. (The trauma measures were administered a few years following the MRI scanning procedures and rely on the accurate self-report of trauma)

Conclusions: Child hood trauma can have long lasting effect on brain anatomy making it a potentially important explanatory variable for neuro- anatomical observations in first episode psychosis.

Clinical implications: Explore trauma history in individuals presenting with psychosis routinely.

summary of the article:

Childhood trauma and hippocampal and amygdalar volumes in first-episode psychosis. Hoy K, Barrett S, Shannon C, Campbell C, Watson D, Rushe T, Shevlin M, Bai F, Cooper S, Mulholland C.Schizophr Bull. 2012 Nov;38(6):1162-9

Read the previous blog on related topic:


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