Increased resting hippocampal and basal ganglia perfusion in people at ultra high risk for psychosis: replication in a second cohort

Paul Allen, Matilda Azis, Gemma Modinos, Matthijs G. Bossong, Ilaria Bonoldi, Carly Samson, Matthew Kempton , Oliver Howes, James Stone, Matthew Broome, Anthony A. Grace, Fernando Zelaya, Philip McGuire

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Abstract

We recently reported that resting hippocampal, basal ganglia and midbrain perfusion is elevated in people at ultra-high risk (UHR) for psychosis. The present study sought to replicate our previous finding in an independent UHR cohort, and examined the relationship between resting perfusion in these regions, psychosis and depression symptoms, and traumatic experiences in childhood. Pseudo-Continuous Arterial Spin Labelling (p-CASL) imaging was used to measure resting cerebral blood flow (rCBF) in 77 UHR for psychosis individuals and 25 healthy volunteers in a case-control design. UHR participants were recruited from clinical early detection services at three sites in the South of England. Symptoms levels were assessed using the Comprehensive Assessment of At Risk Mental States (CAARMS), the Hamilton Depression Scale (HAM-D), and childhood trauma was assessed retrospectively using the Childhood Trauma Questionnaire (CTQ). Right hippocampal and basal ganglia rCBF was significantly increased in UHR subjects compared to controls, partially replicating our previous finding in an independent cohort. In UHR participants, positive symptoms were positively correlated with rCBF in the right pallidum. CTQ scores were positively correlated with rCBF values in the bilateral hippocampus and negatively associated with rCBF in the left prefrontal cortex. Elevated resting hippocampal and basal ganglia activity appears to be a consistent finding in individuals at high risk for psychosis, consistent with data from preclinical models of the disorder. The association with childhood trauma suggests that its influence on the risk of psychosis may be mediated through an effect on hippocampal function.

© 2017, published by Oxford University Press. The attached document (embargoed until 27/12/2018) is an author produced version of a paper, uploaded in accordance with the publisher’s self- archiving policy. The final published version (version of record) is available online at the link below. Some minor differences between this version and the final published version may remain. We suggest you refer to the final published version should you wish to cite from it.
Original languageEnglish
JournalSCHIZOPHRENIA BULLETIN
Early online date27 Dec 2017
DOIs
Publication statusPublished - 1 Dec 2018

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