4.7 Article

Reduced connectivity of the auditory cortex in patients with auditory hallucinations: a resting state functional magnetic resonance imaging study

Journal

PSYCHOLOGICAL MEDICINE
Volume 40, Issue 7, Pages 1149-1158

Publisher

CAMBRIDGE UNIV PRESS
DOI: 10.1017/S0033291709991632

Keywords

Functional connectivity; primary auditory cortex; schizophrenia; secondary auditory cortex

Funding

  1. NHMRC [236025, 400317]
  2. Garnett Passe and Rodney Williams Memorial Foundation
  3. MHRI
  4. Cognitive Neurobiology of Psychosis Platform at Neurosciences Victoria

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Background. Previous research has reported auditory processing deficits that are specific to schizophrenia patients with a history of auditory hallucinations (AH). One explanation for these findings is that there are abnormalities in the interhemispheric connectivity of auditory cortex pathways in AH patients; as yet this explanation has not been experimentally investigated. We assessed the interhemispheric connectivity of both primary (A1) and secondary (A2) auditory cortices in n=13 AH patients, n=13 schizophrenia patients without auditory hallucinations (non-AH) and n=16 healthy controls using functional connectivity measures from functional magnetic resonance imaging (fMRI) data. Method. Functional connectivity was estimated from resting state fMRI data using regions of interest defined for each participant based on functional activation maps in response to passive listening to words. Additionally, stimulus-induced responses were regressed out of the stimulus data and the functional connectivity was estimated for the same regions to investigate the reliability of the estimates. Results. AH patients had significantly reduced interhemispheric connectivity in both A1 and A2 when compared with non-AH patients and healthy controls. The latter two groups did not show any differences in functional connectivity. Further, this pattern of findings was similar across the two datasets, indicating the reliability of our estimates. Conclusions. These data have identified a trait deficit specific to All patients. Since this deficit was characterized within both A1 and A2 it is expected to result in the disruption of multiple auditory functions, for example, the integration of basic auditory information between hemispheres (via A1) and higher-order language processing abilities (via A2).

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