M146. NEUROCHEMICAL MODULATION OF AUDITORY CORTEX FUNCTIONAL CONNECTIVITY IN PATIENTS WITH AUDITORY VERBAL HALLUCINATIONS
Author(s) -
Sarah Weber,
Helene Hjelmervik,
Alexander R. Craven,
Erik Johnsen,
Rune A. Kroken,
ElseMarie Løberg,
Lars Ersland,
Kristiina Kompus,
Kenneth Hugdahl
Publication year - 2020
Publication title -
schizophrenia bulletin
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.823
H-Index - 190
eISSN - 1745-1701
pISSN - 0586-7614
DOI - 10.1093/schbul/sbaa030.458
Subject(s) - neurochemical , hallucinating , neuroscience , psychology , temporal lobe , superior temporal gyrus , psychosis , prefrontal cortex , auditory hallucination , auditory cortex , inhibitory postsynaptic potential , functional magnetic resonance imaging , audiology , cognition , epilepsy , medicine , psychiatry , computer science , artificial intelligence
Background Auditory hallucinations have been linked to aberrant functioning of the left superior temporal gyrus (STG) and are associated with impaired cognitive control regulated by areas in the prefrontal cortex. However, the mechanisms behind these dysfunctions are still unclear. Methods The current study combined resting state connectivity fMRI with MR spectroscopy (MRS) in a sample of 81 psychosis patients to explore how neurochemical correlates of auditory hallucinations modulate left STG functioning. The analyses were focused on glutamate (Glu) and gamma-aminobutyric acid (GABA), two neurotransmitters with excitatory and inhibitory functions, respectively, since these have previously been implicated in psychosis. Results Glu and GABA showed differential relationships with left STG connectivity in patients with and without hallucinations. Specifically, Glu concentration in the anterior cingulate cortex (ACC) was positively related to functional connectivity between the left and right temporal lobe in hallucinating patients only. In contrast, GABA concentration in the ACC was negatively related to connectivity between the left and right temporal lobe in non-hallucinating patients only. Discussion These findings support a recently proposed model of interhemispheric temporal lobe miscommunication in auditory hallucinations and indicate prefrontal neurochemical modulation as a potential underlying mechanism. The results can further be integrated with previously suggested excitatory/inhibitory imbalances as neurochemical modulators in AVH.
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