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The neural basis of auditory hallucinations (AH) in patients with schizophrenia is poorly characterized. Functional imaging studies investigate either the "state" dimension (i.e., the measurement of changes in brain area activation at the precise moment of AH onset) or the "trait" dimension (i.e., the neural correlates of the propensity to hallucinate). A corollary of AH (particularly acoustic-verbal) is the activation of brain regions involved in the auditory perception of speech (auditory cortex). One theory is that patients with schizophrenia with AH may have a deficit in processing their internal speech (i.e., external attribution to internal verbal content). However, there is little clinical data on the specific role of the mesencephalic region of the inferior colliculi (IC) in the formation of these symptoms. Preliminary research has shown intense expression of dopamine D2 receptors, particularly on glutamatergic neurons in mouse ICs. Thus, ICs receive numerous inhibitory dopaminergic inputs, likely involved in signal optimization and modulation. The study authors hypothesize that AHs are the result of a defect in signal inhibition by the IC, which lose their function as perceptual filters.
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Specific inclusion criteria for the group (SCZ+/HA+) • Patient with a PANSS score (question P3 regarding hallucinations) ≥ 4 (corresponds to PANSS (P3) 4, 5, 6, and 7 patients) AND having experienced hallucinations in the past 15 days.
Specific inclusion criteria for the control group
• Patient with a PANSS score (question P3 regarding hallucinations) = 1) AND having not experienced any hallucinations in the past 15 days.
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40 participants in 2 patient groups
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Martin Pastre
Data sourced from clinicaltrials.gov
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