Clin Psychopharmacol Neurosci.
2018 Aug;16(3):324-332. 10.9758/cpn.2018.16.3.324.
Neural Signature for Auditory Hallucinations in Schizophrenia: A High-Resolution Positron Emission Tomography Study with Fludeoxyglucose (¹â¸F)
- Affiliations
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- 1Department of Psychiatry, Gachon University Gil Medical Center, Gachon University School of Medicine, Incheon, Korea.
- 2Neuroscience Research Institute, Gachon University, Incheon, Korea.
- 3Department of Biomedical Engineering, Gachon University, Incheon, Korea.
- 4Research Institute for Advanced Industrial Technology, Korea University, Sejong, Korea.
- 5Department of Computer Science and Engineering & Center for Advanced Image and Information Technology, Chonbuk National University, Jeonju, Korea.
- 6Department of Psychiatry, Maeumsarang Hospital, Wanju, Korea.
- 7Research Institute of Clinical Medicine of Chonbuk National University-Biomedical Research Institute of Chonbuk National University Hospital, Jeonju, Korea. chungyc@jbnu.ac.kr
- 8Department of Radiology, Chonbuk National University Medical School, Jeonju, Korea.
- 9Department of Psychiatry, Chonbuk National University Medical School, Jeonju, Korea.
- KMID: 2419987
- DOI: http://doi.org/10.9758/cpn.2018.16.3.324
Abstract
OBJECTIVE
Auditory hallucinations (AHs) are a core symptom of schizophrenia. We investigated the neural signature of AHs by comparing hallucinating patients with schizophrenia with non-hallucinating patients with schizophrenia.
METHODS
We recruited hallucinating patients with schizophrenia meeting the criteria for persistent, prominent, and predominant AHs (n=10) and non-hallucinating patients with schizophrenia (n=12). Various clinical assessments were performed incluing Psychotic Symptom Rating Scale for Auditory Hallucinations. Using fludeoxyglucose (¹â¸F) positron emission tomography, regional differences in neural activity between the groups were analyzed.
RESULTS
The regions of interest analysis showed significantly lower standardized uptake value ratio (SUVR) in the superior, middle, and inferior frontal gyri, and higher SUVR in the putamen in patients with AHs versus patients without AHs. These findings were confirmed in the voxel-wise analysis.
CONCLUSION
Our findings indicate that hypoactivity in the frontal and cingulate gyri, coupled with hyperactivity in the temporal gyrus and putamen, may contribute to the pathophysiology of AHs.
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