Yingying Tang1, Tianhong Zhang1, Bradley Edelman2, Botao Zeng3, Shanshan Zhao4, Chunyan Li4, Kaiming Zhuo3, Zhenying Qian4, Hui Li4, Qian Guo4, Huiru Cui4, Yikang Zhu4, Lijuan Jiang4, Chunbo Li1, Dehua Yu5, Jijun Wang6. 1. Shanghai Key Laboratory of Psychotic Disorders, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, PR China; Department of EEG and Imaging, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, PR China. 2. Department of Biomedical Engineering, University of Minnesota, Minneapolis, MN, USA. 3. Department of EEG and Imaging, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, PR China. 4. Shanghai Key Laboratory of Psychotic Disorders, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, PR China. 5. Department of Psychiatry, Yangpu Hospital, Medical School of Tongji University, Shanghai 200090, PR China. Electronic address: ydh@tongji.edu.cn. 6. Shanghai Key Laboratory of Psychotic Disorders, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, PR China; Department of EEG and Imaging, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, PR China. Electronic address: jijunwang27@gmail.com.
Abstract
BACKGROUND: Deficits in gamma-aminobutyric acid (GABA) inhibitory neurotransmission have been associated with pathophysiological mechanisms underlying schizophrenia. However, little is known about whether these deficits occur before or after the onset of psychosis. METHOD: We recruited 16 drug-naive subjects at ultra-high risk of psychosis (UHR), 17 schizophrenia patients and 28 healthy controls. Cortical inhibition was determined using transcranial magnetic stimulation (TMS) over the left primary motor cortex. TMS markers such as short-interval cortical inhibition (SICI), cortical silent period (CSP) and intracortical facilitation (ICF) were obtained from each subject. While SICI can reflect GABA type A (GABAA) mediated inhibition, CSP is thought to indicate GABA type B (GABAB) mediated inhibitory circuits. RESULTS: As compared with healthy controls, UHR subjects showed a prolonged CSP with no change in SICI, whereas schizophrenia patients demonstrated both a prolonged CSP and a reduced SICI. No group differences were found for ICF. CSP in schizophrenia patients also had a positive correlation with positive symptom score of the positive and negative symptom scale (PANSS). CONCLUSIONS: Cortical inhibitory deficits among UHR subjects were relatively limited compared to those among schizophrenia patients. Alterations might occur in some subgroup of GABA-mediated neurotransmitter systems before the onset of psychosis, while alterations in both GABAA and GABAB networks might contribute to full-blown psychosis.
BACKGROUND:Deficits in gamma-aminobutyric acid (GABA) inhibitory neurotransmission have been associated with pathophysiological mechanisms underlying schizophrenia. However, little is known about whether these deficits occur before or after the onset of psychosis. METHOD: We recruited 16 drug-naive subjects at ultra-high risk of psychosis (UHR), 17 schizophreniapatients and 28 healthy controls. Cortical inhibition was determined using transcranial magnetic stimulation (TMS) over the left primary motor cortex. TMS markers such as short-interval cortical inhibition (SICI), cortical silent period (CSP) and intracortical facilitation (ICF) were obtained from each subject. While SICI can reflect GABA type A (GABAA) mediated inhibition, CSP is thought to indicate GABA type B (GABAB) mediated inhibitory circuits. RESULTS: As compared with healthy controls, UHR subjects showed a prolonged CSP with no change in SICI, whereas schizophreniapatients demonstrated both a prolonged CSP and a reduced SICI. No group differences were found for ICF. CSP in schizophreniapatients also had a positive correlation with positive symptom score of the positive and negative symptom scale (PANSS). CONCLUSIONS: Cortical inhibitory deficits among UHR subjects were relatively limited compared to those among schizophreniapatients. Alterations might occur in some subgroup of GABA-mediated neurotransmitter systems before the onset of psychosis, while alterations in both GABAA and GABAB networks might contribute to full-blown psychosis.
Authors: Xiaoming Du; Peter Kochunov; Ann Summerfelt; Joshua Chiappelli; Fow-Sen Choa; L Elliot Hong Journal: Brain Stimul Date: 2016-11-12 Impact factor: 8.955