Guowei Wu1, Yunxia Wang2, Tumbwene E Mwansisya3, Weidan Pu1, Huiran Zhang1, Chang Liu1, Qing Yang4, Eric Y H Chen5, Zhimin Xue1, Zhening Liu6, Baoci Shan7. 1. Institute of Mental Health, Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, China. 2. Key Laboratory of Nuclear Radiation and Nuclear Energy Technology, Institute of High Energy Physics, Chinese Academy of Sciences, Beijing 100049, China; National Laboratory of Pattern Recognition, Institute of Automation, Chinese Academy of Sciences, Beijing 100190, China. 3. Institute of Mental Health, Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, China; College of Health Sciences, University of Dodoma, P.O. Box 395, Dodoma, Tanzania. 4. Department of Psychiatry, Yale School of Medicine, New Haven, CT 06520, USA. 5. Department of Psychiatry, University of Hong Kong, Hong Kong, China. 6. Institute of Mental Health, Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, China; State Key Laboratory of Medical Genetics, Central South University, Changsha, Hunan 410011, China. Electronic address: zningl@163.com. 7. Key Laboratory of Nuclear Radiation and Nuclear Energy Technology, Institute of High Energy Physics, Chinese Academy of Sciences, Beijing 100049, China; Beijing Engineering Research Center of Radiographic Techniques and Equipment, Beijing 100049, China. Electronic address: shanbc@ihep.ac.cn.
Abstract
BACKGROUND: Schizophrenia (SZ) and bipolar I disorder (BD) share many overlapping clinical features, confounding the current diagnostic systems. Recent studies suggest the posterior cingulate (PCC) and medial prefrontal (MPFC) cortices that are involved in SZ and BD pathophysiology. However, the roles of PCC and MPFC in providing specific distinctive and shared neural substrates between these two disorders remain largely unknown. Examining the neurophysiologic mechanism of these diseases may help explain the clinical observations and differentiate the two disorders. METHODS: We used the Dynamic Casual Modeling (DCM), which is capable of eliciting hidden neuronal dynamics and reveal cross-regulation of multiple neuronal systems, to characterize the pattern of disrupted effective connectivity in the left PCC-MPFC circuit during working memory tasks in 36 SZ and 20 BD patients as well as 29 healthy controls. RESULTS: Compared to the healthy controls, both SZ and BD patient groups exhibited significant negative effective connectivity from the left MPFC to PCC. The negative effective connectivity was more remarkable in schizophrenic patients. Only patients with BD differed from healthy controls with positive effective connectivity from the left PCC to MPFC. CONCLUSIONS: Whole brain analysis revealed deactivation of the left PCC and MPFC across all patient groups. This study provides new insight that changes in effective connectivity of the left MPFC to left PCC circuit during working memory processing may be a core pathophysiological feature distinguishing SZ from BD.
BACKGROUND:Schizophrenia (SZ) and bipolar I disorder (BD) share many overlapping clinical features, confounding the current diagnostic systems. Recent studies suggest the posterior cingulate (PCC) and medial prefrontal (MPFC) cortices that are involved in SZ and BD pathophysiology. However, the roles of PCC and MPFC in providing specific distinctive and shared neural substrates between these two disorders remain largely unknown. Examining the neurophysiologic mechanism of these diseases may help explain the clinical observations and differentiate the two disorders. METHODS: We used the Dynamic Casual Modeling (DCM), which is capable of eliciting hidden neuronal dynamics and reveal cross-regulation of multiple neuronal systems, to characterize the pattern of disrupted effective connectivity in the left PCC-MPFC circuit during working memory tasks in 36 SZ and 20 BD patients as well as 29 healthy controls. RESULTS: Compared to the healthy controls, both SZ and BD patient groups exhibited significant negative effective connectivity from the left MPFC to PCC. The negative effective connectivity was more remarkable in schizophrenicpatients. Only patients with BD differed from healthy controls with positive effective connectivity from the left PCC to MPFC. CONCLUSIONS: Whole brain analysis revealed deactivation of the left PCC and MPFC across all patient groups. This study provides new insight that changes in effective connectivity of the left MPFC to left PCC circuit during working memory processing may be a core pathophysiological feature distinguishing SZ from BD.
Authors: Hamdi Eryilmaz; Alexandra S Tanner; New Fei Ho; Adam Z Nitenson; Noah J Silverstein; Liana J Petruzzi; Donald C Goff; Dara S Manoach; Joshua L Roffman Journal: Neuropsychopharmacology Date: 2016-04-22 Impact factor: 7.853
Authors: José M Goikolea; Danai Dima; Ramón Landín-Romero; Imma Torres; Giuseppe DelVecchio; Marc Valentí; Benedikt L Amann; Caterina Mar Bonnín; Peter J McKenna; Edith Pomarol-Clotet; Sophia Frangou; Eduard Vieta Journal: Schizophr Bull Date: 2019-03-07 Impact factor: 9.306