Shugan Jieyu Capsule (SG), a Chinese herbal medicine mainly composed of Acanthopanax and Hypericum perforatum, has been used to ameliorate cognitive impairments and emotional problems induced by post-stroke depression (PSD), while the altered brain dynamics underlying the ameliorative effects of SG have remained unclear. Our study focused on investigating the potential neurobiological mechanisms of SG in improving the cognitive function of PSD patients via restingstate functional magnetic resonance imaging (fMRI). Fifteen PSD patients (mean ages: 64.13 ± 6.01 years) were instructed to take 0.72 g of SG twice a day for 8 weeks. PSD patients underwent fMRIs, the 24-item Hamilton Depression Scale (HAMD-24) and the Montreal Cognitive Assessment (MoCA) at baseline and the end of intervention, and these assessments were also performed on twenty-one healthy controls (HC) (mean ages: 60.67 ± 6.95 years). Additionally, the dynamic amplitude of low-frequency fluctuations (dALFF) and functional connectivity (dFC) were determined to reveal changes in dynamic functional patterns. We found that taking SG significantly reduced the depressive symptoms assessed by HAMD-24 and improved cognitive functions assessed by MoCA in PSD patients. Furthermore, at baseline, PSD patients showed decreased dALFF in the right precuneus and increased dFC between the right precuneus and left angular gyrus, compared with HC. After intervention, the dALFF and dFC variances of the abnormal patterns were reversed. Additionally, the dALFF variance in the right precuneus was positively correlated with MoCA scores in PSD patients after SG treatment. Collectively, our results indicate that SG may improve the cognitive function of PSD patients through alteration of brain dynamics. Our findings lay a foundation for the exploration of the neurobiological mechanisms of SG in ameliorating symptoms of PSD patients.

Background: Stroke with basal ganglia damage (SBG) is a neurological disorder characterized by cognitive impairment. The neurobiological mechanism of cognitive impairment in stroke patients with basal ganglia damage (SBG patients) remains unclear. This study aimed to explore the underlying neurobiological mechanism of cognitive impairment in SBG patients using resting-state functional magnetic resonance imaging (rs-fMRI). Methods: The differences in functional connectivity (FC) between 14 SBG patients (average age: 61.00 ± 7.45 years) and 21 healthy controls (HC) (average age: 60.67 ± 6.95 years) were examined using voxel-mirrored homotopic connectivity (VMHC) and degree centrality (DC). Moreover, we compared the cognitive functions of SBG patients with HC using the Chinese Revised Wechsler Adult Intelligence Scale (WAIS-RC) and Wechsler Memory Scale (WMS). Results: Full-scale intelligence quotient (FIQ) (t = 2.810, p < 0.010) and memory quotient (MQ) (t = 2.920, p < 0.010) scores of SBG patients were significantly lower than those of HC. Compared with HC, significantly decreased VMHC values in the bilateral angular gyrus, supramarginal gyrus, inferior frontal gyrus, middle temporal gyrus, hippocampus, precuneus, precentral gyrus, and middle occipital gyrus and decreased DC values in the right supramarginal gyrus, bilateral angular gyrus, and right postcentral gyrus were observed in SBG patients. Moreover, the VMHC values in the angular gyrus, inferior frontal gyrus, supramarginal gyrus, and middle temporal gyrus and the DC values in the right supramarginal gyrus were significantly correlated with cognitive functions in all participants. Conclusion: Our findings may provide a neural basis for cognitive impairments in SBG patients. Furthermore, local abnormalities of functional networks and interhemispheric interaction deficits may provide new ideas and insights for understanding and treating SBG patients' cognitive impairments.

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Background: Functional near-infrared spectroscopy (fNIRS) has many advantages over other neuroimaging modalities for routine measurement of task-dependent cortical activation, but most fNIRS studies of schizophrenia have used letter fluency tasks (LFTs). Further, performances on category fluency tasks (CFTs) and LFTs may be distinct in Chinese patients due to the unique semantic features of Chinese written characters. To identify unique disease biomarkers measurable by fNIRS in Chinese schizophrenia patients, this study compared cortical oxygenated hemoglobin changes ([oxy-Hb]) during a Chinese LFT and CFT between patients and healthy controls.Methods: Inpatients of the Second Affiliated Hospital of Xinxiang Medical University were recruited from Match 2020 to July 2021. The Positive and Negative Symptom Scale (PANSS) was used to evaluate psychiatric symptoms. Dynamic changes in [oxy-Hb], an indicator of neural activity, were measured during CFT and LFT performance by 52-channel fNIRS.Results: Forty-seven schizophrenia inpatients and 29 healthy controls completed all tests. Schizophrenia patients showed significant cortical activation at 15 channels covering the left hemisphere and 17 channels over the right hemisphere during the CFT. During the LFT, activity was significantly increased at only six channels, all over the left hemisphere (FDR P &lt; 0.05). In healthy controls, significant [oxy-Hb] increases were found at 24 channels over the left hemisphere and 19 channels over the right hemisphere during CFT. While during the LFT, the significant increases were found at 7 channels all over the left hemisphere (FDR P &lt; 0.05). When years of education was included as a covariate, the schizophrenia group demonstrated no significant hypoactivation relative to healthy controls at any channel after FDR correction (FDR P &lt; 0.05) during CFT while demonstrated significant hypoactivation at channel 11 during LFT (FDR P &lt; 0.05). There were no significant associations between PANSS scores and [oxy-Hb] changes after FDR correction (FDR P &lt; 0.05).Conclusions: Left lateralization during CFT was reduced among schizophrenia patients and may be related to the semantic deficit. The Chinese-CFT could be a more sensitive indicator of frontal-temporal dysfunction in schizophrenia.