Brain imaging abnormalities are present in schizophrenia (SZ) and bipolar disorder (BD), demonstrating disease-specific changes, yet they also share similarities in certain brain regions or functional characteristics, with SZ potentially exhibiting more extensive brain damage compared to BD. Structural magnetic resonance imaging (MRI) studies demonstrated widespread gray matter reductions in SZ, particularly in the prefrontal and temporal lobes. In BD, gray matter thickening was observed in the prefrontal lobes during manic episodes, while a reduction in gray matter was noted in the amygdala and hippocampus during depressive episodes. Both SZ and BD exhibited increased ventricular volume and reduced overall brain volume. Functional MRI studies revealed reduced functional connectivity in the prefrontal and temporal lobes in SZ, with decreased global and local efficiency in brain regions such as the hippocampus and cingulate gyrus. BD showed enhanced connectivity in the anterior cingulate gyrus and the default mode network (DMN). Both SZ and BD demonstrated altered functional connectivity in areas such as the striatum, salience network, central executive network and DMN. Diffusion tensor imaging studies showed decreased fractional anisotropy (FA) in the corpus callosum of SZ, with a decrease in FA in the left fronto-occipital fasciculus in BD. Both SZ and BD exhibited reduced FA in the uncinate fasciculus and corpus callosum. Magnetic resonance spectroscopy revealed decreased concentrations of glutathione, N-acetylaspartate (NAA) and inositol in the anterior cingulate gyrus of SZ. In BD, glutathione and inositol concentrations were elevated in the anterior cingulate gyrus, while NAA levels decreased during depressive episodes and increased during remission. Both SZ and BD showed increased levels of glutamate and gamma-aminobutyric acid in the prefrontal cortex. This article provides a review of the current evidence on the differences and similarities in multimodal magnetic resonance brain imaging between SZ and BD, aiming to offer a reference for future exploration of neuroimaging biomarkers and the neurobiological mechanisms of SZ and BD.

Brain imaging abnormalities are present in schizophrenia (SZ) and bipolar disorder (BD), demonstrating disease-specific changes, yet they also share similarities in certain brain regions or functional characteristics, with SZ potentially exhibiting more extensive brain damage compared to BD. Structural magnetic resonance imaging (MRI) studies demonstrated widespread gray matter reductions in SZ, particularly in the prefrontal and temporal lobes. In BD, gray matter thickening was observed in the prefrontal lobes during manic episodes, while a reduction in gray matter was noted in the amygdala and hippocampus during depressive episodes. Both SZ and BD exhibited increased ventricular volume and reduced overall brain volume. Functional MRI studies revealed reduced functional connectivity in the prefrontal and temporal lobes in SZ, with decreased global and local efficiency in brain regions such as the hippocampus and cingulate gyrus. BD showed enhanced connectivity in the anterior cingulate gyrus and the default mode network (DMN). Both SZ and BD demonstrated altered functional connectivity in areas such as the striatum, salience network, central executive network and DMN. Diffusion tensor imaging studies showed decreased fractional anisotropy (FA) in the corpus callosum of SZ, with a decrease in FA in the left fronto-occipital fasciculus in BD. Both SZ and BD exhibited reduced FA in the uncinate fasciculus and corpus callosum. Magnetic resonance spectroscopy revealed decreased concentrations of glutathione, N-acetylaspartate (NAA) and inositol in the anterior cingulate gyrus of SZ. In BD, glutathione and inositol concentrations were elevated in the anterior cingulate gyrus, while NAA levels decreased during depressive episodes and increased during remission. Both SZ and BD showed increased levels of glutamate and gamma-aminobutyric acid in the prefrontal cortex. This article provides a review of the current evidence on the differences and similarities in multimodal magnetic resonance brain imaging between SZ and BD, aiming to offer a reference for future exploration of neuroimaging biomarkers and the neurobiological mechanisms of SZ and BD.

Negative symptoms of schizophrenia profoundly affect patients' social function and life quality, and traditional treatments have limited efficacy in improving these symptoms. In recent years, non-invasive brain stimulation techniques such as repetitive transcranial magnetic stimulation (rTMS), transcranial direct current stimulation (tDCS), transcranial alternating current stimulation (tACS), and transcranial random noise stimulation (tRNS) have shown potentiality in alleviating negative symptoms. However, the selection of stimulation targets remains an area of active research, as different targets may yield varying therapeutic outcomes. Therefore, identifying the most appropriate treatment targets is crucial for improving negative symptoms. This article reviews the targets selection and therapeutic effects of different non-invasive brain stimulation techniques for ameliorating negative symptoms, to provide guidance for target selection in clinical treatment.

Schizophrenia is a chronic disabling disease of unknown etiology. Its neuroimaging abnormalities have been confirmed by a large number of studies. However, when these structural abnormalities occur and how they develop over time are unclear. The relationship between structural abnormalities and antipsychotic treatment needs to be further explored. Longitudinal studies on the brain structure of clinical high risk for psychosis, first-episode schizophrenia and chronic schizophrenia, exploring the influence of drug therapy on them, are helpful to construct the trajectories of brain structure changes in the whole course of schizophrenia and dynamically track the brain structure changes, so as to further explore the pathophysiology of schizophrenia. This article reviews the longitudinal research progress of brain structure changes in patients with schizophrenia.

Schizophrenia is a chronic disabling disease of unknown etiology. Its neuroimaging abnormalities have been confirmed by a large number of studies. However, when these structural abnormalities occur and how they develop over time are unclear. The relationship between structural abnormalities and antipsychotic treatment needs to be further explored. Longitudinal studies on the brain structure of clinical high risk for psychosis, first-episode schizophrenia and chronic schizophrenia, exploring the influence of drug therapy on them, are helpful to construct the trajectories of brain structure changes in the whole course of schizophrenia and dynamically track the brain structure changes, so as to further explore the pathophysiology of schizophrenia. This article reviews the longitudinal research progress of brain structure changes in patients with schizophrenia.

Objective:To explore differences of resting brain regional homogeneity (ReHo) between patients with major depressive disorder (MDD) and their siblings.Methods:From January to December 2013, the resting-state functional magnetic resonance imaging (fMRI) data of 87 patients with MDD and 21 healthy siblings were collected.DPABI v5.1 software was used to preprocess the resting-state fMRI data, and ReHo maps of each subject was obtained. A two-sample t-test was used to compare differences between the patients with MDD and their siblings in ReHo values throughout the brain. ReHo values within the significant brain regions were extracted out, and used to calculate Spearman correlation with the total score of 17-items Hamilton depression rating scale(HAMD-17) in the patients with MDD and their siblings respectively.The software of SPSS 20.0 was used for statistical analysis. Results:The patients with MDD exhibited lower ReHo values in the precuneus extending to the posterior cingulate cortex (PCu/PCC) compared with their siblings (cluster-size=126 voxel, cluster-level PFDR=0.033; MNI: x=-4, y=-58, z=38, t=4.30). ReHo values of the PCu/PCC in patient with MDD were positively correlated with the severity of depressive symptoms ( r=0.255, P=0.021). Conclusion:Compared with the siblings, local brain activity of the PCu/PCC in the patients with MDD was decreased, and related to the severity of depressive symptoms. It is helpful to further reveal the intrinsic neural mechanism of MDD.

A 51-year-old schizophrenic patient with long-term clozapine treatment developed intestinal obstruction combined with infection. Subsequently, the patient′s clozapine plasma concentration abnormally increased to 3 094.80 μg/L (reference range 350-600 μg/L), accompanied with pulmonary infection. Patient′s symptoms showed significant improvement after clozapine was discontinued, along with intravenous fluid reinfusion and antibiotic treatment. This current article also provided a literature review of 16 reported cases of infection with abnormally elevated clozapine plasma concentration. Clozapine plasma concentration and blood routine should be monitored in clozapine users, and adverse reactions should be treated in time. For clozapine users with infection but normal leukocyte count, multiple bacterial infection indicators such as the neutrophil proportion and C-reactive protein should begiven comprehensive consideration, and antibiotics should be used when appropriate. If clozapine plasma concentration is abnormally high, clozapine can be discontinued and intravenous fluid reinfusion can accelerate clozapine elimination. After the patient′s condition stabilizes, clozapine could be reused.

Major depressive disorder is a prevalent and burdensome mental illness that exhibits a high degree of heritability. Despite this, the underlying neural mechanisms that contribute to its development remain unclear. To enhance our comprehension of the pathology and susceptibility mechanisms of major depressive disorder, this study aims to compare the neuroimaging characteristics of patients diagnosed with major depressive disorder and their first-degree relatives. The objective of this study is to conduct a comprehensive analysis and synthesis of brain functional images of individuals diagnosed with major depressive disorder, including those in the acute and remission stages, as well as their first-degree relatives, utilizing various prevalent neuroimaging modalities. Additionally, this study aims to identify potential avenues for future research in this area. This study shows that abnormalities in local brain functional activity and functional interactions of the cortical-limbic-cerebellar circuits are critical in intrinsic neural mechanisms of depression and their first-degree relatives, and this circuits is also a potential target for antidepressants. Future studies are needed to further clarify the role of unbalanced cortical-limbic-cerebellar circuits in the disease process of depression.

A 51-year-old schizophrenic patient with long-term clozapine treatment developed intestinal obstruction combined with infection. Subsequently, the patient′s clozapine plasma concentration abnormally increased to 3 094.80 μg/L (reference range 350-600 μg/L), accompanied with pulmonary infection. Patient′s symptoms showed significant improvement after clozapine was discontinued, along with intravenous fluid reinfusion and antibiotic treatment. This current article also provided a literature review of 16 reported cases of infection with abnormally elevated clozapine plasma concentration. Clozapine plasma concentration and blood routine should be monitored in clozapine users, and adverse reactions should be treated in time. For clozapine users with infection but normal leukocyte count, multiple bacterial infection indicators such as the neutrophil proportion and C-reactive protein should begiven comprehensive consideration, and antibiotics should be used when appropriate. If clozapine plasma concentration is abnormally high, clozapine can be discontinued and intravenous fluid reinfusion can accelerate clozapine elimination. After the patient′s condition stabilizes, clozapine could be reused.

Major depressive disorder is a prevalent and burdensome mental illness that exhibits a high degree of heritability. Despite this, the underlying neural mechanisms that contribute to its development remain unclear. To enhance our comprehension of the pathology and susceptibility mechanisms of major depressive disorder, this study aims to compare the neuroimaging characteristics of patients diagnosed with major depressive disorder and their first-degree relatives. The objective of this study is to conduct a comprehensive analysis and synthesis of brain functional images of individuals diagnosed with major depressive disorder, including those in the acute and remission stages, as well as their first-degree relatives, utilizing various prevalent neuroimaging modalities. Additionally, this study aims to identify potential avenues for future research in this area. This study shows that abnormalities in local brain functional activity and functional interactions of the cortical-limbic-cerebellar circuits are critical in intrinsic neural mechanisms of depression and their first-degree relatives, and this circuits is also a potential target for antidepressants. Future studies are needed to further clarify the role of unbalanced cortical-limbic-cerebellar circuits in the disease process of depression.