Anhedonia is one of the core symptoms of major depressive disorder, and its underlying mechanisms remain unclear. The regulation of the reward process in brain regions, such as the hippocampus, amygdala, striatum, ventral tegmental brain, and prefrontal lobe, may play a role in anhedonia. This study has concluded the changes in relevant brain regions in reward anticipation, decision-making, and feedback processes. The neuroimaging mechanisms of inflammation, neurotransmitter metabolism, and gene expression on depression anhedonia symptoms were reviewed.

Alexithymia refers to a deficiency of emotional structure, but the neurologic and psychological mechanisms of non-suicidal self-injury (NSSI) in adolescents are still unclear. The neural basis of alexithymia may play a role in adolescents′ NSSI by affecting the function of emotion regulation and emotion expression. At the same time, NSSI is also considered to be a non-adaptive emotional regulation mode for alexithymia individuals, which interacts with personality factors and psychosocial factors. This study explored the neuropsychological mechanism of alexithymia in adolescent NSSI from the perspective of emotional function, and provided theoretical basis for early identification and precise intervention of alexithymia and adolescent NSSI.

Anhedonia is one of the core symptoms of major depressive disorder, and its underlying mechanisms remain unclear. The regulation of the reward process in brain regions, such as the hippocampus, amygdala, striatum, ventral tegmental brain, and prefrontal lobe, may play a role in anhedonia. This study has concluded the changes in relevant brain regions in reward anticipation, decision-making, and feedback processes. The neuroimaging mechanisms of inflammation, neurotransmitter metabolism, and gene expression on depression anhedonia symptoms were reviewed.

Alexithymia refers to a deficiency of emotional structure, but the neurologic and psychological mechanisms of non-suicidal self-injury (NSSI) in adolescents are still unclear. The neural basis of alexithymia may play a role in adolescents′ NSSI by affecting the function of emotion regulation and emotion expression. At the same time, NSSI is also considered to be a non-adaptive emotional regulation mode for alexithymia individuals, which interacts with personality factors and psychosocial factors. This study explored the neuropsychological mechanism of alexithymia in adolescent NSSI from the perspective of emotional function, and provided theoretical basis for early identification and precise intervention of alexithymia and adolescent NSSI.

Objective:To investigate the functional connectivity of default mode network (DMN) and limbic system, the expression level of inflammatory cytokine and their correlation in bipolar disorder type Ⅱ(BDⅡ) patients with depressive episodes.Methods:Thirty-three BD Ⅱ patients with depressive episodes and forty-six healthy controls were recruited to complete the resting-state functional magnetic resonance imaging (rs-fMRI). After image preprocessing, the DMN and limbic system were extracted from the image data by independent component analysis (ICA), so as to compare the differences of functional connectivity of resting brain network between the patients and the controls.Serum levels of inflammatory cytokines interleukin-6 (IL-6), interleukin-8(IL-8), interleukin-10(IL-10), tumor necrosis factor-α (TNF-α), and C-C motif chemokine ligand 4 (CCL4) in patients and healthy controls were detected.The correlation between functional connectivity of different brain regions and inflammatory cytokines was analyzed.SPSS 17.0 software was used for data statistical analysis.The two samples were compared using t-test or Mann-Whitney U-test, and Spearman was used for correlation testing. Results:In BDⅡ patients, the functional connectivity of the right medial prefrontal cortex(cluster-size=7 voxel, cluster-level PGRF<0.05, MNI: x=6, y=54, z=9, t=-3.765) and the left superior frontal gyrus(cluster-size=10 voxel, cluster-level PGRF<0.05, MNI: x=-21, y=54, z=15, t=-4.139) in DMN decreased, while the left cerebellum Ⅳ and Ⅴ lobules of limbic system (cluster-size=21 voxel, cluster-level PGRF<0.05, MNI: x=-15, y=-24, z=-30, t=4.468) and cerebellar tonsil of left cerebellum posterior lobe(cluster-size=8 voxel, cluster-level PGRF<0.05, MNI: x=-15, y=-51, z=-45, t=4.138) in the limbic system increased.Compared with the healthy controls, the serum levels of IL-10(7.39 (6.33, 9.32) pg/mL vs 6.54 (5.84, 7.39) pg/mL, Z=-2.937, P=0.003)and CCL4 (39.31 (25.77, 68.70) pg/mL vs 31.30 (20.32, 40.89) pg/mL, Z=-2.209, P=0.027) were higher in BDⅡ patients.The functional connectivity of the left cerebellum Ⅳ and Ⅴ lobules was positively correlated with the serum levels of IL-10 ( r=0.432, P=0.031) and that of the cerebellar tonsil of left cerebellum posterior lobe was positively correlated with the serum levels of IL-10 ( r=0.429, P=0.032) and CCL4 ( r=0.402, P=0.046). Conclusion:The functional connectivity of DMN and limbic system in BDⅡ patients with depressive episode is abnormal in resting-state fMRI.The expression level of inflammatory cytokines in patients' serum increases, and has correlation with the functional connection of limbic system.

Major depressive disorder(MDD) is a kind of mental disorder with depression and decreased interest as the main clinical manifestations. The pathogenesis of MDD is unclear, and MDD is characterized by high incidence, high recurrence rate and high suicide rate. At present, the hypothesis of monomamine mechanism can not fully clarify its pathological characteristics, and a considerable number of patients with depression do not respond well to existing antidepressants. N-methyl-D-aspartate receptor (NMDAR) antagonist and γ-aminobutyric acid A(GABAA) receptor positive allosteric regulator have a potential rapid antidepressant effect, which may be a breakthrough in the pathogenesis and clinical treatment of depression. NMDAR has bidirectional regulation, when proper activation of NMDAR can promote dendrite development, neuronal growth and long-term potentiation, but overstimulation of NMDAR can cause toxic reaction, leading to synaptic atrophy and neuronal death. In addition, inflammation can induce changes in NMDAR function and lead to depressive symptoms. At present, ketamine, a new antidepressant NMDAR antagonist, may plays a role in rapid antidepressant and delayed recurrence of depression by increasing the release of BDNF, activating the signal pathway of mammalian target of rapamycin complex 1(mTORC1), and promoting protein synthesis and synaptic plasticity. Thus, ketamine has the effect of rapid antidepressant and delaying the recurrence of depression. However, due to the large variability of NMDAR gene in patients with MDD, its potential functional polymorphism affects clinical symptoms and drug sensitivity. Therefore, by analyzing the latest research at home and abroad, this review comprehensively summarizes the pathogenesis of NMDAR dysfunction, the pathogenesis of MDD, antidepressant treatment and clinical application status, in order to provide theoretical basis for clinical accurate treatment of MDD patients in the future.

The purpose of this article is to provide references for understanding the current provision of bipolar disorder with mixed features as well as future efforts in clinical practice. The article is to review the profile of assessment， management and treatment of suicide risk in bipolar disorder with mixed features. And this review also provides a theoretical framework toward future targeted therapeutic interventions and guidance for bipolar disorder with mixed features.

This paper aims to explore the main points of diagnosis， treatment and misdiagnosis of conversion disorder characterized by paroxysmal abdominal pain. The general hospitals had a high misdiagnose rate and no effective symptomatic treatment for conversion disorder patients with physical discomfort as main symptoms， which leading to heavy physical and mental burden of patients and waste of medical resources， so this paper retrospectively analyzed the etiology， diagnostic process， treatment and therapeutic effect of a case of conversion disorder with paroxysmal abdominal pain as the main symptom. Case analysis showed that the physical discomfort as chief complain of conversion disorder patients affected the rate of early correct diagnosis and treatment， so clinicians' ability of diagnosis and differential diagnosis of conversion disorder needs to be strengthened. At the same time， cognitive behavioral therapy （CBT） is effective in the clinical treatment and recurrence prevention of conversion disorder.

Patients with major depressive disorder (MDD) have a cognitive impairment, and part of the cognitive impairment persists in the remission stage, which restricts the overall patient's comprehensive recovery. Brain-derived neurotrophic factor (BDNF) and its related gene expression play important roles in neuronal genesis, synaptic plasticity and dendritic growth in the brain, and are closely related to the pathogenesis of MDD and its cognitive impairment. Therefore, this article reviews the latest research on the mechanism of cognitive impairment of MDD affected by BDNF from the aspects of gene inheritance, such as BDNF expression, gene polymorphism and epigenetic inheritance, in order to provide a theoretical basis for further exploring the mechanism of cognitive impairment of MDD.

Patients with major depressive disorder (MDD) have a cognitive impairment, and part of the cognitive impairment persists in the remission stage, which restricts the overall patient's comprehensive recovery. Brain-derived neurotrophic factor (BDNF) and its related gene expression play important roles in neuronal genesis, synaptic plasticity and dendritic growth in the brain, and are closely related to the pathogenesis of MDD and its cognitive impairment. Therefore, this article reviews the latest research on the mechanism of cognitive impairment of MDD affected by BDNF from the aspects of gene inheritance, such as BDNF expression, gene polymorphism and epigenetic inheritance, in order to provide a theoretical basis for further exploring the mechanism of cognitive impairment of MDD.