Objective:To compare the differences in prefrontal activation patterns between major depressive disorder and schizophrenia during the eye basic emotion discrimination task (EBEDT).Methods:Using functional near infrared spectroscopy (fNIRS) technology and block design, the changes of prefrontal lobe oxyhemoglobin (Oxy-Hb) concentrations under EBEDT in 40 patients with major depressive disorder, 47 patients with schizophrenia and 55 normal controls were compared. Subsequently, employing years of education as a covariate, an analysis of covariance was performed on the EBEDT behavioral results and the changes in prefrontal Oxy-Hb concentrations in the three groups.The statistical software was SPSS 25.0.Results:(1)The correct number of EBEDT in schizophrenia group (13.93±7.67) was significantly lower than that in major depressive disorder group (19.26±8.07) and normal control group (21.79±6.36)(both P<0.05), and the EBEDT reaction time in schizophrenia group ((3.97±1.77) s) was significantly longer than those in major depressive disorder group ((3.21±1.27) s) and normal control group ((2.63±0.62) s)(both P<0.05).(2)During the EBEDT task block, the normal control group showed increased activation levels in the frontal polar region, Broca's area, anterior motor cortex and supplementary motor area (SMA) compared with the control block( t=2.02-3.18, all P<0.05); and the schizophrenia group showed increased activation levels in the frontal eye field compared with the control block( t=2.26, P=0.03); while the major depressive disorder group exhibited decreased activation levels in the entire prefrontal lobe compared with the control block( t=-3.47--2.34, all P<0.05). (3)During the emotion recognition task of EBEDT, the activation levels of the frontal polar area (ch37), dorsolateral prefrontal cortex (ch31), Broca's area (ch49, ch51, ch53), and SMA (ch1, ch47, ch52) were significantly different among the major depressive disorder, schizophrenia and normal controls( F=3.23-5.53, all P<0.05). Further pairwise comparisons showed that the activation levels in all the above pathways were lower in the major depressive disorder group than those in the normal control group, and the activation levels in Broca's area (ch53) and SMA area (ch52) were lower in the schizophrenia group than those in the normal control group, while the activation levels in the frontal polar area (ch37) and Broca's area (ch49) were lower in the major depressive disorder group than those in the schizophrenia group(all P<0.05). Conclusions:In EBEDT, the activation patterns of the prefrontal cortex are different between patients with major depressive disorder and patients with schizophrenia. Patients with major depressive disorder have a decrease in prefrontal cortex activation, while patients with schizophrenia have an increase in the frontal eye field activation.The activation levels in prefrontal cortex of both patients group are lower than that of normal controls. Meanwhile, the prefrontal cortex activation level of patients with major depressive disorder is lower than that of patients with schizophrenia.

Oromandibular dystonia (OMD) is a type of Meige syndrome, which is characterized by involuntary repeated abnormal postured contraction of bilateral masticatory muscles, orbicularis oris muscles and mimetic muscles. Involved nerves are buccal branch of facial nerve, mandibular marginal branch and/or mandibular branch of trigeminal nerve. At present, the pathogenesis of OMD is still unclear, and no specific treatment for OMD is noted. This article reviews the pathogenesis, clinical manifestations, classifications, diagnoses, differential diagnoses and treatments of oromandibular dystonia in order to strengthen the understanding of the disease.

Objective To retrieve,evaluate and summarize the relevant evidences of oral health manage-ment in the community elderly people to provide reference for community medical staffs.Methods The evi-dences on oral health management of the comunity elderly people were systematically retrieved from various guide websites and Chinese and English databases.The retrieval limit was from the database establishment to September 2021.The research group conducted the evaluation and extracted the evidences according to the rel-evant literature evaluation criteria.Results A total of 17 literatures were included,including 5 guidelines,4 expert consensuses and 8 systematic reviews.A total of 28 pieces of evidences were summarized from the five aspects of assessment and examination,daily life management,management of special oral problems,denture management,and education and training.Conclusion Community medical staffs should fully consider the clin-ical situation,department resources and patient wishes,and conduct the evidence application to increase the o-ral health level of the community elderly people.

Objective:To explore the correlation between clinical phenotypes and genotypes among 46 children with SCN1A-related developmental epileptic encephalopathy (DEE). Methods:Clinical data of 46 children with DEE and SCN1A variants identified at the Guangzhou Women and Children′s Medical Center between January 2018 and June 2022 were collected. The children were grouped based on their age of onset, clinical manifestations, neurodevelopmental status, and results of genetic testing. The correlation between SCN1A genotypes and clinical phenotypes was analyzed. Results:Among the 46 patients, 2 children (4.35%) had developed the symptoms before 3 months of age, 42 (91.30%) were between 3 to 9 months, and 2 cases (4.35%) were after 10 months. Two cases (4.35%) presented with epilepsy of infancy with migrating focal seizures (EIMFS), while 44 (95.7%) had presented with Dravet syndrome (DS), including 28 cases (63.6%) with focal onset (DS-F), 13 cases (29.5%) with myoclonic type (DS-M), 1 case (2.27%) with generalized type (DS-G), and 2 cases (4.55%) with status epilepticus type (DS-SE). Both of the two EIMFS children had severe developmental delay, and among the DS patients, 7 cases had normal development, while the remaining had developmental delay. A total of 44 variants were identified through genetic sequencing, which included 16 missense variants and 28 truncating variants. All EIMFS children had carried the c. 677C>T (p.Thr226Met) missense variant. In the DS group, there was a significant difference in the age of onset between the missense variants group and the truncating variants group ( P < 0.05). Missense variants were more common in D1 (7/15, 46.7%) and pore regions (8/15, 53.3%), while truncating variants were more common in D1 (12/28, 42.9%). Children with variants outside the pore region were more likely to develop myoclonic seizures. Conclusion:The clinical phenotypes of DEE are diverse. There is a difference in the age of onset between individuals with truncating and missense variants in the SCN1A gene. Missense variants outside the pore region are associated with a higher incidence of myoclonic seizures.

Mechanical allodynia (MA), including punctate and dynamic forms, is a common and debilitating symptom suffered by millions of chronic pain patients. Some peripheral injuries result in the development of bilateral MA, while most injuries usually led to unilateral MA. To date, the control of such laterality remains poorly understood. Here, to study the role of microglia in the control of MA laterality, we used genetic strategies to deplete microglia and tested both dynamic and punctate forms of MA in mice. Surprisingly, the depletion of central microglia did not prevent the induction of bilateral dynamic and punctate MA. Moreover, in dorsal root ganglion-dorsal root-sagittal spinal cord slice preparations we recorded the low-threshold Aβ-fiber stimulation-evoked inputs and outputs of superficial dorsal horn neurons. Consistent with behavioral results, microglial depletion did not prevent the opening of bilateral gates for Aβ pathways in the superficial dorsal horn. This study challenges the role of microglia in the control of MA laterality in mice. Future studies are needed to further understand whether the role of microglia in the control of MA laterality is etiology-or species-specific.
Mice ; Animals ; Hyperalgesia/metabolism* ; Microglia/metabolism* ; Disease Models, Animal ; Spinal Cord/metabolism* ; Spinal Cord Dorsal Horn/metabolism* ; Ganglia, Spinal/metabolism*