Migraine is a complex neurological disorder with unknown etiology,involving genetic and environmental factors.The pathogenesis of migraine is closely related to the activation of microglia and inflammatory factors.ATP is a ligand for the P2X receptor(P2XR),a ligand gated ion channel(LGIC)widely expressed in neurons and gli-al cells.This review elucidates that P2X(P2X3,P2X4,P2X7)receptors regulate the activation of microglia and release of inflammatory factors through different signaling pathways,mediating neuropathic pain and migraine occur-rence,providing potential targets for the treatment of migraine.

Chronic migraine is a common episodic brain dysfunction disorder, which often progresses from migraine and is frequently accompanied by sleep disorders, anxiety, depression or obesity. Extensive connections exist between the hypothalamus and other components of the central nervous system; through integrating pain signals, neural conduction and inflammatory pathways, the hypothalamus becomes an important hub for migraine chronicization. This review, combined with clinical imaging evidence, analyzes the pathogenic mechanisms of chronic migraine and its complications from perspective of the hypothalamus as the higher neural center, so as to provide useful references for prevention and treatment of chronic migraine.

Chronic migraine is a common episodic brain dysfunction disorder, which often progresses from migraine and is frequently accompanied by sleep disorders, anxiety, depression or obesity. Extensive connections exist between the hypothalamus and other components of the central nervous system; through integrating pain signals, neural conduction and inflammatory pathways, the hypothalamus becomes an important hub for migraine chronicization. This review, combined with clinical imaging evidence, analyzes the pathogenic mechanisms of chronic migraine and its complications from perspective of the hypothalamus as the higher neural center, so as to provide useful references for prevention and treatment of chronic migraine.

Ferroptosis is a novel type of oxidatively regulated cell death driven by iron-dependent lipid peroxidation.As the main site of iron utilization and oxidative metabolism,mitochondria are the main source of intracellular reactive oxy-gen species.Ferroptosis is associated with the severe impairment of mitochondrial structure and function,bioenergetics,and metabolism.Alzheimer disease(AD)is a devastating progressive neurodegenerative disease with the main clinical manifestation of decline in memory and cognitive function.Emerging evidence suggests that mitochondrial dysfunction plays a significant role in the process of ferroptosis in AD.This article elaborates on the mechanism of ferroptosis,mito-chondrial dysfunction and its role in ferroptosis in AD,and the treatment of AD,in order to provide a new perspective for exploring new strategies for the prevention and treatment of AD.

Cerebral venous sinus thrombosis(CVST)is a special type of cerebrovascular disease,and the common autoimmune diseases that can cause CVST are systemic lupus erythematosus and antiphospholipid syndrome,and the combination of CVST with Sj?gren's syndrome is not common in clinical practice.The authors reported the case data of a patient with Sj?gren's syndrome combined with CVST and discussed the possible pathogenesis,treatment and prognosis,with the aim of providing some guidance for the diagnosis and treatment of this type of patient.

Compared with conventional cardiopulmonary resuscitation (CCPR), extracorporeal cardiopulmonary resuscitation (ECPR) can improve the survival rate of patients with cardiac arrest, and reduce the risk of reperfusion injury. However, it is still difficult to avoid the risk of secondary brain damage. Low temperature management has good neuroprotective potential for ECPR patients, which minimizes brain damage. However, unlike CCPR, ECPR has no clear prognostic indicator. The relationship between ECPR combined with hypothermia management-related treatment measure and neurological prognosis is not clear. This article reviews the effect of ECPR combined with different therapeutic hypothermia on brain protection and provides a reference for the prevention and treatment of neurological injury in patients with ECPR.
Humans ; Brain ; Cardiopulmonary Resuscitation ; Brain Injuries ; Hypothermia, Induced ; Heart Arrest

ObjectiveTo explore the diagnoses of diseases and functioning of speech fluency disorder, analyze the main assessment content, and construct framework of intervention solution based on International Classification of Diseases 11th Revision (ICD-11), International Classification of Functioning, Disability and Health (ICF) and International Classification of Health Interventions (ICHIβ-3). MethodsThe diagnoses of diseases and functioning was discussed with ICD-11 and ICF. The assessment tools were analyzed with ICF. A holistic intervention solution was constructed with ICF and ICHIβ-3. ResultsSpeech fluency disorder is classified as 6A01.1 developmental speech fluency disorder for ICD-11. The related diseases include 6A01.0 developmental speech sound disorder, 6A01.2 developmental language disorder, cerebral palsy, MA80.0 aphasia, MA80.1 dysphasia and MA80.2 dysarthria, etc. For ICF, the categories related to speech fluency disorder might be s3 structures invovled in voice and speech; b3 voice and speech functions, especially b330 fluency and rhythm of speech functions; d1 learning and applying knowledge, d3 communication, especially d330 speaking and d355 discussion, d7 interpersonal interactions and relationships, and d9 community, social and civic life. A holistic intervention solution for speech fluency disorder was developed, involving in body structure, body function, activities and participation, and environmental factors, including assessment, training and treatment, educational counseling, and psychological and social support, etc. ConclusionA framework of diagnosis, assessment and rehabilitation has been constructed for speech fluency disorder.

ObjectiveTo discuss the diagnosis, assessment and rehabilitation for children with cerebral palsy complicated with speech disorder based on the tools of World Health Organization Family of International Classifications (WHO-FICs). MethodsThe diagnosis of speech disorder after cerebral palsy was classified using International Classification of Diseases, 11th Revision (ICD-11). The disorders of speech function were classified using International Classification of Functioning, Disability and Health (ICF). A structured speech function rehabilitation solution was developed based on the International Classification of Health Interventions (ICHIβ-3). ResultsAccording to ICD-11, cerebral palsy was classified as 08 Neurological Disorder, which was further classified as 8D20.0 Spastic Unilateral Cerebral Palsy and 8D20.1 Spastic Bilateral Cerebral Palsy (8D20.10 Spastic Quadriplegic Cerebral Palsy and 8D20.11 Spastic Bilateral Cerebral Palsy), with the speech disorders involving 6A00 Disorders of Intellectual Development, 6A01 Developmental Speech or Language Disorders, MA80 Speech Disturbances, MA81 Speech Dysfluency and MA82 Voice Disturbances. For ICF, the speech disorders mainly involved s1 structures of the nervous system, s3 structures invoved in voice and speech, b3 voice and speech functions, d1 learning and applying knowledge, and environment and individual factors; and could be further classified as b310 voice functions, b320 articulation functions, and b330 fluency and rhythm of speech functions. Based on ICHIβ-3, a rehabilitation solution was developed, involving the areas of body structure and function, activity and participation, and environmental factors. ConclusionBased on ICD-11, ICF and ICHIβ-3, a methodological system of assessment and interventions for speech disorders after cerebral palsy has been systematically constructed, including diagnosis of disease, assessment, intervention and coding of speech disorder.

Objective To investigate the establishment of focal cerebral ischemia model in rabbits with the improved suture method.Methods A total of 45 healthy and clean adult New Zealand rabbits were divided into either a sham operation group (n =5) or a model group (n =40) using random number table method before modeling,and the sex was not limited.The self-made head ends of 2-0 fishing lines dipped in paraffin were used as the sutures.The external carotid artery was cut and inserted into a intracranial artery through the internal carotid artery and blocked the origin of middle cerebral artery.The neurological function score was performed after 6 h.The neurological deficit scores ≥2 was successful modeling.The rabbits were killed by anesthesia.The brain slices were stained with 2％ 2,3,5-triphenyl tetrazolium chloride solution.The infarct foci were observed.The diameters of suture head and the depth of suture insertion were compared in the model rabbits with successful modeling,failure,and death in the model group.Results There were 40 rabbits in the model group,six of them died,including 4 died of subarachnoid hemorrhage within 4 h after operation,and 2 died from anesthetic accident.The mortality rate was 15.0％.Seven rabbits failed,mainly because of cerebral vasospasm and the insertion depth of suture was insufficient.Twenty-seven had successful modeling,and the success rate was 67.5％.All the rabbits in the sham operation group survived.The diameter of the suture head and insertion depth in the successful modeling rabbits were compared with the death and failure outcome in rabbits.The difference was statistically significant (diameter:0.52 ± 0.14 mm vs.0.45 ±0.40 mm and 0.58 ±0.17 mm;depth:5.49 ±0.17 cm vs.6.04 ± 0.11 cm and 4.26 ±0.30 cm;all P ＜ 0.05).Conclusions The improved suture method can successfully prepare the focal cerebral ischemia model of middle cerebral artery in rabbits.The method is simple.Its repeatability and practicability are better.

Objective To evaluate comprehensively the efficacy and safety of citalopram combined with risperidone in the treatment of refractory depression.Methods Computer-aided information retrieval was made by using such databases as PubMed,Cochrane Library,Embase,CBM,CNKI,VIP,WanFang and Lancet as well,at the same time,manual data retrieval was also made by searching related literature from both published and unpublished papers,and both at home and abroad.The time span for information retrieval was from the inception to December 2016.After 2 reviewers screened independently the retrieved literature in accordance with the included and excluded selection criteria,and collected the retrieved papers and evaluated methodological the quality of the retrieved literature,meta-analysis was performed by using RevMan 5.3 software.Results Finally,a total of 8 randomized controlled trials (RCTs) involving 711 patients were included in the study.Meta-analyses showed that the effective rate and cure rate of the citalopram combined with risperidone group were respectively [OR =3.47,95％ CI (2.33,5.16)] (P ＜ 0.01) and [OR =2.48,95％CI (1.64,3.76)] (P ＜0.01),which were superior to those of the simple citalopram group.Following treatment of 2,4,6 and 8 weeks,HAMD scores of the experimental group were respectively [SMD =0.65,95％CI (0.39,0.92),P ＜0.01;SMD =0.59,95％ CI (0.34,0.84),P ＜0.01;SMD =0.62,95％ CI (0.24,0.99),P =0.001;SMD =0.78,95％ CI (0.27,1.29),P =0.003].After treatment of 2,4 and 6 weeks,HAMA scores of the experimental group were respectively[SMD =0.51,95％ CI (0.09,0.92),P =0.02;SMD=0.34,95％CI (0.09,0.58),P=0.007;SMD=0.54,95％CI (0.15,0.93),P=0.007],which were also superior to those of the simple citalopram group.Following treatment of 4 and 6 weeks,TESS scores of the experimental group were respectively [SMD =-0.37,95％ CI (-1.66,0.92),P =0.580;SMD =-0.19,95％ CI (-0.90,0.51),P =0.590].There was no statistical significance when comparisons were made between the 2 groups.Conclusions Current evidence shows that citalopram combined with risperidone could produce good effects on refractory depression,without obvious adverse reactions.For this reason,risperidone could be supplemented clinically,so as to enhance therapeutic efficacy in the treatment of refractory depression.