Bipolar affective disorder (BPAD) is a chronic psychiatric condition with high heritability (60-85%) and significant phenotypic variability, complicating its etiological understanding. Genome-wide association studies (GWAS) have revealed genetic overlaps with diverse traits, suggesting pleiotropy. This study aimed to identify shared genetic factors and infer causal relationships using large-scale GWAS data.BPAD GWAS summary statistics were obtained from the UK Biobank via the Complex Trait Genetics Virtual Lab (CTG-VL) platform. Genetic correlations with 1,504 traits were estimated using linkage disequilibrium score regression (LDSC), with quality filters ensuring heritability (h² > 0.05, p < 0.05). The latent causal variable (LCV) model was applied to assess genetic causal proportion (GCP), distinguishing vertical from horizontal pleiotropy. Multiple testing was corrected using false discovery rate (FDR < 5%).Seventy-five traits showed significant genetic correlations with BPAD (FDR < 5%). Among these, 47 exhibited strong causal associations (|GCP| > 0.6; FDR < 5%), and 28 showed partial genetic causality (|GCP| < 0.6; FDR < 5%). Our results showed that the genetic variants affecting BPAD risk had positive and negative effects on other complex phenotypes. For example, we found that genetic predisposition to BPAD increased the risk of depression, excessive worry, and altered blood levels of vitamin C and calcium. On the other hand, we found that genetic variants influencing the use of certain supplements and medications, such as glucosamine/chondroitin, multivitamin mineral preparations, vitamin D, clopidogrel, and nicorandil, as well as the exposure to gas or solid fuel cooking/heating, decreased BPAD risk. Additionally, we detected that genetic variants affecting some mental, work, living, dietary, and physical health factors also increased BPAD risk. Our study provides novel insights into the potential causal determinants of BPAD and suggests new avenues for future research to elucidate the biological mechanisms and pathways involved in this disorder.

AIMS:To investigate the relationship between the neutrophil:lymphocyte ratio (NLR) in peripheral venous blood and the degree of vascular reflow following mechanical thrombectomy in patients with acute ischemic stroke (AIS) and anterior circulation large vessel occlusion. MATERIALS AND METHODS:Patients with successful reflow were divided into two groups: i) partial reflow group (mTICI = 2b) and ii) complete reflow group (mTICI = 3) according to the modified thrombolysis in cerebral infarction classification (mTICI). Basic clinical data, disease characteristics, interventional therapy and prognosis for patients in the two groups were compared, and the association with the degree of postoperative reflow determined using multivariate logistic analysis. RESULTS:Univariate analysis of 21 cases of partial reflow and 45 cases of complete reflow showed statistically significant differences in the preoperative NLR, occluded vessel location, thrombus burden, puncture to recanalization time, thrombus removal times, and prognosis at 90 days post operation (p < 0.05 for all comparisons). Compared with patients with partial reflow, patients with complete reflow had lower NLR, more occluded vessels in the middle cerebral artery, lower thrombus burden, shorter operation time, fewer thrombectomy time and better clinical prognosis. DISCUSSION AND CONCLUSION:Multivariate logistic regression analysis thus shows that NLR and a low thrombus burden are independent prediction factors for complete reflow in this collective of AIS patients. Patients with anterior circulation AIS coupled with low NLR and low thrombus burden prior to mechanical thrombectomy are more likely to achieve complete reflow.

Cerebral palsy (CP) is a complex neurological disorder characterized by motor and postural impairments, often stemming from prenatal or perinatal brain injury. Despite extensive research, the precise genetic mechanisms underlying CP remain elusive.Here, we employed genome-wide Summary-data based MR (SMR) and Mendelian randomization (MR) analysis to investigate the potential causal role of genes within the complement system in neuronal development and plasticity (CSNDP) pathway in CP pathogenesis. Leveraging summary-level data from large-scale GWAS and quantitative trait locus (QTL) studies, we assessed the associations of CSNDP-related gene expression, DNA methylation, and protein abundance with CP susceptibility.Our analysis identified several putatively causal genes associated with CP risk, including CX3CL1 and TYRO3, both implicated in neuroinflammation and synaptic modulation. Colocalization analysis provided strong evidence for shared genetic variants driving the association of CX3CL1 and TYRO3 with CP risk. Furthermore, druggability assessment revealed the potential therapeutic targets of CX3CL1 and TYRO3, supporting their relevance in CP treatment strategies. Phenome-wide association studies demonstrated no significant adverse effects of drugs targeting CX3CL1 and TYRO3 on other disease traits, suggesting their safety profile.Our findings shed light on the molecular underpinnings of CP and highlight the potential of targeted interventions within the CSNDP pathway.

Second-generation antidepressants (SGADs) often cause neurological side effects (SEs). This meta-analysis seeks to quantify the short-term rates of neurological SEs related to routinely used second-generation antidepressants used to treat major depressive disorder (MDD). A search of the PubMed, EMBASE,Cochrane Library databases and Web of Science was done to uncover double-blind, randomized, placebo-controlled studies evaluating the effectiveness of frequently used SGADs medicines in people with MDD. Qualifying studies were required to concentrate on the use of SGADs routinely used in MDD and to uncover data on treatment-emergent neurological SEs occurring within 12 weeks of therapy. Overall, 143 RCT studies containing 188 treatment arms were included in the meta-analyses. Most SGADs increased the risk of neurological SEs compared to placebo. The least tolerated antidepressants on the neurological tract were desvenlafaxine (OR=1.98; CI 0.85-4.65; p-value=0.12) and venlafaxine (OR=1.15; CI 0.96-1.38; p-value=0.13). Agomelatine, bupropion and vortioxetine exhibited reduced neurological SEs, showing diminished risk in insomnia (OR=0.56; CI 0.36-0.88; p-value=0.01), somnolence (OR=0.46; CI 0.27-0.79; p-value=0.01), vision blurred (OR=0.43; CI 0.19-0.96; p-value=0.04), respectively. Most SGADs did not or just marginally increased the risk of headache compared to placebo. In conclusion, frequently used SGADs demonstrated distinct patterns of neurological SEs, which physicians should consider when prescribing antidepressants to promote treatment adherence and favorable outcomes in patients with MDD.

BACKGROUND:Atopic dermatitis (AD) is a common chronic inflammatory skin disease that affects adults worldwide. Recent evidence suggests that AD may be associated with cognitive dysfunction, but the results of individual studies have been inconsistent. This systematic review and meta-analysis aimed to evaluate the association between AD and cognitive dysfunction in middle-aged and older adults.METHODS:To find relevant research, a comprehensive search of electronic databases from the beginning to March 2023 was carried out. Data were taken from studies that were eligible, and a meta-analysis was done to determine the pooled hazard ratio (HR) and 95% confidence interval (CI).RESULTS:We searched three databases and found a total of 15 studied arms included in 5 cohort studies with over 8.5 million participants were included in the analysis. The results showed that individuals with AD had a higher risk of developing dementia of all-cause dementia (pooled hazard ratio (HR) = 1.16; 95% CI, 1.10-1.23,P<0.001) and the Alzheimer type (pooled HR = 1.28; 95% CI, 1.01-1.63,P<0.001) but not vascular dementia (pooled HR = 1.42; 95% CI, 0.99-2.04,P<0.001). Subgroup analyses showed that the association between atopic dermatitis and all-cause dementia was significant in Europe (P = 0.004) but not in Asia (P = 0.173) and was significant in prospective cohort studies (P<0.001) but not in non-prospective cohort studies (P = 0.068). Sensitivity analysis and publication bias detection confirmed the reliability of the overall findings.CONCLUSIONS:In conclusion, this study demonstrated that AD was associated with increased risk of cognitive dysfunction, particularly dementia of the Alzheimer type and all-cause dementia, in middle-aged and older participants. Further research is needed to understand the mechanisms behind this association and its potential implications for clinical practice.SYSTEMATIC REVIEW REGISTRATION:PROSPERO, identifier (CRD42023411627).

Background: Cataract has been shown to be associated with an increased risk of cognitive impairment. However, the results of previous studies have been inconsistent. This systematic review and meta-analysis aimed to investigate the association between cataract and the incidence of cognitive impairment in older adults.Methods: A comprehensive search of electronic databases from inception to January 2023 was performed to identify relevant studies. Data were extracted from eligible studies and a meta-analysis was performed to calculate the pooled hazard ratio (HR) and 95% confidence interval (CI).Results: We included 13 studies with 25 study arms involving a total of 798,694 participants. Compared with participants without cataract, those with cataract had a higher risk of developing all-cause dementia (pooled HR: 1.22; 95 % CI: 1.08-1.38; I2 =86 %; 9 studies), Alzheimer's disease dementia (pooled HR: 1.18; 95 % CI: 1.07-1.30; I2 =0 %; 9 studies), vascular dementia (pooled HR: 1.21; 95 % CI: 1.02-1.43; I2 =77 %;3 studies) and mild cognitive impairment (pooled HR: 1.30; 95% CI: 1.13-1.50; I2 =0%;2 studies). There was no significant association between cataract and mixed dementia (pooled HR: 1.03; 95 % CI: 0.52-2.04; I2 =78 %;2 studies). We assessed the risk of bias of the included studies using the Newcastle-Ottawa Scale and found that most of them had a low or moderate risk of bias. The number of studies in each meta-analysis ranged from two to nine, with more studies available for all-cause dementia and Alzheimer's disease dementia than for vascular dementia and mixed dementia.Conclusions: The findings suggest that cataract may be associated with cognitive impairment in older adults. However, the causal relationship between cataract and cognition remains unclear and requires further investigation.

Background: Hereditary spastic paraplegia 4 (SPG4) caused by spastin (SPAST) gene mutations accounts for 40-45% of hereditary spastic paraplegia (HSP) cases. To search for more genetic evidences for the pathogenesis of HSP, the SPAST genotype and clinical phenotype of a Chinese Han SPG4 family were analysed in this study.Methods: The clinical data of the proband and his family members were collected. Whole genomic DNA was extracted from peripheral blood, and the gene detection and pathogenicity analysis of mutations were conducted using whole-exome sequencing technology. Suspected pathogenic mutations were identified. Verification within this family was conducted by Sanger sequencing.Results: Eight (4 males and 4 females) of 20 members in 4 generations had SPG4. All patients presented with the high feet arches (pes cavus), the abnormal gait, the active tendon reflexes of the upper limbs, the hyperreflexia of the lower limbs, and the positive ankle clonus and Babinski's signs bilaterally. In the proband, we found a heterozygous mutation c.1495C > T in SPAST gene, which was associated with the autosomal dominant SPG4. Both the daughters and granddaughters of the proband in this family were verified to carry this mutation. The clinical characteristics of the SPG4 patients in this family are in line with the simple type of HSP. Heterozygous c.1495C > T is a pathogenic mutation in this family.Conclusion: In this study, we identified a c.1495C > T mutation in the SPAST gene in a Han Chinese family, enriching the mutation spectrum of SPG4.

BackgroundBullous pemphigoid (BP) is a rare autoimmune skin condition that causes large fluid-filled blisters on the skin, especially in older adults. BP has been linked to various diseases and medications, but its association with cognitive outcomes is unclear.MethodsWe conducted a systematic review and meta-analysis of studies investigating the association between BP and cognitive outcomes, such as all-cause dementia, Alzheimer's disease, and vascular dementia in middle-aged and older adults. We searched PubMed, Embase, and Web of Science databases for relevant studies published up to March 2023. We included studies that reported odds ratios (ORs) or hazard ratios (HRs) with 95% confidence intervals (CIs) for the association between BP and cognitive outcomes. We pooled the ORs, or HRs using random-effects models and performed subgroup and sensitivity analyses to explore potential sources of heterogeneity.ResultsThe study selection process identified 13 studies for inclusion in the analysis, 11 studied arms of which used a case-control design and 7 studied arms of which used a cohort design. The studies were conducted primarily in Europe, with a few from Asia and the United States. The meta-analysis found that BP was associated with higher odds of all-cause dementia in middle-aged and older participants in both cohort studies(HR = 1.41,95% CI: 1.20-1.66, P = 0.000) and case-control (OR = 4.25, 95% CI, 2.73-6.61; P = 0.000). The study found no significant publication bias in the included studies. The meta-regression analyses identified some subgroups associated with significantly reported odds ratios in case-control association analysis, including Europe, BP diagnosed based on clinical, histology, immunofluorescence, and both adjustment status of NO and YES.ConclusionsOur meta-analysis suggests that BP is associated with an increased risk of all-cause dementia in middle-aged and older adults. Further studies are needed to elucidate the underlying mechanisms and causal relationship between BP and cognitive outcomes.

目的 研究时间飞跃法磁共振血管成像(TOFMRA)结合三维动脉自旋标记技术(3D-ASL)在脑动脉狭窄及闭塞疾病中的诊断价值.方法 选取2018年1月-2020年12月在我院诊治的150例脑动脉狭窄及闭塞疾病患者为研究对象,均采用TOF MRA、3D-ASL成像以及TOF MRA结合3D-ASL技术进行诊断,以数字减影血管造影(DSA)为金标准,比较不同成像技术的诊断效能、诊断不同脑动脉狭窄程度及闭塞的准确率、与DSA诊断结果的一致性以及3D-ASL成像技术下不同标记后延迟(PLD)时间责任颈内动脉供血区与镜像侧脑血流量(CBF).结果 TOFMRA结合3D-ASL成像诊断脑动脉狭窄及闭塞的敏感度、特异度、准确性、阳性预测值、阴性预测值均高于TOFMRA、3D-ASL成像技术(P＜0.05);TOFMRA结合3D-ASL诊断成像技术诊断1、2级动脉狭窄的准确率高于TOFMRA、3D-ASL成像技术(P＜0.05);三种方法诊断3、4级动脉狭窄及闭塞的准确率比较,差异无统计学意义(P＞0.05);TOF MRA结合3D-ASL的准确率与DSA诊断结果具有高度一致性,且一致性高于TOF MRA、3D-ASL单独检测(P＜0.05);3D-ASL成像技术下,PLD为1.5 s时,闭塞侧颈内动脉供血区CBF值低于镜像侧(P＜0.05),但PLD为2.0s时,闭塞侧颈内动脉供血区CBF值与镜像侧比较,差异无统计学意义(P＞0.05).结论 TOF MRA结合3D-ASL对脑动脉狭窄及闭塞具有较高的诊断价值,可提升血管低狭窄程度的诊断准确率,评估闭塞脑血流灌注情况,两者联合可提高诊断效能,为临床介入治疗提供参考依据.

Background: Purpurogallin (PPG) has been testified to have neuroprotective effects. This study intends to probe the neuroprotection of PPG on cerebral ischemia/reperfusion (I/R) injury and its potential mechanism. Methods: C57/B6 mice, BV2 microglia and HT22 hippocampal neurons were used for in-vivo and in-vitro ex-periments. I/R injury models were constructed using middle cerebral artery occlusion (MCAO/R) and oxygen -glucose deprivation/reoxygenation (OGD/R), respectively. The expression of apoptosis and inflammatory pro-teins, and endoplasmic reticulum (ER) stress proteins were gauged by Western blotting (WB). The contents of inflammatory cytokines in OGD/R-induced BV2 microglia were testified by enzyme-linked immunosorbent assay (ELISA). Cell counting kit-8 (CCK-8), TUNEL assay and flow cytometry (FCM) were utilized to examine the viability and apoptosis of cells. The neurological, learning and memory functions were evaluated by the modified neurological severity score (mNSS) and water maze experiment. 2, 3, 5-triphenyltetrazole chloride (TTC) staining was utilized to calculate the volume of cerebral infarction and cerebral edema in the peri-infarct area. Apoptosis-related proteins, inflammation-related proteins and ER stress proteins were gauged by WB. ELISA was conducted to verify inflammatory cytokines. Results: PPG treatment notably abated the expression of ER stress proteins and inflammatory factors in OGD/R-induced BV2 microglia and boosted HT22 neuron's viability and eased their apoptosis in comparison to the control group. In vivo, PPG treatment signally lessened cerebral infarct area, cerebral edema, and neurological deficit scores in MCAO/R mice. Additionally, PPG caused a dramatic decline in neuronal apoptosis and levels of ER stress proteins and inflammatory factors in the brain's peri-infarct region of MCAO/R mice. Mechanically, PPG blocked the TLR4/NF-kappa B pathway in OGD/R-induced BV2, HT22 neurons, and the MCAO/R mice. Conclusion: PPG attenuates brain I/R damage probably by suppressing ER stress and neuroinflammation via inactivation of the TLR4/NF-kappa B pathway, suggesting that PPG may be a candidate drug for treating cerebral I/R injury.

目的:观察椎基底动脉扩张延长症患者的临床症状,并分析其影响因素.方法:回顾性分析本院2015年1月—2021年10月收治的100例椎基底动脉扩张延长症患者的临床资料,统计患者临床症状,根据有无临床症状分为症状组和无症状组,通过单因素和二元Logistic回归分析法分析临床症状的危险因素.结果:100例患者中,78例患者出现临床症状,发生率为78.00％,以短暂性脑缺血发作(42.31％)和后循环梗死(23.08％)为主.症状组C-反应蛋白、中性粒细胞与淋巴细胞比值、基底动脉偏移度分级、基底动脉直径以及高血压、椎动脉优势、血管内高信号征比例均明显高于无症状组(P<0.05).二元Logistic回归分析结果显示,高血压、基底动脉直径、血管内高信号征以及椎动脉优势是影响椎基底动脉扩张延长症患者出现临床症状的独立危险因素(P<0.05).结论:椎基底动脉扩张延长症患者临床症状发生率较高,以短暂性脑缺血发作和后循环梗死为主,高血压、基底动脉直径、血管内高信号征以及椎动脉优势是影响椎基底动脉扩张延长症患者出现临床症状的主要危险因素.

Abstract The function of polypyrimidine tract-binding protein 2 (PTBP2) is the regulator of neuronal fate during central nervous system development. The possible relationship between the PTBP2 and the pathogenesis of amyotrophic lateral sclerosis (ALS) hasn’t been known. In this study, we observed and analyzed the expression and distribution of PTBP2, as well as the possible relationship between PTBP2 expression and distribution and the neural cell death in both SOD1 wild-type (WT) and Tg(SOD1*G93A)1Gur (TG) mice applying the immunofuorescence analysis and western blot analysis. Our data demonstrated that the PTBP2 expression and distribution significantly increased in the AH, the LH, and the surrounding CC region at the pre-onset, onset, and progression phases of ALS. PTBP2 protein isn't just expressed in mature neurons, yet additionally, in neuronal precursor cells, astrocytes, microglia. The increment of PTBP2 distribution was closely related to the death of neural cells at the development of ALS. PTBP2-expressing motor neurons were lost during the ALS disease process. Together, these results defined PTBP2 as a candidate therapeutic target for ALS, providing novel insights into mechanisms of vulnerability to motor neurons in ALS.

Dysregulation of microRNAs (miRNAs) is involved in abnormal development and pathophysiology in the brain.Although miR-20b plays essential roles in various human diseases, its function in cerebral ischemic stroke remains unclear.A cell model of oxygen glucose deprivation/reoxygenation (OGD/R) and A rat model of middle cerebral artery occlusion/reperfusion (MCAO/R) were constructed.qRT-PCR and western blot were used to evaluate the expression of miR-20b and TXNIP.Cell viability was detected by MTT assay, and cell apoptosis was evaluated by flow cytometry.Targetscan and Starbase were used to predict the potential targets of miR-20b.Luciferase reporter assay was applied to determine the interaction between miR-20b and TXNIP.Rescue experiments were conducted to confirm the functions of miR-20b/TXNIP axis in cerebral ischemic stroke.MiR-20b was significantly downregulated after I/R both in vitro and in vivo.Upregulation of miR-20b inhibited OGD/R-induced neurons apoptosis and attenuated ischemic brain injury in rat model.Bioinformatic prediction suggested that TXNIP might be a target of miR-20b, and luciferase reporter assay revealed that miR-20b negatively regulated TXNIP expression by directly binding to the 3'-UTR of TXNIP.Downregulation of TXNIP inhibited OGD/R-induced neurons apoptosis in vitro and ischemic brain injury in vivo.Rescue experiments indicated that downregulation of TXNIP effectively reversed the effect of miR-20b inhibitor in neurons apoptosis after OGD/R-treatment and ischemic brain injury in a mouse model after MCAO/R-treatment.Our study demonstrated that upregulation of miR-20b protected the brain from ischemic brain injury by targeting TXNIP, extending our understanding of miRNAs in cerebral ischemic stroke.

Background Ischemic stroke is a destructive cerebrovascular disorder related to oxidative stress; NOX2 is a major source for ROS production; and miR-126a-5p is involved in several diseases, such as abdominal aortic aneurysm. We investigated the role of miR-126a-5p in regulating NOX2 in ischemic stroke. Methods MiR-126a-5p and NOX2 were examined in the brains of rats subjected to cerebral ischemia/reperfusion (I/R) by RT-PCR and Western blot. MiR-126a-5p agomir was delivered to examine the effects of miR-126a-5p on I/R injury. The neurological deficit, infarct volume, and brain water content were evaluated. NOX activity, ROS production, and MDA and SOD levels were detected to assess oxidative stress. H&E staining was used to examine cell state. Apoptosis was evaluated by TUNEL, caspase-3 activity, and cleaved-caspase-3 protein level. The relationship between miR-126a-5p and NOX2 was analyzed by bioinformatics and luciferase reporter assay. MiR-126a-5p mimic, miR-126a-5p inhibitor, or pcDNA-NOX2 were transfected in SH-SY5Y cells to further assess the effects of miR-126a-5p on OGD/R-induced cells injury. Results NOX2 was upregulated and miR-126a-5p was down-regulated in the brains of I/R rats. MiR-126a-5p agomir obviously reduced the neurological deficit, infarct volume, brain water content, oxidative stress, and apoptosis in I/R rats. MiR-126a-5p targeted NOX2 directly and regulated NOX2 negatively. Moreover, miR-126a-5p mimic elevated cell viability and inhibited oxidative stress and apoptosis in OGD/R-treated SH-SY5Y cells, while miR-126a-5p inhibitor had the opposite effects. NOX2 overexpression antagonized the protective effects of miR-126a-5p mimic on OGD/R-induced cell injury. Conclusion MiR-126a-5p is a novel potential target for ischemic stroke therapy due to its protection against cerebral I/R injury via directly targeting NOX2.

目的 研究脑卒中偏瘫患者周围神经的神经电生理变化.方法 选择南昌大学第三附属医院脑卒中偏瘫患者180例,3～7 d、6个月进行肢体神经传导、针极肌电图、交感神经皮肤反应(SSR)测定.结果 180例患脑卒中偏瘫患者急性期1例检测出双侧腓肠神经传导速度减慢,针极肌电图正常;病程6个月时,56例出现NCV异常,运动神经总异常率为3.6％,感觉神经总异常率6.4％,SCV异常率高于MCV异常率.肌电图:①患侧:21例出现插入电位延长,18例有自发电位;②健侧:4例出现插入电位及自发电位.SSR:脑卒中偏瘫患者急性期、病程6个月时,健侧、患侧SSR潜伏期、波幅与正常值比较差异有统计学意义(P<0.05),而健侧潜伏期、波幅及患侧潜伏期、波幅比较差异无统计学意义(P>0.05).6个月与急性期对比,患侧及健侧下肢、健侧上肢潜伏期差异有统计学意义(P<0.01),患侧上肢潜伏期及所有肢体波幅差异无统计学意义(P>0.05).结论 脑卒中偏瘫患者在病程6个月出现周围神经损害,SCV异常率高于MCV异常率,而在急性期出现SSR抑制、自主神经功能异常.

目的:分析丙戊酸钠(VPA)对继发性癫痫患者神经元特异性烯醇化酶(NSE)和血清酸性钙结合蛋白(s-100β)水平的影响,探讨NSE和S-100β 水平在VPA用药中的指导意义.方法:选择神经内科收治的继发性癫痫患者36例为观察组,给予丙戊酸钠缓释片口服治疗.在治疗前和服用药物3个月后检测血清NSE和s-100β 含量.同时选择门诊健康体检者30例为对照组.结果:观察组患者血清NSE和s-100β 水平均明显高于对照组,差异有统计学意义(P<0.05);观察组服用VPA3个月后,血清NSE和s-100β水平均明显降低,差异有统计学意义(P<0.05).结论:血清NSE和s-100β 水平与癫痫发作有关,且长期服用VPA能降低血清NSE和s-100β 水平.

目的 观察经颅多普勒超声(c-TCD)和经胸壁心脏超声发泡试验(c-TTE)对诊断偏头痛合并卵圆孔未闭(PFO)的应用价值,以及对确诊卵圆孔未闭的偏头痛患者行卵圆孔未闭封堵术后的疗效评估价值.方法 选取2013年11月-2017年4月我院收治的偏头痛患者,进行c-TCD联合c-TTE检查,筛查出阳性结果者,进一步行经食道心脏超声(TEE)确诊卵圆孔未闭,对确诊卵圆孔未闭的偏头痛患者行卵圆孔未闭封堵术,术后随访病例,同时进行c-TCD、c-TCD联合c-TTE检查.结果 386例患者c-TCD检查阳性率38.56％,c-TCD联合c-TTE检查阳性率32.64％,差异无统计学意义;其中37例患者接受介入封堵术治疗10例患者偏头痛症状完全消失,14例患者症状明显改善;6个月内随访,21例患者两项检查结果均为阴性;16例c-TTE仍为阳性,但气泡量均有明显减少(1级),其中11例c-TCD为阳性结果,均为少量气栓影(1级).结论 c-TCD联合c-TTE可运用于偏头痛并卵圆孔未闭诊断,且半定量方法可提高PFO确诊及术后治疗效果评价的敏感性和准确性.

目的 探讨抗N-甲基-D-天冬氨酸(NMDA)受体脑炎的临床特点 、诊断及治疗,提高对该疾病的认识.方法 报道1例抗NMDA受体脑炎患者的临床表现及诊治过程,并总结其临床特征.结果 患者为青年女性,表现为精神行为异常及抽搐,意识障碍及通气不足.脑脊液中抗NMDA受体抗体阳性.联合静脉用免疫球蛋白 、激素冲击及血浆置换等治疗,患者临床痊愈.结论 抗NMDA受体脑炎是一种自身免疫性的 、能用血清学方法诊断的疾病.早期明确诊断和给予及时治疗,预后良好.

目的 比较前列地尔注射液与银杏达莫注射液治疗早期急性脑梗死的疗效.方法 选取70例早期急性脑梗死患者,比较前列地尔与银杏达莫对患者神经功能恢复的疗效及不良反应.结果 两组药物治疗均有显著疗效,其中前列地尔注射液组患者神经功能恢复较早,有较好的治疗效果,两组用药的治疗疗效经分析有统计学差异(P＜ 0.05).结论 前列地尔注射液组优于银杏达莫治疗组,对早期急性脑梗死有较好的治疗作用,值得临床推广应用.