OBJECTIVE:Although up to 45% of patients with psoriatic arthritis (PsA) have a family history of psoriatic disease, it is unclear whether this family history contributes to a distinct PsA phenotype and/or the timing of disease onset. We aimed to identify differences in onset, domain involvement, and disease activity based on family history of psoriatic disease. METHODS:A total of 843 patients with PsA were enrolled in an observational, longitudinal registry. Demographics, medical history, family history, and psoriatic phenotype and activity were collected. RESULTS:Of the total, 379 patients (45.0%) had at least one first-degree relative (FDR) or second-degree relative (SDR) with psoriatic disease. Those with a family history developed psoriasis and PsA earlier than those with no family history (psoriasis: mean 27.6 vs 32.2 years [P < 0.01]; PsA: mean 37.6 years vs 40.3 years [P < 0.01]) and were more likely to have entheseal involvement (36.7% vs 30.0%; P < 0.05). Patients with an FDR or SDR with PsA were diagnosed with psoriasis and PsA earlier than those with an FDR or SDR with psoriasis alone, followed by those with no family history (psoriasis: mean 26.3 vs 27.8 vs 32.2 years, respectively [P < 0.01]; PsA: mean 36.5 vs 37.9 vs 40.3 years, respectively [P = 0.01]). CONCLUSION:In this cohort, patients with PsA with a family history of psoriatic disease were diagnosed with psoriasis and PsA earlier and were more likely to have entheseal involvement compared to those without a family history. Further research incorporating molecular and immune features is needed to investigate genetic, environmental, and epigenetic factors that impact PsA phenotype and severity, as well as the transition from psoriasis to PsA.

OBJECTIVES:Although genetic risk factors, such as HLA-DRB1 alleles, contribute to the pathogenesis of rheumatoid arthritis (RA), the concordance rate in monozygotic (MZ) twins is low, suggesting that other factors are involved in disease development. Further, the relative contribution of nongenetic elements in identical twins has not been characterised. Here, we aimed to characterise host and microbial biomarkers of RA by studying MZ twins discordant for disease using a multiomics approach. METHODS:Eight pairs of MZ twins discordant for RA (N = 16) were enrolled in the United States (US). The gut microbiome was assessed using shotgun metagenomic sequencing. Autoantibodies, cytokines, and plasma proteins were measured in both plasma and faeces. Levels of short-chain fatty acids (SCFAs) from serum and faeces were quantified using gas chromatography mass spectrometry (GC-MS). Metagenomic data from a UK twin registry (TwinsUK) (N = 14) were used to validate findings in the US population. RESULTS:Although microbiome diversity and composition did not differ between twins, we observed a significant decrease in the SCFA-producing bacteria Blautia faecis and significantly lower concentrations of faecal butyrate and propionate in affected RA twins in the US. TwinsUK showed a similar reduction in the SCFA-producers Gemmiger formicilis and Faecalicatena fissicatena, as well as bacterial SCFA metabolism pathways. CONCLUSIONS:Multiomics biomarkers differentiate MZ twins discordant for RA. Faecal butyrate and propionate, as well as SCFA-producing bacteria, were decreased in affected twins. We found a similar decrease in SCFA-producing taxa in affected twins in a geographically distinct cohort in the UK. Our results suggest that, if further validated in larger cohorts, multiomics approaches may improve our understanding of RA pathogenesis and, potentially, contribute to more accurate diagnostics and coadjuvant therapies.

Abstract Genetic and environmental influences contribute to Crohn’s disease (CD) development. However, the relationship between these two factors is unclear, limiting insights into CD pathophysiology, as well as interventions to prevent disease. To address this knowledge gap, we performed a longitudinal study of entire multiplex families to identify relatives discordant between their genetic risk for disease, as calculated by an IBD polygenic risk score (PRS), and their CD status. Fecal specimens were collected quarterly (up to 32 months) for assessment of intestinal inflammation by fecal calprotectin assays and gut microbiome composition by 16S sequencing. We evaluated 8 candidate IBD PRS, and the best performing score across all families was used to rank each subject by genetic risk. Untargeted fecal metabolomic analysis was performed on a single specimen chosen from each of the 5 subjects that best represented the following categories: CD+/high PRS, CD-/high PRS, CD+/low PRS, and CD-/low PRS. To avoid potential confounders, we excluded the following specimens: elevated calprotectin, collected < 3 months since antibiotic use, or from pediatric subjects, who may still develop CD. From these 20 samples, 12 fecal specimens (3 from each category) were each gavaged into 5 germ-free IL-10 deficient mice (male, SvEv129, 7.5-12 weeks old). As a control, 4 other mice were gavaged with a fecal slurry from age- and sex-matched Murine Pathogen Free 129S6/SvEvTac mice. Mice were maintained in isolator cages with sterile food, water, and bedding. A score evaluating weight loss, pellet consistency, and fecal blood was used to measure disease activity over time. We studied 396 fecal specimens from 52 subjects across four multigenerational families. We found low microbiome diversity and an altered microbial composition based on 16S sequencing of 12 CD-affected subjects compared to unaffected relatives. Among subjects with CD, we observed an inverse correlation between microbiome diversity and PRS that included CD-relevant genetic variants. There was no relationship between PRS and microbiome diversity among unaffected relatives or with a PRS using ulcerative colitis-specific genetic variants. Among relatives with high PRS, those protected from disease (i.e., CD-/high PRS) had high relative abundance of multiple fecal metabolites (Figure 1). Germ-free IL-10 deficient mice gavaged with these fecal specimens showed reduced disease activity - on par with mice treated with human inocula from those with no CD or low PRS (Figure 2). In contrast, mice colonized with CD+/high PRS inocula displayed high disease activity immediately following gavage. In conclusion, our findings suggest the presence of a CD-protective factor within the gut microbiome of unaffected relatives with high PRS that is transferable and that mitigates disease activity in an IBD mouse model. Figure 1 Fecal small molecules that characterize Crohn’s disease risk in multiplex families. 10 subjects with high genetic risk for CD, half with disease and half without, underwent untargeted metabolomic analysis by hybrid liquid chromatography-mass spectrometry. For each subject, the single optimal specimen was identified from longitudinal sampling to avoid sampling near antibiotic use or with intestinal inflammation (determined by the biomarker, fecal calprotectin). Unsupervised clustering analysis of the 460 differentially abundant metabolites (p Figure 2 Disease activity index (DAI) over time by different inocula. DAI differs based on treatment inocula (p=0.001) as determined by two-way ANOVA testing. Pairwise t-tests show that this difference is driven primarily by the DAI induced by the CD, high PRS inocula compared to other human inocula groups (p=0.002-0.009). DAI in the CD-protected group (no CD, high PRS) is on par with mice treated with No CD and Low PRS inocula.

Gerstmann-Sträussler-Scheinker syndrome (GSS) is a rare genetic prion disease caused by a mutation in the prion protein (PRNP) gene. It is typically characterized by progressive cerebellar ataxia and slowly progressive dementia. We present a case study of the GSS from China in which a 45-year-old male with a progressive gait and balance disorder developed cerebellar ataxia onset but was misdiagnosed as spinocerebellar ataxia (SCA) for 2 years. The patient's clinical, electrophysiological, and radiological data were retrospectively analyzed. Examination revealed ataxia, dysarthria, muscle weakness, areflexia in lower limbs, including a pyramidal sign, whereas cognitive decline was insignificant. His late mother had a similar unsteady gait. An electroencephalogram (EEG) showed normal findings, and 14-3-3 protein was negative. A brain MRI was performed for global brain atrophy and ventricular enlargement. Positron emission tomography-computed tomography (PET-CT) (18F-fluoro-2-deoxy-d-glucose, FDG) images showed mild to moderate decreased glucose metabolism in the left superior parietal lobe and left middle temporal lobe. According to genetic testing, his younger brother also had the P102L variant in the PRNP gene. This single case adds to the clinical and genetic phenotypes of GSS.

Introduction Psoriatic arthritis (PsA) is a complex, immune-mediated disease associated with skin psoriasis that, if left untreated, can lead to joint destruction. Up to 30% of patients with psoriasis progress to PsA. In most cases, psoriasis precedes synovio-entheseal inflammation by an average of 5–7 years, providing a unique opportunity for early and potentially preventive intervention in a susceptible and identifiable population. Guselkumab is an effective IL-23p19 inhibitor Food and Drug Administration (FDA)-approved for treatment of moderate-to-severe psoriasis and PsA. The Preventing Arthritis in a Multicentre Psoriasis At-Risk cohort (PAMPA) study aims to evaluate the efficacy of guselkumab in preventing PsA and decreasing musculoskeletal power Doppler ultrasound (PDUS) abnormalities in a population of patients with psoriasis who are at-increased risk for PsA progression. Methods and analysis The PAMPA study is a multicentre, randomised, double-blind, placebo-controlled, interventional, preventive trial comparing PDUS involvement and conversion to PsA in patients with psoriasis at-increased risk for progression treated with guselkumab compared with non-biological standard of care. The study includes a screening period, a double-blind treatment period (24 weeks) and an open-label follow-up period (72 weeks). At baseline, 200 subjects will be randomised (1:1) to receive either guselkumab 100 mg (arm 1) or placebo switching to guselkumab 100 mg starting at week 24 (arm 2). Arm 3 will follow 150 at-risk psoriasis patients who decline biological therapy and randomisation. Changes from baseline in the PDUS score at week 24 and the difference in proportion of patients transitioning to PsA at 96 weeks will be examined as the coprimary endpoints. Ethics and dissemination Ethics approval for this study was granted by the coordinating centre’s (NYU School of Medicine) Institutional Review Board (IRB). Each participating site received approval through their own IRBs. The findings will be shared in peer-reviewed articles and scientific conference presentations. Trial registration number NCT05004727 .

目的 观察龟鹿二仙胶加味方联合泼尼松片治疗Duchenne型肌营养不良(Duchenne mus-cular dystrophy,DMD)的 疗效.方法 将49例DMD患者随机分为观察组(19例)、对照组(30例).观察组采用龟鹿二仙胶加味方联合泼尼松片的中西医结合治疗方案,对照组仅用泼尼松片治疗.治疗前及连续治疗3个月后,分别观察自汗盗汗、步行异常等临床症状的改善情况,并检测血清肌酸激酶(creatine kinase,CK)、乳酸脱氢酶(lactic dehydrogenase,LDH)、肌酸激酶同工酶(creatine kinase-MB,CK-MB)水平.结果 连续治疗3个月后,观察组自汗盗汗、步行异常评分显著升高(P＜0.05),两组治疗前后自汗盗汗、步行异常、睡眠质量异常、乏力懒言评分差值的差异具有统计学意义(P＜0.05).观察组治疗后CK、CK-MB水平均显著下降(P＜0.05),两组治疗前后LDH、CK-MB差值的差异具有统计学意义(P＜0.05).结论 龟鹿二仙胶加味方联合泼尼松片不仅改善DMD患者的临床症状,而且修复其血清CK、CK-MB的异常.

目的:分析104例痉挛性斜颈的临床特点、A型肉毒毒素的临床疗效及其与临床特点相关性.方法:回顾分析我院2012年1月至2019年12月住院的符合痉挛性斜颈诊断标准的患者104例,统计患者临床特点;分析A型肉毒毒素疗效在不同性别、年龄、体质指数、教育年限、病程、临床分型、注射次数、注射总量、平均每次注射剂量、注射方式各方面的差异性及治疗后不良反应的发生情况.结果:痉挛性斜颈患者男:女=1∶1.36,年龄以40～50岁为主,且以40 ～ 50岁发病较多,病程(56.84±82.19)个月,发病到确诊间隔时间(22.75±57.44)个月,疾病早期易误诊为颈椎病;易合并精神情绪类疾病;其病因与劳累、情绪异常、饮酒和相关部位的外伤等有关,69.23％的患者在日常生活中起病,64.42％患者情绪激动、劳累或者行走时症状明显;A型肉毒毒素治疗有效率97.22％,A型肉毒毒素疗效与年龄、性别、体质指数、教育年限、病程、临床分型、注射次数、注射总量、平均每次注射剂量之间均无统计学差异(P＞0.05);不良反应发生率10.58％.结论:痉挛性斜颈女性多于男性,年龄多在40～50岁;痉挛性斜颈的临床诊断较困难,病程长,发病多与劳累、情绪等因素有关,早期应防止误诊.A型肉毒毒素治疗痉挛性斜颈有效率较高且不良反应较少,多次注射未见疗效明显降低,但是否有其他影响因素不能肯定.

临床思维是临床医师根据患者情况进行正确决策的能力,正确的临床思维是临床工作的基础.在中西医结合临床神经病学专业研究生的临床思维培养中,从临床理论教学、临床实践教学、临床科研教学3个维度综合培养研究生的临床思维,对研究生的角色快速转变和临床思维能力培养具有重要意义.

目的 通过分析2009-2018年发表的肝豆状核变性中文文献,了解其发展脉络,追踪该领域的研究热点和学术前沿.方法 以CNKI期刊全文数据库为数据源,采用文献计量学方法,利用网络分析工具CiteSpace对2009-2018年发表的916篇文献的载文量、研究机构、基金资助和关键词等进行可视化分析.结果 期刊年度载文量总体呈下降趋势;916篇文献共有137项各类基金资助,资助比例较低;安徽中医药大学神经病学研究所附属医院发文贡献度最大;发文量≥15篇的高产作者共有16位,其中韩咏竹、鲍远程、胡纪源、杨文明和杨任民发文量位居前列;高频关键词包括“铜蓝蛋白”“青霉胺”“铜代谢障碍”“诊断”“误诊”“儿童”等.研究热点和学术前沿包括病因病理研究、诊断分型研究、治疗和疗效评价研究3个方面.结论 肝豆状核变性研究取得了一定的研究成果,形成了相对固定的核心作者和研究团队.应进一步加强机构间合作,促进作者间的合作与交流.

目的 总结分析神经梅毒误诊和(或)漏诊原因.方法 选取2011年7月至2018年5月安徽中医药大学神经病研究所附属医院诊治的22例神经梅毒患者作为研究对象.对其临床分型、冶游史问诊、诊断、是否合并他神经系统疾病等进行比较分析.结果 出院诊断分型与文献Fisher概率P＞0.05,入院诊断、修正诊断一致性检验(Kappa=0.353,P＜0.05),优势性检验P＜0.05,前后冶游史问诊一致性检验(Kappa=0.009,P＞0.05),优势性检验P＜0.05.有、无症状神经梅毒并存疾病的Fisher概率P＜0.05.结论 神经梅毒临床表现不典型或无症状,加上多数患者隐瞒冶游史,极易造成误诊和(或)漏诊,临床应注重神经梅毒定性、定位分析,常规进行血液和(或)脑脊液的筛查.

神经心理学是研究人类心理活动神经机制、高级认知功能的一门学科,是通过研究脑损害患者高级认知功能,加深对脑的各种疾病症状谱认识,通过神经心理学检测为认知功能康复寻找突破口.更为重要的是,脑结构和功能的问题是当今科学时代的研究热点,神经心理学研究对脑科学发展具有重要的意义.中医院校毕业的学生主要从事临床中医医疗工作,服务对象是病人,而病人的神经心理变化,直接关系到就诊的最终预后,故学习神经心理学对于医学生有着重要意义.神经心理学涉及神经病学、精神病学、心理学等多学科,具有更新较快、实践性强等特点,如何让医学生在轻松易懂的过程中学好神经心理学,是每一位教学工作者一直努力追求的.论文从中医院校的神经心理学教学中目前存在问题、对策措施及教学效果进行思考和建议.

Objective To report a case of peripheral neuropathy secondary to copper deficiency (CD) by long‐term decoppering chelation in Wilson′s disease (WD) to enhance understanding of the disease, and to pay more attention to individualized treatment of WD. Methods A case of WD diagnosed 12 years ago confirmed by gene detection and since then treated with anti‐copper agent was diagnosed as CD based peripheral neuropathy and significant neutropenia and followed up for six months, and the clinical manifestations, laboratory examination, electrophysiology, imaging features were summarized. The related literatures were reviewed. Results A total of 16 cases of WD complicated with CD were reviewed and analyzed, including seven males and nine females aged 13-56 years. All of them were treated with zinc for 1-38 years, and nine cases with peripheral neuropathy. Hematological indicators can be significantly improved and neurological symptoms can be partially alleviated after stopping copper removal treatment. Conclusions Peripheral neuropathy in a WD with treatment‐related CD may occur in blind treatment, irregular treatment monitoring and without individualized treatment adjustment. It is necessary to monitor blood routine, copper and zinc metabolism regularly and advocate individualized treatment of WD.

Wilson’s disease (WD) is an autosomal recessive disease of impaired copper metabolism. Previous study demonstrated that WD with corpus callosum abnormalities (WD-CCA) was limited to the posterior part (splenium). This study aimed to compare clinical features between WD-CCA and WD without corpus callosum abnormalities (WD-no-CCA). Forty-one WD patients who had markedly neurological dysfunctions were included in this study. We retrospectively reviewed clinical, biochemical characteristics and MRI findings in the 41 WD patients. All patients were assessed using the Unified Wilson’s Disease Rating Scale. Nine patients had corpus callosum abnormalities, 4 of 9 patients had abnormal signal in the genu and splenium, 5 of 9 patients had abnormal signal only in the splenium. WD-CCA had longer course (9.9 ± 4.0 years vs. 3.4 ± 3.6 years, p<0.01), more severe neurological dysfunctions (37.6 vs. 65.9, p<0.01) and higher psychiatric symptoms scores (11.2 vs. 22.5, p<0.01) than WD-no-CCA. The MRI findings indicated that WD-CCA had higher ratio than WD-no-CCA in globus pallidus (88.9% vs. 43.8%, p = 0.024) and thalamus (100% vs. 59.4%, p = 0.038). The index of liver function and copper metabolism had no significant in WD-CCA and WD-no-CCA patients. Our findings indicate Wilson’s disease can involve the posterior as well as the anterior part of CC and patients with CC involvement had more extensive brain lesions, more severe neurological dysfunctions and psychiatric symptoms.

目的 探讨肝豆状核变性(WD)肝硬化失代偿期患者的预后及影响预后的相关因素.方法 回顾性分析2012年10月至2015年12月住院的67例WD合并肝硬化失代偿期患者的临床资料,根据生存结局分为存活组和死亡组,比较两组一般资料、生化指标、并发症、Child-Turcotte-Pugh(CTP)分值、终末期肝病模型(MELD)分值.结果 死亡组患者16例,存活组患者51例,死亡组患者白蛋白(ALB)、胆碱酯酶(CHE)、血清钠均较存活组患者低,BMI、TBil、PT、国际标准比值(INR)、血氨、透明质酸(HA)、铜蓝蛋白(CP)、CTP分值、MELD分值均较存活组患者高,差异均有统计学意义(均P＜0.05);死亡组患者更容易出现中等量以上的腹水、肝性脑病(HE)(均P＜0.05);CTP分级(A级、B级、C级)及MELD分值(＜5分和＞5分)对于3年内患者的预后预测具有统计学差异(均P＜0.01);经Cox比例风险模型分析,TBil、CHE、肝性脑病是WD肝硬化失代偿期患者预后的相对独立危险因素(P＜0.05).结论 WD肝硬化失代偿期患者出现高水平TBil、低水平CHE及肝性脑病,提示预后较差,CTP系统及MELD模型均能用于评估患者的预后.

目的:观察多中心Wilson病(WD)患者在中西医结合长期驱铜治疗前后WD综合评定量表(Globle Asessment Scale,GAS)各项目评分的改变并评估其疗效,为建立疗效好、不良反应小的WD长期综合治疗方案提供循证医学依据.方法:参与研究的4个中心共纳入1001例WD确诊患者,随机分成青霉胺(PCA)组、二巯基丁二酸(DMSA)组、肝豆片组和中西医结合组(肝豆片+PCA/DMSA)4组(各组按1∶1∶1∶3平行设计,各组的条件除了治疗方案不同外,其他条件完全相同).在首次入院时、维持治疗1年时(第2次入院时)、维持治疗2年时(第3次入院时)进行GAS量表各项目(GAS-L、C、M、O项目及神经功能)评分,通过治疗前后自身比较及组间比较,评估各组患者的疗效.结果:各治疗组WD患者GAS各项目评分均较治疗前明显降低,在维持治疗2年时的疗效较维持治疗1年时更为明显,尤以中西医结合组评分改善最显著.结论:4种长期驱铜治疗方法均可改善WD患者的病情,中西医结合长期驱铜治疗的疗效更为显著,是目前WD患者长期治疗最有效的方案.

目的:了解肝豆状核变性(hepatolenticular degenemtion,HLD)下丘脑-垂体-肾上腺轴(the hypothalamic–pituitary–adrenal axis,HPA)分泌功能.方法:选取未经治疗的HLD患者组45例和健康对照组25例,用化学发光免疫分析法分别测定血浆中促肾上腺皮质激素(adrenocorticotropic hormone,ACTH)、血清皮质醇(COR)、24h尿游离皮质醇(UFC),用比色法测24小时尿17-羟皮质类固醇(17-hydroxy-cortico-steroid,17-OHCS)、17-酮类固醇(17-ketos-teroide,17-KS),比较两组之间上述指标有无差异.并对10例患者进行ACTH刺激试验,比较刺激前后COR、17-OHCS、血嗜酸性粒细胞计数.结果:未经治疗的HLD患者组ACTH、COR,24hUFC,17-OHCS、17-KS均明显低于正常组,10例HLD患者ACTH刺激试验,刺激后COR、17-OHCS、血嗜酸性粒细胞计数均明显升高,显示肾上腺对外源性ACTH的刺激反应活跃.结论:HLD患者垂体分泌功能下降并存在继发性肾上腺皮质功能减退.

总结了40例肝豆状核变性(WD)患者继发口腔真菌感染的临床特点及“三黄液”口腔护理的疗效.15例为WD肝硬化失代偿患者,25例为WD脑型患者,WD脑型患者均有假性球麻痹表现.使用“三黄液”口腔护理,5d治愈率为12.5％,10d治愈率为65％,15d治愈率为95％.认为WD肝硬化失代偿及WD脑型患者更易合并口腔真菌感染,使用“三黄液”口腔护理能有效治疗WD患者口腔真菌感染.

Objective To investigate the correlation between self -efficacy and the life quality in patients with Wilson ’ s disease ( WD).Methods TheGeneral Self-Efficacy Scale ( GSES) and the WHO Quality of Life Scale ( WHOQOL-BREF) were used for inves-tigation among 215 WD patients as WD group and 190 healthy people as the control group in order to study the correlation between self -effi-cacy and the life quality in patients with WD.Results According to GSES,the score in WD group was significantly lower than that in the control group (2.344 ±0.4978 vs.2.611 ±0.4912,t=5.407, P<0.05).According to WHOQOL -BREF, the total score in WD group was significantly lower than that in the control group (76.46 ±13.20 vs.91.26 ±16.95,t=9.835, P<0.05),so it was with all the items of the life quality scale ( P<0.05 ).The score on the self-efficacy had the positive correlation with that of the total score on the life quality to-gether with items ( P<0.05 ).Conclusion The self-efficacy and life qualityin patients with Wilson ’ s disease are significantly lower than those for healthy people.Their self-efficacy is positively related with the quality of life , which means the better self -efficacy they have , the better their quality of life is.

Objective To assess the clinical features of Wilson disease ( WD ) patients with freezing of gait ( FOG) , in order to facilitate recognition of the WD with FOG.Methods The age, course of disease, clinical symptoms characteristics, imaging features, apeutic efficacy of 25 cases of WD with FOG were analyzed.Results Twenty-five patients with WD with FOG offen onset in youth, and have long course of the disease.The gait movement in 25 patients had difficulty in starting, turning to, but smoothly when the obstacle was encountered, usually associated with severe dystonia and cirrhosis. The other clinical features included speech disorders, multiple abnormal involuntary movements, psychiatric symptoms, etc.MRI findings showed that the symmetrical abnormal signal of bilateral lenticular nucleus, brain stem ( midbrain, pons) , thalamus, part of it had cerebral cortex atrophy. After short-term treatment of copper-cleaning agents combined with bromocriptine, Piribedil sustained-release tablets, FOG could be improved in 18 cases, the effective rate was 72%.And clozapine was added in patients with no obvious improvement, and then 4 cases improved, the total effective rate was 88%.Conclusions WD with FOG is later than other types of WD in age of onset.FOG is rare in the onset of WD patients, and offen associated with multiple focal and generalized dystonia.Treatment of copper-cleaning agents combined with dopamine receptor agonists and clozapine have effect on WD with FOG in short term.

Objective:To study the clinical significance of electroencephalograms(EEG) in patients with hepatolenticular degeneration(HD) known as Wilson’s disease and hepatic encephalopathy(HE) . Methods:EEG data of 26 cases was retrospectively analyzed .Results:EEG abnormalities with the clinical stages of hepatic encephalopathy have a significant relationship ,and the more severe clinical symptoms , the more EEG changes .Conclusion:EEG can be used as a diagnostic indicator and an important means of monitoring changes in the condition of patients with HE .