Role of the globus pallidus in motor and non-motor symptoms of Parkinson's disease

The globus pallidus plays a pivotal role in the basal ganglia circuit. Parkinson's disease is characterized by degeneration of dopamine-producing cells in the substantia nigra, which leads to dopamine deficiency in the brain that subsequently manifests as various motor and non-motor symptoms. This review aims to summarize the involvement of the globus pallidus in both motor and non-motor manifestations of Parkinson's disease. The firing activities of parvalbumin neurons in the medial globus pallidus, including both the firing rate and pattern, exhibit strong correlations with the bradykinesia and rigidity associated with Parkinson's disease. Increased beta oscillations, which are highly correlated with bradykinesia and rigidity, are regulated by the lateral globus pallidus. Furthermore,bradykinesia and rigidity are strongly linked to the loss of dopaminergic projections within the cortical-basal ganglia-thalamocortical loop. Resting tremors are attributed to the transmission of pathological signals from the basal ganglia through the motor cortex to the cerebellum-ventral intermediate nucleus circuit. The cortico–striato–pallidal loop is responsible for mediating pallidi-associated sleep disorders. Medication and deep brain stimulation are the primary therapeutic strategies addressing the globus pallidus in Parkinson's disease. Medication is the primary treatment for motor symptoms in the early stages of Parkinson's disease, while deep brain stimulation has been clinically proven to be effective in alleviating symptoms in patients with advanced Parkinson's disease,particularly for the movement disorders caused by levodopa. Deep brain stimulation targeting the globus pallidus internus can improve motor function in patients with tremordominant and non-tremor-dominant Parkinson's disease, while deep brain stimulation targeting the globus pallidus externus can alter the temporal pattern of neural activity throughout the basal ganglia–thalamus network. Therefore, the composition of the globus pallidus neurons, the neurotransmitters that act on them, their electrical activity,and the neural circuits they form can guide the search for new multi-target drugs to treat Parkinson's disease in clinical practice. Examining the potential intra-nuclear and neural circuit mechanisms of deep brain stimulation associated with the globus pallidus can facilitate the management of both motor and non-motor symptoms while minimizing the side effects caused by deep brain stimulation.

Procedural learning changes in patients with Wilson's disease

In the present study, we compared explicit memory performance, using the Wechsler Memory Scale and implicit memory performance, using the Nissen software version of the serial reaction time task, in patients with Wilson＇s disease to normal controls. The Wilson＇s disease patients exhibited deficits in explicit memory tasks, such as figure recall and understanding memory. Moreover, the Wilson＇s disease patients exhibited deficits in implicit memory tasks, including significantly prolonged response times. These findings indicate that Wilson＇s disease patients have explicit and implicit partial memory impairments.

Adenyl cyclase activator forskolin protects against Huntington's disease-like neurodegenerative disorders

Long term suppression of succinate dehydrogenase by selective inhibitor 3-nitropropionic acid has been used in rodents to model Huntington＇s disease where mitochondrial dysfunction and oxidative damages are primary pathological hallmarks for neuronal damage. Improvements in learning and memory abilities, recovery of energy levels, and reduction of excitotoxicity damage can be achieved through activation of Adenyl cyclase enzyme by a specific phytochemical forskolin. In this study, intraperitoneal administration of 10 mg/kg 3-nitropropionic acid for 15 days in rats notably reduced body weight, worsened motor cocordination（grip strength, beam crossing task, locomotor activity）, resulted in learning and memory deficits, greatly increased acetylcholinesterase, lactate dehydrogenase, nitrite, and malondialdehyde levels, obviously decreased adenosine triphosphate, succinate dehydrogenase, superoxide dismutase, catalase, and reduced glutathione levels in the striatum, cortex and hippocampus. Intragastric administration of forskolin at 10, 20, 30 mg/kg dose-dependently reversed these behavioral, biochemical and pathological changes caused by 3-nitropropionic acid. These results suggest that forskolin exhibits neuroprotective effects on 3-nitropropionic acid-induced Huntington＇s disease-like neurodegeneration.

A review of computational modeling and deep brain stimulation:applications to Parkinson’s disease

Biophysical computational models are complementary to experiments and theories,providing powerful tools for the study of neurological diseases.The focus of this review is the dynamic modeling and control strategies of Parkinson’s disease(PD).In previous studies,the development of parkinsonian network dynamics modeling has made great progress.Modeling mainly focuses on the cortex-thalamus-basal ganglia(CTBG)circuit and its sub-circuits,which helps to explore the dynamic behavior of the parkinsonian network,such as synchronization.Deep brain stimulation(DBS)is an effective strategy for the treatment of PD.At present,many studies are based on the side effects of the DBS.However,the translation from modeling results to clinical disease mitigation therapy still faces huge challenges.Here,we introduce the progress of DBS improvement.Its specific purpose is to develop novel DBS treatment methods,optimize the treatment effect of DBS for each patient,and focus on the study in closed-loop DBS.Our goal is to review the inspiration and insights gained by combining the system theory with these computational models to analyze neurodynamics and optimize DBS treatment.

Longitudinal observation of ten family members with idiopathic basal ganglia calcification: A case report

BACKGROUND Familial idiopathic basal ganglia calcification (FIBGC) is a rare autosomal dominant disorder that causes bilateral calcification of the basal ganglia and/or cerebellar dentate nucleus, among other locations. CASE SUMMARY The aim of this study is to report 10 cases of FIBGC observed in a single family. Seven patients showed calcification on their computed tomography scan, and all of these patients carried the SLC20A2 mutation. However, individuals without the mutation did not show calcification. Three patients among the 7 with calcification were symptomatic, while the remaining 4 patients were asymptomatic. Additionally, we longitudinally observed 10 subjects for ten years. In this paper, we mainly focus on the clinical course and neuroradiological findings in the proband and her son.CONCLUSION The accumulation of more case reports and further studies related to the manifestation of FIBGC are needed.

Idiopathic basal ganglia calcification associated with new MYORG mutation site:A case report

BACKGROUND Idiopathic basal ganglia calcification(IBGC)is a neurodegenerative disease characterized by symmetrical calcification of basal ganglia and other brain region,also known as Fahr’s disease.It can be sporadic or familial,and there is no definite etiology at present.With the development of neuroimaging,the number of reports of IBGC has increased in recent years.However,due to its hidden onset,diverse clinical manifestations,and low incidence,it is likely to be misdiagnosed or ignored by potential patients and their family.CASE SUMMARY We report a case of a 61-year-old man who presented with symptoms of dysphagia and alalia.His computed tomography scan of the brain revealed bilateral symmetric calcifications of basal ganglia,cerebellum,thalamus,and periventricular area.The genetic test showed a new mutation sites of MYORG,c.1438T>G mutation and c.1271_1272 TGGTGCGC insertion mutation.He was finally diagnosed with IBGC.CONCLUSION It is important to detect MYORG mutation when IBGC is suspected,especially in those without an obvious family history,for better understanding of the underlying mechanism and identifying potential treatments.

Dynamic Cerebral Microdialysis during Pallidotomy and Thalamotomy in Parkinson’s Disease: A Preliminary Neurochemical Study

In Parkinson’s disease (PD), dopaminergic neurons reduce the regulation of glutamatergic (glutamate-Glu) input from the cortex to neostriatum (caudate and putamen nuclei) consequently leading to a hyperactivity of globus pallidus internae (GPi) neurons that release gamma-amino-butyric acid (GABA) into the thalamic ventrolateral (VL) nucleus. The objective of the present experiment was to measure changes in GABA and Glu in the caudate and the thalamus of 2 patients during the application of electrical stimuli following either a pallidotomy or a thalamotomy. Proper insertion of the electrode was tested by applying high frequency electrical pulses (HFEP). During these procedures, we obtained neurochemical information placing cerebral (CMD) microdialysis probes in caudate nucleus and VL nucleus of ipsi- and contra-lateral thalamus. In VL thalamus, extracellular GABA decreased during HFEP, tending to reach previous levels once HFEP was finalized. Following the pallido- or thalamotomy GABA decreased again. Similarly, in the contralateral VL thalamus, extracellular GABA levels showed a similar but less pronounced profile but did not show any decrement after the lesion. Caudate Glu decreases when HFEP is applied to the GPi and recovers to previous levels after HFEP, but did not decrease again after lesion (GPi-tomy), instead it continued to rise. These results suggest that HFEP exerts a similar but reversible biochemical effect as thermopallido- or thermothalamotomy on GABA extracellular concentration in the ipsilateral VL thalamus. We also observe a distant effect of HFEP, but not of thermolesion, on contralateral thalamic GABA and ipsilateral caudate Glu.

Temporal Aspects of Global Coherence during Discourse Production in Early Stage Parkinson’s Disease

Introduction: Parkinson’s Disease (PD) is a devastating neurodegenerative disease that significantly influences motor performance. Recent studies suggest expressive language deficits may also exist among individuals with PD even though the condition is primarily known for changes in motor skills. The purpose of this pilot study was to examine the influence of early stage PD on global coherence or the ability to maintain consistency of a theme or topic. Methods: Discourse samples were collected from eleven individuals with PD and compared to eleven matched controls to examine measures of global coherence. Two-minute speech samples describing a “typical day” were transcribed and rated on mean global coherence and percentage high global coherence. Results: Greater declines in global coherence were observed among individuals with PD, however, comparisons of both mean global coherence ratings and percentage high global coherence were not statistically significant between the two groups. A significant downward linear trend was observed for both mean global coherence ratings and percentage high coherence among all participants indicating decreases in global coherence over time. Conclusion: Approaches to the study of global coherence as a measure of expressive language performance should consider the temporal changes especially among neurological conditions known to reduce expressive language ability.

HBGH患者血清CGN、SDC-1水平与病情及疾病转归的关系

目的 探讨血清扣带蛋白(CGN)、多配体聚糖-1(SDC-1)水平与高血压性基底节脑出血(HBGH)患者病情及疾病转归的关系。方法 选取2019年2月至2022年2月连云港市第二人民医院(下称该院)收治的123例HBGH患者为研究对象,另选择该院同期行健康体检的体检健康者120例为健康组。检测两组纳入对象血清CGN、SDC-1表达水平。根据疾病转归情况将患者分为好转组92例,恶化组31例。采用受试者工作特征(ROC)曲线及曲线下面积(AUC)分析血清CGN、SDC-1表达水平对HBGH患者疾病转归的预测价值。结果 重度组血清CGN、SDC-1表达水平均高于中度组、轻度组,且中度组血清CGN、SDC-1表达水平均高于轻度组,差异有统计学意义(P<0.05),3组HBGH患者血清CGN、SDC-1表达水平均高于健康组,差异有统计学意义(P<0.05)。恶化组血清CGN、SDC-1表达水平高于好转组,差异有统计学意义(P<0.05)。血清CGN、SDC-1预测HBGH患者疾病转归的AUC分别为0.742(95%CI:0.792~0.697)、0.861(95%CI:0.906~0.910),两者联合预测的AUC为0.917(95%CI:0.962~0.870)。恶化组出血量、破入脑室情况明显高于好转组,入院格拉斯哥昏迷量表(GCS)评分低于好转组,差异有统计学意义(P<0.05)。多因素Logistic回归分析显示,血清CGN≥51.63 pg/mL(OR=3.815)、血清SDC-1≥450.67μg/L(OR=4.230)、入院GCS评分≤8分(OR=5.333)是HBGH患者疾病转归的影响因素(P<0.05)。结论 血清CGN、SDC-1表达水平升高与HBGH患者病情加重、疾病转归恶化密切相关,二者对HBGH患者疾病转归具有一定预测价值。

体位性低血压与脑小血管病综合评分的相关性研究

目的探究脑小血管病(cerebral small vessel disease,CSVD)患者体位性低血压(orthostatic hypotension,OH)的有无及其类型与CSVD综合评分之间的关系。方法连续入组2021年3月至2023年9月期间的CSVD住院患者460例,根据有无OH及不同OH亚型将所有受试者分为无OH组、早期OH(early OH,EOH)组及延迟/持续OH(delayed/prolonged OH,DPOH)组。采用0~4分的五分制评分方法评估CSVD综合评分。分别分析不同OH分组与腔隙、脑白质高信号(white matter hyperintensities,WMH)评分、脑微出血(cerebral microbleeds,CMBs)、基底节区血管周围间隙(basal ganglia-perivascular spaces,BG-PVS)及CSVD综合评分的相关性。结果入组患者中EOH和DPOH的发生率分别为10.00%和17.17%。各组间存在腔隙的比例、BG-PVS等级及CSVD综合评分的分布差异有统计学意义(P<0.01),校正年龄、性别、高血压及卧位舒张压后,DPOH是腔隙(OR=2.421,95%CI:1.372~4.271,P=0.002)、严重BG-PVS(OR=1.714,95%CI:1.074~2.740,P=0.024)及更高CSVD综合评分(OR=1.791,95%CI:1.140~2.818,P=0.012)的独立危险因素。结论在CSVD患者中,DPOH较EOH更多见,且是CSVD综合评分增加的独立危险因素。

假性甲状旁腺功能减退症致Fahr综合征一例

患者男性,19岁,因发作性意识丧失伴四肢抽搐10年,加重1月余,于2022年4月15日入院。患者入院前10年无明显诱因突发意识丧失后摔倒,伴四肢强直性抽搐、双眼上翻、牙关紧闭,2~3 min后自行缓解,无舌咬伤、大小便失禁,无恶心、呕吐,此后1个月内发作2次,当地医院诊断为“癫痫”,予丙戊酸钠(具体剂量不详)口服,规律服药期间每年发作1~2次;3年前调整药物为丙戊酸镁0.25 g/晚口服,仍每年发作1~2次;1个月前癫痫发作频率增加,1个月内发作2次,外院头部CT显示双侧额叶灰白质交界区、基底节区多发对称性钙化灶(图1)。

内侧苍白球的神经元分型及其在运动障碍相关疾病中功能的研究进展

基底神经节在运动调控中起重要作用,内侧苍白球是基底神经节的重要输出核团之一,其功能异常可导致运动障碍相关疾病(如帕金森病),并可作为临床治疗的靶核团。内侧苍白球神经元根据形态、标志物、神经递质与受体不同分为不同的亚群,其分布和生理功能也有所不同。不同神经元亚群接受纹状体、外侧苍白球和丘脑底核等上游神经核团的输入,下游主要投射到外侧缰核和丘脑。由此形成具有神经元亚群特异性介导的神经通路,并在运动调控和运动障碍相关疾病如帕金森病及非运动症状中起重要作用。这为基底节在运动和非运动功能调控及其疾病治疗方面提供了新的研究视角,本研究对此进行综述。

正常和帕金森病患者基底神经节的转录差异分析

目的分析人基底神经节各核团的分子标志物以及不同核团间、不同性别、疾病相关的差异表达,探讨差异表达基因的生物学功能。方法针对来源于10具人尸脑45个基底神经节核团样本,按是否有神经疾病分为对照组和帕金森病组,对照组按性别分为女性和男性组,提取各样本RNA进行高通量转录组测序。生物信息学分析鉴定对照组各核团的分子标志物、不同核团间、不同性别以及帕金森病相关的差异表达基因,并对差异表达基因进行基因富集分析和功能注释。结果测序分析发现,top差异表达基因包含尾状核的DRD1、FOXG1、FAM183A;黑质的SLC6A3、EN1、SLC18A2、TH;苍白球的MEPE、FGF10;底丘脑的SLC17A6、PMCH、SHOX2等。其中,壳核top差异表达基因与尾状核存在部分重叠,如DRD1、FOXG1等。对照组不同核团间鉴定出大量差异表达基因,尾状核与苍白球间存在数量最多的差异表达基因(9321),其次是壳核与苍白球间(6341),尾状核与黑质间(6054)。黑质与底丘脑间存在数量最少的差异表达基因(44)。基因富集分析发现,尾状核与苍白球间下调基因显著富集在神经元髓鞘形成、细胞迁移调节等;壳核与苍白球上调基因富集在化学突触传递、膜电位调节、金属离子转运、神经递质转运等,而下调基因富集在神经元髓鞘形成、细胞黏附等;尾状核与黑质上调基因富集在化学突触传递、轴突传导等,而下调基因富集在神经元髓鞘形成等。另外,尾状核、壳核、黑质、苍白球和底丘脑分别鉴定到性别差异上调基因468、548、1402、333和341个,以及下调基因756、988、2532、444和1372个。基因富集分析发现,上调基因大多富集在免疫反应相关通路,下调基因富集在化学突触传递等。最后,尾状核、壳核、黑质、苍白球和底丘脑分别鉴定出帕金森病特异上调基因709、852、276、507和416个,以及下调基因830、2014、1218、836和1730个。基因富集分析发现,上调基因大多富集在凋亡信号调节,下调基因大多富集在化学突触传递、动作电位调节等。结论我们发现并分析了人基底神经节不同核团的分子标志物、核团间差异、性别差异和帕金森病的相关差异。

Properties of oscillatory neuronal activity in the basal ganglia and thalamus in patients with Parkinson’s disease

Background:The cardinal features of Parkinson’s disease(PD)are bradykinesia,rigidity and rest tremor.Abnormal activity in the basal ganglia is predicted to underlie the mechanism of motor symptoms.This study aims to characterize properties of oscillatory activity in the basal ganglia and motor thalamus in patients with PD.Methods:Twenty-nine patients with PD who underwent bilateral or unilateral electrode implantation for subthalamic nucleus(STN)DBS(n=11),unilateral pallidotomy(n=9)and unilateral thalamotomy(n=9)were studied.Microelectrode recordings in the STN,globus pallidus internus(GPi)and ventral oral posterior/ventral intermediate of thalamus(Vop/Vim)were performed.Electromyography of the contralateral limbs was recorded.Single unit characteristics including interspike intervals were analyzed.Spectral and coherence analyses were assessed.Mean spontaneous firing rate(MSFR)of neurons was calculated.Analysis of variance and χ^(2) test were performed.Results:Of 76 STN neurons,39.5% were 4–6 Hz band oscillatory neurons and 28.9% were β frequency band(βFB)oscillatory neurons.The MSFR was 44.2±7.6 Hz.Of 62 GPi neurons,37.1% were 4–6 Hz band oscillatory neurons and 27.4% were βFB neurons.The MSFR was 80.9±9.6 Hz.Of 44 Vop neurons,65.9% were 4–6 Hz band oscillatory neurons and 9%were βFB neurons.The MSFR was 24.4±4.2 Hz.Of 30 Vim oscillatory neurons,70% were 4–6 Hz band oscillatory neurons and 13.3% were β FB neurons.The MSFR was 30.3±3.6 Hz.Further analysis indicated that proportion of βFB oscillatory neurons in STN and GPi was higher than that of similar neurons in the Vop and Vim(P<0.05).Conversely,the proportion of 4–6 Hz band oscillatory neurons and tremor related neurons in the Vim and Vop was higher than that of STN and GPi(P<0.05).The highest MSFR was for GPi oscillatory neurons whereas the lowest MSFR was for Vop oscillatory neurons(P<0.005).Conclusion:The alterations in neuronal activity in basal ganglia play a critical role in generation of parkinsonism.β oscillatory activity is more prominent in basal ganglia than in thalamus suggesting that the activity likely results from dopaminergic depletion.While both basal ganglia and thalamus have tremor activity,the thalamus appears to play a more important role in tremor production,and basal ganglia β oscillatory activity might be the trigger.

缺血性脑卒中的中医治疗的研究进展

缺血性脑卒中(IS)是一种常见的脑血管疾病,由于其高致残率、高复发率、高死亡率的特点,患者生命健康和生存质量受到严重危害。近年来中医疗法广泛应用于IS的临床治疗中,且取得良好效果。本文对近年IS的中医治疗的研究进展作一综述。

帕金森病动作语言障碍及相关神经联动机制研究进展

动作语言涉及运用与动作概念有关的词汇进行语言活动的行为。在动作语言加过程中,额叶皮质会将储存的运动相关信息投射到基底节,基底节进行信息处理并与颞叶储存的概念和语义信息整合后,再投射回额叶皮质,实现动词内在动作意义激活。帕金森病的病理基础是基底节损伤,患者在早期认知功能尚可时就可能出现动作语言处理不同程度的受损。本文通过对帕金森病动作语言相关的神经基础机制研究进行回顾和总结,以期为现有的帕金森病临床语言康复提供新的思路和启示。

异动症的发病机制研究进展

中国帕金森病患者数量居世界首位,是目前亟需解决的沉重负担。帕金森病目前尚无有效治疗措施,半个世纪以来,以左旋多巴制剂为主的多巴胺替代疗法一直是帕金森病治疗的“金标准”,但在短暂的治疗蜜月期后,可导致基底神经节代谢通路功能异常而诱发异动症,致使帕金森病症状更难控制并可能致残,严重损害患者的精神和生活质量。异动症的病理生理学机制非常复杂,涉及神经元机制和非神经元机制。该文综述了异动症发病机制的研究进展,并探讨了左旋多巴神经元毒性的争议,为帕金森病/异动症的治疗方案提供科学理论和干预思路。

心率变异性与扩大的血管周围间隙脑部分布关系研究

背景扩大的血管周围间隙(EPVS)与认知功能障碍、情感障碍、脑卒中及卒中后不良结局等密切相关,尽早发现并给予处理极为重要。目的探讨心率变异性(HRV)与EPVS脑部分布之间的关系。方法选取2020年1月至2022年5月在郑州大学第二附属医院神经内科住院治疗并完成24 h动态心电图监测和脑部核磁共振(MRI)的患者199例为研究对象。评估患者EPVS负荷,根据EPVS分数对基底节区EPVS(BG-EPVS)及半卵圆中心EPVS(CS-EPVS)严重程度进行分组:轻度BG-EPVS组(Potter评分1分,126例)、中度BG-EPVS组(Potter评分2分,46例)、重度BG-EPVS组(Potter评分3~4分,27例);轻度CS-EPVS组(Potter评分1分,131例)、中度CSEPVS组(Potter评分2分,45例)、重度CS-EPVS组(Potter评分3~4分,23例)。根据BG-EPVS与CS-EPVS数量划分EPVS优势模型:模型1(BG>CS,119例)、模型2(BG=CS,20例)、模型3(BG<CS,60例)。比较各组的一般资料与HRV指标,采用Spearman秩相关分析探讨HRV指标与EPVS的相关性,将单因素分析中有统计学意义的HRV指标纳入多因素Logistic回归分析探讨EPVS严重程度及优势模型的独立影响因素。结果轻、中、重度BGEPVS组患者年龄、目标区间内正常间隔连续差的均方根(rMSSD)、总功率(TP)比较,差异有统计学意义(P<0.05);其中重度BG-EPVS组年龄高于轻度BG-EPVS组(P<0.05),重度BG-EPVS组rMSSD、TP低于轻度BG-EPVS组(P<0.05)。Spearman秩相关分析结果显示,HRV指标中的rMSSD、>50 ms的相邻正常间隔的百分比(PNN50)、TP与BG-EPVS严重程度呈负相关(r_(s)=-0.357、-0.153、-0.169,P<0.05);目标区间内每5 min正常间隔标准差的平均值(SDNNindex)、rMSSD与EPVS优势模型呈正相关(r_(s)=0.155、0.262,P<0.05)。校正混杂因素后的多因素Logistic回归分析结果显示,rMSSD是BG-EPVS严重程度的独立影响因素〔OR=0.983,95%CI(0.972,0.994),P=0.002〕;rMSSD是EPVS优势模型的独立影响因素〔OR=1.017,95%CI(1.006,1.028),P=0.003〕。结论rMSSD分别与BG-EPVS严重程度、优势模型呈负相关和正相关,是BG-EPVS严重程度及EPVS优势模型的独立影响因素,提示rMSSD下降时自主神经系统失衡,可能引起血脑屏障破坏或脑中代谢废物清除减少,rMSSD参与BG-EPVS形成的病理生理学机制。

纹状体神经元在运动启动中的作用

适时、适度的运动启动对于我们的日常生活至关重要。纹状体(striatum)作为基底节神经环路的主要输入核团在运动启动(movement initiation)过程中发挥重要的调节作用,其损伤往往会导致运动障碍性疾病。因此本文围绕纹状体神经元在运动启动中的重要作用机制以及目前常用的运动启动评价方式进行综述,概括了多种运动模型理论依据及不足,并以此为基础提出一种新模型来解释纹状体神经元对运动启动的调控作用,为运动启动相关障碍性疾病的机制研究拓宽思路。

获得性肝脑变性1例

目的探讨获得性肝脑变性的诊断及治疗方法。方法2021年2—3月于蚌埠市第三人民医院就诊的获得性肝脑变性1例,对其进行病例分析,结合相关文献探讨该病诊断和治疗方法。结果男性,56岁,因“言语不清伴右肢无力1年,加重伴步态不稳半年”入院。既往有肝硬化、脾脏切除术史多年。头颈磁共振可见大脑脚及丘脑区对称性短TI信号影,颈髓内长T2影。血微量元素:全血锰44.1μg/L↑,全血锌3.54 mg/L↓,全血铁241.82μg/L↓。血氨:69μmol/L。诊断为获得性肝脑变性,予以保肝、对症治疗,病人症状好转出院。结论获得性肝脑变性起病隐匿,临床上容易被神经内科医师所忽视,诊断需结合其慢性肝病史、神经系统体征、头颅磁共振特征性表现以及血微量元素测定等综合判定。其治疗目前仍缺乏有效手段,治疗原发病、控制慢性肝病是基础。