ObjectiveIn patients with multiple system atrophy (MSA), the hot cross bun sign (HCBS) has been associated with disease severity in MSA. This study is aimed at investigating the prevalence of HCBS and its potential risk factors in Chinese MSA patients.Materials and MethodsA total of 175 MSA patients who met "possible" or "probable" diagnostic criteria were included in this cross-sectional study. The Unified MSA Rating Scale (UMSARS), Nonmotor Symptoms Scale (NMSS), Hamilton Depression Rating Scale-17 (HDRS-17), Hamilton Anxiety Scale (HAMA), and Montreal Cognitive Assessment (MoCA, permission has been granted) were compared between MSA patients with and without HCBS (defined as pontine cruciform hyperintensity on T2-weighted fluid-attenuated inversion recovery [T2-FLAIR] sequences). Binary logistic regression analysis was used to identify the independent risk factors for the presence of HCBS.ResultsHCBS was identified in 110 of 175 patients (62.86%). Univariate analysis revealed significant relationships between HCBS and female, cerebellar subtype, REM sleep behavior disorder (RBD), higher UMSARS-IV score, and moderate-to-severe white matter hyperintensities (WMHs). The occurrence of HCBS in MSA was independently associated with the MSA-C subtype (OR = 6.05, 95%CI = 2.55-14.38), RBD (OR = 2.56, 95%CI = 1.06-6.20), higher UMSARS-IV scores (OR = 2.48, 95%CI = 1.42-4.35), and moderate-to-severe WMH (OR = 4.10, 95%CI = 1.14-14.75).ConclusionsHCBS is a common neuroimaging observation in MSA patients. Our research shows that the MSA-C subtype, RBD, greater disability severity (as assessed by UMSARS-IV), and moderate-to-severe WMH are independent risk factors for HCBS. Higher UMSARS-IV scores were substantially linked to the presence of HCBS, but there was no association between the severity grade of HCBS and the degree of disability. The prevalence of HCBS and its clinical correlates in a Chinese MSA cohort are demonstrated cross-sectionally in this study, especially with regard to subtype, RBD, disability, and WMH burden.

BACKGROUND:Early differentiation of multiple system atrophy (MSA) from Parkinson's disease (PD) remains difficult, particularly within two years of symptom onset, when diagnostic uncertainty has major implications for prognosis, referral, and trial enrolment. Because MSA is rare, previous biomarker studies have often been limited by relatively small samples and restricted multicentre validation. We aimed to determine the diagnostic performance of plasma neurofilament light chain (NfL) for differentiating MSA from PD and to assess the incremental value of glial fibrillary acidic protein (GFAP), total tau (t-tau), and phosphorylated tau at threonine 217 (p-tau217). METHODS:In this multicentre cross-sectional diagnostic study, participants were enrolled from five movement-disorder referral centres in China between Jan 1, 2018, and June 30, 2024, and were divided by enrolment period into discovery and temporally separated validation datasets. Plasma NfL, GFAP, t-tau, and p-tau217 were measured using light-initiated chemiluminescence assays. Group comparisons used age- and sex-adjusted models, and discrimination was assessed using receiver-operating-characteristic analysis with sensitivity, specificity, predictive values, and robustness analyses. FINDINGS:The analysis included 2408 participants: 782 (32.5%) with PD, 796 (33.1%) with MSA, and 830 (34.5%) healthy controls. NfL was the best single biomarker for differentiating MSA from PD in the discovery dataset (AUC 0.920, 95% CI 0.903-0.936). The discovery-derived cutoff of 41.3 pg/mL yielded sensitivity of 90.5% and specificity of 83.4% in the discovery dataset, and sensitivity of 86.7% and specificity of 85.5% in the validation dataset (AUC 0.924, 95% CI 0.898-0.948). In the early-stage subgroup, NfL retained strong performance (AUC 0.943, 95% CI 0.915-0.966). Integrated multimarker models provided limited incremental discrimination over NfL alone. INTERPRETATION:Plasma NfL may support the differentiation between clinically diagnosed MSA and PD, including early in the disease course. The limited added value of multimarker panels supports a simpler and more immediately translatable NfL-first strategy for diagnostically uncertain parkinsonism. FUNDING:National Natural Science Foundation of China; the Capital's Fund for Health Improvement and Research; Beijing Natural Science Foundation; Beijing Municipal Science and Technology Commission; Beijing Neurosurgical Institute; Beijing Traditional Chinese Medicine Science and Technology Development Fund.

BackgroundPrevious experimental studies have suggested synergistic effects of Panax notoginseng saponins combined with antiplatelet agents in ischemic stroke. However, large-scale real-world clinical evidence regarding the efficacy and safety of this combination remains limited. This study aimed to explore the efficacy and safety of Xuesaitong soft capsule plus antiplatelet agents in ischemic stroke patients.MethodsThis multicenter, controlled, retrospective real-world study included 38,652 patients with ischemic stroke who received either antiplatelet agents (aspirin and/or clopidogrel) alone (control group, N = 37,249) or Xuesaitong soft capsule plus antiplatelet agents (observational group, N = 1,403). Propensity score matching (PSM) was initially performed at a 1:20 ratio (N = 1,401 in the observational group vs. N = 27,955 in the control group). A 1:4 PSM sensitivity analysis was subsequently performed to evaluate the robustness of the findings (N = 1,401 in the observational group vs. N = 5,604 in the control group).ResultsAfter 1:20 matching, the 1-year major adverse cardiovascular and cerebrovascular event (MACCE) incidence was lower in the observational group than in the control group (14.99% vs. 18.71%) (P < 0.001). The 2- and 3-year MACCE incidences showed the same trend (both P < 0.001). Subgroup analyses indicated that the reduction in 1-year MACCE incidence was greater in patients aged 45–64 years, treated within 2 weeks after stroke onset, with MACCE occurring within 1 month after treatment, and without hypertension, hyperlipidemia, or coronary heart disease (all P < 0.05). The incidence of adverse events of special interest was lower in the observational group than in the control group (18.56% vs. 21.82%) (P = 0.004). The 1:4 PSM sensitivity analysis confirmed the robustness of the findings, with lower 1-year MACCE incidence in the observational group than in the control group (14.99% vs. 18.58%) (P = 0.002).ConclusionXuesaitong soft capsule combined with antiplatelet agents is associated with lower MACCE incidence and gastrointestinal adverse events compared to antiplatelet agents alone in ischemic stroke patients.

In this study, we used the Mendelian randomization (MR) method to systematically examine whether there is a bidirectional causal relationship between amyotrophic lateral sclerosis (ALS) and Alzheimer's disease (AD), Parkinson's disease (PD), frontotemporal dementia (FTD), multiple system atrophy (MSA), and dementia with Lewy bodies (DLB). We analyzed data from 6,44,924 participants using MR to evaluate causality. We employed inverse variance weighted and MR-Egger regression tests for MR analysis. Additionally, we performed sensitivity analyses using the MR-Egger test and Mendelian Randomization Pleiotropy RESidual Sum and Outlier. The inverse variance weighted analysis found no evidence of a risk effect between ALS and the neurodegenerative diseases AD, PD, FTD, MSA, and DLB. However, the MR-Egger analysis showed that both AD (odds ratio: 1.079, 95% confidence interval: 1.017-1.145, P = .029) and PD (odds ratio: 1.210, 95% confidence interval: 1.046-1.401, P = .020) have a risk effect on ALS, indicating that AD and PD increase the risk of ALS. Our MR analysis suggests that AD and PD may have a potential causal relationship with ALS. Conversely, ALS does not appear to have a causal relationship with the other neurodegenerative diseases examined (FTD, MSA, DLB).

Spatial metabolomics is an emerging technology that integrates mass spectrometry imaging (MSI) with metabolomics, offering a novel visual perspective for traditional metabolomics analysis. This technology enables in-depth analysis in three dimensions: qualitative, quantitative, and localization of metabolites. Spatial metabolomics precisely reflects the characteristics of metabolic network changes in metabolites within entire tissues or specific micro-regions. It provides a detailed understanding of the pharmacodynamic material basis and mechanisms of action. These capabilities suggest that spatial metabolomics can offer significant technical support for studying the complex pathophysiology of mental disorders. Although the mechanisms underlying mental disorders have been reviewed multiple times, this paper provides a comprehensive comparison between traditional metabolomics and spatial metabolomics. It also summarizes the latest progress and challenges of applying spatial metabolomics to the study of mental disorders and traditional Chinese medicine.

The incidence of Neurodegenerative Diseases is on the rise, paralleling the societal trend of an aging population and the extension of the average life expectancy. NDs frequently manifest varying levels of chronic fatigue, a phenomenon whose underlying mechanisms remain obscure. This condition significantly impairs the quality of life for patients and presents a formidable challenge to our nation’s healthcare system. This paper delves into the potential mechanisms, assessments, and therapeutic approaches for Parkinson’s Disease and Multiple System Atrophy in the context of chronic fatigue. The objective of this study is to enhance the understanding of chronic fatigue in NDs, as well as to contribute to the advancement of its diagnosis and treatment methodologies.

BACKGROUND:Parkinson's disease (PD) is a common neurodegenerative disorder. The role of protein post-translational modifications (PTMs), especially small ubiquitin-like modifier (SUMO) conjugation (SUMOylation), in PD pathogenesis remains unclear. This study aimed to investigate the relationship between SUMOylation and PD. METHODS:The analysis included the GSE22491 dataset, GSE18838 dataset, and 189 SUMO related genes. Differentially expressed genes (DEGs) between the PD group and the control group were identified in GSE22491; these were then intersected with SUMO related genes to identify candidate genes. Machine learning was used to select biomarkers consistent across both datasets, which were validated in GSE6631. Further analyses included back propagation (BP) neural network analysis, enrichment analysis, immune infiltration analysis, regulatory network construction, drug prediction, and molecular docking. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to validate the biomarkers. RESULTS:An overlap analysis of 3,222 DEGs and 189 SUMO related genes identified 25 candidate genes. Subsequent validation using the GSE22491 and GSE18838 datasets narrowed these biomarkers down to SUMO3 and SEH1L, which are involved in pathways (such as the nuclear pore pathway) associated with PD. Significant positive correlations were observed between specific immune cell subtypes and both biomarkers. Based on these correlations, relevant transcription factors (ZNF394, IRF4, FOXM1, EGR1) and drugs (Cianidanol, Methylmethanesulfonate, Valproic acid) were predicted. Additionally, RT-qPCR results confirmed that SUMO3 is significantly downregulated in PD. CONCLUSION:SUMO3 and SEH1L were identified as novel biomarkers for PD, offering potential targets for early diagnosis and therapy in PD.

Multiple system atrophy (MSA) is a progressive neurodegenerative disease characterized by its aggressive nature. Its main clinical features include autonomic dysfunction, Parkinson’s disease, and cerebellar ataxia. We conducted a comprehensive review of the existing literature, exploring studies and reports related to the mechanisms and treatment of multiple system atrophy related neurogenic bladder. Our aim is to provide a detailed and up-to-date overview of its underlying pathophysiology and current therapeutic strategies. Neurogenic bladder, a common manifestation of MSA, often goes untreated or mistreated, significantly affecting patients’ quality of life. Early-stage bladder dysfunction is frequent in MSA patients and correlates with disease severity. The mechanisms of MSA related neurogenic bladder are related to the autonomic nervous system, somatic nerves, frontal cortex, brainstem, and sacral medulla center. Currently, treatment for MSA related neurogenic bladder is mainly symptomatic, and specific drugs are lacking. Further in-depth research is needed to develop more effective therapeutic options that improve patients' quality of life and reduce the risk of complications.

BACKGROUND:Dysfunction of the cholinergic system is implicated in the pathophysiology of Multiple System Atrophy (MSA). However, in vivo assessment of cholinergic pathways originating from the nucleus basalis of Meynert (NBM) and pedunculopontine nucleus (PPN), and their clinical relevance remains inadequately characterized. OBJECTIVES:To utilize diffusion MRI and free-water (FW) image model to characterize cholinergic system degeneration in MSA and examine its association with clinical features. METHODS:We included 103 MSA patients and 44 healthy controls who underwent diffusion MRI. Probabilistic tractography reconstructed three major cholinergic pathways: a medial NBM projection via cingulum, a lateral NBM projection via external capsule, and PPN-thalamus pathway. FW imaging quantified microstructural integrity using FW fraction (FWf) and corrected axial diffusivity (cAxD). These DWI-based metric were analyzed to (1) differentiate patients from controls and (2) examine the associations with clinical features in MSA. RESULTS:Compared to controls, MSA patients showed higher FWf values in both the lateral NBM and PPN-thalamus pathways. Receiver operating characteristic analysis showed that the FWf-based model best differentiated MSA from controls (AUC = 0.89 [0.76-1.00]), with PPN-thalamus FWf being the most discriminative feature. Across all three cholinergic pathways, higher FWf values were associated with longer disease duration, and PPN-thalamus FWf values specifically correlated with total Unified Multiple System Atrophy Rating Scale scores. CONCLUSION:Cholinergic pathway damage is a prominent pathological feature of MSA, with PPN-thalamus pathway showing particular vulnerability (as indicated by increased FWf) and strong clinical relevance. This FWf elevation likely related to neuronal degeneration or neuroinflammatory changes driven by α-synuclein pathology.

皮质基底节变性是一种罕见、起病隐匿的神经系统变性病,其常见的临床表现为非对称性肌强直及失用.陈志刚教授结合古代医家论述及其临床经验,提出中医脑病"脑气-脑髓-脑神"一体论的核心辨治体系,指出脑气紊乱、毒邪留滞脑髓、脑神失用是本病发生的病理基础.治法以理气、祛毒,益髓充脑为主,具有较好疗效.附1则验案以佐证.

Objective To investigate the risk factors for fatigue impairment in patients with multiple system atro-phy(MSA).Methods A total of 101 patients with MSA were enrolled,and according to the score of Fatigue Severity Scale(FSS),they were divided into non-fatigue group(<4 points)with 41 patients and fatigue group(≥4 points)with 60 patients.A binary logistic regression analysis was used to screen for the risk factors for fatigue in patients with MSA.Results There were significant differences in sex,course of disease,clinical classification,urinary retention,UMSARS-I,UMSARS-II,UMSARS-I+II,UMSARS-IV,bradykinesia,myotonia,ataxia,abnormal gait and posture,and ESS score be-tween the patients with different between fatigue levels(P<0.05).The binary logistic regression analysis showed that UMSARS-I and ESS scores were independent risk factors for fatigue in MSA patients(P<0.05).Conclusion Fatigue im-pairment in patients with MSA is caused by multiple factors,among which UMSARS-I and ESS scores are independent risk factors for fatigue in MSA.

目的 探讨脑白质高信号(WMH)严重程度与多系统萎缩(MSA)临床症状的相关性.方法 收集2017年1月至2021年12月北京中医药大学东方医院收治的85例合并WMH的MSA患者,采集患者年龄、性别、病程等一般临床资料.根据Fazekas量表对患者白质高信号进行分级,并将患者分为轻度WMH组(Fazekas量表评分≤2分)和中重度WMH组(Fazekas量表评分≥3分).应用Heohn-Yahr(H-Y)分级、统一多系统萎缩评估量表(UMSARS)评估患者运动症状,采用蒙特利尔认知评估量表(MoCA)评估认知功能,采用非运动症状量表(NMSS)评估患者非运动症状.采用Spearman相关性分析WMH与临床症状的相关性,采用多元线性回归分析WMH严重程度与NMSS和MoCA的关系.结果 与轻度WMH患者相比,中重度WMH的MSA患者起病年龄、NMSS评分更高,MoCA评分低(P＜0.05).两组间H-Y分级、UMSARS评分比较差异无统计学意义(P＞0.05).多元线性回归分析结果显示,在校正年龄、病程、卒中史、高血压、糖尿病、心脏病、吸烟、饮酒史后,WMH 对 MoCA 有负向影响(β=-1.836,95％CI:-3.452～-0.221;t=-2.264,P＜0.05),而 WMH 对NMSS评分总分无统计学影响(P＞0.05).Spearman相关性分析显示NMSS子项中心血管症状(r=0.267,P＜0.05)、睡眠/疲乏(r=0.347,P＜0.05)以及情绪/认知(r=0.225,P＜0.05)子项分数均与WMH严重程度有相关性.结论 WMH与MSA部分临床症状存在相关性,且MSA临床症状的风险程度与WMH的严重程度相关.

路易体痴呆是一种神经变性性痴呆,主要表现为波动性认知功能障碍、视幻觉及帕金森综合征.本课题组提出了从脑髓—脑神—脑气的角度辨治路易体痴呆,认为脑为髓海,根于肾,是脑的物质基础;脑神是大脑内各种精神活动的集合,包括认知、情感、思维等,是脑功能的体现;脑气则是连接脑髓和脑神的枢纽,可充脑髓,养脑神.肾虚髓空是本病发生的基础,随疾病进展,正虚邪盛,痰瘀内生,日久酝酿成毒留滞于脑,造成髓损神伤,脑气紊乱,病人出现一系列肢体运动、官窍及认知问题;病至晚期正虚积损,元神不复,造成形神衰惫.在治疗方面,以补肾益髓,养神复意,调补脑气为主,同时应在辨证过程中注意痰浊瘀毒的有无,把握好标本虚实,兼以祛毒化浊、固本培元.

目的 观察温肾健脑方治疗多系统萎缩非运动症状的临床疗效.方法 将2019 年1 月—2021 年10 月北京中医药大学东方医院诊治的60 例多系统萎缩患者随机分为治疗组和对照组各30 例.对照组维持既往抗帕金森治疗,治疗组在维持既往抗帕金森治疗的基础上给予温肾健脑方口服,2 组均治疗6 个月.观察2 组患者治疗前后非运动症状筛查量表(NMSS)、膀胱过度活动量表(OABSS)、疲乏量表(FSS)、匹兹堡睡眠质量指数量表(PSQI)评分变化,评估治疗6 个月后临床疗效.结果 2 组患者治疗前后NMSS评分比较差异均无统计学意义(P均>0.05),治疗组NMSS中尿频及夜尿增多症状明显改善(P均<0.05).治疗6 个月后,对照组中肝肾不足型患者NMSS评分明显升高(P<0.05),治疗组中肝肾不足型患者NMSS评分明显降低(P<0.05).2 组患者治疗后OABSS评分、FSS评分、PSQI评分均较治疗前明显降低(P均<0.05),且治疗组OAB-SS评分与PSQI评分明显低于对照组(P均<0.05).治疗组临床总有效率为26.7％(8/30),高于对照组的3.3％(1/30),差异有统计学意义(P<0.05).结论 温肾健脑方可以改善多系统萎缩患者尿频、夜尿增多、膀胱过度活动综合征、疲乏以及睡眠障碍,尤对肝肾不足证效果佳.

神经系统变性病是一类慢性起病、进行性发展的神经系统疾病,与神经元的丢失及损伤密切相关,因其发病机制复杂且临床表现多样,西医尚缺乏特异性的治疗手段.中医学重要理论分支络病学说,认为"初为气结在经,久则血伤入络",其研究内容涵盖了络脉病变和由络脉病变引起的继发脏腑组织病变,这与神经系统变性病从脑络病渐及全身络脉受累的病理演化过程相符.本研究通过回顾络的起源与分类,并从络探讨神经系统变性病的病因病机,总结以络病学说为指导治疗神经系统变性病的方法和用药规律,以期为中医临床论治神经系统变性病提供新的思路和指导.

线粒体脑肌病是一种罕见、累及多系统的致命性神经系统疾病.陈志刚教授结合古人论述及临床经验,提出以脑气、脑髓、脑神经损伤为中心的线粒体脑肌病的核心病机体系,指出脑气不足、脑气紊乱是线粒体脑肌病发生的基础;虚气留滞导致伏邪内生,痰、瘀、毒邪阻遏脑髓进而影响脑髓功能;脑髓失养而脑神失用,表现为精神、智能障碍.治疗上采用补益脑气、益精填髓、充养脑神为主.本研究从脑气-脑髓-脑神多角度阐述线粒体脑肌病的临床特点.

目的 采用Meta分析法探讨解毒通络疗法治疗脑卒中的有效性及安全性.方法 计算机检索中国知网、万方数据知识服务平台、维普网、中国生物医学文献数据库、PubMed、Embase、the Cochrane Library中公开发表的解毒通络疗法治疗脑卒中有效性及安全性的随机对照试验,检索时限为2011 年1 月—2023 年1 月.对照组采用常规西医治疗,治疗组在对照组基础上采用解毒通络疗法.采用RveMan 5.3 统计学软件进行Meta分析.结果 最终纳入文献14 篇,共包含1 572 例患者.Meta分析结果显示,治疗组有效率高于对照组[RR =1.22,95%CI(1.16,1.29),P<0.001].治疗组治疗后美国国立卫生研究院卒中量表(NIHSS)评分低于对照组[MD =-2.38,95%CI(-2.64,-2.12),P<0.001];治疗组缺血性脑卒中[MD =-2.36,95%CI(-2.65,-2.08)、出血性脑卒中[MD =-2.46,95%CI(-3.07,-1.84)]NIHSS评分均低于对照组(P<0.001).治疗组治疗后日常生活活动能力量表(ADL)评分高于对照组[MD =8.93,95%CI(6.83,11.02)],血清超敏C反应蛋白[MD =-2.22,95%CI(-2.60,-1.85)]、总胆固醇[MD =-0.33,95%CI(-0.49,-0.17)]、三酰甘油[MD =-0.16,95%CI(-0.25,-0.06)]、低密度脂蛋白胆固醇[MD =-0.33,95%CI(-0.43,-0.22)]水平低于对照组(P<0.01).仅2 篇文献报道了轻度不良反应,且样本量较少.对纳入文献的NIHSS评分、ADL评分采用逐一剔除法进行敏感性分析,合并效应量值并未发生较大改变,提示本研究结果较稳定.结论 现有证据表明在常规西医基础上加用解毒通络疗法治疗脑卒中的疗效显著,可有效改善患者神经功能及血脂,减轻炎性反应,提高患者日常生活活动能力,且具有一定安全性.

正常的步态功能是一个由感觉、认知及运动功能共同参与的过程,需将外部感觉信息和涉及皮质、皮质下、脑干及脊髓结构的神经网络相结合[1-2].步态随着年龄的增加而逐渐下降,并预示着认知功能下降、跌倒和死亡的风险[3-4].脑小血管病( cer-ebral small vessel disease, CSVD )系指由颅内小动脉、小静脉、穿支动脉及毛细血管等小血管的结构或功能性病变所致的综合征.其影像学诊断标准包括以下几点,如脑白质高信号( white matter hyperinten-sity,WMH)、近期皮质下小梗死、腔隙、血管周围间隙、脑微出血和脑萎缩[5].

目的 运用数据挖掘方法分析中医药治疗脑卒中后抑郁的病因病机、用药规律.方法 收集中国知识资源总库(CNKI)、万方数据知识服务平台(Wanfang Data)、维普中文期刊服务平台(VIP)、中国生物医学文献数据库(CBM)自建库起至2021年7月中医药治疗脑卒中后抑郁的相关文献,以统一标准录入Microsoft Excel构建规范化数据库,通过SPSS 20.0、IBM SPSS Modeler 18.0软件进行数据挖掘,统计药物及其四气、五味、归经的频次,并分析研究用药规律.结果 本研究共纳入306篇文献,使用中药方315次.共有154首方剂,常用方剂包括柴胡舒肝散、柴胡龙骨牡蛎汤、逍遥散、血府逐瘀汤、补阳还五汤、丹栀逍遥散、归脾汤、解郁通络汤等.共涉及181味中药,高频药物(频次≥30)共计33味,主要包括柴胡、甘草、川芎、郁金、当归、白芍、茯苓、石菖蒲、半夏、香附、陈皮等.药性以温性为主,药味以辛、苦、甘为多,归经以肝经、脾经、肺经为主,药物功效分析显示排名前三位为补虚药、活血化瘀药、理气药.关联规则分析获得二项关联规则22条、三项关联规则119条,聚类分析获得3个核心聚类群.结论 脑卒中后抑郁与肝、脾、肺密切相关,正虚是其病因基础,主要病机是血瘀气郁、痰阻窍闭、正虚风动,以扶正祛邪、气血兼顾为指导原则,多采用活血化瘀行气、开窍化痰息风、清热安神补虚之法,为中医药治疗脑卒中后抑郁提供了参考方案.

快速眼动睡眠行为障碍(RBD)是以快速眼动(REM)期发生的肌肉迟缓丧失及异常行为为特征的疾病,主要表现为REM期肌肉失迟缓,出现与生动梦境相关的异常肢体活动.西医治疗方法主要包括氯硝西泮和褪黑素,但其治疗作用有限.中医方面对于本病的认识尚不明确,陈志刚教授结合临床经验,认为本病发病与肾相关,当从脑髓-神-气体系探讨核心病机.其中脑髓是基础结构,脑气是维持脑功能活动的物质之一,脑神是脑功能的外在体现,脑髓损伤,脑气不足,则神乱梦魇.本文基于脑髓-神-气体系,探讨本病中医病机,为中医药诊疗提供思路和参考.