神经康复和脑卒中课件.pptx

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1、神经康复和脑卒中神经康复定义1.康复医学（rehabilitation medicine）：残疾和功能障碍的预防、诊断评估、功能修复、治疗和处理2.神经康复（neurorehabilitation）：神经系统疾病所致障碍的康复预防、康复评定和康复治疗；包括感觉、运动、自主神经和高级神经功能障碍的康复西方康复概念的演变1.康复概念起源n 古希腊希波克拉底（Hippocrates，460337 BC）时代n 中世纪欧洲“rehabilitation”指教徒因触犯戒律而被驱逐教门，待禁令解除后重归教门的过程n 近代国际上残疾人重新获得所失去的权利回归社会n 1910年倡导者将残疾人的医疗福利事业称为

2、“rehabilitation”2.康复方法：滑轮悬挂肢体、步行训练和抗阻力练习等运动方法中国康复概念的演变1.康复概念起源n 成书于西汉时期(20725 BC)的黄帝内经记载了功能恢复的理论和方法n 1000余年前就开始应用姿势和呼吸练习治疗疾病n 古代典籍里“康复”是指恢复健康和平安2.康复方法：应用针灸、导引（体操、气功、自我按摩）和熨（热敷）等手段促进功能恢复，同时辅以饮食和精神调理康复发展的阶段1.物理治疗学阶段（18801919年）n 原理：利用物理因子包括人工（光、电、磁等）和自然（气候、日光和海水等）两大类，进行单纯性康复治疗，如矫正体操、直流电和达松阀等n 学会名称：按摩师学

3、会康复发展的阶段2.物理医学阶段（19201945）n 原理：用物理学的方法诊断和治疗疾病阶段n 物理医学的形成：第一次世界大战（1914年8月-1918年11月）后，应用物理学的方法进行疾病的治疗，同时实施残疾状况和程度的诊断和预防n 学会名称：1938年美国物理治疗师学会成立，1943年英国成立了物理医学会康复发展的阶段3.物理医学与康复医学阶段（1946至今）n 第二次世界大战（1939年9月1945年8月）后，Rusk等人大力提倡康复医学，把战伤的康复经验运用于和平年代，使物理医学逐渐完善发展形成了现代康复医学n 学会名称：1947年成立了美国物理医学与康复医学委员会，1951年成立了

4、国际物理医学与康复学会，1969年国际康复医学会成立康复目标1.功能恢复：康复的目标不是治愈疾病，而是在躯体、个体活动能力和社会参与能力等方面达到最大程度的功能恢复2.能力恢复：功能恢复不等于能力的恢复，更强调能力恢复康复基本原则1.综合训练：保存和恢复机体的运动、感知、语言、心理、生活、职业和社会等方面的功能，重视功能检查和评定2.全面康复：从生理、心理、职业和社会生活等方面进行系统性康复，达到医疗康复、教育康复、职业康复和社会康复3.重返社会：最大限度地恢复其受限或丧失的功能，接受正常或相对正常的社会物质和精神生活，重新参加社会生活，履行其社会职责康复主要内容1.康复预防n 一级预防（初级

5、预防）：预防躯体功能和结构的缺失和异常，是康复预防的基础和关键，是最高级的预防，可减少70病残的发生n 二级预防（次级预防）：预防个体功能活动受限，在预防的同时进行康复治疗，是最重要的预防n 三级预防：预防个体社会参与能力的局限性，保存和提高其残存的能力，最大程度地减少社会参与能力的局限性，使其回归社会康复主要内容1.康复功能评定：综合评定患者受损功能的状况、程度、水平和康复治疗效果，实时指导康复治疗2.康复治疗：通过康复训练，预防疾病所致功能障碍的发生和降低其残疾程度。康复治疗贯穿于功能恢复的始终三级康复1.一级康复（早期康复）：在患者病情允许和机体可耐受的情况下，急性期临床治疗的同时进行早

6、期康复干预（急诊室或神经内科）2.二级康复（恢复期康复）：康复训练目的主要为促进机体功能代偿，降低伤残程度（康复病房或康复中心）3.三级康复（社区康复）：社区康复医生在二级康复的基础上，根据患者居住环境制定康复计划并负责实施训练或居家康复（社区或家中）神经康复机理1.神经可塑性定义：神经系统的结构和功能随内外环境的变化发生适应性改变的过程称为神经可塑性（neural plasticity），包括神经结构和功能的可塑性2.神经可塑性作用：神经系统损伤后所发生的神经可塑性是神经损伤后功能康复的理论基础3.康复训练：促进神经功能重建中枢神经系统功能重建1.损伤区周围组织的功能重建：神经功能的恢复是由

7、于病灶周围未受损皮质功能的重建，而且该功能重建具有训练依赖性2.损伤区对侧相应部位的功能重建：Fabisch报道患者因严重癫痫发作而切除左侧大脑半球，其右侧肢体部分运动功能出现自然恢复和言语功能的保留，而且经过功能训练可恢复其右手功能中枢神经系统结构重建1.潜伏神经通路的开放：潜伏通路是指在发育过程中已然存在，在正常情况下不发挥主导作用，在主导通路损伤后可显现其功能2.失神经敏感：神经元解除受控于其他神经元的调控作用，表现为突触后膜神经递质的反应性异常增强，称失神经敏感3.神经轴突的再生：损伤临近区的正常神经元以发芽的形式再生，并向靶组织或其他神经元延伸形成新的突触影响脑可塑性的因素1.保护受

8、损神经细胞：减少神经细胞损伤，促进神经元网络重建，可增强其抗损伤能力。2.改善损伤区的微环境和外环境：改善和调控损伤区微环境、外部环境的刺激及功能训练可改善缺失功能的恢复3.神经干细胞移植：移植后的神经干细胞具有向病变部位迁移的特性，随之分化为特异性的神经细胞，参与宿主神经的网络重建脑可塑性与功能重建的相关性1.功能重建的最佳表现形式是以损伤同侧皮质功能激活的优势化2.功能磁共振成像和经颅磁刺激对失语和失用的研究结论相一致康复训练与脑可塑性1.通过强制性诱导运动疗法训练，可明显促进脑卒中恢复期功能改善2.康复训练可广泛激活大脑皮质，包括双侧的次级感觉区和运动前区以及对侧的主要感觉运动区3.康复

9、治疗前运动诱发的激活区域主要在健侧皮质，治疗后主要转移至患侧皮质，同时伴随运动功能评分增高神经康复的方法1.物理疗法（physical therapy,PT）2.作业疗法（occupational therapy,OT）3.语言治疗（speech therapy,ST）4.心理治疗（psychological therapy,PT）5.康复工程（rehabilitation engineering,RE）6.职业疗法（vocational rehabilitation，VR）7.传统康复（traditional rehabilitation,TR）8.康复护理（rehabilitation n

10、ursing,RN）物理疗法1.物理治疗：应用物理因子的作用提高健康水平、防治疾病和促进机体康复，包括预防作用和综合治疗作用2.体育疗法：通过特定的体育方法治疗疾病和恢复机体功能3.运动疗法：为缓解症状和改善功能而进行的全身或局部运动，是物理疗法的主要方法之一物理疗法运动疗法1.按运动方式分类n 被动运动：由外力作用于人体某一部分所引起的运动，一般用于维持正常或增大已受限的关节功能活动范围；n 主动运动：依靠患者自身的肌力进行运动，患者肌力在3级以上者，均可进行主动运动物理疗法运动疗法2.按肌肉收缩方式分类n 等长运动（isometric exercise）：关节活动和肌肉长度无明显变化的运动

11、，等长阻力训练是增加肌力最为迅速的方法n 等张运动（isotonic exercise）：关节角度发生变化和肌肉明显缩短的运动n 等速运动（isokinetic exercise）：借助特定仪器以恒定的速率运动，肌肉收缩力与所受阻力呈正相变化物理疗法运动疗法3.按神经生理学治疗分类n 本体感觉神经肌肉促进疗法：刺激本体感觉（肌肉牵张、关节挤压和牵引等）辅以特殊运动模式（螺旋、对角线状运动等）促进运动功能恢复n Bobath疗法：通过反射抑制模式（RIP）抑制异常姿势和运动，促进正常的感觉和运动模式。RIP为对抗因肌肉痉挛所致的异常姿势而进行的一种被动运动物理疗法运动疗法3.按神经生理学治疗分类

12、n Brunnstrom疗法：主要利用联合反应和异常协同动作的治疗体系。该方法主要用于脑卒中后偏瘫的评估和治疗，尤以评估系统著称。以此评估方法为基础，形成了西方的FuglMeyer评估方法和东方的上田敏评估法n Rood疗法：在特定的皮肤区域施加强度不同的浅感觉或特殊感觉刺激，调整传入神经的兴奋性，以达到神经兴奋的促通作用作业疗法1.日常生活作业活动：维持日常生活自理和保持健康所必需的活动2.工作作业活动：通过职业活动，创造价值，取得报酬，自给自立，抚养家庭3.消遣性作业活动：利用业余和闲暇时间，以个人兴趣和爱好所进行的各类活动语言治疗1.语言治疗目的：主要提高言语的理解和表达能力；调整患者言

13、语交流的心理和情感障碍；巩固言语训练效果2.常用方法：发音器官锻炼以及语言、用语、命名、读字、会话和阅读等练习心理治疗1.运用心理学理论、方法和技术，改善患者的认知、行为和人格等异常，促进心理健康和协调发展的过程2.一般可分为支持疗法、行为治疗、催眠疗法、生物反馈疗法和社会心理治疗等其他治疗1.职业疗法：残疾人通过社会给予的特殊帮助和自身职业技能培训，享受健全人同等劳动权利和履行其社会义务的过程2.康复工程：工程技术人员应用全面康复知识和工程理论，与康复工作者和残疾人及其家属密切合作，以各种工艺技术为手段，极大的恢复其残疾功能其他治疗1.传统康复治疗：利用传统中医针灸、按摩和推拿等疗法，促进康

14、复2.康复护理：在康复治疗过程中积极采用护理措施（体位处理、心理支持、膀胱和肠道护理等），促进患者康复，预防继发性残疾神经康复评定1.概念：功能障碍的状况、水平、残存功能、损伤程度、康复治疗效果和预后进行客观和准确的评估2.评定项目：运动功能评定，日常生活活动能力评定，神经电生理检查，语言能力评定，心理测验神经康复评定运动功能评定1.肌力评定：n 手法检查和分级：临床常用的手法检查和肌力分级是由K.W.Lovett于1916年提出，并以此为基础进行了实用性修改n 器械检查：3级以上肌力较精细的定量评定，须用专门器械进行肌力测试，包括等长、等张和等速肌力检查神经康复评定运动功能评定2.关节活动度

15、检查：n 发现影响关节活动的因素n 判定障碍程度n 寻找治疗方法神经康复评定运动功能评定3.步态检查：n 短腿步态：双下肢长度差值超过3.5 cmn 关节强直步态：下肢各关节挛缩强直时出现的步态n 关节不稳步态：先天性髋脱位时步态左右摇晃呈鸭步n 疼痛步态：为尽量缩短痛肢的支撑期，使对侧下肢的摆动呈跳跃式快速前进且步幅缩短呈短促步神经康复评定运动功能评定3.步态检查：n 肌肉软弱步态：胫前肌无力的跨阈步态和双髋外展肌损伤的鸭步n 肌痉挛步态：偏瘫步态、脑瘫和高位截瘫的步态n 小脑性共济失调步态：步态蹒跚、躯干左右摇晃和前后倾斜呈醉汉步态n 前冲步态（慌张步态）：帕金森氏病或其他基底节病变n 奇

16、异步态：用已知步态无法解释者应考虑癔病性步态神经康复评定运动功能评定4.运动功能评估量表：n Fugl-Meyer评定法：瑞典出生后移居美国的PT Signe Brunnstrom于20世纪50年代提出了脑卒中评定与治疗方法n MAS评定法：1985年澳大利亚的Carr JH 等发表了卒中患者运动评估量表评定法，也是运动再学习治疗法，主要用于评估患者功能活动能力而不是单纯的协同运动模式神经康复评定日常生活活动能力评定（ADL）1.ADL定义：评估残疾人日常生活的各项基本功能状况，明确日常生活方式、活动量、难以完成的项目和功能障碍程度等2.ADL内容：床上活动；轮椅活动；自理活动；阅读和书写；使

17、用电灯和电话；使用钱币；行走；上下楼梯；外出乘车3.ADL分级：五级20项日常生活活动能力分级法是我国康复医学试用教材中介绍的分级方法神经康复评定神经电生理检查1.EMG检查：神经肌电图是神经康复中必不可少的检测和评定手段2.检查项目：肌电图检查，神经传导速度检查，诱发电位检查神经康复评定语言能力评定1.语言行为：是一种综合力较强和表现力丰富的大脑功能表现，病态性语言行为的临床评定是进行神经语言康复研究中最基本的手段2.语言检查法：n 北京大学第一医院高素荣编制的汉语失语检查法(ABC)n 中国康复研究中心失语症检查(CRRCAE)神经康复评定心理测验1.智力测验：韦氏智力测验2.神经心理测验

18、：Bender-Gestat test3.人格评估：明尼苏达多相人格测验，艾森克人格问卷4.记忆力测验：修订韦氏记忆量表5.其他测验：汉密尔顿焦虑量表（HAMA），汉密尔顿抑郁量表(HAMD)脑卒中 偏瘫康复(脑卒中)1.康复治疗开始时间：当患者生命体征平稳，神经系统症状不再进展 48 小时以后开始介入康复治疗2.康复治疗强度：n 脑卒中患者病情稳定(生命体征稳定，症状体征不再进展)后应尽早介入康复治疗n 脑卒中患者的康复训练强度要考虑到患者的体力、耐力和心肺功能情况，在条件许可的情况下，适当增加训练强度是有益的偏瘫康复（脑卒中）3.肌力训练：强化肌力训练对脑卒中患者运动功能恢复有积极作用n

19、给予适当的渐进式抗阻训练，进行肌力强化训练n 肌电生物反馈疗法与常规康复治疗相结合n 功能电刺激治疗偏瘫康复（脑卒中）4.痉挛的防治：痉挛是速度依赖的紧张性牵张反射过度活跃的表现，是脑卒中后患者一个最重要的损害n 痉挛的治疗应该是阶梯式的n 治疗痉挛首选无创的治疗方法n 全身性肌肉痉挛的患者，建议使用口服抗痉挛药物n 对局部肌肉痉挛建议使用 A 型肉毒毒素n 难治性肌肉痉挛可以试用鞘内注射巴氯芬或者选择性脊神经后根切断术、脊髓背根入口区破坏等Outcome after mobilization within 24 hours of acute stroke:a randomized contr

20、olled trialPhysical therapists guideline adherence on early mobilization and intensity of practice at dutch acute stroke units:a country-wide surveyACTIVLIM-Stroke:a crosscultural Rasch-built scale of activity limitations in patients with strokeDiscrepancy between cardiac and physical functional res

21、erves in strokeEffects of telerehabilitation on physical function and disability for stroke patients:a randomized,controlled trialPatient-reported auditory functions after stroke of the central auditory pathwayThe feasibility of cardiopulmonary exercise testing for prescribing exercise to people aft

22、er strokeEffects of robot-assisted gait training on cardiopulmonary fitness in subacute stroke patients:a randomized controlled studyAngiogenesis:a harmonized target for recovery after strokeAngiogenic Response to Ischemic Brain Injury:A Multipurpose PathwayAngiogenic Response to Ischemic Brain Inju

23、ry:A Multipurpose PathwayIt is clear that 1.Angiogenesis genes are upregulated within minutes of the onset of cerebral ischemia in rodents2.Angiogenic proteins remain increased in the area of ischemia for days to weeksAngiogenic Response to Ischemic Brain Injury:A Multipurpose PathwayIt is unclear1.

24、Whether the angiogenic response leads to the development of functional new blood vessels that improve brain function after stroke2.Clinical and experimental studies in other vascular beds have emphasized the potential for adverse consequences related to neovascularizationAngiogenic Response to Ische

25、mic Brain Injury:A Multipurpose PathwayIt is likely that the“proangiogenic state,”induced in response to an ischemic insult,has multiple purposes in the hours to weeks after the injury:First,the growth factors expressed may promote survival of the endothelial,glial,and neuronal cell types in the pen

26、umbral areaSecond,the neovascularization may act to remove damaged tissue Angiogenic Response to Ischemic Brain Injury:A Multipurpose PathwayIt is likely that the“proangiogenic state,”induced in response to an ischemic insult,has multiple purposes in the hours to weeks after the injury:Lastly,the pr

27、oangiogenic state may create a“vascular niche”in which neural stem cells are generated and allowed to migrate.Growth FactorsNumerous growth factors have been implicated in the recov-ery process after ischemic stroke:1.Basic fibroblastic growth factor2.Brain-derived neurotrophic factor(BDNF),3.Vascul

28、ar endothelial growth factor(VEGF)4.Granulocyte colony-stimulating factor5.Other neurotrophinsGrowth FactorsNeurotrophins promote recovery by enhancing:1.Angiogenesis2.Neurogenesis3.Synaptogenesis4.Neuronal plasticityGrowth FactorsVEGF1.The most commonly studied proangiogenic molecule in stroke is V

29、EGF.2.Although touted for its neuroprotective and neurogenic properties,VEGF can worsen edema and hemorrhage after stroke through its enhancement of vascular permeability and this effect is dose-related.3.However,a great deal of evidence exists that the proangiogenic and vascular permeability effect

30、s of VEGF can be“uncoupled.”Growth Factors VEGF Differential expression of the various isoforms of VEGF may be important in this process after stroke:1.VEGF-B promotes cell survival without the predominant vascular permeability2.Angiogenic effects demonstrated with the better studied VEGF-A isoformG

31、rowth Factors BDNF1.BDNF is a member of the neurotrophin family that is widely expressed and has many functions extending beyond its neuronal effects.2.After experimental ischemia,higher levels of BDNF in the brain improved functional recovery,whereas BDNF knock down worsened functional outcome.Grow

32、th Factors BDNF1.A unique aspect of BDNF biology was the identification of its involvement in the crosstalk between the constituents of the neurovascular unit to promote recovery after central nervous system ischemic insults.2.BDNF has been reported to regulate the expression of VEGF.BDNF has been i

33、mplicated in cardiovascular development and found to induce a robust angiogenic effect in endothelial cells comparable to that of VEGF.Nonpharmacologic Interventions That ImproveRecovery:Effect on AngiogenesisExercise/Physical Therapy1.Exercise preconditioning induces tolerance to brain ischemia thr

34、ough many proposed mechanisms,including induction of VEGF and stimulation of angiogenesis and neurogenesis.2.Physical activity after stroke has also been shown to induce angiogenesis and improve long-term outcome as well.Nonpharmacologic Interventions That ImproveRecovery:Effect on AngiogenesisExerc

35、ise/Physical TherapyThe most important finding was that:Inhibition of endothelial nitric oxide synthase or angiogenesis(with endostatin)abolished the beneficial effects of exercise on outcome.Nonpharmacologic Interventions That ImproveRecovery:Effect on AngiogenesisPeripheral/Transcranial Magnetic S

36、timulation 1.Electric stimulation resulted in decreased apoptosis and inflammation and increased angiogenesis in the ischemic cortex.2.These effects were accompanied by a robust increase in neurotrophic factors,including VEGF and BDNF,and the antiapoptotic effect was abolished by inhibiting Akt acti

37、vation.Nonpharmacologic Interventions That ImproveRecovery:Effect on AngiogenesisPeripheral/Transcranial Magnetic StimulationThe importance of angiogenesis was further implicated in the positive response to peripheral stimulation when mice treated with a specific inhibitor of VEGF receptor-2 had dec

38、reased neuroblast migration toward the injured area.Nonpharmacologic Interventions That ImproveRecovery:Effect on AngiogenesisLow-Level Laser Therapy1.Light therapy has been shown to reduce infarct size and improve outcome when administered at least 6 hours after experimental stroke onset.2.Experts

39、in the technique have agreed on a critical role of VEGF and angiogenesis to the protection afforded by light therapy.3.Laser therapy is currently in clinical trials for promotion of recovery after ischemic stroke.Repurposed Pharmacological Interventions That Improve Stroke RecoveryStatinsStatins hav

40、e been shown to limit the ischemic insult and improve functional outcome and recovery after experimental ischemia.The observed improved outcome has been attributed to the statins ability to induce in the ischemic border zone as follows:1.Neurogenesis2.Neuroprotection3.Neuroplasticity4.AngiogenesisRe

41、purposed Pharmacological Interventions That Improve Stroke RecoveryStatinsData from in vitro and ex vivo angiogenesis research support a biphasic dose-dependent effect of statins in angiogenesis：1.The lower concentrations have a proangiogenic effect.2.The higher concentrations produce an antiangioge

42、nic response in endothelial cells.3.In a striking contrast to the proangiogenic effect of statins in models of ischemia,statins have been shown to have an antiangiogenic effect in both cancer and inflammation settings.4.It can be concluded that statins have a dose-and context-dependent modulatory ef

43、fect on angiogenesis.Repurposed Pharmacological Interventions That Improve Stroke RecoveryAngiotensin II Receptor Type 1 Antagonists1.A meta-analysis of clinical trials using these agents in various disease states pointed to a small,but significant,increase in the incidence of lung cancer in treated

44、 patients.2.Angiotensin ii receptor type 1 antagonists have been shown to be both pro-and antiangiogenic,depending on the situation(ischemia or not)and tissue involved.3.In a recent set of experiments done in a rat model of ischemic stroke,treatment with candesartan after 3 hours of temporary middle

45、 cerebral artery occlusion resulted in improved long-term functional outcomes and a proangiogenic state.4.This acute treatment was subsequently shown to be associated with increased VEGF expression in both the ischemic and nonischemic hemispheres at 24 hours after treatment and increased vascular de

46、nsity in both hemispheres at 7 days.Repurposed Pharmacological Interventions That Improve Stroke Recovery1.Angiotensin II Receptor Type 1 Antagonists2.Most believe that angiogenesis only occurs in the ipsilateral hemisphere after stroke and experimental studies compare only the cortical tissue in th

47、e 2 sides for evidence to support this claim.3.It is well known,however,that ischemic injury in the brain can result in diaschisis and functional MRI studies in human stroke victims have consistently shown involvement of the contralesional hemisphere in recovery.4.It is possible that induction of an

48、giogenesis in the striatum of the contralesional hemisphere is important to functional recovery after ischemic stroke by improving recruitment of neuroblasts to the area of recovery.Consequences of Impaired Angiogenesis1.As commented in a recent review,diabetic and/or hypertensive patients may devel

49、op dysfunctional vasculature after stimulation of angiogenesis in the recovering penumbra after stroke,and this can be detrimental.2.There is strong evidence that hyperglycemia-mediated oxidative damage to microvascular endothelial cells triggers a cascade of events that causes excessive angiogenesi

50、s and result in vascular proliferative retinopathy.3.These immature vessels then break and leak worsening vascular and neuronal damage.Consequences of Impaired Angiogenesis1.The effect of hyperglycemia in the cerebral vasculature,especially after an ischemic event,is less clear.2.We reported extensi