周围性面神经麻痹的针刺时机探析

周围性面神经麻痹是临床常见的多发病,在治疗上多采用针刺治疗,而针刺的时机异同,会直接影响病患的恢复效果。现代医学研究普遍认为,急性期面瘫,面神经炎症,多发生水肿,不应尽快针刺治疗;而针灸临床多数报道表明,早期给予针刺,能有效提高临床有效率。因此,对于针刺时机则需进一步加强其标准化。本文则主要通过对近几年文献的检索,探索最佳针刺时机在面神经麻痹中的临床应用。     

运用彭静山教授“一点二穴三线四面取穴法”针刺治疗难治性面瘫

彭静山教授提出“一点二穴三线四面”八字取穴法。笔者运用此八字取穴法指导针灸临床取穴治疗难治性面瘫,临床效果显著。本文列举临床典型病例,详细阐述取穴和针刺治疗方法,并对治疗机理进行论述。对于难治性面瘫,单纯毫针针刺治疗效果有一定局限性,以“一点二穴三线四面”八字取穴法为基础,取穴点以透刺连接构成线、面,以芒针联合透刺法为主要治疗方法,可强化治疗效果、提高临床效应。     

电针傍刺经筋结点治疗缺血性脑卒中急性期上肢偏瘫的临床研究

目的通过观察电针傍次上肢经筋结点治疗缺血性脑卒中急性期上肢偏瘫的临床疗效,探讨电针傍次经筋结点治疗缺血性卒中急性期肢体瘫痪的作用机制。方法60例缺血性卒中急性期偏瘫的患者采用SPSS软件随机数字生成器分为治疗组与对照组各30例。治疗组采用电针傍刺上肢经筋结点治疗,对照组采用电针上肢常规经穴治疗。分别于治疗前后观察评价两组上肢的肌力(MMT徒手肌力评定法)、关节活动度(ROM关节活动度评定法)、运动功能(Fugl-Meyer运动功能评分量表、ARAT上肢动作研究量表)、临床神经功能缺损程度(NIHSS量表)确定疗效。结果两组患者治疗后ROM评分下降,Barthel指数、Fugl-Meyer评分、ARAT评分均上升。治疗组较对照组ROM评分、Barthel指数、Fugl-Meyer评分、ARAT评分改善更优(P<0.05);疗程结束后治疗组肌力经MMT评定后有效率为90%,高于对照组的76.67%(P<0.05);治疗组疗效经神经功能缺损程度评价有效率为93.33%,高于对照组76.67%(P<0.05)。结论电针傍刺经筋结点与常规针刺治疗都可以改善缺血性卒中急性期上肢瘫痪,但电针傍刺经筋结点治疗效果更佳。     

针刺联合优质护理干预对周围性面神经麻痹急性期患者的影响

目的分析针刺联合优质护理干预对周围性面神经麻痹急性期患者的影响。方法以2016年1月—2019年2月60例周围性面神经麻痹急性期患者为研究对象,患者按照护理方法不同,将其分为对照组、观察组各30例患者,对照组进行神经内科的常规护理,观察组进行针刺联合优质护理干预,对2组患者临床疗效和护理满意度等进行观察。结果对照组总有效率为70%,观察组总有效率为96.6%(P<0.05)。对照组护理满意度为63.3%,观察组护理满意度为96.6%(P<0.05)。结论周围性面神经麻痹急性期患者临床治疗中,针刺联合优质护理干预的应用,可以提升患者临床疗效,降低患者住院时间,实现其护理满意度的提升。     

C19orf12 mutation causing mitochondrial membrane-protein Associated Neurodegeneration masquerading as spastic paraplegia

Mitochondrial Membrane-protein Associated Neurodegeneration (MPAN) is a rare disease, caused by C19orf12 mutations and up to 29 different mutations have been described. We report a young woman presented with spastic paraparesis due to C19orf12 gene. MPAN presenting like Hereditary spastic paraplegia-43 is rare and the genetic mutation had been described only once in the literature.     

肌电生物反馈对痉挛型脑瘫患儿下肢运动功能影响的Meta分析

目的:应用Meta分析评价肌电生物反馈治疗痉挛型脑瘫的作用。方法:检索PubMed、Embase、Cochrane图书馆及中国生物医学文献数据库、CNKI、维普、万方数据库中2009年1月~2019年6月关于肌电生物反馈治疗痉挛型脑瘫的随机对照试验,利用RevMan 5.3软件进行Meta分析。结果:纳入10项随机对照试验,共613个病例;肌电生物反馈可以改善脑瘫患儿踝关节活动度(MD=5.06,95%CI=4.01~6.10,P<0.01),改善粗大运动功能(GMFM D区MD=3.75,95%CI=2.75~4.75,P<0.01;GMFM E区MD=6.04,95%CI=4.82~7.26,P<0.01),改善腓肠肌痉挛程度(MD=5.19,95%CI=-0.52^-0.39,P<0.01)。结论:肌电生物反馈在改善脑瘫患儿下肢运动功能方面具有一定效果,但所纳入研究的方法有局限性,还需更严格的设计和高质量的研究方法进一步证明。     

The neurophysiology of deforming spastic paresis: A revised taxonomy

This paper revisits the taxonomy of the neurophysiological consequences of a persistent impairment of motor command execution in the classic environment of sensorimotor restriction and muscle hypo-mobilization in short position. Around each joint, the syndrome involves 2 disorders, muscular and neurologic. The muscular disorder is promoted by muscle hypo-mobilization in short position in the context of paresis, in the hours and days after paresis onset: this genetically mediated, evolving myopathy, is called spastic myopathy. The clinician may suspect it by feeling extensibility loss in a resting muscle, although long after the actual onset of the disease. The neurologic disorder, promoted by sensorimotor restriction in the context of paresis and by the muscle disorder itself, comprises 4 main components, mostly affecting antagonists to desired movements: the first is spastic dystonia, an unwanted, involuntary muscle activation at rest, in the absence of stretch or voluntary effort; spastic dystonia superimposes on spastic myopathy to cause visible, gradually increasing body deformities; the second is spastic cocontraction, an unwanted, involuntary antagonist muscle activation during voluntary effort directed to the agonist, aggravated by antagonist stretch; it is primarily due to misdirection of the supraspinal descending drive and contributes to reducing movement amplitude; and the third is spasticity, one form of hyperreflexia, defined by an enhancement of the velocity-dependent responses to phasic stretch, detected and measured at rest (another form of hyperreflexia is “nociceptive spasms”, following flexor reflex afferent stimulation, particularly after spinal cord lesions). The 3 main forms of overactivity, spastic dystonia, spastic cocontraction and spasticity, share the same motor neuron hyperexcitability as a contributing factor, all being predominant in the muscles that are more affected by spastic myopathy. The fourth component of the neurologic disorder affects the agonist: it is stretch-sensitive paresis, which is a decreased access of the central command to the agonist, aggravated by antagonist stretch. Improved understanding of the pathophysiology of deforming spastic paresis should help clinicians select meaningful assessments and refined treatments, including the utmost need to preserve muscle tissue integrity as soon as paresis sets in.     

针药结合治疗脑卒中后假性球麻痹吞咽障碍研究进展

吞咽障碍是脑卒中后常见的并发症之一,目前针药结合治疗本病具有较好的临床疗效。综述近年来针药结合治疗脑卒中后假性球麻痹吞咽障碍的文献,以期对本病未来的临床工作有些许启发。目前以针药结合为主治疗本病的方法包括毫针结合内服中药、穴位贴敷、穴位注射、中药穴位离子导入以及毫针与中药以其他形式的结合,包括中药药棒、药枕、中药点舌、氧驱雾化吸入、灌肠等。针药结合治疗本病具有同效相须、异效互补、反效制约的治疗特点,也存在不少问题亟待解决。