Gracies J M, Elovic E, McGuire J, Simpson D M
Department of Neurology, Mount Sinai Medical Center, New York, NY 10029, USA.
Muscle Nerve Suppl. 1997;6:S61-91.
Spasticity is a velocity-dependent increase in stretch reflex activity. It is one of the forms of muscle overactivity that may affect patients with damage to the central nervous system. Spasticity monitoring is relevant to function because the degree of spasticity may reflect the intensity of other disabling types of muscle overactivity, such as unwanted antagonistic co-contractions, permanent muscle activity in the absence of any stretch or volitional command (spastic dystonia), or inappropriate responses to cutaneous or vegetative inputs. In addition, spasticity, like other muscle overactivity, can cause muscle shortening, which is another significant source of disability. Finally, spasticity is the only form of muscle overactivity easily quantifiable at the bedside. Under the name pharmacological treatments of spasticity, we understand the use of agents designed to reduce all types of muscle overactivity, by reducing excitability of motor pathways, at the level of the central nervous system, the neuromuscular junctions, or the muscle. Pharmacologic treatment should be an adjunct to muscle lengthening and training of antagonists. Localized muscle overactivity of specific muscle groups is often seen in a number of common pathologies, including stroke and traumatic brain injury. In these cases, we favor the use of local treatments in those muscles where overactivity is most disabling, by injection into muscle (neuromuscular block) or close to the nerve supplying the muscle (perineural block). Two types of local agents have been used in addition to the newly emerged botulinum toxin: local anesthetics (lidocaine and congeners), with a fully reversible action of short duration, and alcohols (ethanol and phenol), with a longer duration of action. Local anesthetics block both afferent and efferent messages. The onset of action is within minutes and duration of action varies between one and several hours according to the agent used. Their use requires resuscitation equipment available close by. When a long-lasting blocking agent is being considered, we favor the use of transient blocks with local anesthetics for therapeutic tests or diagnostic procedures to answer the following questions: Can function be improved by the block? What are the roles played by overactivity and contracture in the impairment of function? Which muscle is contributing to pathologic posturing? What is the true level of performance of antagonistic muscles? A short-acting anesthetic can also serve as preparation to casting or as an analgesic for intramuscular injections of other antispastic treatment. Alcohol and phenol provide long-term chemical neurolysis through destruction of peripheral nerve. Experience with ethanol is more developed in children using intramuscular injection, while experience with phenol is greater in adults with perineural injection. In both cases, there are anecdotal reports of efficacy but studies have rarely been controlled. Side effects are numerous and include pain during injection, chronic dysesthesia and chronic pain, and episodes of local or regional vascular complications by vessel toxicity. In the absence of controlled studies, a theoretical comparison of neurolytic agents with botulinum toxin is proposed. Neurolytic agents may be preferred to botulinum toxin on a number of grounds, including earlier onset, potentially longer duration of effect, lower cost, and easier storage. Conversely, pain during injection, tissue destruction with chronic sensory side effects, and lack of selectivity on motor function with neurolytic agents may favor the use of botulinum toxin. Neurolytic agents and botulinum toxin may be used in combination, the former for larger proximal muscles and the latter for selective injection into distal muscles. In the future, neurolytic agents may prove more appropriate in very severely affected patients for whom the purposes of the block are comfort and hygiene. (ABSTRACT TRUNCATED)
痉挛是一种与速度相关的牵张反射活动增强。它是肌肉过度活动的一种形式,可能影响中枢神经系统受损的患者。痉挛监测与功能相关,因为痉挛程度可能反映其他致残性肌肉过度活动的强度,如不必要的拮抗肌共同收缩、在无任何牵张或自主指令时的持续性肌肉活动(痉挛性肌张力障碍),或对皮肤或自主神经输入的不适当反应。此外,与其他肌肉过度活动一样,痉挛会导致肌肉缩短,这是另一个导致残疾的重要原因。最后,痉挛是唯一一种在床边易于量化的肌肉过度活动形式。在痉挛的药物治疗方面,我们理解使用旨在通过降低中枢神经系统、神经肌肉接头或肌肉水平的运动通路兴奋性来减少所有类型肌肉过度活动的药物。药物治疗应作为肌肉延长和拮抗肌训练的辅助手段。特定肌肉群的局部肌肉过度活动常见于多种常见病症,包括中风和创伤性脑损伤。在这些情况下,我们倾向于通过肌肉注射(神经肌肉阻滞)或靠近供应肌肉的神经注射(神经周围阻滞),对过度活动最致残的肌肉进行局部治疗。除了新出现的肉毒杆菌毒素外,还使用了两种局部药物:局部麻醉剂(利多卡因及其同类物),作用完全可逆且持续时间短;酒精(乙醇和苯酚),作用持续时间较长。局部麻醉剂可阻断传入和传出信息。起效时间在数分钟内,根据所用药物不同,作用持续时间在1至数小时之间。使用时需要在附近配备复苏设备。当考虑使用长效阻滞剂时,我们倾向于使用局部麻醉剂进行短暂阻滞,用于治疗试验或诊断程序,以回答以下问题:阻滞能否改善功能?过度活动和挛缩在功能损害中起什么作用?哪些肌肉导致了病理性姿势?拮抗肌的实际功能水平如何?短效麻醉剂还可作为石膏固定的准备或用于其他抗痉挛治疗的肌肉注射镇痛。酒精和苯酚通过破坏周围神经提供长期化学性神经溶解作用。儿童使用肌肉注射乙醇的经验更多,而成人使用神经周围注射苯酚的经验更丰富。在这两种情况下,都有疗效的传闻报道,但很少有对照研究。副作用众多,包括注射时疼痛、慢性感觉异常和慢性疼痛,以及因血管毒性导致的局部或区域血管并发症。在缺乏对照研究的情况下,对神经溶解剂与肉毒杆菌毒素进行了理论比较。基于多种原因,神经溶解剂可能比肉毒杆菌毒素更受青睐,包括起效更早、潜在作用持续时间更长、成本更低和储存更方便。相反,注射时疼痛、伴有慢性感觉副作用的组织破坏以及神经溶解剂对运动功能缺乏选择性,可能更倾向于使用肉毒杆菌毒素。神经溶解剂和肉毒杆菌毒素可联合使用,前者用于较大的近端肌肉,后者用于选择性注射到远端肌肉。未来,神经溶解剂可能被证明更适合那些病情非常严重、阻滞目的是为了舒适和卫生的患者。(摘要截选)