痉挛的传统药物治疗。第一部分:局部治疗。

Muscle & nerve. Supplement Pub Date : 1997-01-01
J M Gracies, E Elovic, J McGuire, D M Simpson
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引用次数: 0

摘要

痉挛是拉伸反射活动的速度依赖性增加。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,因为痉挛的程度可能反映其他致残类型的肌肉过度活动的强度,如不必要的对抗性共同收缩,在没有任何拉伸或意志指令的情况下的永久性肌肉活动(痉挛性肌张力障碍),或对皮肤或植物输入的不适当反应。此外,痉挛和其他肌肉过度活动一样,会导致肌肉缩短,这是导致残疾的另一个重要原因。最后,痉挛是唯一一种在病床旁容易量化的肌肉过度活动形式。在痉挛的药理学治疗下,我们理解使用药物来减少所有类型的肌肉过度活动,通过减少运动通路的兴奋性,在中枢神经系统,神经肌肉连接,或肌肉的水平。药物治疗应作为肌肉延长和拮抗剂训练的辅助手段。局部肌肉过度活动的特定肌群是经常看到在一些常见的病理,包括中风和创伤性脑损伤。在这种情况下,我们倾向于在那些过度活动最致残的肌肉中使用局部治疗,通过注射到肌肉中(神经肌肉阻滞)或靠近供应肌肉的神经(神经周围阻滞)。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(利多卡因和同类药物),具有短时间的完全可逆作用,以及酒精(乙醇和苯酚),具有较长的作用时间。局部麻醉剂同时阻断传入和传出信息。作用的开始在几分钟内,作用的持续时间根据所使用的药物在一到几个小时之间变化。它们的使用需要附近可用的复苏设备。当考虑使用长效阻断剂时,我们倾向于在治疗试验或诊断过程中使用瞬态阻滞与局部麻醉剂,以回答以下问题:阻滞能改善功能吗?过度活动和挛缩在功能损害中起什么作用?哪块肌肉导致了病态的姿势?拮抗肌的真实水平是什么?短效麻醉剂也可用作铸造前的准备,或作其他抗痉挛治疗中肌内注射的止痛剂。酒精和苯酚通过破坏周围神经提供长期的化学神经松解作用。使用肌肉内注射的儿童对乙醇的经验更成熟,而使用神经周围注射的成人对苯酚的经验更丰富。在这两种情况下,都有关于疗效的轶事报道,但研究很少受到控制。副作用很多,包括注射时疼痛,慢性感觉不良和慢性疼痛,以及由血管毒性引起的局部或区域血管并发症。在缺乏对照研究的情况下,建议将神经溶解剂与肉毒杆菌毒素进行理论比较。与肉毒杆菌毒素相比,神经溶解剂可能更受欢迎,原因包括起效早、可能持续时间长、成本低、易于储存。相反,注射时的疼痛、组织破坏和慢性感觉副作用,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。在未来,神经溶解剂可能被证明更适合于非常严重的患者,因为他们的目的是舒适和卫生。(抽象截断)
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Traditional pharmacological treatments for spasticity. Part I: Local treatments.

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)

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