Neurophysiological and Neuroanatomical Background of Spasticity: Surgical Implication for Dorsal Rhizotomy in Cerebral Palsy.

Marc Sindou, Anthony Joud, George Georgoulis
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Abstract

Spasticity arises from the exaggeration of the monosynaptic reflex, attributed to the loss of inhibitory influences from descending supraspinal structures, though not exclusively. Defined by its resistance to muscle stretching, spasticity yields two significant outcomes. Firstly, muscles tend to remain in a shortened position, restricting movement. Secondly, hypertonia, coupled with a lack of mobilization, leads to soft tissue changes, including a loss of viscoelasticity. This non-velocity-dependent biomechanical aspect limits movements, even at slow velocities, rendering them unresponsive to antispastic agents. Proactively addressing hypertonia/spasticity is crucial to prevent the fixation of disorders and the potential irreducibility of this vicious circle. Understanding the role of the reticular formation, its afferent projections, and efferent pathways is essential for comprehending circadian tone variations and the variability in clinical presentations among patients. The mechanism of hypertonia in children with cerebral palsy is twofold: a neural component due to spasticity (velocity dependent) and a biomechanical component linked to soft tissue changes. Although clinically challenging to differentiate, this distinction is crucial, as only the former responds to antispastic treatments, while the latter requires physiotherapy. Additionally, spasticity is often accompanied by dystonia, a sustained hypertonic state induced by voluntary motion attempts. Distinguishing spasticity from dystonia is essential, as dorsal rhizotomy minimally affects the dystonic component. Spasticity, by opposing muscle stretching and lengthening, leads to muscles remaining in a shortened position, resulting in soft tissue changes and contracture, ultimately restricting movements. Hypertonia and lack of mobilization create a vicious circle, culminating in severe locomotor disability due to irreducible musculotendinous retraction and joint ankylosis/bone deformities. These evolving consequences must be carefully considered during a child's assessment for decision-making. The hypotonic effects of lumbosacral dorsal rhizotomy, acting not only at a segmental level on the lower limbs but also supra-segmentally through the reticular formation, are also discussed.

痉挛的神经生理学和神经解剖学背景:脑瘫背神经根切断术的手术意义。
痉挛是由单突触反射的夸大引起的,归因于下行棘上结构的抑制性影响的丧失,尽管不是唯一的。痉挛的定义是对肌肉拉伸的抵抗,痉挛产生两个重要的结果。首先,肌肉往往保持在一个缩短的位置,限制运动。其次,高张力,加上缺乏动员,导致软组织的变化,包括粘弹性的丧失。这种非速度依赖的生物力学方面限制了运动,即使在缓慢的速度下,也使它们对抗痉挛剂没有反应。主动解决高张力/痉挛对于防止疾病的固定和这种恶性循环的潜在不可还原性至关重要。了解网状结构的作用,它的传入投射和传出通路对于理解昼夜节律音调的变化和患者临床表现的可变性至关重要。脑瘫儿童高张力的机制是双重的:痉挛引起的神经成分(速度依赖)和与软组织改变有关的生物力学成分。虽然临床上很难区分,但这种区别是至关重要的,因为只有前者对抗痉挛治疗有反应,而后者需要物理治疗。此外,痉挛常伴有肌张力障碍,这是一种由自主运动引起的持续高张力状态。区分痉挛和肌张力障碍是必要的,因为背根切断术对肌张力障碍的影响最小。痉挛,通过相反的肌肉拉伸和延长,导致肌肉保持在一个缩短的位置,导致软组织改变和挛缩,最终限制运动。高张力和缺乏活动形成恶性循环,最终导致肌肉腱不可还原的收缩和关节强直/骨畸形导致严重的运动障碍。在对儿童进行决策评估时,必须仔细考虑这些不断变化的后果。腰骶背根切断术的低张力效应,不仅在节段水平上作用于下肢,而且通过网状结构也作用于节段上。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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