Sindou Marc, Joud Anthony, Georgoulis George
University of Lyon, Lyon, France.
Groupe ELSAN, Clinique Bretéché, Nantes, France.
Adv Tech Stand Neurosurg. 2025;51:15-39. doi: 10.1007/978-3-031-86441-4_3.
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.
痉挛源于单突触反射的亢进，这归因于上位脊髓结构下行抑制性影响的丧失，但并非完全如此。痉挛的定义是其对肌肉拉伸的抵抗，会产生两个显著后果。首先，肌肉倾向于保持缩短状态，限制运动。其次，张力亢进加上缺乏活动，会导致软组织变化，包括粘弹性丧失。这种非速度依赖性的生物力学方面限制了运动，即使在缓慢速度下也是如此，使它们对抗痉挛药物无反应。积极应对张力亢进/痉挛对于预防疾病的固定以及这个恶性循环的潜在不可逆转性至关重要。了解网状结构的作用、其传入投射和传出通路对于理解昼夜节律变化以及患者临床表现的变异性至关重要。脑瘫患儿张力亢进的机制有两方面：由于痉挛导致的神经成分（速度依赖性）和与软组织变化相关的生物力学成分。尽管临床上难以区分，但这种区分至关重要，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，这是一种由试图进行自主运动诱发的持续性张力亢进状态。区分痉挛和肌张力障碍至关重要，因为背根切断术对肌张力障碍成分影响极小。痉挛通过对抗肌肉拉伸和延长，导致肌肉保持缩短状态，从而引起软组织变化和挛缩，最终限制运动。张力亢进和缺乏活动形成恶性循环，最终由于不可逆转的肌腱回缩和关节强直/骨骼畸形导致严重的运动障碍。在对儿童进行评估以做决策时，必须仔细考虑这些不断演变的后果。还讨论了腰骶部背根切断术的低张力效应，其不仅在节段水平作用于下肢，还通过网状结构在节段以上起作用。
