{"title":"Neurophysiological and Neuroanatomical Background of Spasticity: Surgical Implication for Dorsal Rhizotomy in Cerebral Palsy.","authors":"Marc Sindou, Anthony Joud, George Georgoulis","doi":"10.1007/978-3-031-86441-4_3","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":72077,"journal":{"name":"Advances and technical standards in neurosurgery","volume":"51 ","pages":"15-39"},"PeriodicalIF":0.0000,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Advances and technical standards in neurosurgery","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1007/978-3-031-86441-4_3","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
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.