Muscle contracture and passive mechanics in cerebral palsy

Abstract

Skeletal muscle contractures represent the permanent shortening of a muscle-tendon unit, resulting in loss of elasticity and, in extreme cases, joint deformation. They may result from cerebral palsy, spinal cord injury, stroke, muscular dystrophy, and other neuromuscular disorders. Contractures are the prototypic and most severe clinical presentation of increased passive mechanical muscle force in humans, often requiring surgical correction. Intraoperative experiments demonstrate that high muscle passive force is associated with sarcomeres that are abnormally stretched, although otherwise normal, with fewer sarcomeres in series. Furthermore, changes in the amount and arrangement of collagen in the extracellular matrix also increase muscle stiffness. Structural light and electron microscopy studies demonstrate that large bundles of collagen, referred to as perimysial cables, may be responsible for this increased stiffness and are regulated by interaction of a number of cell types within the extracellular matrix. Loss of muscle satellite cells may be related to changes in both sarcomeres and extracellular matrix. Future studies are required to determine the underlying mechanism for changes in muscle satellite cells and their relationship (if any) to contracture. A more complete understanding of this mechanism may lead to effective nonsurgical treatments to relieve and even prevent muscle contractures.

The Energy of Muscle Contraction. I. Tissue Force and Deformation During Fixed-End Contractions

“…There are a range of muscle conditions and impairments that are associated with increases in fibrotic tissue, changing muscle stiffness, and this energetic framework now provides an approach for us to understand how such conditions lead to loss of muscle function. For instance, altered material properties of muscle tissue post stroke (Lee et al, 2015 ) and with cerebral palsy (Lieber and Fridén, 2019 ) have been linked to increases in collagenous connective tissue within the muscle (Lieber and Ward, 2013 ). Whilst it is possible to measure proxies of muscle tissue stiffness with shear wave ultrasound elastography (Lee et al, 2015 ), it is difficult to partition these changes between the passive stiffness of the fibres, or the stiffness of the base material.…”

Change in popliteal angle and hamstrings spasticity during childhood in ambulant children with spastic bilateral cerebral palsy. A register-based cohort study

“…3). This may indicate that there are additional factors than an increased stretch reflex registered as spasticity contributing to muscle contractures [14,26,[40][41][42]. Reduced active terminal knee extension, either due to reduced selective motor control, muscle weakness or immobilization, may be contributing factors [6].…”

“…In addition Gough and Shortland [39] suggested that in CP there might be multifactorial impairments of muscle growth which may lead to impaired muscle adaptation during growth [39]. Recent published papers have also shown increased arrangement of collagen in the extra cellular matrix, and factors within the contractile elements in the muscles which may contribute to muscle contractures [14,26,40,42].…”

Serial sarcomere number is substantially decreased within the paretic biceps brachii in individuals with chronic hemiparetic stroke

“…For example, at this point, only a single published study has calculated serial sarcomere number (i.e., measured both sarcomere length and fascicle length in vivo ) under conditions in which a human muscle has chronically been placed at a shortened position 32 . In this case, the calf muscles in children with cerebral palsy with equinus contractures (functionally shortened muscle-tendon units that are more resistant to stretch 30,31 ) severe enough to require surgical intervention did not “re-optimize” to the shorter muscle lengths imposed by the participants’ chronically plantarflexed joint posture. Rather, the soleus muscles in these children had sarcomeres substantially longer (4.07µm 32 ) than optimal length (2.70µm 33 ).…”

“…Sarcomere length measurements in living human subjects have traditionally been limited to biopsy or intraoperative studies, (i.e. during distraction surgeries for limb discrepancy 13 , tendon transfer surgeries 34,35 , or muscle lengthening in children with cerebral palsy 30 ) and only recently have become measurable via minimally or non-invasive techniques 36,37 . As a result, the authors estimated serial sarcomere number for control participants by combining fascicle length measures obtained from typically developing children via ultrasound with sarcomere lengths measured from adult cadavers via dissection.…”