No abstract

Children with spastic cerebral palsy (CP) have small, weak muscles. However, change in muscle size due to resistance training in this group is unknown. We investigated the effect of plantarflexor strengthening on muscle volume, gait, and function in 13 ambulant children with spastic CP (seven males, six females; mean age 10y 11mo, SD 3y 0mo, range 6y 11mo–16y 11mo; eight with diplegia, five with hemiplegia; Gross Motor Function Classification System level I, six; level II, five; level III, two). Assessments were performed before training, 5 and 10 weeks into training, and at a 3‐month follow‐up. Medial and lateral gastrocnemius volumes were computed from three‐dimensional ultrasound images. The number of unilateral heel raises able to be achieved on each side was assessed. Function was measured using three‐dimensional gait analysis, the ‘timed up and go’ test, the Gillette Functional Assessment Questionnaire, and the Functional Mobility Scale. Training involved heel raises or Thera‐Band resistance, 4 times a week for 10 weeks. Medial and lateral gastrocnemius volumes increased by 17 and 14% at week 5 (p=0.03, p=0.028). This increase was maintained at week 10 and follow‐up (medial gastrocnemius p=0.001, p<0.001; lateral gastrocnemius p=0.006, p=0.007). Heel raises (mean number) increased by week 5 (p=0.002). This was maintained at week 10 and follow‐up (p<0.001; p<0.001). No significant change in measured function was observed. Muscle volume increased in response to training in children with spastic CP. The role of progressive strength training in maintaining long‐term function is discussed.

No abstract

Skeletal muscle deformity is common in children with spastic cerebral palsy (CP), but the underlying mechanisms are unclear. This review explores some possible factors which may influence the development of muscle deformity in CP. Normal muscle function and growth appear to depend on the interaction of neuronal, endocrinal, nutritional, and mechanical factors, and also on the development of an appropriate balance between muscle protein synthesis and degradation, and between the development of contractile and non-contractile components. In this context, the changes seen in muscle in children with CP are reviewed and discussed. It is suggested that the development of muscle deformity in children with CP may be related to a multifactorial impairment of muscle growth, on which adaptation of the extracellular matrix due to altered loading may be imposed.Why do children with spastic cerebral palsy (CP) develop muscle deformity? We generally associate the development of deformity with the presence of spasticity and a consequent resistance of muscle to passive stretch, but the aetiology may be more complex. Children with CP show an early reduction in gastrocnemius muscle belly size, 1 an alteration in gene expression within the flexor carpi ulnaris, 2 an increase in sarcomere length, and an alteration in the extracellular matrix of semitendinosus.3 It is likely that the development of muscle deformity in spastic CP is related to a number of factors, but without detailed evidence are we able to speculate as to how it may occur? In this review, the factors influencing protein turnover in skeletal muscle are discussed, followed by an outline of the development of muscle innervation and of muscle fibre growth. Muscle changes in spastic CP are then discussed, following which some possible mechanisms which lead to the development of muscle deformity in CP are suggested.Neuronal innervation, mechanical demands, paracrine and endocrine factors, and nutrition influence skeletal muscle protein synthesis and degradation, which in turn determine muscle fibre size and metabolism. [4][5][6] The contractile proteins in the sarcomere, myosin and actin, are supported by larger proteins such as titin and nebulin, 7 which connect the actin and myosin, via the Z-disc and costameres, to the basal lamina and hence, via the endomysium, perimysium, and epimysium, to the tendon. Muscle fibres thus exist in a three-dimensional connective tissue framework which provides support, allows transmission of force, and appears to monitor muscle activity levels, particularly at the level of the Z-disc. 8,9 The balance between the development of muscle fibres and of the extracellular matrix in muscle appears to be determined by the interaction of neuronal, mechanical, and growth factors.

Ambulant young people with cerebral palsy (CP) have reduced muscle volumes in their lower limbs (as low as 50% of their weight‐matched typically‐developing peers). Yet, they may complete a ‘timed up‐and‐go’ test at similar speeds to unaffected persons. Perhaps, these individuals are able to maintain high levels of function because their muscle deficits have not fallen below the threshold values required to perform certain motor tasks. This is consistent with data from studies of progressive strengthening in children with mild CP. These programmes improve muscular output but have limited immediate effect on functional capacity. Sarcopenia is responsible for much of the loss of muscle mass in the typically developing adult. The decline in muscle mass begins in the mid‐twenties and occurs rapidly after the 7th decade. It is possible that the muscle deficits characteristic of young people with CP, coupled with the decline of muscle properties in adulthood, contribute to an early loss of mobility in this group. In the typically developing elderly, progressive strengthening is thought to extend mobility. Perhaps, the real value of strengthening programmes in CP is to improve muscular reserve in the short‐term and to maintain muscle mass above critical thresholds in the long‐term.

This study is the first to investigate the effects of surgery on muscle belly volume and length in the human subject. The study indicates that VP surgery is not an agent of long-term muscle atrophy in individuals with SDCP with plantarflexion deformities.

Due to an error in the December 2001 version of this article the corrected version is published below. Ultrasound images were obtained of the medial gastrocnemius at different ankle joint positions with the knee extended. Fascicle length and deep fascicle angle were measured in five normally developing adults (mean age 33 years, age range 24 to 36 years) and in five normally developing children (mean age 7.8 years, age range 7 to 11 years), and in seven children with spastic diplegia (mean age 10 years, age range 6 to 13 years). These architectural variables were similar in the groups of normally developing adults and children. Importantly, no statistical difference could be found between the normally developing children and those with diplegia for fascicle length. Deep fascicle angles were reduced significantly in the clinical group at a particular ankle joint angle but not at the resting angles. The difference in deep fascicle angles is explained as a function of resting muscle length and is not attributed any clinical importance. Our results do not explain the structural origin of muscle contracture explicitly. However, they do indicate that most of the fixed shortness in the medial gastrocnemii of ambulant children with spastic diplegia is not due to reduced muscle fibre length. We suggest that muscle contracture may be better explained in terms of shortness of the aponeuroses of pennate muscles, such as the medial gastrocnemius, through reduced muscle fibre diameter.

No abstract