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3. Winsler A, Hutchison LA, De Feyter JJ, et al. Child, family, and childcare predictors of delayed school

Should children with cerebral palsy exercise? UNNI G NARAYANAN Department of Surgery & Child Health Evaluative Sciences, The Hospital for Sick Children, Bloorview Research Institute, University of Toronto, Toronto, ON, Canada. doi: 10.1111/dmcn.12765 This commentary is on the original article by Balemans et al. on pages 660–667 of this issue.

Should children with cerebral palsy (CP) exercise? Surely they should. The received wisdom on the value of exercise has approached the level of self-evident. That is, until Van Wely et al.1 reported that a 6-month home-based programme of physical activity, comprising lifestyle counseling and fitness training – including strengthening and anaerobic exercises – neither increased physical fitness nor improved physical activity in ambulant children with CP, when compared with traditional physiotherapy. In fact, in this randomized trial, neither group demonstrated any meaningful improvements in any of the outcome measures at the end of the 6-month programme, let alone 12 months from baseline. This was a disappointing finding. After all, there is indisputable evidence that children with CP are less fit, less strong, and less active than their typically developing peers.2 How, then, could a programme designed to increase fitness fail to show any benefits, even in the context of a welldesigned trial? Perhaps the data deserved further scrutiny. The investigators observed wide variation in responses among participants, prompting them to perform subgroup analyses of the secondary outcomes of the original trial, to explain why some children seemed to benefit while others did not. They explored, longitudinally, the association between changes in fitness (aerobic, anaerobic, and muscle strength) and changes in mobility capacity (gross motor function measure [GMFM] and 1-min walk test) over time. Their findings, reported by Balemans et al.3 were equivocal. In children with unilateral CP, the changes in different aspects of fitness were associated neither with each other nor with measures of mobility. However, in children with bilateral CP, changes in aerobic fitness were associated with changes in anaerobic fitness, and weakly associated with changes in muscle strength. In multivariate analyses, anaerobic fitness and knee strength were the most important determinants of improvements in GMFM, while

anaerobic fitness and hip abductor strength was associated with increased walking capacity. The rationale for such secondary analyses is understandable, but must be considered cautiously in the face of an increased probability of finding significant associations merely by chance. In children with bilateral CP, the observed improvements in fitness, GMFM, and walking capacity were modest at best, and, arguably, of little clinical significance. The 6-month supervised home programme, with components of fitness, strength training, as well as counseling, can hardly be dismissed as an inadequate ‘dose’ of exercise. If the intensity and duration of such a programme are inadequate, how feasible would it be for children with CP to access or participate in an ‘adequate’ exercise programme outside the context of a controlled trial? On the other hand, perhaps the benefits of exercise lie elsewhere. The intended goal of the intervention programme was to increase physical activity. It could be argued that participation in the programme was, in itself, successful in increasing participants’ physical activity, even if no measurable functional gains resulted. It would be interesting to know what participants thought of the programme. In a separate report, the intervention group did demonstrate higher levels of social participation in domestic life after 12 months than their counterparts in the comparison group.4 So, should we recommend exercise for children with CP and, if so, for what benefits exactly? The literature suggests that aerobic exercise can improve physiological outcomes in children with CP, but evidence that these changes have any meaningful impact on outcomes of activity and participation remains elusive.5 This trial does not change that conclusion; therefore, the answer to the question has to be no (at least not yet) if those outcomes are the ultimate and only goals of exercise. It is plausible that, for most children with CP, the largest benefits of exercise might be of a preventative nature. The apparent negative outcome (no change) in this trial might, over time, be proven to be a positive one, if exercise contributes to preserving function and mobility, which are otherwise known to deteriorate during adolescence and young adulthood, or contribute to long-term health benefits. Commentaries


Since these benefits are based on ‘common-sense’ rather than ‘evidence’, we should recommend exercise for children with CP no less (or no more) than we do for all children, while we continue to study the long-term

impacts of exercise, along with how best to create opportunities for children with CP and other developmental disabilities that allow them to effectively and sustainably engage in healthy lifestyles.

REFERENCES 1. Van Wely L, Balemans AC, Becher JG, Dallmeijer AJ.

3. Balemans AC, Van Wely L, Becher JG, Dallmeijer AJ.

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Associations between fitness and mobility capacity in

cerebral palsy did not improve physical activity: a rando-

school-aged children with cerebral palsy: a longitudinal

mised trial. J Physiother 2014; 60: 40–9.

analysis. Dev Med Child Neurol 2015; 57: 660–667.

ipation, self-perception and quality of life: a randomized controlled trial. Clin Rehabil 2014; 28: 972–82. 5. Rogers A, Furler BL, Brinks S, Darrah J. A systematic review







2. Carlon S, Taylor N, Dodd K, Shields N. Differences

4. Van Wely L, Balemans AC, Becher JG, Dallmeijer AJ.

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in habitual physical activity levels of young people with

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AACPDM evidence report. Dev Med Child Neurol 2008;

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tematic review. Disabil Rehabil 2013; 35: 647–55.

Trunk control for reaching: growing into or out of dysfunction? SANDRA SAAVEDRA University of Hartford, Rehabilitation Sciences, West Hartford, CT, USA. doi: 10.1111/dmcn.12732 This commentary is on the original article by van Balen et al. on pages 668–676 of this issue.

Deficits in postural control are a hallmark of cerebral palsy (CP), yet little is known about the trajectory of early postural development in children with CP due to the difficulty of diagnosis before 1.5 to 2 years of age. This hampers efforts to improve rehabilitation and services for children during the early years when their nervous systems are most receptive to activity-based interventions. Knowledge of the time course, processes, and interactions of postural development with functional skills is essential for understanding current treatment responses and for developing strategies for better outcomes for these children. The article by van Balen et al.1 is of great interest because it offers a rare glimpse into longitudinal postural reactions in a group of young infants at high risk for neurological deficits. They report that postural reactions during reach did not differ between infants at high risk and typically developing infants at 4 and 6 months of age, while at 18 months the infants at high risk showed significant deficits in timing and coordination of postural muscles during reach. The authors conclude that the infants at high risk ‘grew into postural deficit’. These findings suggest that neural connections to trunk muscles, similar to corticospinal connections for upper extremity function,2 may be intact at birth but susceptible to activity-dependent remodeling during the first years of life. There are several issues that need consideration before fully embracing these conclusions. (1) Inclusion criteria for 598 Developmental Medicine & Child Neurology 2015, 57: 593–599

the group at risk required ‘definitely abnormal general movements’ at 10 weeks of age. This raises a question about why, if general movements were abnormal, their movements for postural reactions during reach were ‘virtually similar’ to typically developing infants at 4 and 6 months of age. Were postural responses the same or does the method of evaluation lack the sensitivity to differentiate between high risk and typically developing at early ages when infants have noisy data due to variability of performance? Ultimately we must ask, did the infants at high risk ‘grow into their dysfunction’ or did the typically developing infants ‘grow out of their dysfunction’? The results reported for direction specificity suggest the latter while results for anticipatory reactions and latency of onset suggest the former. (2) This study used only three observational episodes: 4, 6, and 18 months. Increased frequency of observation is necessary to examine the true trajectory of postural development and isolate other contributing factors.3 (3) There were no measures indicating age of onset for independent sitting. While children in the two groups were the same chronological age, they were most likely at different developmental stages of postural control especially by the time they were 18 months of age. (4) The methods used for electromyography (EMG) could have contributed to sparse information. Collecting bilateral EMG from trunk muscles would allow greater opportunity to record direction specificity, and recruitment order. The adult-like 100ms window for anticipatory responses could have biased the results against the group at high risk who showed increasing latency of responses with age. The authors entice us with the ambiguity of questions faced by clinicians and researchers. The need to pose challenging situations to stimulate postural activity is countered by the need to provide adequate postural support to allow infants to learn fine motor and cognitive skills. What

Should children with cerebral palsy exercise?

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