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Orthoses at rest more commonly known as night splints, are they clinically relevant for the Cerebral Palsy population?

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Typically resting AFOs are requested to prevent ankle equinus contractures in growing CP children, by providing the necessary stretch stimulus that allows the muscle to lengthen in line with bone growth. The theory is sustained muscle stretch stimulates an increase in muscle length by addition of sarcomeres in spastic calf muscles, specifically the gastrocnemius. Numerous studies however support that elongation may be partially or shared between connective tissue and the muscle belly itself.

Growing evidence reveals clinical effectiveness of passive stretching is conflicted, and often yield clinically insignificant or worsening ROM’s overtime whether it be manual, stretching for minutes, or sustained for a duration of hours. Did you read the controversial Cochrane paper? Sustained stretch via orthoses for range is not an evidence-based treatment but is still often applied by the use of a night AFO splinting regime that are part of the general management of CP. In a current NHS climate of savings should we still be issuing resting orthoses, particularly AFO’s for CP?

From an anatomical stand point the night AFO modality is flawed in isolation for gastrocnemius lengthening as the knee needs to be captured in extension. Add in a gaiter and often compliance is a struggle especially in a bilateral situation. Again, papers looking at KAFO regimes for CP, Maas papers come to mind, utilising static and dynamic spring assist have also yielded little positive results, with little or no difference to the control group, and additionally poorly tolerated.

Another theory in the presence of spasticity is based on the potential efficacy of prolonged stretching that affect the stretch reflex. In practice, orthoses may be helpful in downregulating the stretch reflex. This may help to improve active functional performance of activities or increase the ease of ADL’s through the maintenance or improvement of range of movement passively.

A consideration however is with a CP child with a spastic muscle, the increased gain or lower threshold of the stretch reflex may cause the muscle to be activated even during low levels of stretch. If the net result of these factors was an increase in muscle stiffness, this could prevent the muscle from elongating in response to stretch.

A smaller fascicle length and smaller muscle thickness is found in children with CP, however, very little is known about the development of these. ROM of a joint is thought to be the passive slack length of the muscle tendon complex in relation to bone length and by the muscle tendon complex stiffness. The muscle tendon complex stiffness is determined by the size and length of the muscle belly fibres and by the amount and arrangement of connective tissues of the muscle tendon complex. Until we gain improved knowledge of the changes in muscle morphology in the CP child, we are unlikely to gain further insight into the etiology of reduced ROM in this population.

If delivered as part of an overall goal-directed rehabilitation or management programme at your centre, we would love to hear your thoughts on resting AFO provision for CP specifically for prevention of equinus?

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