Neurophysiological mechanisms of hypertonia and hypotonia in children with spastic cerebral palsy: surgical implications.

Abstract

Mechanism of hypertonia in cerebral palsy children is dual: a neural component due to spasticity (velocity dependent) and a biomechanical component linked to soft tissue changes. Their differentiation-which might be clinically difficult-is however crucial, as only the first component will respond to anti-spastic treatments, the second to physiotherapy. Furthermore, spasticity is frequently associated with dystonia, which is a sustained hypertonic state induced by attempts at voluntary motion. Spasticity and dystonia have to be carefully distinguished as dorsal rhizotomy will not significantly influence the dystonic component. Spasticity, which by definition opposes to muscle stretching and lengthening, has two important consequences. First, the muscles tend to remain in a shortened position, which in turn results in soft tissue changes and contracture. The second is that movements are restricted. Thus, both hypertonia and lack of mobilization create a vicious circle leading to severe locomotor disability linked to irreducible musculotendinous retraction and joint ankylosis/bone deformities. These evolving consequences should be highly considered during the child's assessment for decision-making. The hypotonic effects of lumbosacral dorsal rhizotomy, which are not only segmental on the lower limbs but also supra-segmental through the reticular formation, are finally discussed.