Spasticity as part of a central neurological disorder is characterized by a ‘velocity dependent hyperactive stretch-reflex’ [1]. Secondary, morphological adaptations of the muscle-tendon complex reduce the passive joint angle-moment relationship (i.e. passive ROM) [2]. Potentially, joint hyper-resistance, as a result of either the neurological disorder, muscle morphology or both, can be clinically assessed [3]. Botulinum Toxin-A (BoNT-A), in combination with casting and physiotherapy are regularly used as conservative treatment in children with a spastic paresis to improve gait. While in some studies improvements resulting from this approach are reported, large treatment response variability persists [4]. Heterogeneity in treatment effectiveness may be due to a clinical focus at the joint impairment level rather than on the contributing mechanisms of joint hyper-resistance. In recent years great advances have been made in standardized, objective assessments of stretch reflexed induced joint hyper resistance [5]. 3D ultrasound (3DUS), allows morphometry of the muscle-tendon complex in children with spastic paresis [6]. The combination of instrumented assessments of neurological, muscle morphology and gait characteristics following treatment has not been carried out.@en

Selective dorsal rhizotomy (SDR) is a neurosurgical treatment to reduce spasticity in children with cerebral palsy (CP). Where some children show large improvements on domains of motor function and mobility, others do not [1–3]. Since SDR is a highly invasive and irreversible treatment, it is important to select only those candidates who are most likely to benefit from the procedure.@en