This 2003 review by Graham and Selber synthesizes the musculoskeletal pathology, natural history, and management framework for the cerebral palsies. It covers spasticity management (BTX-A, ITB, SDR) and orthopaedic surgery across all three major topographic subtypes. The central argument: the static brain lesion should never be cited without acknowledging the progressive musculoskeletal consequences.
The trainee who understands one thing from this paper: the brain lesion in CP is static, but the musculoskeletal pathology is not. Every management decision — when to inject BTX-A, when to operate, how to plan multilevel surgery — flows from recognizing that contractures, bony torsion, and hip displacement will worsen if left untreated.
When you see a child with spastic diplegia being referred for toe-walking, resist the impulse to simply lengthen the Achilles tendon. That isolated procedure reliably produces crouch gait as proximal deformities progress. The correct approach is full biomechanical assessment and single-event multilevel surgery addressing all levels simultaneously.
When managing a child with spastic quadriplegia, hip surveillance cannot be passive. With a 35–55% prevalence of displacement and a silent early course, systematic screening radiographs are the only way to catch displacement early enough for soft-tissue prevention rather than major reconstruction.
The negative features of the upper motor neurone syndrome (weakness, poor selective motor control) determine whether a child will walk — not spasticity. Aggressively treating spasticity while ignoring strength training addresses the wrong problem.
This 2003 review by Graham and Selber synthesizes the musculoskeletal pathology, natural history, and management framework for the cerebral palsies. It covers spasticity management (BTX-A, ITB, SDR) and orthopaedic surgery across all three major topographic subtypes. The central argument: the static brain lesion should never be cited without acknowledging the progressive musculoskeletal consequences.
The trainee who understands one thing from this paper: the brain lesion in CP is static, but the musculoskeletal pathology is not. Every management decision — when to inject BTX-A, when to operate, how to plan multilevel surgery — flows from recognizing that contractures, bony torsion, and hip displacement will worsen if left untreated.
When you see a child with spastic diplegia being referred for toe-walking, resist the impulse to simply lengthen the Achilles tendon. That isolated procedure reliably produces crouch gait as proximal deformities progress. The correct approach is full biomechanical assessment and single-event multilevel surgery addressing all levels simultaneously.
When managing a child with spastic quadriplegia, hip surveillance cannot be passive. With a 35–55% prevalence of displacement and a silent early course, systematic screening radiographs are the only way to catch displacement early enough for soft-tissue prevention rather than major reconstruction.
The negative features of the upper motor neurone syndrome (weakness, poor selective motor control) determine whether a child will walk — not spasticity. Aggressively treating spasticity while ignoring strength training addresses the wrong problem.