'Botulinum toxin and cerebral palsy: time for reflection?' SIR-We write in response to the above review by Gough et al. 1 We commend Gough, Fairhurst, and Shortland for their timely, balanced, and clearly expressed view of the role of botulinum toxin A (BTX-A) in cerebral palsy (CP) and the Editor of the journal for publication of this important review.The premise that 'the use of BTX-A is based on the concept that muscle fibres in children with spastic CP are short, and that weakening the muscle with BTX-A injections will allow them to be stretched and, thus, to grow longitudinally' is not exactly what we had in mind from our experimental studies in the hereditary spastic mouse, 2 or in pilot work in the use of BTX-A in children with CP. 3 The view that sarcomere numbers are reduced and fibre length decreased in spastic muscle is not well supported by the literature as reviewed by Foran et al. 4 However, there is much stronger evidence for shortening of the muscle belly, with compensatory increased length of the tendon and shortening of the entire muscle-tendon-unit (MTU), all of which result in abnormal posturing and decreased joint range of motion. It was shortening of the MTU as a whole that we and others have investigated in both the hereditary spastic mouse and in children with CP. 2,3 There is evidence in both the hereditary spastic mouse and from musculoskeletal modelling in children, for lengthening of the MTU as a whole, after injection with BTX-A. 5,6 This lengthening may be a passive phenomenon and the result of weakness from BTX-A chemodenervation. There is Level I evidence that this can result in a reduction in spastic equinus and modest improvements in gait. However, the majority of studies to date are very short term and Gough and colleagues are right to draw attention to the broader context of the management of the motor disorder in older children, adolescents, and adults with CP which is dominated much more by weakness than by spasticity. Weakness is much more important as a key issue in bilateral CP (spastic diplegia and spastic quadriplegia) than in unilateral CP (spastic hemiplegia). Therefore, although the use of BTX-A in the management of spastic posturing in the hemiplegic upper limb can be compromised by increased weakness, this is unlikely to be of significance in the longer term. Children with spastic hemiplegia never develop crouch gait, therefore the use of BTX-A for the management of spastic equinus is unlikely to be detrimental in the long term.In bilateral CP, crouch gait is part of the natural history but is also frequently exposed or exacerbated by any intervention which results in weakness of the soleus and reduces the effectiveness of the plantar flexion knee extension couple. Such interventions most definitely include any form of lengthening of the gastrocsoleus, selective dorsal rhizotomy (SDR), intrathecal baclofen (ITB), and chemodenervation with BTX-A. Before the use of BTX-A in the management of spastic equinus in our centre, many children had isolated surgical lengtheni...