Purpose of study: To describe the histological effects of botulinum toxin on gastrocnemius muscle affected by cerebral palsy.

Method: Samples of gastrocnemius were obtained at the time of surgery. Ethical committee approval had been obtained for the study. Details of timing and doses of botulinum toxin previously administered to the muscle were recorded. A variety of immunohistochemical tests were employed to identify any changes in the muscle. Alterations in the distribution of myosin isoforms were identified with antibodies for fast, slow and neonatal myosin. The presence of persistent denervation was inferred from fibres deficient in neuronal nitric oxide synthase (nNOS). Mitochondrial abnormalities were assessed with an NADH stain and the presence of chronic atrophic fibres (nuclear clumps) noted.

Results: Our first case had received 3 botulinum injections over a period of 5 years, the last one 3 years prior to biopsy. Histology showed pronounced abnormalities with a wide variation in fibre size, areas of myofibrillar disruption and 50% of fibres co-expressing fast and slow myosin. Other samples showed less change but showed more frequent nuclear clumps than controls, indicating chronic atrophy and more hybrid fibres than controls, but always less than 10%. Treated muscles also showed a small, variable number of atrophic fibres without nNOS. Treated samples showed no apparent fibre type grouping, a feature associated with collateral sprouting of peripheral nerves following denervation.

Conclusions: Moderate doses of botulinum toxin appear to produce an alteration in muscle histology apparent several years afterwards. No correlation could be found between the timing of the previous injection or the dose of botulinum toxin injected and the severity of the changes. Botulinum toxin remains a valuable aid in the management of spastic muscle. However consideration should be given to other methods of treatment if an effective non surgical alternative exists.

Introduction: Selective dorsal rhizotomy has been used extensively in Europe and North America in the management of spasticity secondary to cerebral palsy. Permanent reduction in lower limb spasticity has been observed with consequent improvements in gait parameters. A decade ago a rhizotomy programme was established in Oswestry to utilise the technique for a carefully monitored group of children with cerebral palsy diplegia.

Methods: Using stringent selection criteria, twenty children underwent selective lumbar dorsal rhizotomy with follow up by means of gait analysis. A permanent reduction in spasticity has been observed with a significant improvement in almost all parameters. We report the need for further bony and soft tissue surgery and our complications. There has been weight gain in the majority of cases. There has been no major spinal deformity.

Conclusion: As a result of our review of the results in the first twenty cerebral palsy diplegic patients we have modified our selection criteria. Exclusion criteria include weakness, not enough spasticity or poor control.

A chance observation of asymmetrical bone ages in a child with spastic hemiplegia stimulated a prospective gathering of bilateral hand radiographs in 33 hemiplegic patients, and on a single occasion in a control group of 23 patients with leg length discrepancy in the absence of neurological disorder. The bone age assessments according to Greulich and Pyle, which by convention has used the left hand only, were done by a single expert observer blinded to the clinical details.

13 hemiplegic patients (39%) had delayed bone ages of 6 months or more. When present it was always delayed on the hemiplegic side. The mean delay for the whole group was 2.5 months, whereas there was no mean difference in the control group (p = 0.001). The oldest bone age with asymmetry was 14.5 years in males and 12 years in females, indicating that when present the delay “catches up” in the last 2-3 years of growth.

In hemiplegia the percentage leg length discrepancy also tends to decrease during later growth, and after 80% of growth the hemiplegic side outgrows the normal leg by a mean of 0.3cm/year. No correlation could be found between the delay of bone age and the severity of either the neurological abnormality or the actual discrepancy of length. The implications for clinical management will be discussed.