Cessation of paraplegic spasms by combined neuromuscular stimulation and standing

University College London (2003) J Physiol 547P, C146

Oral Communications: Cessation of paraplegic spasms by combined neuromuscular stimulation and standing

Jonathan A. Norton*, Duncan E. Wood† and Brian L. Day*

*Human Movement Group, Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, University College London, London WC1N and †Department of Medical Physics and Biomedical Engineering, Salisbury District Hospital, Salisbury, UK

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Patients with complete paraplegia frequently suffer from muscle spasms. In a pilot study, electrical stimulation of the posterior nerve roots was demonstrated to stop spasms in a paraplegic patient (Craggs et al. 2000). In the present study we have investigated whether spasms could be altered by neuromuscular stimulation and/or load-bearing standing. All experiments were approved by the local ethics committee and the patient gave informed consent.

The patient, a 59-year-old male, had a complete spinal cord lesion at the 10/11th thoracic level of 20 years duration and a S2-5 posterior rhizotomy. He commonly experienced dorsiflexion spasms at rest. Kinematic and EMG recordings showed that a spasm involved ankle and knee flexors and extensors bilaterally with an interspasm interval of between 3 and 30 s. The spasms showed significant coherence between muscles at various frequencies within and between legs (Fig. 1).

When he stood with the assistance of 20 Hz stimulation of both quadriceps muscles the spasms stopped entirely. At the end of the stimulated stand the spasms did not reappear for periods up to 7 h, although rapid passive dorsiflexion would restart the spasms with the same resting characteristics as before. Passive standing, without stimulation in a standing frame, stopped the spasms but only for approximately 5 min. The legs bore 68 ± 4 % and 61 ± 1 % body weight (mean ± S.D.) during stimulated and passive standing, respectively. With the subject supine, bilateral stimulation of quadriceps, either on its own or in conjunction with manual pressure applied to the soles of the feet, had no effect on the spasms.

The coherence analysis suggests that components of the spasm arise from common sources, possibly driven by spinal oscillators. The results imply that the spinal circuits responsible receive inputs from the periphery, which are capable of modulating the spasm source. It appears that in this subject spasm suppression is maximally effective when the afferent input is generated by the combination of muscle stimulation and load-bearing standing.

We wish to thank our patient. This work was supported by the UCL Graduate School and MRC.



Where applicable, experiments conform with Society ethical requirements.

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