Dose et al.1 are to be congratulated on their paper describing spinal cord stimulation (SCS) generating activity in spinal networks, and thus emphasising the significance of the undamaged central nervous system in the restoration of function following a central nervous system lesion. After 30 years as the chairman of the scientific committee and trustee of the International Spinal Research Trust, as a lone voice advocating a shift of emphasis from the lesion to the intact central nervous system, with, it has to be said, very little effect, I feel this is a most welcome paper, highlighting as it does the importance of neuromodulation.
However, I would like to put the work of Dose et al.1 in some historical perspective. SCS was, of course, first used in the treatment of chronic pain as a direct result of the seminal work of Melzack and Wall,2 but the first person to demonstrate improvement in neurological deficit with SCS was Cook3 in the early 1970 s. He was carrying out this procedure for pain on a young sufferer with multiple sclerosis when to his great surprise he saw a marked improvement in spasticity with consequent improvement in ambulation. Cook3 had contacted me following a paper in The Lancet4 in which I had suggested that experimental changes in the central nervous following partial denervation and the effect of repetitive stimulation5 suggested an approach to neurological deficit via the intact central nervous system rather than the lesion itself. The speed of change suggested that this was almost certainly due to an increase in inhibition. Cook3 took his observations to the neurologists in his hospital and later to the neurological societies of New York. They refused to even investigate this. I knew the chief of neurology at Cook’s hospital and he told me that the general consensus was that, although Cook’s3 results were remarkable, ‘these things just don’t happen’. Subsequent studies by myself and colleagues6 (summarised in Spinal Cord Dysfunction Volume III) demonstrated, for the first time, recordable and reproducible neurophysiological changes in patients at spinal and brain-stem levels with epidural electrode SCS and eventually led to the formation of the International Neuromodulation Society.
What Cook3 had observed was no more than that reported by Frolich and Sherrington7 in 1902: after decerebration in cat, dog and Macaque, stimulation of the lower thoracic and lumbar region of the spinal cord showed ‘...an effect...constant and regular...evoked marked inhibition of the rigidity...’.
The convention of prior acknowledgement is important, as well as being courteous. Correct referencing demonstrates that the authors have read widely in their subject, indicates support for their hypothesis and adds credibility to their work.
Cook3 deserves much greater recognition.
References
Dose F, Deumens R, Forget P, Taccloa G . Staggered multi-site low frequency electrostimulation effectively induces locomotor patterns in the isolated rat spinal cord. Spinal Cord 2016; 54: 93–101.
Melzack R, Wall PD . Pain mechanism: a new theory. Science 1965; 150: 971–979.
Cook AW, Weinstein SP . Chronic dorsal column stimulation in multiple sclerosis. Preliminary report. N Y State J Med 1973; 73: 2868–2872.
Illis LS . Regeneration in the central nervous system. The Lancet 1973; 301: 1035–1037.
Illis LS . Enlargement of spinal cord synapses after repetitive stimulation of a single posterior root. Nature 1969; 5201: 76–77.
Illis LS Spinal cord dysfunction. In: Illis LS (ed). Functional Stimulation, vol. III. Oxford University Press, 1992.
Frolich A, Sherrington CS . Path of impulses for inhibition under decerebrate rigidity. J Physiol 1902; 28: 14–19.
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Illis, L. Spinal cord stimulation. Spinal Cord 55, 624 (2017). https://doi.org/10.1038/sc.2016.81
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DOI: https://doi.org/10.1038/sc.2016.81