Extrapolation of neuroscience research to the non-surgical management of compressive neuropathies

Abstract

Invited Commentary on: ‘Pain science and mobilisation of painful compressive Neuropathies’, Zusman The merit of this review is that it brings new and potentially important findings from neuroscience experiments to the attention of clinicians who might use movement-based treatment modalities in their management of common entrapment neuropathies. As nicely summarised in the review, Gupta and Steward propose that compressive peripheral neuropathy is a Schwann cell-mediated disease in the absence of axonal damage. Although Schwann cell-mediated changes indeed occur in their model of chronic nerve compression, the statements regarding axonal integrity are based on the quantitative evaluation of myelinated fibres which remained unchanged. For unmyelinated fibres, Gupta’s group report an increase in number of C-fibres. In a recent study using the same chronic nerve compression model, other authors provided evidence for a reduction of unmyelinated fibres distal to the injury in the innervated skin. Because determining axonal integrity with nerve biopsies in humans has obvious feasibility constraints, biopsy data are only available for severe compression neuropathies. These data support a degenerative– regenerative response of the unmyelinated fibre population. The exact nature and cause of nerve fibre depletion, and the possible contribution to neuropathic pain mechanisms, need to be carefully investigated before discarding the possibility of axonal loss in chronic nerve compression. Because of the lack of adequately powered randomised clinical trials, neurodynamics and many other areas of physiotherapy have embraced pain science research to underpin their application. Although largely unproven, various theories anchored in these more basic sciences have been proposed to promote the use of movement in the management of neuropathies. At first sight, the findings from Gupta and colleagues that mechanical stimulation may lead to dedifferentiation, proliferation, and apoptosis of Schwann cells, together with the down-regulation of myelin forming proteins and up-regulation of GAP43, appear to undermine a movement-based approach. A question which remains, however, is to what extent the in vitro models using laminar fluid flow chambers and in vivo models using silastic tubes resemble the sliding of nerves as they occur with normal movement. The rodent’s sciatic nerve may indeed slide through the tube immediately following the application of the tube, but at least in the silastic tube experiments we are currently conducting the formation of granulation tissue proximal and distal to the tube prevents the nerve from sliding through the tube. As such, it remains unclear whether longitudinal and transverse sliding within physiological ranges initiates these Schwann cell-mediated changes. If the advocated movement-based interventions do indeed stimulate the Schwann cells to the extent that a cascade of responses is initiated as outlined above, one would expect a deterioration of symptoms following treatment. Clinical trials have not reported such worsening. As mentioned above, large randomised clinical trials are not yet available, but a recent systematic review of the smaller trials concluded that the positive trends towards pain and symptom reduction, improved sensation, and improved function and strength, make nerve gliding techniques a reasonable option in the treatment of carpal tunnel syndrome (CTS). Although the common view is that the natural history of CTS is favourable, close inspection of the data reveals only marginal improvements in symptom severity, function, and neurophysiological findings over a 10–15 month period. Developing an effective treatment with low monetary and temporal costs is therefore important. As indicated in the review, George et al. indeed reported that the immediate effects of mobilisation of the median nerve in patients with CTS were not superior to a specific mobilisation. It should be noted, however, that the cited reference was an abstract which only reported preliminary findings in a small sample. More recently, the same research group demonstrated significantly larger hypoalgesia to temporal summation for mobilisation of the median nerve compared to a control treatment in asymptomatic participants and patients with CTS, suggesting a potential specific mechanism of action. The immediate analgesic effects were similar to those observed following spinal manual therapy. Two large-scale randomised clinical trials to investigate the effects of movement-based interventions for CTS and cervical radiculopathy are currently being conducted in our centre. These trials will raise the level Correspondence to: M W Coppieters, School of Health and Rehabilitation Sciences, Building 84A, The University of Queensland, St Lucia, Qld 4072, Australia. Email: m.coppieters@uq.edu.au Coppieters and Schmid Commentaries