• M Koltzenburg and J Scadding.
• Institute of Neurology, University College London and National Hospital for Neurology and Neurosurgery, London, UK. M.Koltzenburg@ich.ucl.ac.uk
• Curr. Opin. Neurol. 2001 Oct 1; 14 (5): 641-7.

AbstractDamage to peripheral nerves triggers a cascade of events in axotomized sensory neurones that are generally believed to be responsible for the generation of neuropathic pain. Recent data in animal models show that alterations in the properties of undamaged neurones that project into a damaged nerve can also play an important role. These new findings could explain some of the enigmatic clinical signs and symptoms of pain following nerve injury such as the spread of symptoms into areas not affected by the primary lesion. The basis by which uninjured nerves could be affected is a reduced supply of neurotrophic factors, an abnormal interaction in the Remak bundles of partially denervated Schwann cells and unmyelinated axons, or the byproducts of Wallerian degeneration.

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