Peripheral nerves respond to injury in a unique fashion. Changes in the local milieu of the injured nerve trunk may determine both the likelihoods of regeneration and the production of neuropathic pain. For example, changes in local blood flow within this microenvironment may reflect several interesting features of the repair process. Crushed and sectioned nerves develop hyperemia, or rises in local blood flow rather than ischemia, and these rises appear to be mediated by one of several mechanisms. Firstly, vasa nervorum, the blood vessels that supply nerve trunks, are innervated by peptidergic fibers that may participate in "neurogenic" inflammation, as occurs in other innervated tissues. Secondly, following a nerve section or crush, early rises in blood flow may be mediated by local deposition of calcitonin gene-related peptide and nitric oxide from axonal end bulbs. Thirdly, brisk angiogenesis accompanies a proliferative phase in the proximal nerve stump that accompanies mast cell proliferation and axonal sprouting. Axonal sprouting, in turn, may be supported by local trophic factors, and the success of subsequent regrowth down the distal nerve stump may be determined by the microenvironment it encounters on its road to recovery. Better understanding of these and other events in injured nerve trunks is needed to help solve the two cardinal problems of peripheral nerve injuries: functional disability from impaired regeneration and the development of disabling neuropathic pain.
Biomedical Reviews 1997; 8: 37-54.
Email this article (Login required) 
