Abstract
The main elements of neurogenic inflammation in the skin – antidromic vasodilatation, axon reflex flare and neurogenic plasma extravasation – are briefly described. New evidence is presented for a contribution from small myelinated fibres, as well as unmyelinated fibres, to antidromic vasodilatation. The mechanisms underlying flare are discussed and it is argued that weak coupling between C-fibre terminals must be important in determining the extent of spread of vasodilatation. The extent to which neurogenic factors contribute to a range of inflammatory models and to inflammatory disease states is discussed; it is argued that the importance of neurogenic mechanisms may have been underestimated.