The effect of cold on nerve fibre populations may be quite selective.
Thus it was possible in the present study, with precise timing of a no
n-freezing cold nerve injury, to destroy myelinated fibres, but leave
unmyelinated fibres intact, The aetiology of this cold-induced selecti
ve peripheral nerve pathology remains controversial, but recent eviden
ce suggests that ischaemia plays an important role. To investigate thi
s matter further, me have sought to determine whether ischaemia alone
might account for such discrete nerve pathology, in a series of non-fr
eezing cold injury paradigms. Compared with previous 'pure' ischaemic
peripheral nerve models, notable differences were found in the present
paradigms (early post-ischaemic luxury perfusion and severe nerve pat
hology), suggesting a multifactorial aetiology, Nonetheless a tight co
rrelation was evident, with increasing duration of cold injury resulti
ng in a progressively more severe reduction in post-cold nerve blood h
ow Given these findings, we would propose that the pathological basis
of non-freezing cold nerve injury is one of ischaemia, accelerated and
enhanced by direct cold injury.