Cold-induced neuropathy may play a dominant role in the long-term sequelae with cold sensitivity after local cold injuries (LCIs). Somatosensory functions were assessed and nerve conduction velocity (NCV) and motor distal delay (MDD) were measured in the limbs of 31 Norwegian former soldiers with persistent cold intolerance 3-4 years after the primary LCI. NCV measurements were performed in 24 lower and 16 upper extremities. NCV was related to degree of overall subjective complaints quantified by means of a visual analogue scale (VAS). Motor (MNCV) and sensory conduction velocity (SNCV) in the lower extremities and SNCV in the hands were significantly decreased compared with controls. MDD was pathologically increased in the feet. NCV of the forearms ranged from normal to significant reduction. The more pronounced effect on the lower extremities may be caused by deeper cooling of the calves compared with forearms for several reasons. No significant associations were found between VAS and NCV except for the right median nerve. NCV measurements may provide objective findings in cold-injured patients and in those with few or no conspicuous clinical signs.

The present findings may demonstrate important neurovascular reactions to local frostbite and may explain human sequelae following frostbite.

Rapid rewarming of in vivo frozen arteries in warm water (42 degrees C) did not prevent immediate vasoparalysis and degeneration of sympathetic nerves. However, nerve regeneration occurred earlier and with higher tissue nerve densities as compared to tissue that had been slowly rewarmed. Myointimal hyperplasia was less pronounced after rapid rewarming. Abnormal sympathetic nerve function and myointimal hyperplasia, as observed in this study, may contribute to a greater understanding of sequelae in the human body following frostbite.