Experimental Cold Injury to Peripheral Nerve

Abstract

Focal non-freezing injury to rat sciatic nerve resulted in nerve conduction block and cessation of axoplasmic transport. Rats showed early functional recovery but subsequently developed a slowly progressive sciatic nerve paralysis. Horseradish peroxidase studies revealed prominent nerve oedema with early enhanced pinocytosis and later, passive leakage through damaged endoneurial capillaries. Detailed microscopy indicated a striking selective vulnerability to cold based on nerve fibre diameter. Unmyelinated fibres were spared while large myelinated nerve fibres showed severe axonal degeneration. Paranodal and segmental demyelination were infrequent findings and may have resulted from early axonal swelling. Possible pathogenic mechanisms to explain the degeneration of myelinated fibres in hypothermic injury are discussed. It is concluded that the gradient of clinical severity seen in limb hypothermic injuries has a pathological correlate in peripheral nerve.

Cold-Induced Perturbation of Cutaneous Blood Flow in the Rat Tail: A Model of Nonfreezing Cold Injury

“…Numerous animal studies have focused on vascular and neural dysfunctions associated with exposures to nonfreezing cold (for example, Blackwood and Russell, 1943;Das et al, 1991;Denny-Brown et al, 1945;Endrich et al, 1990;Gilliatt and Kennett, 1987;Nukada et al, 1981;Peyronnard et al, 1977); however, with the exception of the Blackwood and Russell, study results of those animal studies are not necessarily pertinent to the unique human NFCI condition as they do not indicate a discernible progression of stages following cold exposure analogous to the syndrome described in humans. Taken together with data from other cold injury studies employing the rat tail model, which show that the tail exhibits distinctive stages of loss of thermal sensitivity followed by enhanced thermal sensitivity (Ahlers et aL, 1990) and manifests differential stages of characteristic neural dysfunctions (Shurtleff et al, 1993: Van Orden et al, 1990, the perturbations in cutaneous blood flow observed in the present study suggest that the rat tail may be an extremely functional and valid model of human NFCI.…”

Nerve conduction velocity in human limbs with late sequelae after local cold injury

“…Following a non-freezing cold injury (trench foot, immersion foot) neuropathy may develop and persist without limb swelling or histological abnormalities of blood vessels and muscles [6][7][8]. The detailed pathogenesis is still unclear [9], but thick, myelinated nerve fibres seem to be especially vulnerable to cooling [10][11][12]. In frostbite, formation of ice crystals may cause general necrosis and degeneration of all nerve fibres.…”

“…In frostbite, formation of ice crystals may cause general necrosis and degeneration of all nerve fibres. It has been suggested [11] that a continuum exists between the relatively mild, hypothermic lesion of trench foot, the intermediate syndrome of immersion foot and the severe, necrotic lesion of frostbite. These clinical conditions seem to correlate with the histopathological changes in peripheral nerves, progressively involving myelinated fibres, unmyelinated fibres and finally the entire endoneurium.…”

Nonfreezing Cold-Induced Injuries

“…Original animal studies that modelled NFCI, demonstrated that cold temperatures near the freezing point were more likely to cause injury when the extremities were wet than when they were dry [14]. Established NFCI is associated with histological and/or clinical evidence of nerve damage [16,17].…”