nerve crush injury indicated that animals which received
treatment with hyperbaric oxygen at pressures of at least 2.5
atmospheres absolute (ATA) experienced enhanced regeneration
of the crushed nerve during the first few days following injury and
treatment (Haapaniemi et al., 1998). Bajrovic´ et al. (2002) found
that, when using a similar model, HBO therapy did not dose
dependently effect regeneration and when examining a crush of
the sural nerve, HBO did not effect regeneration in distal axons in
comparison to the control group. Research focusing on recovery of
motor functioning after a nerve crush injury has been inconclusive
as well. For instance, functional recovery following a nerve crush
injury and HBO therapy was not improved by treatment
(Haapaniemi et al., 2002), yet Zamboni et al. (1995) found that
when the sciatic nerve was transected and then repaired HBO
significantly improved motor functioning. Finally, in a commonly
used model of neuropathic pain, the chronic constriction injury of
the sciatic nerve, it was found that HBO improved blood flow,
decreased edema, and prevented cellular damage of the mitochondria
and other organelles as compared to animals which did
not receive treatment (Mychaskiw et al., 2005). Surprisingly, this
study did not quantify the effects of HBO treatment on pain, and no
other study has attempted to utilize this model or examine
neuropathic pain and HBO.