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The potential therapeutic effect of hyperbaric oxygen (HBO) after rat peroneal nerve crush was evaluated. Animals were given 100% oxygen at 2.5 atmosphere absolute for 90 minutes twice daily for 1 week and then once daily for 1 week. Edema increased in crushed nerves compared with control nerves, but no effect was associated with the administration of HBO. Gait analysis demonstrated injury at 1, 7, and 14 days after nerve crush, but no difference was found at 22 and 28 days after injury (analysis of variance: P < .001, 10 animals per group). Eight weeks after injury, nerve stimulation and muscle force measurements were 114 g for the injured group and 146 g for the control group (P < .001). There were no HBO-associated changes in gait parameter or nerve/muscle force measurements. This study demonstrated that rat peroneal nerve crush injury causes acute intraneural edema and temporary decrement of gait parameters. Elicited nerve stimulation demonstrated persistent loss of force 4 weeks after normalization of gait, but no HBO effect.

The potential benefit of brain-derived neurotrophic factor (BDNF) on motor-nerve regeneration after transection injury in 24 adult rats was evaluated after entubulation repair. Gait analysis for ankle angle and tension transduction device (TTD) strain-gauge measurements yielded functional evaluation of regeneration. The BDNF (15 mg/mL) or phosphate buffered saline (control) was injected into the silicone elastomer (Silastic) channel. Gait analysis performed 0, 2, 4, 6, 10, and 12 weeks after injury demonstrated a significant difference between uninjured and injured legs of 23 and 43 degrees, respectively (P<.001, analysis of variance). The TTD evaluation 13 weeks after injury demonstrated a significant decrease in force development of injured compared to uninjured legs, 148 and 58 g, respectively (P<.001). No functional benefits were demonstrated between BDNF-treated versus control-treated animals in either model for a single exposure to BDNF.

Rat peroneal nerves were transected and entubulated with a Silastic channel. The experimental group was treated with hyperbaric oxygen to evaluate changes in acute edema, functional recovery, and histology. Hyperbaric oxygen was administered with 100% O2 at 2.5 atmospheres absolute for 90 minutes twice a day for 1 week and then four times a day for 1 week. Acute edema changes based on nerve water weight and transfascicular area measurements were greater in injured than in uninjured nerves but demonstrated no differences between hyperbaric oxygen-treated and -untreated groups 2, 8 and 16 days after surgery. Functional evaluation with gait analysis demonstrated significant changes between injured and uninjured group 1, 3, 7, and 13 weeks after injury but no differences between hyperbaric oxygen-treated and -untreated groups. Thirteen weeks after the initial injury, elicited muscle force measurements demonstrated no significant improvement from hyperbaric oxygen treatment of injured nerves. Histologic evaluation of nerve area, myelinated axon number, myelinated axon area, myelin thickness, and blood vessel number and area revealed no significant differences between hyperbaric oxygen-treated and -untreated groups. Hyperbaric oxygen was not associated with improvement of nerve regeneration with any of the outcome variables in this model.

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