The high prevalence of spontaneous activity demonstrates that denervation of the skeletal muscles served by motor neurons below the level of the lesion occurs in individuals with chronic complete SCI. The electrophysiological testing revealed the striking absence of sensory and motor nerve conduction and aberrant neuromuscular junction transmission. It is important to understand the mechanisms that underlie the profound reduction of the functional integrity of the peripheral nervous system to maximize the restoration of movement, particularly should descending neural control be reestablished by a future therapy.

Chemotherapy drugs have neurotoxicity associated with treatment, which can become a doselimiting problem when clinical presentation is severe. However, there is no effective therapy to circumvent the neurotoxicity of anti-cancer drug treatment. In this study, we utilized a newly designed mouse model of cisplatin-induced peripheral neuropathy to determine both the severity of neurotoxicity induced by drug treatment and the effectiveness of the Rho kinase inhibitor Y-27632 in post-treatment recovery. Sensory nerve conduction studies revealed a significant increase in mean distal (peak) latency with cisplatin treatment, indicating a deterioration of sensory nerve function. Also, hind paw touch sensitivity decreased steadily with increasing cumulative dose of cisplatin. Histological and immunohistochemical analyses of the sural nerve using neuronal marker protein gene product 9.5 (PGP 9.5) demonstrated abnormal nerve fiber morphology in cisplatin-treated mice. Remarkably, post-treatment with Y-27632 improved the sural nerve distal (peak) latency and sensory threshold to return to pre-treatment levels. Sural nerve histology worsened in the absence of Y-27632 during recovery. These studies suggest that Rho kinase inhibitor Y-27632 can initiate regeneration of damaged nerves following cisplatin treatment.

There is increasing interest in using mouse models for electrodiagnostic research. Studying transgenic mice with various pathologies, add to our knowledge of the natural history of a disease. It is imperative, however, to compare disease models to the appropriate control. Therefore, in order for these animals to be used in electrodiagnostic research, reference values must be set. If reference values are not available, the validity of data is highly questionable. We propose a method of obtaining mixed nerve action potentials and collect reference values from the sural nerve of mice. The results were a mean peak latency of 1.74 ms on the right and 1.89 ms on the left. The mean amplitude was 17.0 μV on the left and 21.6 μV on the right. In future studies, these reference values can be useful tools in analysis of murine subjects.

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