The natural history of diabetes neuropathy is progressive and irreversible loss of sensibility in the feet, leading to ulceration and/or amputation in 15% of patients. The prevalence of neuropathy is more than 50% in those who have been diabetic for 20 years. Decompression of the tibial and peroneal nerves in those with diabetic neuropathy improves sensation in 70% of patients. The impact of this surgery on the development of ulcers and amputations in both the operated and the contralateral, nonoperated limb was evaluated in a retrospective analysis of 50 patients with diabetes a mean of 4.5 years (range, 2-7 years) from the date of surgery. No ulcers or amputations occurred in the index limb of these patients. In contrast, there were 12 ulcers and 3 amputations in 15 different patients in contralateral limbs. This difference was significant at P < 0.001. It is concluded that decompression of lower extremity nerves in diabetic neuropathy changes the natural history of this disease, representing a paradigm shift in health care costs.

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Cisplatin produces a dose-dependent and dose-limiting peripheral neuropathy in patients. This study tested the hypothesis that this clinical neuropathy results from the chronic compression of peripheral nerves rendered susceptible to injury because of cisplatin-induced microtubular dysfunction. A quantitative model of cisplatin neurotoxicity was developed by administering cisplatin to rats and measuring the neuropathy by hindlimb walking track assay. The study aims were: (1) to characterize neuropathy induced by cisplatin in the adult rat; (2) to evaluate the role of decompressive surgery in the prevention of cisplatin neuropathy; and (3) to determine whether decompressive surgery was an effective treatment for established neuropathy. The assay demonstrated an increased print length in animals after 8 weeks of cisplatin (p < 0.01). This neuropathy progressed for 6 weeks after cisplatin was stopped, and reversed slowly over 3 months. These abnormalities were prevented by early tarsal tunnel decompression. Decompressive surgery was also beneficial, if performed early in the course of the neuropathy; abnormalities reversed in 5 weeks and remained normal for the remainder of the study. Control animals had progressive abnormalities which slowly resolved over a period of 18 weeks after discontinuing cisplatin. However, decompressive surgery performed after the neuropathy was established did not alter the neuropathic walking-track pattern. These studies provide insight into the etiology and possible therapeutic approaches to cisplatin neuropathy. Although further studies are required, they suggest that, in selected patients, decompressive surgery may have a role in the prevention or early treatment of cisplatin-induced neuropathy. Patients with underlying clinical or subclinical compressive neuropathies could be at high risk for the development of cisplatin neuropathy, and quantitative monitoring of neuropathies may be useful.

A pyridoxine (B6) dietary deficiency was studied in female adult Sprague-Dawley rats by hind-limb walking-track analysis. Serum levels of pyridoxine and three metabolites were quantified by high-pressure liquid chromatography with fluorescence measurement. Morphometric analysis of the sciatic and posterior tibial nerves (from within the tarsal tunnel) was performed after 1 year on a diet deficient in vitamin B6. The B6-deficient rats developed abnormal walking-track patterns by 8 months, and these track parameters were different from age- and sex-matched normal diet control rats at the p < 0.05 level. Adding B6 at 10 parts per million to the diet then partially corrected these parameters, whereas the addition of 30 parts per million B6 corrected the abnormal pattern completely. Serum pyridoxal concentration correlated with the functional parameters, dropping from a mean of 115 mg per liter to 39.5 mg per liter (p < 0.05), and correcting with the B6 additive. Morphometric analysis demonstrated that the B6-deficient nerve from the tarsal tunnel had a decreased nerve fiber density (p < 0.001), with a normal total myelinated nerve fiber number, and an increased axon-to-myelin ratio (p < 0.003). It is concluded that a diet totally deficient in vitamin B6 results in a peripheral neuropathy.