Pyridoxine metabolism in carpal tunnel syndrome with and without peripheral neuropathy.

The role of insufficient pyridoxine as an etiologic factor in the development of carpal tunnel syndrome (CTS) has been reported and has led to the empirical use of pyridoxine to treat CTS. Previous studies have not employed standardized electrodiagnostic criteria to objectively determine the presence of CTS or to rule out peripheral neuropathy (PN). The present study categorized subjects with symptoms suggestive of CTS into four groups by standardized electrodiagnostic criteria: (1) CTS, (2) PN, (3) CTS and PN, (4) normal. At least seven subjects were in each group. Erythrocyte glutamine oxaloacetic acid transaminase (EGOT) activity with and without in vitro enhancement with pyridoxal phosphate was used as a means of identifying subjects with and without pyridoxine metabolic abnormalities. A significant difference in pyridoxine metabolic activity (PMA) was found between groups by both chi square (p less than 0.05) and analysis of variance (p less than 0.05). Further evaluation showed that this difference was associated with the presence or absence of PN (p less than 0.05). There was no difference in PMA when groups were separated on the basis of CTS. Results showed that a PMA abnormality was a factor highly correlated with the presence of PN but not CTS. This finding suggested that the positive response reported previously in subjects with CTS taking supplemental pyridoxine may actually be related to an unrecognized PN, which was compounding the symptomatology.