The effect of diphenylhydantoin on nerve conduction velocity

Clinical and Electrophysiologic Evaluation of Peripheral Nerve Function in Chronic Phenytoin Therapy

“…High serum concentrations of phenytoin exert an immediate and reversible effect on peripheral nerve conduction that must be distinguished from permanent electrophysiologic changes of chronic peripheral neuropathy (Morrell et al, 1958;Hopf, 1968;Birket-Smith and Krogh, 1971;Marcus et al, 1981). Many of the reports on chronic phenytoin neuropathy have not taken this phenomenon into account (Brumlik and Moretti, 1966;DeCastro et al, 1972;Encinoza, 1974). Only Eisen et al (1974) considered separately those patients with blood phenytoin levels above 20 pg/ml.…”

“…The majority of patient:, included in previous studies were taking other anticonvulsants in addition to phenytoin (Brumlik and Moretti, 1966;Lovelace and Horwitz, 1968;Eisen et al, 1974;Encinoza, 1974;Chokroverty and Sayeed, 1975). The possible contribution of the other anticonvulsants to the development of the neuro-Epilepsio, Vol.…”

“…Widely differing findings regarding clinical neuropathy and electrophysiologic abnormalities resulting from anticonvulsant therapy have been reported. The incidence of clinical neuropathy has ranged from 0 (Encinoza, 1974) to 33% (Eisen et al, 1974) and that of electrophysiologic abnormalities has varied from 0 (Brumlik and Moretti, 1966) to 89% (Eisen et al, 1974). It seems possible that phenytoin serum levels, duration of phenytoin (Dilantin) therapy, folate deficiency, and the potential effect of other anticonvulsants might have contributed in varying, but unmeasured, degrees to the divergent results obtained.…”

Topical Phenytoin in Neuralgic Pain, Peripheral Modulation of Central Sensitization: Two Case Reports

“…Effects of phenytoin on peripheral nervous system read-outs have been described since nearly half a century, based on a number of different studies and models [56][57][58][59]. Treatment in sciatic nerve rat and frog models with phenytoin, even at subclinical concentrations of 5 mg/ml, caused a significant decrement in the amplitude and increment in the latency of the compound action potential [1,60].…”

Motor and sensory conduction velocities and electromyographic findings in man before and after carbamazepine treatment

“…Furthermore, decreased C,, increased amplitude and duration of motor potentials by electromyography and also clinically overt neuropathy have been re-peatedly described (6,7,8,9), although in a single study C, was found to be normal (10) in patients on long-term DPH-treatment. Furthermore, decreased C,, increased amplitude and duration of motor potentials by electromyography and also clinically overt neuropathy have been re-peatedly described (6,7,8,9), although in a single study C, was found to be normal (10) in patients on long-term DPH-treatment.…”