Motor nerve conduction study in patients on diphenylhydantoin therapy.

Chokroverty, S; Sayeed, Z A

doi:10.1136/jnnp.38.12.1235

Cited by 31 publications

(17 citation statements)

References 12 publications

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“…Three had absent reflexes and all three had been treated for more than 10 years. Some reduction in nerve conduction velocity has also been demonstrated in patients receiving the drug for many years, even without abnormal signs (Lovelace and Horwitz, 1968;DeCastro et al, 1972;Eisen et al, 1974;Encinoza, 1974;Chokroverty and Sayeed, 1975).…”

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confidence: 98%

“…Diphenyihydantoin (DPH) may produce mild peripheral neuropathy in patients who have received the drug for several years (Lovelace and Horwitz, 1968;Eisen et al, 1974;Chokroverty and Sayeed, 1975). Lower limb areflexia, loss of vibration sensation, and occasional slight disturbances of other sensory modalities occur.…”

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confidence: 99%

“…Thus, in 50 unselected patients, Lovelace and Horwitz (1968) found that lower limb reflexes were absent in 18 % of patients treated for more than five years, but in 50 % of those treated for more than 15 years. Chokroverty and Sayeed (1975) examined 35 patients on DPH therapy. Three had absent reflexes and all three had been treated for more than 10 years.…”

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confidence: 99%

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Acute conduction velocity changes in guinea-pigs after administration of diphenylhydantoin

Quesne¹,

Goldberg²,

Vajda³

1976

Journal of Neurology, Neurosurgery & Psychiatry

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SYNOPSIS Motor nerve conduction velocity was measured after dosing guinea-pigs with 200-400 ,umol/kg diphenylhydantoin (DPH) daily for three to four days. Conduction velocity fell by a mean value of 13% in animals that achieved plasma DPH levels over 200 ftmol/l. There was no change in velocity with DPH levels below this value.Diphenyihydantoin (DPH) may produce mild peripheral neuropathy in patients who have received the drug for several years (Lovelace and Horwitz, 1968;Eisen et al., 1974;Chokroverty and Sayeed, 1975). Lower limb areflexia, loss of vibration sensation, and occasional slight disturbances of other sensory modalities occur. The motor system is rarely involved and never severely. The incidence of abnormal signs appears to be related to the duration of therapy, rather than to the dose taken. Thus, in 50 unselected patients, Lovelace and Horwitz (1968) found that lower limb reflexes were absent in 18 % of patients treated for more than five years, but in 50 % of those treated for more than 15 years. Chokroverty and Sayeed (1975) Horwitz, 1968;DeCastro et al., 1972;Eisen et al., 1974;Encinoza, 1974;Chokroverty and Sayeed, 1975).In distinction from a mild chronic effect on peripheral nerve function after exposure to DPH for many years, the drug appears to have an acute effect on conduction velocity when given in high doses. When intravenous DPH was given to rabbits Morrell et al. (1958) found some increase in conduction time (Accepted 14 May 1976.) in the posterior tibial nerve, as well as effects on other parameters of nerve excitability. In man, Hopf (1968) found that after treatment for 11 days there was an increase in the range of conduction velocity in the ulnar nerve. There was no effect on maximal velocity, thus suggesting that the smaller and slower conducting fibres were more affected. Birkett-Smith and Krogh (1971) measured motor nerve conduction velocity in a series of patients with high DPH levels in the serum and repeated the estimation about a week later, when the serum level had fallen after reduction in the dose. In patients with initial DPH concentrations above 30 mg/l (120 ,4mol/l) maximal nerve conduction velocity was reduced and when the measurement was repeated the velocity had increased in all. The increase ranged from 0.9 to 14.3 m/s.

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Acute conduction velocity changes in guinea-pigs after administration of diphenylhydantoin

Quesne¹,

Goldberg²,

Vajda³

1976

Journal of Neurology, Neurosurgery & Psychiatry

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“…The following factors were considered: a majority of the patients (16) were on anticonvulsive treatment with diphenylhydantoin, which in long-term treatment has been suspected of causing a slowing in motor nerve conduction velocity (Chokroverty and Rubino, 1974;Eisen et al, 1974). In the present study the slowing of sensory conduction velocity was, however, present to the same degree in the treated and the non-treated group (P>0.2).…”

Section: Discussionmentioning

confidence: 56%

Peripheral nerve involvement in Batten-Spielmeyer-Vogt's disease.

Lyon¹

1975

Journal of Neurology, Neurosurgery & Psychiatry

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“…This has been observed most for phenytoin (PHT) [2,3], but the same effect has recently also been seen in subjects treated with other AEDs [4]. Evoked potential (EP) studies have shown that central conduc tion can also be altered by AEDs.…”

Section: Introductionmentioning

confidence: 91%

Effects of Long-Lasting Antiepileptic Therapy on Brainstem Auditory Evoked Potentials

Medaglini¹,

Filippi²,

Smirne³

et al. 1988

Neuropsychobiology

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The brainstem auditory evoked potentials of 84 epileptic patients in chronic monotherapy with carbamazepine (n = 36), phenobarbital (n = 19), Na-valproate (n = 20) or progabide (n = 9) were studied. The mean values of I–III and I–V interpeak latencies (IPLs) were respectively 2.16 ± 0.11 and 4.03 ± 0.17 in the control group, 2.31 ± 0.09 and 4.17 ± 0.16 in the valproic group, 2.30 ± 0.17 and 4.19 ± 0.20 in the carbamazepine group, 2.17 ±0.16 and 4.10 ± 0.18 in the phenobarbital group and 2.16 ± 0.11 and 4.12 ± 0.17 in the progabide group. The prolongation of I–III and I–V IPLs was statistically significant only for the valproic acid and carbamazepine groups. Neither duration of the epilepsy and treatment and frequency of seizures nor the serum drug levels were correlated with I–V IPL values.

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Motor nerve conduction study in patients on diphenylhydantoin therapy.

Cited by 31 publications

References 12 publications

Acute conduction velocity changes in guinea-pigs after administration of diphenylhydantoin

Acute conduction velocity changes in guinea-pigs after administration of diphenylhydantoin

Peripheral nerve involvement in Batten-Spielmeyer-Vogt's disease.

Effects of Long-Lasting Antiepileptic Therapy on Brainstem Auditory Evoked Potentials

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