NO EFFECT OF LONG-TERM VIGABATRIN TREATMENT ON CENTRAL-NERVOUS-SYSTEMCONDUCTION IN PATIENTS WITH REFRACTORY EPILEPSY - RESULTS OF A MULTICENTER STUDY OF SOMATOSENSORY AND VISUAL-EVOKED POTENTIALS
F. Mauguiere et al., NO EFFECT OF LONG-TERM VIGABATRIN TREATMENT ON CENTRAL-NERVOUS-SYSTEMCONDUCTION IN PATIENTS WITH REFRACTORY EPILEPSY - RESULTS OF A MULTICENTER STUDY OF SOMATOSENSORY AND VISUAL-EVOKED POTENTIALS, Epilepsia, 38(3), 1997, pp. 301-308
Purpose: In dogs, vigabatrin (VGB) has been associated with intramyeli
nic edema producing delayed central conduction in somatosensory and vi
sual evoked potentials (SEP, VEP). No such effects have been reported
in humans. We assessed whether abnormalities of central conduction cou
ld be detected prospectively in patients with epilepsy treated with VG
B as long-term add-on medication. Methods: Two hundred one patients wi
th refractory partial epilepsy were enrolled and monitored for as long
as 2 years. VGB was added to the treatment at an average dose of 2-3g
/day. Conduction in somatosensory and visual pathways was assessed by
median nerve SEP and pattern VEP recordings performed at inclusion and
once every 6 months. The upper limit and test-retest variability of E
P latencies were evaluated at time of enrollment in the patient group.
Prolonged N13-N20 or P14-N20 SEP intervals and P100 VEP latency >2.5
SD above the baseline mean, observed on repeated runs in the same sess
ion and exceeding the test-retest variability at enrollment were consi
dered to indicate central conduction slowing. Results: One hundred nin
e patients completed the 2-year study period, and 92 discontinued VGB,
of whom 37 were monitored with regard to EP until the end of the stud
y. No consistent change in SEP or VEP was observed in the entire group
during VGB treatment. The number of occasional EP values outside the
baseline range in patients treated with VGB similar to that in patient
s whose VGB treatment had been discontinued. Conclusions: We detected
no evidence of changes in SEP and VEP attributable to altered neuronal
conduction in the CNS during long-term VGB treatment.