4-Aminopyridine (4-AP) and Visual Evoked Potentials (VEP)

Rationale: 4-Aminopyridine (Fampyra®) has been approved for the symptomatic treatment of impaired gait in multiple sclerosis. It has been suggested that it acts by blocking voltage-gated potassium channels in demyelinated axons, thereby preserving the action potential and improving nerve conduction.

Method: We investigated the effects of 4-AP on VEP in 9 patients with MS (2 men, 7 women, mean age 52 ± 10 years, duration of disease 8.9 ± 4.5 years, EDSS 5.4 ± 0.6). Each patient received 4-AP 10 mg bid for 2 weeks. Clinical evaluation and VEP recording was performed both at baseline and after two weeks of treatment.

Results: The mean VEP P100 latency for 18 eyes increased non-significantly from baseline (117.1 ms ± 12.0) to (118.6 ms ± 13.0) at follow-up. At baseline, VEPs were delayed in 10/18 eyes, whereas at follow-up 8/18 eyes were delayed. Mean latency, duration, and amplitude were not changed. Relative to baseline, P100 latency increased by ≥1 ms in 8 eyes, was unchanged in 5, and decreased by ≥1 ms in 5. No differences in the effect of 4-AP on P100 in patients with demyelination versus those without were found.

Discussion: In this small study we did not find a significant acceleration effect on VEP latency after 4-AP. In particular, an effect of 4-AP on nerve conduction speed in cases of apparent demyelinative alteration could not be verified.