Several clinical trials have demonstrated that 4-aminopyridine (4-AP), a potassium channel-blocking agent, improves symptoms in patients with central demyelination multiple sclerosis (MS) (Fujihara et al.). 4-AP probably produces larger action potentials in demyelinated nerve fibres or enhances central or peripheral synaptic transmission. Bever et al. (1994) suggested that demyelination exposes axonal potassium channels that decrease action-potential duration and amplitude, thus impairing action-potential propagation; in order to confirm this hypothesis Bever et al. (1994-1996) tested patients with MS with 4-AP and 3,4 diaminopyridine (3,4 DAP) because of their potassium channel blocker function and reported a clinically important motor improvement. Stefoski et al. (1991) demonstrated the efficacy of a single oral dose of 4-AP in enhancing MS patients' performances. Because of both MS and chronic inflammatory demyelinating polyneuropathy (CIDP), we studied the symptomatic effect of 3,4-dyaminopiridine in CIDP patients. Thirteen patients participated in the study; for each patient we performed a clinical and neurophysiological evaluation before and l h after a single oral dose of 3,4 DAP (20 mg). Electrical stimuli were delivered to the median, ulnar, and peroneal nerves. We measured latency and amplitude of proximal and distal motor potentials, motor conduction velocity, latency and dispersion of the F wave. We found no significant changes in the electrophysiological data of peripheral motor nerve function. Similarly, using 3,4 DAP in MS patients, Sheean et al. (1998) found no electrophysiological changes.
|Issue number||4 SUPPL.|
|Publication status||Published - 2000|
ASJC Scopus subject areas
- Clinical Neurology