To the Editor: Most symptoms of multiple sclerosis, such as paresis, ataxia, and hypoesthesia, are derived from conduction block at the demyelinated portion of nerve fibers.1 Conduction block is generated because of an initial lack of sodium channels in the newly exposed axolemma. The axolemma under the normal myelin sheet has a relatively low voltage-gated sodium channel density, which may be insufficient for action-potential propagation.2 Demyelination decreases the safety factor of action-potential propagation for at least two different reasons: 1) the electrical capacity of the demyelinated membranes increases and, consequently, more current is needed for a constant potential change; and 2) the local potential may be insufficient to depolarize the subsequent node because of leakage across the neuron. In the normal axon, the safety factor for saltatory conduction is 3 to 5. In the demyelinated axon, the safety factor is typically reduced to near 1. This is a critical level; small improvement in the safety factor may cause a successful conduction and, conversely, a small decrease will result in conduction block.