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To the Editor:
The article by Katz et al.1 illustrates the important concept that not every immune-mediated motor neuropathy demonstrates evidence of conduction block on routine nerve conduction studies (NCS). However, one should question whether they are justified in proposing different disease entities simply based on electrophysiologic appearances. In fact, multifocal acquired motor axonopathy (MAMA) may have the same pathophysiology as multifocal neuropathy with conduction block. NCS detect myelin dysfunction when there is a significant change in waveforms across an affected nerve segment. In their study, root stimulation studies were not performed. Therefore, a proximal conduction block at nerve root level may have been overlooked and the response to treatment may have been misinterpreted.2
Myelin dysfunction often results from an immune attack against nerve sites with a less robust blood–nerve barrier: the proximal nerve roots and the distal segment of the axon.3 Myelin dysfunction can occur at either site or both. The rate and degree of centripetal spread depends on the severity of the immune response. Those with greater degrees of centripetal spread will enter the nerve segments most often evaluated by routine NCS. Those with more indolent courses may not spread to these segments; thus, overt evidence of myelin dysfunction may be missed. Katz et al.1 likely examined patients with an indolent disease course (duration, 3 to 19 years). These patients could be further subdivided into those with pure distal involvement (treatment nonresponders) and those with both proximal and distal involvement (treatment responders).
Consider a simple model of two independent nodes of Ranvier: one proximal, one distal. Failure at both nodes results in a markedly reduced probability of signal transmission success (probability product rule).4 Conversely, improvement at one site has a more significant impact when two nodes are affected. Evidence of radicular involvement was …
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