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Conduction slowing in diabetic distal polyneuropathy
Author(s) -
Herrmann David N.,
Ferguson Michele L.,
Logigian Eric L.
Publication year - 2002
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.10204
Subject(s) - amyotrophic lateral sclerosis , compound muscle action potential , nerve conduction velocity , pathophysiology , axon , polyneuropathy , medicine , cardiology , motor nerve , diabetic neuropathy , diabetes mellitus , neuroscience , electrophysiology , anatomy , endocrinology , biology , disease
The pathophysiologic significance of motor conduction slowing observed in diabetic distal symmetrical polyneuropathy (DSP) remains controversial. We have used multiple linear regression analysis of compound muscle action potential (CMAP) amplitude vs. motor conduction velocity (CV) and distal latency (DL) in 57 patients with diabetic DSP and 34 patients with amyotrophic lateral sclerosis (ALS) to determine whether motor conduction slowing in diabetic DSP is due mainly to loss of large axons as in ALS or whether there is an additional demyelinative component. We found amplitude‐dependent slowing of CV and DL in both diabetic DSP and ALS in the upper and lower extremities, consistent with a loss of large myelinated fibers. However, in diabetic DSP, there was also significant amplitude‐independent slowing in intermediate but not distal nerve segments, supportive of an additional demyelinative component. CMAP amplitude vs. CV and DL regression analyses using ALS as a control group for relatively pure axon loss may provide pathophysiologic information about motor nerves in other neuropathic disorders. © 2002 Wiley Periodicals, Inc. Muscle Nerve 26: 232–237, 2002