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Superficial radial sensory nerve potentials in immune-mediated and diabetic neuropathies.

Tamura N, Kuwabara S, Misawa S, Mori M, Nakata M, Hattori T

Department of Neurology, Chiba University School of Medicine, Inohana, Japan. nonnon@graduate.chiba-u.jp

OBJECTIVE: The pattern of abnormal median-normal sural sensory nerve action potential (SNAP) is frequently found in acute/chronic inflammatory demyelinating polyneuropathy (AIDP/CIDP), whereas sural/radial SNAP amplitude ratio is sensitive to detect dying-back degeneration. To investigate whether radial SNAP and its amplitude ratio to median or sural SNAP provide additional particular patterns of sensory nerve involvement. METHODS: Superficial radial, median, and sural SNAPs were recorded in 63 normal subjects and in 132 patients with AIDP/CIDP (n = 22), diabetic neuropathy (n = 83), or other axonal polyneuropathy (n = 27). Median/radial and sural/radial amplitude ratios were examined. RESULTS: In normal subjects, median/radial ratio was 0.96 +/- 0.05 (mean +/- SEM), and sural/radial ratio was 0.50 +/- 0.03. Compared with normal controls, the median/radial ratio was lower in patients with AIDP/CIDP (0.64 +/- 0.11; P < 0.001) or diabetic neuropathy (0.75 +/- 0.04; P = 0.08), but similar in those with other neuropathy (0.94 +/- 0.10). The sural/radial ratio was higher in the AIDP/CIDP group (0.71 +/- 0.08; P = 0.10), and lower in the diabetic (0.36 +/- 0.03; P < 0.001) and other axonal neuropathy groups (0.40 +/- 0.07; P = 0.08). CONCLUSIONS: AIDP/CIDP is associated with a reduced median/radial ratio and increased sural/radial ratio, probably reflecting demyelination predominant in the distal nerve terminals. Diabetic neuropathy is characterized by decreases in both median/radial and sural/radial ratios, presumably due to coexistence of carpal tunnel pathology and dying-back degeneration. SIGNIFICANCE: Comparison of multiple SNAP amplitudes provides information about characteristic distribution patterns of sensory nerve involvement in peripheral neuropathies.

Published 12 September 2005 in Clin Neurophysiol, 116(10): 2330-3.
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