Median-radial sensory nerve comparative studies in the detection of median neuropathy at the wrist in diabetic patients
Introduction
Nerve conduction abnormalities across the carpal tunnel (median neuropathy at the wrist) are frequently found in patients with diabetes (Albers et al., 1996, Perkins et al., 2002), whereas this may not be associated with typical symptoms of carpal tunnel syndrome. Pathological studies in diabetic neuropathy have shown axonal degeneration presumably caused by microangiopathy (Dyck and Giannini, 1996), but other multiple factors including metabolic abnormalities should contribute to development of diabetic neuropathy (Brismar et al., 1987, Sima, 1996). Fundamental metabolic factors are activation of the polyol pathway and impaired Na+–K+ pump function, presumably leading to axonal edema, a decrease in trans-axonal Na+ gradient, and reduced nodal Na+ currents (Brismar et al., 1987, Brismar, 1993, Misawa et al., 2004, Misawa et al., 2006a).
Previous electrophysiological studies showed that within a month after insulin administration or treatment with aldose reductase inhibitors, there was an improvement in nerve conduction particularly across the common entrapment sites (Kitano et al., 2004, Kikkawa et al., 2005, Misawa et al., 2006b): in median nerve studies, distal latencies and sensory nerve conduction velocities changed significantly. These findings are consistent with a hypothesis that intra-axonal Na+ accumulation and axonal edema mediated by hyperglycemia increase pressure of the carpal tunnel (Misawa et al., 2006b).
Median-ulnar comparative studies (MUCS), as well as median-radial comparative studies (MRCS), were developed as sensitive measures of nerve conduction slowing across the carpal tunnel (Jackson and Clifford, 1989, Preston et al., 1994). The comparison can, however, be made only when ulnar nerve conduction is normal. Because diabetes can involve the multiple common entrapment sites, concomitant Guyon’s canal lesion (ulnar nerve compression at the wrist) may reduce the ability to detect abnormality by MUCS. The aim of this study is to compare the utility of MUCS and MRCS in the detection of median neuropathy at the wrist in diabetic patients, and to study a relationship between carpal tunnel slowing and changes in nodal Na+ currents.
Section snippets
Subjects
This study enrolled 120 consecutive diabetic patients (72 men and 48 women; 16 type 1 and 104 type 2 diabetes), who were referred to EMG clinic, Chiba University Hospital in 2006. We excluded patients with renal failure, because serum K+ levels can significantly alter the membrane potential and axonal excitability properties (Kiernan et al., 2002, Kuwabara et al., 2007). Patients’ age ranged from 27 to 87 years (mean, 62 years; SD, 13 years), and the mean duration of diabetes was 15 years
Median-radial and median-ulnar comparative studies (MRCS and MUCS)
Table 1 shows results of MRCS and MUCS in normal controls, and in patients with diabetes or idiopathic carpal tunnel syndrome (CTS). In normal subjects, the median-radial and median-ulnar latency differences did not significantly correlate with age gender, and body mass index. In patients, findings were similar for MRCS and MUCS. In MRCS, raw latencies of median SNAP were longer for the diabetes and CTS groups than for the normal groups (p < 0.001), whereas radial latencies were longer for only
Discussion
Our results show that median-radial comparative studies (MRCS) appear to be the most sensitive test in the detection of nerve conduction slowing across the carpal tunnel in patients with diabetes mellitus. Moreover, findings of the latent addition studies raise the possibility that the conduction slowing is associated with, or enhanced by, metabolic factors mediated by hyperglycemia. In diabetic patients, assessment of nerve conduction at the common entrapment sites is important, because this
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