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Spinal somatosensory conduction in diabetes

Department of Neurology, Stanford University Medical Center, Stanford, CA.

The velocity bf impulse conduction was compared in peripheral nerve, spinal cord, and supraspinal segment of the somatosensory pathway in 15 diabetic subjects (mean age, 34.3 ± 12.4 years) with little or no evidence of polyneuropathy, and in 15 age-matched normal controls. Motor and sensory conduction velocities (CVs) were slower in the diabetic subjects, and the latencies of F waves and somatosensory evoked potentials (SEPs) from arm and leg were longer (p <0.001 in each case), showing a relationship to duration of disease (0.51 <Irl <0.84, p <0.001 in each case). Indirect estimates of spinal somatosensory conduction velocity (SSCV) were slower in the diabetic subjects (39.4 ± 13.3 m/sec versus 54.2 ± 10.5 m/sec, p <0.001), but conduction in the supraspinal segment (cervical cord to cortex) was identical in the two groups (5.6 ± 1.3 m/sec versus 5.6 ± 0.8 m/sec, p <0.1). In relationship to peripheral nerve CV, the incidence of subnormal SSCV in the diabetic subjects could not be fully explained on the basis of: (1) a passive consequence of peripheral neuropathy, (2) a sensory distal axonopathy, or (3) a primary diabetic myelopathy. We conclude that 40% of diabetics have subclinical electro-physiologic dysfunction of the posterior columns of the spinal cord, which may contribute to the lower-extremity sensory symptoms that are so prevalent in this disorder.

Address correspondence and reprint requests to Dr. Dorfman, Department of Neurology, Stanford University Medical Center, Stanford, CA 94305.

This investigation was supported by a grant from the Kroc Foundation and by USPHS Training Grant No. NS-07012.

Accepted for publication October 1, 1980.

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