Spinal somatosensory conduction in diabetes.
The velocity of 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 less than 0.001 in each case), showing a relationship to duration of disease (0.51 less than lrl less than 0.84, p less than 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 less than 0.001), but conduction in the supraspinal segment (cervical cord to cortex) was identical in the two groups (5.6 +/- 1.3 msec versus 5.6 +/- 0.8 msec, p less than 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 electrophysiologic 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.
D000293:Adolescent; D000328:Adult; D003920:Diabetes Mellitus / Q000503:physiopathology*; D003922:Diabetes Mellitus, Type 1 / Q000503:physiopathology; D004558:Electric Stimulation; D005071:Evoked Potentials; D005260:Female; D006801:Humans; D008297:Male; D008475:Median Nerve / Q000503:physiopathology; D008875:Middle Aged; D009431:Neural Conduction; D012677:Sensation; D013003:Somatosensory Cortex / Q000503:physiopathology; D013116:Spinal Cord / Q000503:physiopathology*; D013979:Tibial Nerve / Q000503:physiopathology