Fifty-four diabetic patients with or without clinical evidence of neuropathy and with no clinical evidence of CNS dysfunction were studied by somatosensory-evoked potentials after electrical stimulation of the median nerve at the wrist and recorded from the scalp electrode against a noncephalic reference. Peripheral conduction index, calculated as the distance from the wrist to the C7 spinous process divided by the P9 latency, was significantly decreased (P <0.01) in diabetic patients (69.81 ± 6.47 m/s) compared with 28 age-matched nondiabetic subjects (76.85 ± 5.65 m/s). The P11–P13 interpeak latency, representative of the transit time from the dorsal column at the level of the sensory input into the cervical cord to the brain stem along the somatosensory pathways (CCT1), and the P13-N19 interpeak latency, representative of the transit time from the brain stem to the somatosensory cortex (CCT2), were significantly increased in diabetic patients (CCT1, 2.51 ± 0.63 ms; CCT2, 5.76 ± 0.92 ms) compared with nondiabetic subjects (CCT1, 2.28 ± 0.36 ms, P <0.05; CCT2, 5.18 ± 0.51 ms, P <0.01). We conclude that, in diabetic patients, neurophysiological abnormalities may be present in two distinct parts of the CNS and the peripheral nervous system.

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