Collier A, Reid W, McInnes A, Cull R E, Ewing D J, Clarke B F
Diabetic and Dietetic Department, Royal Infirmary, Edinburgh, U.K.
Diabetes Res Clin Pract. 1988 Sep 5;5(3):171-5. doi: 10.1016/s0168-8227(88)80084-6.
Using somatosensory and visual evoked potential techniques we have looked for evidence of central neuropathy in a group of insulin-dependent diabetics with mild peripheral neuropathy. The N9, N13, and N20 components of the somatosensory evoked potential were significantly (P less than 0.001) delayed in the diabetic group compared with the control subjects. There was a small but non-significant increase in the interpeak N13-9 and N20-13 latencies in the diabetic group. The visual evoked potential (P100) showed a small but insignificant delay. The delay in cerebral evoked potentials was mostly attributable to peripheral neuropathic damage and no firm evidence was obtained in favour of central diabetic neuropathy.
