NEUROPHYSIOLOGICAL IMPAIRMENTS IN IDDM PATIENTS DURING EUGLYCEMIA ANDHYPOGLYCEMIA

OBJECTIVE- To test the hypothesis that latencies of evoked potentials in IDDM patients are delayed compared with healthy control subjects du ring euglycemia, and that insulin-induced hypoglycemia causes further latency delays of evoked potentials to occur. RESEARCH DESIGN AND METH ODS- we recruited 23 IDDM patients (27.9 +/- 1.6 yr of age, HbA1c 6.7 +/- 0.3%, without sensory or autonomic neuropathy) and 26 unequivocall y healthy subjects who were carefully matched for sex, age, and body m ass index to serve as the control group (18 men and 8 women, 28.4 +/- 1.6 yr of age, 22.6 +/- 0.7 kg/m2), for a controlled, prospective stud y. Sequential euglycemichypoglycemic clamps were performed with stable glycemic plateaus of 5.6, 3.3, 2.2, and 1. 7 mM, at which the patient s' and healthy control subjects' neurophysiological functions were eva luated. The methodological armamentarium included the measurement of b rainstem auditory, middle-latency auditory, and somatosensory evoked p otentials that assessed conduction velocity in corresponding neural st ructures and information processing in die midbrain and auditory corte x. RESULTS- Multiple analysis of variance revealed a significant overa ll difference of brainstem auditory evoked potential latencies during euglycemia between the study group and healthy control group (F = 3.41 , P < 0.03), which was mainly attributable to latency delays of wave I II (F = 6.60, P < 0.02), V (F = 9.19, P < 0.01), and interpeak latency I-V (F = 2.82, P < 0.07). Repeated analysis of variance measures dete cted a significant latency delay of the major wave P. of the middle-la tency auditory evoked potentials during hypoglycemia (F = 4.4, P < 0.0 2), which rapidly returned to normal after reinstitution of euglycemia . CONCLUSIONS- In IDDM patients, chronic, structural CNS changes alrea dy appear at the brainstem level during euglycemia. Functional, revers ible CNS changes, however, seem to emerge during acute deviation from glucose homeostasis in more rostral brain regions.