GLUCOSE THRESHOLD FOR CEREBRAL DYSFUNCTION DURING HYPOGLYCEMIA IN IDDDM

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Clinical observation suggests that cognitive function can remain impaired after hypoglycemia, despite normalization of plasma glucose. To determine that such a delay occurs, and whether it is influenced by the duration of hypoglycemia, we compared P300 latency (prolongatin is a marker of hypoglycemic cognitive dysfunction), after different periods of hypoglycemia. 17 normal volunteers had 2 hypoglycemic clamp studies. Plasma glucose was lowered to 50mg/dl for 60 min or 180 min. P300 latency was measured at baseline, during hypoglycemia and during glucose recovery. All subjects showed P300 prolongation during hypoglycemia, No change was seen during 3 euglycemic control studies. Despite euglycemia restoration, P300 latency remained prolonged in 13/17 subjects following the 60 min hypoglycemic clamp and all subjects after 180 min of hypoglycemia. The delay was related to the duration of preceding hypoglycemia; it was 2217 min after 60 mins and 4916 min after 180 mins of hypoglycemia (p=0.008). We conclude that hypoglycemia induced cognitive impairment continues after normoglycemia is reestablished and the duration of continuing impairment is proportional to the duration of antecedent hypoglycemia.