GLUCOSE THRESHOLD FOR CEREBRAL DYSFUNCTION DURING HYPOGLYCEMIA IN IDDDM

临床观察表明，认知功能可能会继续受损 低血糖后，尽管血糖正常化。要确定 这样的延迟是否发生，以及它是否受到 低血糖，我们比较了P300潜伏期(延长是一个标志 低血糖认知功能障碍)，在不同时期 低血糖症。17名正常志愿者进行了2项降糖钳夹试验。 将血糖降至50 mg/dl，持续60分钟或180分钟。P300 在基线、低血糖和血糖期间测量潜伏期 恢复。 所有受试者在低血糖时均出现P300延长，无明显变化 在3项正常血糖对照研究中可见。 尽管正常血糖恢复，但P300潜伏期在13/17年仍延长 受试者在60min的降糖钳夹下，所有受试者在60min后 低血糖180分钟。延误与持续时间有关。 低血糖前，60min后2217min，4916min后 低血糖180min(p=0.008)。 我们的结论是，低血糖导致的认知损害在 正常血糖重新建立，持续损害的持续时间 与既往低血糖的持续时间成正比。

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.