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首页> 外文期刊>Metabolic brain disease >Cognitive, neurophysiologic and metabolic sequelae of previous hypoglycemic coma revealed by hyperinsulinemic-hypoglycemic clamp in type 1 diabetic patients
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Cognitive, neurophysiologic and metabolic sequelae of previous hypoglycemic coma revealed by hyperinsulinemic-hypoglycemic clamp in type 1 diabetic patients

机译：患有1型糖尿病患者的高胰岛素血症降血性肠道揭示了先前低血糖昏迷的认知，神经生理学和代谢后遗症

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摘要

To examine the relationship between electroencephalographic (EEG) activity and hypoglycemia unawareness, we investigated early parameters of vigilance and awareness of various symptom categories in response to hypoglycemia in intensively treated type 1 diabetic (T1DM) patients with different degrees of hypoglycemia unawareness. Hypoglycemia was induced with a hyperinsulinemic-hypoglycemic clamp in six T1DM patients with a history of hypoglycemia unawareness previous severe hypoglycemic coma (SH) and in six T1DM patients without (C) history of hypoglycemia unawareness previous severe hypoglycemic coma. Cognitive function tests (four choice reaction time), counterregulatory responses (adrenaline), and symptomatic responses were evaluated at euglycemia (90 mg/dl) and during step-wise plasma glucose reduction (68, 58 and 49 mg/dl). EEG activity was recorded continuously throughout the study and analyzed by spectral analysis. Cognitive function deteriorated significantly at a glucose threshold of 55 +/- 1 mg/dl in both groups (p = ns) during hypoglycemia, while the glucose threshold for autonomic symptoms was significantly lower in SH patients than in C patients (49 +/- 1 vs. 54 +/- 1 mg/dl, p < 0.05, respectively). In SH patients, eye-closed resting EEG showed a correlation between the mean dominance frequency and plasma glucose (r = 0.62, p < 0.001). Theta relative power increased during controlled hypoglycemia compared to euglycemia (21.6 +/- 6 vs. 15.5 +/- 3% Hz p < 0.05) and was higher than in the C group (21.6 +/- 6 vs. 13.8 +/- 3%, p < 0.03). The cognitive task beta activity was lower in the SH group than in the C group (14.8 +/- 3 Hz, vs. 22.6 +/- 4 vs. p < 0.03). Controlled hypoglycemia elicits cognitive dysfunction in both C and SH patients; however, significant EEG alterations during hypoglycemia were detected mainly in patients with a history of hypoglycemia unawareness and previous severe hypoglycemic coma. These data suggest that prior episodes of hypoglycemic coma modulate brain electric activity.
机译：为了检查脑电图（EEG）活性和低血糖无意之间的关系，我们调查了对各种症状类别的早期参数，以应对低血糖治疗的1型糖尿病（T1DM）患者不同程度的低血糖无意识的患者。在六个T1DM患者中，用高胰岛素血症 - 低血糖钳诱导低血糖胰蛋白酶患者，其患有历史的低血糖无知的历史，以前严重的低血糖COMA（SH）和六个T1DM患者没有（c）低血糖无知的历史，以前的严重降血糖昏迷。在Euglycemia（90mg / dL）和逐步血浆葡萄糖还原（68,58和49mg / dl）时评估认知函数测试（四种选择反应时间），对应反应（肾上腺素）和对症反应。在整个研究中不断记录EEG活性，并通过光谱分析分析。在低血糖期间，在两组（P = NS）中，在两组（P = NS）的葡萄糖阈值下的认知函数显着恶化，而SH患者的自主主义症状的葡萄糖阈值显着低于C患者（49 +/- 1与54 +/- 1 mg / dl，p <0.05分别）。在SH患者中，眼睛闭合的休息EEG显示平均优势频率和血浆葡萄糖（r = 0.62，p <0.001）之间的相关性。与晚期（21.6 +/- 6，15.5 +/- 3％Hz P <0.05）相比，在受控低血糖期间增加的相对功率增加（21.6 +/- 3％）并高于C组（21.6 +/- 6与13.8 +/- 3 ％，p <0.03）。 SH组中的认知任务β活性比C组（14.8 +/- 3 Hz，与22.6 +/- 4与P <0.03）较低。受控低血糖引发C和SH患者的认知功能障碍;然而，主要在低血糖缺血性历史和以前严重的降血糖昏迷的患者中检测到低血糖期间的显着的EEG改变。这些数据表明，钙血糖彗态的事先发作调制脑电活动。

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