Howorka K, Heger G, Schabmann A, Skrabal F, Pumprla J
Department of Biomedical Engineering and Physics, University of Vienna, Allgemeines Krankenhaus, Vienna, Austria.
Acta Diabetol. 1998 Apr;35(1):1-8. doi: 10.1007/s005920050093.
To assess the relationship between symptom perception and neurophysiological characteristics in hypoglycaemia unawareness, we investigated the awareness of symptoms, objective changes of autonomic function and counter-regulatory neuroendocrine responses to hypoglycaemia in intensively treated type I (insulin-dependent) diabetic patients with different degrees of hypoglycaemia unawareness. Hypoglycaemia (venous plasma glucose below 2.2 mmol/l) was induced with an intravenous insulin bolus in subjects with a history of repeated severe hypoglycaemia and hypoglycaemia unawareness (n = 10) and in a comparable group with good awareness of hypoglycaemia (n = 8). Autonomic symptoms, selected parameters of autonomic function and counter-regulatory hormones were assessed serially. Although hypoglycaemia was more pronounced in unaware patients (1.6 vs 2.0 mmol/l, P = 0.05), their induced adrenaline response was markedly impaired (delta adrenaline: 1.25+/-1.10 vs 2.55+/-1.46 nmol/l, P = 0.05). Astonishingly, differences between both patient groups in the course of autonomic function changes did not reach the level of significance (P = 0.35-0.92), although the unaware group reported markedly fewer autonomic symptoms, both neurogenic (P = 0.001) and neuroglycopenic (P = 0.04) than the aware group. This study indicates that in hypoglycaemia unawareness even extensive changes in autonomic function are not sufficient for the perception of hypoglycaemia and confirms that the central nervous system plays an important role in the awareness of hypoglycaemia.
为评估低血糖无意识状态下症状感知与神经生理特征之间的关系，我们调查了强化治疗的不同程度低血糖无意识的Ⅰ型（胰岛素依赖型）糖尿病患者对低血糖症状的感知、自主神经功能的客观变化以及对低血糖的反调节神经内分泌反应。对有反复严重低血糖和低血糖无意识病史的受试者（n = 10）以及低血糖意识良好的对照组受试者（n = 8）静脉注射胰岛素推注诱发低血糖（静脉血浆葡萄糖低于2.2 mmol/l）。连续评估自主神经症状、自主神经功能的选定参数和反调节激素。尽管无意识患者的低血糖情况更严重（1.6 vs 2.0 mmol/l，P = 0.05），但其诱发的肾上腺素反应明显受损（肾上腺素变化量：1.25±1.10 vs 2.55±1.46 nmol/l，P = 0.05）。令人惊讶的是，尽管无意识组报告的神经源性（P = 0.001）和神经低血糖性（P = 0.04）自主神经症状明显少于意识组，但两组患者在自主神经功能变化过程中的差异未达到显著水平（P = 0.35 - 0.92）。这项研究表明，在低血糖无意识状态下，即使自主神经功能发生广泛变化也不足以感知低血糖，并证实中枢神经系统在低血糖感知中起重要作用。
