New pathophysiological problems : Two confusing manifestations in the diagnosis of brain death.

在我们对脑死亡患者进行的一系列研究中，我们发现了另外两个重要事实，即用我们的血管加压素（ADH）和儿茶酚胺方法维持长期稳定的循环。一个事实是，下丘脑激素仍然存在于脑死亡患者的血清中，尽管他们符合脑死亡的所有标准，甚至在诊断后几天。另一种是脑死亡患者出现由疼痛刺激和/或各种自主运动引起的身体运动。这两个事实可能与脑死亡的定义相矛盾;“整个大脑所有功能的不可逆停止”。本研究旨在解释这两个事实的意义，并通过本研究得到以下结果：##结果I ##脑死亡患者血清中CRH、GRH和LH-RH的检测时间长达17天。然而，所有的脑在脑死亡后最多7天表现出坏死性自溶。这表明 ...更多信息 硒激素应该来自下丘脑以外的任何其他组织。胰岛素诱导的低血糖和精氨酸输注的下丘脑刺激试验显示，下丘脑没有CRH、ACTH、皮质醇或GRH的反应性分泌。脑死亡后血清内源性ADH水平迅速下降，尽管血清渗透压异常高，但从未升高。这意味着脑死亡后，下丘脑既不会产生ADH，也不会从上神经系统向脑垂体发出命令。这些结果与脑死亡的概念并不矛盾。结果2各种脊反射在脑死亡后即刻暂时消失，但在脑死亡后5 ~ 10天又可出现。尸检显示脊髓坏死性自溶，从上颈髓开始，向下发展至不同水平。然而，所有这些都被认为是来自残留的完整脊髓。我们在国际上首次发现了被动屈颈引起的一种新的自主神经反射，它以血压显著升高和心动过速等血流动力学反应为特征。这种反射在脑死亡中很常见（12例中有10例），而在脑死亡以外的任何其他患者中从未见过。此外，即使在上胸脊髓退化的患者中也可以看到这种反射，并且被神经节阻滞剂完全抑制。因此，该反射被认为是脑死亡的特异性反射，并且是包括交感神经节的外周自主神经反射。刺激正中神经的体感诱发电位中，N13峰起初明显，但在脑死亡后7 ~ 10天逐渐消失。N13峰被认为来自上颈脊髓。提示脊髓坏死性自溶发生在脑死亡后2 ~ 3天，而下段脊髓坏死性自溶发生在脑死亡后7 ~ 10天。少

We found another two important facts during our series of studies in the brain dead patients with long-term stable circulation maintained by our vasopressin(ADH)and catecholamine method. One fact is that hypothalamic hormones still present in the serum of brain dead patients, though they met all the criteria of brain death, even several days after the diagnosis. The other is that body movement induced by painful stimuli and/or various types of voluntary movement are seen in brain dead patients. These two facts might contradict to the definition of the brain death ; "irreversible cessation of all functions of entire brain". In this study, we aimed to explain the meaning of these two facts.We have got following results through this study :## Results I ## Hypothalamic hormones, such as CRH, GRH and LH-RH, were detected in the serum of brain dead patients as long as 17 days after brain death. All brains, however, showed necrotic autolysis at most 7 days after brain death. This suggests the … More se hormones should be derived from any other tissues than the hypothalamus. Hypothalamic stimulation tests by insulin-induced hypoglycemia and arginine infusion showed absence of reacting secretion of CRH, ACTH, cortisol or GRH from hypothalamus. The serum endogenous ADH level decreased rapidly just after the brain death and had never increased in spite of abnormally high serum osmotic pressure. This means neither production of ADH in the hypothalamus nor commands from the upper nervous system to the pituitary gland is seen after brain death. These results do not contradict to the concept of brain death.## Results 2 ## Various spinal reflexes disappeared temporally just after the brain death but were frequently observed again 5 to 10 days after brain death. Autopsy showed necrotic autolysis of the spinal cord which started from the upper cervical cord and developed downward to various level. All of them, however, were thought to be derived from the residual intact cord. We found a new autonomic reflex elicited by passive neck flexion for the first time in the world which is characterized by hemodynamic response such as marked increase of blood pressure and tachyeardia. This reflex was seen frequently in brain death(in 10 of 12 cases)and never seen in any other patients than brain death. Furthermore, this reflex was seen even in patients whose upper thoracic cord were degenerated, and depressed completely by a ganglion blocker. This reflex, therefore, is considered specific for brain death and to be a peripheral autonomic reflex including sympathetic ganglia. In the somatosensory evoked potential by stimulating the nervus medianus, the N13 peak, which was initially seen obviously, became dull gradually and disappeared 7 to 10 days after brain death. The N13 peak is thought to be derived from the upper cervical spinal cord. This suggests that the necrotic autolysis of the spinal cord is caused within 2 or 3 days after brain death and that of the lower cord 7 to 10 days later. Less