Kalimo H, Olsson Y
Acta Neurol Scand. 1980 Dec;62(6):345-56. doi: 10.1111/j.1600-0404.1980.tb03047.x.
The neuropathological findings in two cases of irreversible hypoglycemic brain injury are described. A 26-year-old diabetic man injected insulin without adequate food intake and died after 2 months in coma. An 84-year-old nondiabetic man accidentally received 10 mg of glibenclamide and died after 3 months in relatively superficial coma. In the first case, an extensive necrotizing injury with gliosis was present in the cerebral cortex with temporal preponderance, as well as in the amygdalae and hippocampus. Lesions were also present in the putamen and caudate nucleus whereas the globus pallidus and thalamus were less severely destroyed. The distribution of the lesions was therefore somewhat different from that commonly seen in hypoxic-ischemic brain injury, which, together with some previously published data, suggests some difference in the pathogenesis of hypoglycemic vs. hypoxic-ischemic brain injury. In the second case only a slight loss of cortical neurons with secondary gliosis could be attributed to the hypoglycemic insult. This case demonstrates the danger of accidental intake of sulfonylurea preparations, which can cause an irreversible brain injury due to their prolonged hypoglycemic effect.
描述了两例不可逆性低血糖脑损伤的神经病理学发现。一名26岁的糖尿病男性在未摄入足够食物的情况下注射胰岛素,2个月后昏迷死亡。一名84岁的非糖尿病男性意外服用10毫克格列本脲,3个月后在相对浅昏迷状态下死亡。在第一例中,大脑皮质以颞叶为主,杏仁核和海马体出现广泛的坏死性损伤伴胶质细胞增生。壳核和尾状核也有病变,而苍白球和丘脑的损伤较轻。因此,病变的分布与缺氧缺血性脑损伤中常见的分布有所不同,这与一些先前发表的数据一起,提示低血糖性与缺氧缺血性脑损伤的发病机制存在一些差异。在第二例中,仅可将轻度皮质神经元丧失伴继发性胶质细胞增生归因于低血糖损伤。该病例表明意外摄入磺脲类制剂的危险性,因其长效低血糖作用可导致不可逆性脑损伤。