Oehmichen Manfred, Woetzel Fabian, Meissner Christoph
Institute of Legal Medicine of Schleswig Holstein, Lübeck, Germany.
Acta Neuropathol. 2009 Mar;117(3):267-74. doi: 10.1007/s00401-008-0459-y. Epub 2008 Nov 14.
Sudden infant death syndrome (SIDS) is characterized by a lack of any known morphological or functional organ changes that could explain the lethal process. In the present study we investigated the hypothesis of an association between hypoxic/ischemic injury and SIDS deaths. In a previous study, we could demonstrate by quantitative immunohistochemistry a distinct drop in microtubule-associated protein (MAP2) reactivity in neurons of adult, human brains secondary to acute hypoxic-ischemic injuries. Here we applied the same method on sections of the frontal cortex and hippocampus of 41 brains of infants younger than 1 year of age. For each brain area 100 selected neurons were evaluated for their MAP2 reactivity in the different layers of the frontal cortex and in the different segments of the hippocampus. Three groups were compared: (1) SIDS victims (n = 17), (2) infants with hypoxia/ischemia (control group one; n = 14), (3) infants without hypoxic/ischemic injury (control group two; n = 10). The SIDS group and hypoxic/ischemic group exhibited a general reduction in the number of MAP2 reactive neurons in comparison with the non-hypoxic/ischemic injury group. The SIDS group also had a significantly lower (P < 0.05) number of reactive neurons in the CA2 and CA3 areas of the hippocampus than did control group two. No difference was detected between the SIDS group and control group one. The SIDS brains were thus found to display hypoxic/ischemic features without however providing evidence as to the cause of the oxygen reduction.
婴儿猝死综合征（SIDS）的特征是缺乏任何已知的能够解释致死过程的形态学或功能性器官变化。在本研究中，我们调查了缺氧/缺血性损伤与SIDS死亡之间存在关联的假说。在先前的一项研究中，我们通过定量免疫组织化学方法证实，继发于急性缺氧缺血性损伤的成年人类大脑神经元中，微管相关蛋白（MAP2）反应性明显下降。在此，我们将相同的方法应用于41例1岁以下婴儿大脑的额叶皮质和海马体切片。对于每个脑区，在额叶皮质的不同层以及海马体的不同节段中，对100个选定的神经元进行MAP2反应性评估。比较了三组：（1）SIDS受害者（n = 17），（2）缺氧/缺血婴儿（对照组一；n = 14），（3）无缺氧/缺血性损伤的婴儿（对照组二；n = 10）。与无缺氧/缺血性损伤组相比，SIDS组和缺氧/缺血组MAP2反应性神经元数量普遍减少。SIDS组海马体CA2和CA3区的反应性神经元数量也显著低于（P < 0.05）对照组二。SIDS组与对照组一之间未检测到差异。因此，发现SIDS患儿的大脑表现出缺氧/缺血特征，但未提供缺氧原因的证据。
