脑干功能障碍与婴儿突然死亡综合征

目的　 探讨婴儿突然死亡综合征 (SIDS)的病理机制。 方法 　SIDS和对照组各 16例脑标本 ,通过常规神经病理检查、胶原纤维酸性蛋白 ( glialfibrillaryacidicprotein ,GFAP)、酪氨酸羟化酶 (tyrosinehydorxylase ,TH)免疫组织化学染色 ,观察脑组织病理变化、胶质细胞增生和脑干TH活性的改变。 结果 　 16例SIDS中 7例可见白质软化坏死 ,白质区GFAP阳性胶质细胞增生明显 ,与对照组比较差别显著。在SIDS组 ,桥脑滑车神经核、延髓迷走神经核和腹外侧网状结构GFAP阳性胶质细胞明显增加 ,与对照组比较差别显著 ;中脑黑质GFAP阳性胶质细胞虽然也增加 ,但与对照组比较 ,差别不显著。迷走神经核和腹外侧网状结构中或强阳性TH免疫反应在SIDS组明显低于对照组 ,但在中脑黑质和滑车神经核 ,两组间差别不显著。 结论 　慢性缺氧或缺血可能引起脑干儿茶酚胺神经元的改变 ,从而导致睡眠时呼吸或循环中枢调节功能障碍 ,成为SIDS的一个重要促发因素。

Brainstem disorder in sudden infant death syndrome MENG

Objective To investigate the mechanism of sudden infant death syndrome(SIDS).Methods Neuropathological changes and alteration of tyrosine hydorxylase(TH)in the brainstem were investigated in 16 cases of SIDS and 16 controls by neuropathogical examination and glial fibrillary acidic protein (GFAP) and TH immunohistochemical staining.Results Necrotic focus was found in the deep and subcortical white matter in 7 of 16 SIDS cases.The numbers of GFAP positive glia were significantly increases in white matter of SIDS cases,compared with the controls.In SIDS,the numbers of GFAP positive glia were significantly increased in trochlear in the pons,vagal nuclei and area reticularis superficialis ventrolateralis,but not significantly increased in substantia nigra in the midbrain,compared with the controls.The moderate or marked TH positive immunoreactivity in SIDS was signficantly lower in the vagal nuclei and area reticularis superficialis ventrolateralis,but not significantly different in the substantia nigra and trochelear in the pons,compared with the controls.Conclusion These catecholaminergic changes in the brainstem may be caused by chronic hypoxia or repeated ischemia and may lead to disorders in respiratory and cardiovascular control in sleep,which become a predisposing risk factor in some SIDS.