Jew J Y, Sandquist D
Arch Neurol. 1979 Mar;36(3):149-54. doi: 10.1001/archneur.1979.00500390067007.
Hyperbilirubinemia is a recognized etiologic factor in motor and hearing disorders associated with cerebral palsy. Its role in more subtle forms of neurological impairment is more controversial. Using a mutant animal model, which develops symptoms and signs closely resembling the human kernicterus syndrome, neurons of hippocampus, cerebral cortex, cochlear nuclei, losuc ceruleus, and olfactory bulb were examined by electron microscopy. Pathological changes, observed in all areas studied, consisted of mitochondrial and endoplasmic enlargement and vacuolation, with glycogen deposition; increased extracellular space; myelin figures; and degenerating changes in nerve terminals. If we make the assumption that pathologic changes in the human infant with neonatal jaundice are similar to changes in the animal model, then the widespread involvement of CNS neurons in all cortical areas examined may well help to explain the syndromes of minimal cerebral dysfunction reported in clinical studies.
高胆红素血症是与脑瘫相关的运动和听力障碍中一个公认的病因。其在更轻微形式的神经损伤中的作用更具争议性。使用一种突变动物模型，该模型会出现与人类核黄疸综合征极为相似的症状和体征，通过电子显微镜对海马体、大脑皮层、耳蜗核、蓝斑和嗅球的神经元进行了检查。在所研究的所有区域观察到的病理变化包括线粒体和内质网增大及空泡化、糖原沉积、细胞外间隙增加、髓鞘样结构以及神经末梢的退行性变化。如果我们假设新生儿黄疸患儿的病理变化与动物模型中的变化相似，那么中枢神经系统神经元在所有检查的皮质区域的广泛受累很可能有助于解释临床研究中报道的轻度脑功能障碍综合征。
