Rose Jessica, Vassar Rachel
Department of Orthopaedic Surgery, Stanford University School of Medicine, Stanford, CA, USA; Motion Analysis Laboratory, Lucile Packard Children's Hospital, Stanford, CA, USA; Neonatal Neuroimaging Laboratory, Stanford University School of Medicine, Stanford, CA, USA.
Department of Orthopaedic Surgery, Stanford University School of Medicine, Stanford, CA, USA; Neonatal Neuroimaging Laboratory, Stanford University School of Medicine, Stanford, CA, USA.
Semin Fetal Neonatal Med. 2015 Feb;20(1):20-25. doi: 10.1016/j.siny.2014.11.002. Epub 2014 Dec 16.
Advances in the care of neonatal hyperbilirubinemia have led to a decreased incidence of kernicterus. However, neonatal exposure to high levels of bilirubin continues to cause severe motor symptoms and cerebral palsy (CP). Exposure to moderate levels of unconjugated bilirubin may also cause damage to the developing central nervous system, specifically the basal ganglia and cerebellum. Brain lesions identified using magnetic resonance imaging following extreme hyperbilirubinemia have been linked to dyskinetic CP. Newer imaging techniques, such as diffusion tensor imaging or single-photon emission computed tomography, allow quantification of more subtle white matter injury following presumed exposure to unbound bilirubin, and may explain more subtle movement disorders. New categories of bilirubin-induced neurologic dysfunction, characterized by subtle bilirubin encephalopathy following moderate hyperbilirubinemia, have been implicated in long-term motor function. Further research is needed to identify subtle impairments resulting from moderate-severe neonatal hyperbilirubinemia, to understand the influence of perinatal risk factors on bilirubin toxicity, and to develop neuroprotective treatment strategies to prevent movement disorders due to bilirubin toxicity.
新生儿高胆红素血症护理方面的进展已导致核黄疸发病率降低。然而，新生儿暴露于高水平胆红素仍会导致严重的运动症状和脑瘫（CP）。暴露于中等水平的未结合胆红素也可能对发育中的中枢神经系统造成损害，特别是基底神经节和小脑。在极度高胆红素血症后使用磁共振成像识别出的脑损伤与运动障碍型脑瘫有关。更新的成像技术，如扩散张量成像或单光子发射计算机断层扫描，能够对假定暴露于游离胆红素后的更细微的白质损伤进行量化，并可能解释更细微的运动障碍。以中度高胆红素血症后的细微胆红素脑病为特征的新型胆红素诱导的神经功能障碍已被认为与长期运动功能有关。需要进一步研究以确定中度至重度新生儿高胆红素血症导致的细微损伤，了解围产期危险因素对胆红素毒性的影响，并制定神经保护治疗策略以预防因胆红素毒性导致的运动障碍。
