George Timothy M, Cummings Thomas J
Pediatric Neurosurgery Service, Duke University Medical Center, Durham, NC 27710, USA.
Pediatr Neurosurg. 2003 Nov;39(5):234-9. doi: 10.1159/000072867.
One key to predicting optimal outcome of novel treatments, such as fetal surgery, for myelomeningocele is understanding the structure of the placode. We hypothesize that if the placode retains normal patterning and is simply unneurulated, then repair may be effective in preventing secondary injury. Serial sections of human myelomeningocele placodes were characterized using novel immunohistochemical caudal spinal cord markers (H4C4, AC4, NOT, VIN-IS-53, and FP3) and established structural markers (e.g. neurofilament, glial fibrillary acidic protein, or synaptophysin). The myelomeningocele placodes studied exhibited abnormal patterning along the dorsoventral and rostrocaudal axes indicative of a change in pattern determination and a paucity of maturing neurons. In addition, there was significant inflammatory infiltrate, gliosis and fibrosis consistent with secondary injury. Additionally, injury to the placode was also demonstrated. The combination of effects may be contributory to abnormal spinal cord function in myelomeningocele patients.
预测诸如胎儿手术等针对脊髓脊膜膨出的新型治疗的最佳效果的一个关键在于了解神经基板的结构。我们推测，如果神经基板保持正常模式且只是未形成神经，那么修复可能有效地预防继发性损伤。使用新型免疫组织化学尾侧脊髓标志物（H4C4、AC4、NOT、VIN-IS-53和FP3）以及已确立的结构标志物（如神经丝、胶质纤维酸性蛋白或突触素）对人类脊髓脊膜膨出神经基板的连续切片进行特征描述。所研究的脊髓脊膜膨出神经基板在背腹侧和头尾轴上呈现出异常模式，这表明模式决定发生了变化且成熟神经元数量稀少。此外，存在与继发性损伤一致的显著炎症浸润、胶质增生和纤维化。另外，还证实了神经基板受到损伤。这些综合作用可能导致脊髓脊膜膨出患者的脊髓功能异常。
