Okumura Akihisa, Hayashi Masaharu, Tsurui Hiromichi, Yamakawa Yoko, Abe Shinpei, Kudo Takahiro, Suzuki Ryuyo, Shimizu Toshiaki, Shimojima Keiko, Yamamoto Toshiyuki
Department of Pediatrics, Juntendo University Faculty of Medicine, Japan.
Brain Dev. 2013 Mar;35(3):274-9. doi: 10.1016/j.braindev.2012.05.006. Epub 2012 May 26.
We described the clinical course and pathological findings in a child with TUBA1A mutation. MRI revealed marked ventricular dilation with thin cortex, poorly differentiated basal ganglia, agenesis of corpus callosum, cerebellar hypoplasia with preserved vermis at 2 months of age. No gain of developmental milestones was observed until she died with respiratory failure at 23 months of age. A de novo missense mutation of c.1096G>A (G366R) was identified in TUBA1A gene. Pathological findings included a lack in lamination in the cerebral cortex, absent corpus callosum without Probst bundle, blurred demarcation among the striatum, internal capsule and globus pallidus in association with irregular running of myelinated fibers, cerebellar hypoplasia with irregular undulation in the dentate nucleus and inferior olivary nucleus, absent olfactory bulbs and tracts, and pyramidal tract hypoplasia. These findings are consistent with previous reports and will be a clue to diagnosis of TUBA1A mutation.
我们描述了一名患有TUBA1A突变儿童的临床病程和病理发现。磁共振成像(MRI)显示,在2个月大时,患儿存在明显的脑室扩张、皮质变薄、基底神经节分化不良、胼胝体发育不全、小脑发育不全但蚓部保留。直到她在23个月大时因呼吸衰竭死亡,均未观察到发育里程碑的进展。在TUBA1A基因中鉴定出一个新发的错义突变c.1096G>A(G366R)。病理发现包括大脑皮质分层缺失、胼胝体缺如且无普罗布斯特束、纹状体、内囊和苍白球之间界限模糊,伴有有髓纤维走行不规则、小脑发育不全,齿状核和下橄榄核有不规则波动、嗅球和嗅束缺如以及锥体束发育不全。这些发现与先前的报道一致,将为TUBA1A突变的诊断提供线索。