不同部位脑梗死后华勒变性3例报道及文献复习

Wallerian Degeneration after Cerebral Infarction in Different Artery Territory: 3 Case Reports and Literature Review

目的探讨不同部位脑梗死后锥体束华勒变性的发生过程和机制。方法报道3例不同部位脑梗死后华勒变性患者的临床资料,根据临床和影像学特点并结合文献对其进行分析。结果颈内动脉或大脑中动脉供血区急性脑梗死后可出现锥体束和胼胝体华勒变性,表现为同侧锥体束(内囊、大脑脚)与胼胝体出现T2和DWI高信号,ADC低信号,并且DWI和ADC信号改变比T2更明显;而单侧脑桥基底部梗死可于数月后出现双侧脑桥小脑束华勒变性,表现为双侧小脑中脚T2和DWI高信号,ADC等信号。结论脑梗死后华勒变性是疾病的发展过程,应充分认识这一现象,避免临床误诊为新发脑梗死。

Aim To study the process and mechanism underlying Wallerian degeneration of the central nervous system after cerebral infarction in different artery territory. Methods 3 cases of Wallerian degeneration after cerebral infarction in different artery territory were described and analyzed according to the clinical and MR features, combined with the literature on Wallerian degeneration. Results Acute cerebral infarction in the territory of the middle cerebral artery or internal carotid artery would cause ipsilateral corticospinal tract （internal capsule and/or cerebral peduncle） and corpus callosum Wallerian degeneration, with high signals on T2 or diffusion-weighted images, and low signals on ADC map. Moreover, changes in DWI and ADC were more apparent than that in T2. Whereas unilateral paramedian pontine infarction would often cause bilateral Wallerian degeneration of the middle cerebellar peduncles, with high signals on both T2 and diffusion-weighted images and isointensity signals on ADC maps several months after the onset of infarction. Conclusion Wallerian degeneration is a common sequel after stroke, which should be fully understood and not be misdiagnosed as acute cerebral infarction.