Kuhn M J, Mikulis D J, Ayoub D M, Kosofsky B E, Davis K R, Taveras J M
Department of Radiology, St John's Hospital, Southern Illinois University School of Medicine, Springfield 62708.
Radiology. 1989 Jul;172(1):179-82. doi: 10.1148/radiology.172.1.2740501.
The dynamic signal intensity changes at magnetic resonance (MR) imaging in active and chronic wallerian degeneration in the corticospinal tract were evaluated. Forty-three patients with wallerian degeneration seen on MR images after cerebral infarction were studied. When possible, patients with acute stroke were examined with MR imaging prospectively at the onset of symptoms and then at weekly intervals for several months. Focal infarction without distal axonal degeneration is demonstrated for the 1st month following onset of clinical symptoms. At 4 weeks, a well-defined band of hypointense signal appears on T2-weighted images in the topographic distribution of the corticospinal tract. After 10-14 weeks, the signal becomes permanently hyperintense. Over several years, accompanying ipsilateral brain stem shrinkage occurs. The dark signal intensity observed on T2-weighted images between 4 and 14 weeks is believed to result primarily from transitory increased lipid-protein ratio.
对皮质脊髓束中急性和慢性华勒氏变性的磁共振（MR）成像动态信号强度变化进行了评估。对43例脑梗死磁共振图像上出现华勒氏变性的患者进行了研究。可能的情况下，对急性卒中患者在症状发作时进行前瞻性磁共振成像检查，随后数月每周检查一次。临床症状发作后第1个月可见无远端轴突变性的局灶性梗死。4周时，在皮质脊髓束的地形分布中，T2加权图像上出现一条明确的低信号带。10 - 14周后，信号变为永久性高信号。数年后，同侧脑干出现萎缩。4至14周期间T2加权图像上观察到的暗信号强度主要被认为是由于脂质-蛋白质比率暂时增加所致。
