Forbes K P, Pipe J G, Heiserman J E
Division of Neuroradiology (K.P.N.F., J.E.H.) and MRI Department (J.G.P.), Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, AZ.
AJNR Am J Neuroradiol. 2001 Mar;22(3):450-5.
The pathogenesis of cerebral venous infarction (CVI) remains controversial, with uncertainty over whether cytotoxic edema plays a role. Recent animal studies have shown that cytotoxic edema reliably occurs in acute CVI and precedes the onset of vasogenic edema. Our hypothesis was that cytotoxic edema would also occur in acute human CVI and would be detectable as an area of restricted diffusion on diffusion-weighted images.
Twelve subjects with acute cerebral venous thrombosis confirmed by MR venography underwent both conventional MR and echo-planar diffusion-weighted imaging (maximum diffusion sensitivity [b=1000 s/mm(2)]). Images were examined for areas of CVI that were identified as T2 hyperintensity, diffusion hyperintensity, or hemorrhage. The percent change in apparent diffusion coefficient (ADC) and T2 signal as well as the T2/diffusion volume were calculated within areas of edematous CVI. Regression techniques were used to examine the relationship of these variables to symptom duration.
Ten regions of CVI were detected in seven subjects, all showing T2 hyperintensity. Two of these regions were predominantly hemorrhagic and did not display diffusion hyperintensity. The remaining eight regions displayed diffusion hyperintensity that was associated with a decreased ADC. ADC values increased with symptom duration (r(2) = 0.96; P <.006). Both T2 hyperintensity and T2/diffusion volume peaked approximately 2 days after symptom onset.
Restricted water diffusion suggesting cytotoxic edema is commonly found in subjects with acute CVI and decreases over time. This supports an important etiologic role for cytotoxic edema in the pathogenesis of CVI.
脑静脉梗死（CVI）的发病机制仍存在争议，细胞毒性水肿是否起作用尚不确定。最近的动物研究表明，细胞毒性水肿在急性CVI中确实会出现，且先于血管源性水肿发作。我们的假设是，细胞毒性水肿在急性人类CVI中也会发生，并且在扩散加权图像上可作为扩散受限区域被检测到。
12例经磁共振静脉造影证实为急性脑静脉血栓形成的患者接受了常规磁共振成像和回波平面扩散加权成像（最大扩散敏感度[b = 1000 s/mm(2)]）。检查图像中被确定为T2高信号、扩散高信号或出血的CVI区域。计算水肿性CVI区域内表观扩散系数（ADC）和T2信号的百分比变化以及T2/扩散体积。采用回归技术研究这些变量与症状持续时间的关系。
7例患者中检测到10个CVI区域，均显示T2高信号。其中2个区域以出血为主，未显示扩散高信号。其余8个区域显示扩散高信号，且与ADC降低相关。ADC值随症状持续时间增加（r(2) = 0.96；P <.006）。T2高信号和T2/扩散体积均在症状发作后约2天达到峰值。
提示细胞毒性水肿的水扩散受限在急性CVI患者中常见，并随时间降低。这支持细胞毒性水肿在CVI发病机制中起重要病因学作用。
