American Journal of Neuroradiology 22:450-455 (3 2001)
© 2001 American Society of Neuroradiology
ARTICLE
Evidence for Cytotoxic Edema in the Pathogenesis of Cerebral Venous Infarction
a From the 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.
BACKGROUND AND PURPOSE: 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.
METHODS: 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/mm2]). 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.
RESULTS: Ten regions of CVI were detected in seven subjects, all showing T2 hyperintensity. Two of these regions were predominately 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 (r2 = 0.96; P < .006). Both T2 hyperintensity and T2/diffusion volume peaked approximately 2 days after symptom onset.
CONCLUSION: 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.
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