EXPERIMENTAL CEREBRAL VENOUS THROMBOSIS - EVALUATION USING MAGNETIC-RESONANCE-IMAGING

Diffusion-weighted (DWI), dynamic contrast-enhanced (perfusion imaging ), and conventional spin-echo magnetic resonance imaging (MRI) were ap plied to characterize the pathophysiology of cerebral venous thrombosi s (CVT) in the rat. We induced CVT by rostral and caudal ligation of t he superior sagittal sinus (SSS) and injection of a thrombogenic cepha lin suspension. The resulting pathology was monitored in an acute and long-term study group. Evans blue and hematoxylin-eosin staining was p erformed for comparison with MRI data. A subgroup of animals was treat ed with i.v. tissue plasminogen activator (t-PA). Successful thrombosi s of the SSS was confirmed by macropathology or histopathology in all rats. Parenchymal lesions as shown by MRI, however, were present only in animals with additional involvement of cortical cerebral veins (11 of 18 rats). The early pathology was clearly detected with the DWI. Th e apparent diffusion coefficient declined to 56 +/- 7% of control valu e at 0.5 h and slowly increased to 84 +/- 8% by 48 h. Perfusion imagin g showed parasagittal perfusion deficits. Treatment with t-PA partiall y resolved the hyperintensity on DWI. Evidence of blood-brain-barrier disruption was observed 2 to 3 h after induction of CVT. In conclusion , experimental CVT is characterized by early cytotoxic edema closely f ollowed by vasogenic edema. The t-PA treatment partially reversed the DWI signal changes consistent with regional tissue recovery, as shown by histopathology. These results encourage the use of cytoprotective d rugs in addition to anticoagulant or thrombolytic therapy.