A reproducible model of an epidural mass lesion in rodents. Part II: Characterization by in vivo magnetic resonance imaging

Object. The goal of this study was to characterize a novel epidural space-occupying lesion caused by balloon expansion in rodents by using sequential in vivo magnetic resonance (MR) imaging. Methods. Ten Sprague-Dawley rats were intraperitoneally sedated. A trephination was performed over the left parietal cortex to attach a balloon-expansion device, which was secured with dental cement. Measurements were performed using a 1.5-tesla MR imaging device to obtain sequential T-2-weighted and diffusion-weighted (DW) sequences in the coronal plane. A three-dimensional, constructed interference in steady state sequence was used for calculation of the balloon volume. The animal's temperature, heartbeat, and the arterial percentage of oxygen saturation were monitored continuously. After a baseline examination had been performed, the balloon was inflated for a 30-minute period until it reached a maximum volume of 0.3 ml; this procedure was followed by a period of sustained inflation lasting 30 minutes, balloon deflation, and a period of reperfusion lasting 3 hours. After perfusion fixation of the animals, morphometric analysis of the lesion size and examination of the percentage of viable neurons in the hippocampus were performed. Magnetic resonance imaging allowed for the precise visualization of the extension and location of the epidural mass lesion, narrowing of the basal cisterns, and development of a midline shift. A white-matter focus of hyperintensity, consistent with brain edema, developed predominantly in the contralateral temporal lobe. During sustained inflation the volume of the balloon did not change and comprised 5 to 7% of total intracranial volume. During the same period the white-matter edema progressed further but no increased signal was revealed on DW images. After balloon deflation the brain reexpanded to the calvaria and imaging signs of raised intracranial pressure subsided. A cortical area of hyperintensity on T-2-weighted images developed in the parietal lobe in the region of the former balloon compression. This area appeared bright on DW images, a finding that corresponded to an early cytotoxic edema. After deflation white-matter vasogenic edema in the temporal lobes regressed within 3 hours after reperfusion. The cortical edema in the parietal lobe and the ipsilateral basal ganglia became sharply demarcated. The histopathological results (that is, the extent of tissue damage) corresponded with findings of the authors' companion investigation, which appears in this issue. Conclusions. Magnetic resonance imaging allows for a precise and sequential in vivo monitoring of a space-occupying epidural mass lesion and visualizes the time course of vasogenic and cytotoxic brain edema. This rodent model of an epidural mass lesion proved to be reproducible.