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Martin Bendszus, Ralf Burger, Giles Hamilton Vince and Laszlo Solymosi

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 T2-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 T2-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.

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Martin Bendszus and René Chapot

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Ralf Burger, Martin Bendszus, Giles Hamilton Vince, Klaus Roosen and Anthony Marmarou

Object. The goal of this study was to characterize a new model of an epidural mass lesion in rodents by means of neurophysiological monitoring, magnetic resonance imaging, and histopathological analysis.

Methods. Changes in intracranial pressure (ICP), cerebral perfusion pressure (CPP), and laser Doppler flowmetry (LDF) values, intraparenchymal tissue partial oxygen pressure (PtiO2), and electroencephalography (EEG) activity were evaluated in the rat during controlled, epidural expansion of a latex balloon up to a maximum ICP of 60 mm Hg. The initial balloon inflation was followed by periods of sustained inflation (30 ± 1 minute) and reperfusion (180 ± 5 minutes). Histopathological analysis and magnetic resonance (MR) imaging were performed to characterize the lesion.

The time to maximum balloon expansion and the average balloon volume were highly reproducible. Alterations in EEG activity during inflation first appeared when the CPP decreased to 57 mm Hg, the LDF value to 66% of baseline values, and the PtiO2 to 12 mm Hg. During maximum compression, the CPP was reduced to 34 mm Hg, the LDF value to 40% of baseline, and the PtiO2 to 4 to 5 mm Hg. The EEG tracing was isoelectric during prolonged inflation and the values of LDF and PtiO2 decreased due to accompanying hypotonia. After reperfusion, the CPP was significantly decreased (p < 0.05) due to the elevation of ICP. Both the LDF value and EEG activity displayed incomplete restoration, whereas the value of PtiO2 returned to normal. Histological analysis and MR imaging revealed brain swelling with a midline shift and a combined cortical—subcortical ischemic lesion beyond the site of balloon compression.

Conclusions. This novel model of an epidural mass lesion in rodents closely resembles the process observed in humans. Evaluation of pathophysiological and morphological changes was feasible by using neurophysiological monitoring and MR imaging.

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Moritz Scherer, Christine Jungk, Michael Götz, Philipp Kickingereder, David Reuss, Martin Bendszus, Klaus Maier-Hein and Andreas Unterberg


In WHO grade II low-grade gliomas (LGGs), early postoperative MRI (epMRI) may overestimate residual tumor on FLAIR sequences. Consequently, MRI at 3–6 months follow-up (fuMRI) is used for delineation of residual tumor. This study sought to evaluate if integration of apparent diffusion coefficient (ADC) maps permits an accurate estimation of residual tumor early on epMRI.


From a consecutive cohort, 43 cases with an initial surgery for an LGG, and complete epMRI (< 72 hours after resection) and fuMRI including ADC maps, were retrospectively identified. Residual FLAIR hyperintense tumor was manually segmented on epMRI and corresponding ADC maps were coregistered. Using an expectation maximization algorithm, residual tumor segments were probabilistically clustered into areas of residual tumor, ischemia, or normal white matter (NWM) by fitting a mixture model of superimposed Gaussian curves to the ADC histogram. Tumor volumes from epMRI, clustering, and fuMRI were statistically compared and agreement analysis was performed.


Mean FLAIR hyperintensity suggesting residual tumor was significantly larger on epMRI compared to fuMRI (19.4 ± 16.5 ml vs 8.4 ± 10.2 ml, p < 0.0001). Probabilistic clustering of corresponding ADC histograms on epMRI identified subsegments that were interpreted as mean residual tumor (7.6 ± 10.2 ml), ischemia (8.1 ± 5.9 ml), and NWM (3.7 ± 4.9 ml). Therefore, mean tumor quantification error between epMRI and fuMRI was significantly reduced (11.0 ± 10.6 ml vs −0.8 ± 3.7 ml, p < 0.0001). Mean clustered tumor volumes on epMRI were no longer significantly different from the fuMRI reference (7.6 ± 10.2 ml vs 8.4 ± 10.2 ml, p = 0.16). Correlation (Pearson r = 0.96, p < 0.0001), concordance correlation coefficient (0.89, 95% confidence interval 0.83), and Bland-Altman analysis suggested strong agreement between both measures after clustering.


Probabilistic segmentation of ADC maps facilitates accurate assessment of residual tumor within 72 hours after LGG resection. Multiparametric image analysis detected FLAIR signal alterations attributable to surgical trauma, which led to overestimation of residual LGG on epMRI compared to fuMRI. The prognostic value and clinical impact of this method has to be evaluated in larger case series in the future.