Correlation of lesion volume and brain swelling from a focal brain trauma

Abstract

Brain edema and secondary growth of a traumatic brain tissue necrosis are important manifestations of secondary brain damage and of prognostic significance in severe head injury. Aim of the current study was to analyze the interdependency of the resulting brain swelling from the size of the focal traumatic lesion. Male Sprague-Dawley rats were intubated and mechanically ventilated. A trephination was made over the left parietal cortex for induction of a cold lesion. Different injury severities were achieved by variing the contact time of the cooled copper-cylinder and the exposed cortex. Animals were randomized into 12 experimental groups. Hemispheric brain swelling was measured in groups A1-A6 (n = 4-8) by gravimetry 24 hrs after lesions of six increasing severity levels. Correspondingly, in animals of groups B1-B6 (n = 5-7) the volume of necrosis was planimetrically assessed in histological serial sections of the brain obtained 24 hrs after trauma of different severity. In groups A1-A6, hemispheric brain swelling (increase in weight) was growing with increasing contact duration of the cold probe with the exposed cerebral cortex, i.e. from 7.7 ± 0.4% (5 s) to a maximum of 9.9 ± 0.5% (25 s). Longer contact periodes (30 s) were not further effective to increase hemispheric brain swelling. The contact times and extent of swelling were linearly correlated between 5 s and 25 s (r = 0.47; p < 0.01). The volume of necrosis in groups B1-B6 increased from 35.7 ± 3.7 mm3 (5 s) to 106.3 ± 10.3 mm3 (30 s). There was again a linear correlation between the duration of contact of the cold probe (i.e. injury severity) with the brain cortex and the volume of necrosis (r = 0.77; p < 0.01). Accordingly, the lesion volume could be increased in a reproducible manner from 35.7 up to 106.3 mm3 by extending the contact times of the cooling device and cerebral cortex. Hemispheric swelling, predominantly due to vasogenic brain edema, was expanding in relationship with the volume of necrosis. © Springer-Verlag 2003.