Quantitative MRI analysis of brain volume changes due to controlled cortical impact

More than 85% of reported brain traumas are classified clinically as “mild” using GCS; qualitative MRI findings are scarce and provide little correspondence to clinical symptoms. Our goal, therefore, was to establish in-vivo sequellae of traumatic brain injury following lower and higher levels of impact to the frontal lobe using quantitative MRI analysis and a mechanical model of penetrating impact injury. To investigate time-based morphological and physiological changes of living tissue requires a surrogate for the human central nervous system. The present model for TBI was a systematically varied and controlled cortical impact on deeply-anaesthetized Sprague Dawley rats designed to mimic different injury severities. Whole-brain MRI scans were performed on each rat prior to either a lower or a higher level of impact and then at hourly intervals for five hours post-impact. Both brain volume and specific anatomical structures were segmented from MR images for inter-subject comparisons post-registration. Animals subjected to lower and higher impact levels exhibited elevated intracranial pressure (ICP) in the low compensatory reserve (i.e., nearly exhausted) and terminal disturbance (i.e., exhausted) ranges, respectively. There was a statistically-significant drop in cerebrospinal fluid of 35% in the lower impacts and 65% in the higher impacts at Hr5 in comparison to the sham control. There was a corresponding increase in corpus callosum volume starting from Hr1 of 60-110% and 30-40% following the lower and higher impact levels, respectively. A statistically significant change in the abnormal tissue from Hr2 to Hr5 was observed for both impact levels, with greater significance for higher impacts. Furthermore, a statistically significant difference between the lower impacts and the sham controls occurred at Hr3. These results are statistically substantiated by a fluctuation in the physical size of the corpus callosum, a decrease in the volume of CSF, and elevated levels of atrophy in the cerebral cortex.