Neurotrauma Reports · 2021 · 11 citations · 122 references
MedicineNeurobiologyNeuroscienceNeuroanatomyNeuroimmunologyNeurophysiologyBrain ImagingCerebral Cortex AnatomyConcussion PathophysiologyInjury BiomechanicsNeuroinflammationTraumatic Brain InjuryBrain Injury BiomechanicsBrain Injury MechanicsBrain Tissue MechanicsNeuroinflammation After InjuryRodent Brain InjuryRodent NeuroinflammationTraumatic Brain Injury PathologyTraumatic Brain Injury Pathophysiology
Diffuse brain injury is better described as multi-focal, where pathology can be found adjacent to seemingly uninjured neural tissue. In experimental diffuse brain injury, pathology and pathophysiology have been reported far more lateral than predicted by the impact site. We hypothesized that local thickening of the rodent skull at the temporal ridges serves to focus the intracranial mechanical forces experienced during brain injury and generate predictable pathology. We demonstrated local thickening of the skull at the temporal ridges using contour analysis on magnetic resonance imaging. After diffuse brain injury induced by midline fluid percussion injury (mFPI), pathological foci along the anterior-posterior length of cortex under the temporal ridges were evident acutely (1, 2, and 7 days) and chronically (28 days) post-injury by deposition of argyophilic reaction product. Area CA3 of the hippocampus and lateral nuclei of the thalamus showed pathological change, suggesting that mechanical forces to or from the temporal ridges shear subcortical regions. A proposed model of mFPI biomechanics suggests that injury force vectors reflect off the skull base and radiate toward the temporal ridge, thereby injuring ventral thalamus, dorsolateral hippocampus, and sensorimotor cortex. Surgically thinning the temporal ridge before injury reduced injury-induced inflammation in the sensorimotor cortex. These data build evidence for temporal ridges of the rodent skull to contribute to the observed pathology, whether by focusing extracranial forces to enter the cranium or intracranial forces to escape the cranium. Pre-clinical investigations can take advantage of the predicted pathology to explore injury mechanisms and treatment efficacy.
122
The Role of Excitatory Amino Acids and NMDA Receptors in Traumatic Brain Injury
Alan I. Faden, Paul Demediuk, S. Scott Panter et al. · Science · 1989 · 1.5K citations
Traumatic brain injury in the rat: Characterization of a lateral fluid-percussion model
Tracy K. McIntosh, Robert Vink, Iwao Yamakami et al. · Neuroscience · 1989 · 1.1K citations
Medicine, Neurobiology, Neuroscience +11
A fluid percussion model of experimental brain injury in the rat
C. Edward Dixon, Bruce G. Lyeth, John T. Povlishock et al. · Journal of neurosurgery · 1987 · 1K citations