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Published on: August 14, 2019
Diffuse Axonal and Vascular Pathology in the Gyrencephalic Brain after High-Energy Blunt Injury: Clinicopathological
Athanasios S Alexandris1, Karin Rafaels2, Michael Horsmon3
1Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
High-energy blunt force trauma can cause brain injuries, leading to breathing problems and death. This study in pigs shows brainstem damage to axons and blood vessels is linked to respiratory failure after such injuries.
Area of Science:
- Neuroscience
- Pathology
- Trauma Research
Background:
- High-energy blunt force trauma, particularly behind helmet blunt trauma (BHBT), is a poorly understood cause of traumatic brain injury (TBI).
- BHBT is frequently associated with apnea and mortality in humans, suggesting a critical role for brainstem injury.
- Characterizing neuropathologies in BHBT is crucial for understanding acute respiratory decompensation.
Purpose of the Study:
- To characterize neuropathologies in a swine model of high-energy BHBT.
- To investigate the association between these neuropathologies and acute respiratory decompensation.
- To examine the role of brainstem axonal and vascular lesions in apnea following BHBT.
Main Methods:
- Utilized a swine model subjected to high-energy BHBT.
- Euthanized animals within 4 hours post-injury for neuropathological assessment.
- Focused on axonal and vascular pathologies, particularly in the brainstem.
Main Results:
- BHBT frequently caused cranial fractures, subarachnoid hemorrhages, contusions, and diffuse axonal and vascular lesions, especially in the brainstem.
- Absence of spontaneous respiration correlated with impact severity and brainstem lesion severity.
- Diffuse axonal lesions in the medial medulla or vascular lesions in the anteroventral brainstem were linked to adverse outcomes, suggesting brainstem respiratory center involvement.
Conclusions:
- High-energy blunt force TBI induces diffuse axonal and vascular lesions associated with poor outcomes.
- Axons and blood vessels may respond differently to tissue deformation, with vascular markers not being direct surrogates for axonal injury.
- Regional brainstem injuries, both axonal and vascular, play a significant role in acute respiratory decompensation after blunt TBI, even with head protection.
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