Axonal Pathology in Traumatic Brain Injury

By Victoria E. Johnson, W. Stewart, Douglas H. Smith. Experimental Neurology, 2012

1,233 citations recorded by the source corpus.

Over the past 70 years, diffuse axonal injury (DAI) has emerged as one of the most common and important pathological features of traumatic brain injury (TBI). Axons in the white matter appear to be especially vulnerable to injury due to the mechanical loading of the brain during TBI. As such, DAI has been found in all severities of TBI and may represent a key pathologic substrate of mild TBI (concussion). Pathologically, DAI encompasses a spectrum of effects from primary mechanical breaking of the axonal cytoskeleton, to transport interruption, swelling and proteolysis, through secondary physiological changes. Depending on the severity and extent of injury, these changes can manifest acutely as immediate loss of consciousness or confusion and persist as coma and/or cognitive dysfunction. In addition, recent evidence suggests that TBI may induce long-term neurodegenerative processes, such as insidiously progressive axonal pathology. Indeed, axonal degeneration has been found to continue even years after injury in humans, and appears to play a role in the development of Alzheimer’s disease-like pathological changes. Here we review the current understanding of DAI as a uniquely mechanical injury, its histopathological identification, and its acute and chronic pathogenesis following TBI.

Subfields: Epidemiology, Molecular Biology, Neurology

View Paper: https://www.semanticscholar.org/paper/6fdff07fcccb6429453f06a8aae43cdaad508837

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. M. Sofroniew
2. J. Burda

In Neurology

1. J. Burda
2. M. Sofroniew
3. Alexander M. Bernstein
4. M. Pekny
5. M. Pekna

Citations in the corpus

• The New Neurometabolic Cascade of Concussion (2014, neutral): “In vitro stretch injury models demonstrate poststretch axonal undulations and beading—in some cases these would recover, but in others the axonal damage was lasting.(17,18) In addition, recent studies using fluid percussion injury centered over the white matter tracts of the corpus callosum indicate”
• Astrocyte roles in traumatic brain injury (2015, background): “…A uthor M anuscript A uthor M anuscript A uthor M anuscript microscopic level during postmortem evaluation, by vascular breakdown and hallmark diffuse axonal injury that manifests as axonal swellings, plasmalemmal disruption, disconnection and Wallerian degeneration (Johnson et al., 2013).”
• NAD+ metabolism: pathophysiologic mechanisms and therapeutic potential (2020, background): “Axonal degeneration is an early and prominent feature of many neurological disorders, including AD, PD, ALS, ischemic brain and spinal cord injuries, diabetic neuropathy and traumatic brain injury.(483,484) SARM1, as the evolutionary conservative executor of degradation cascade, is required for the ”