Motor Vehicle Crash-Related Subdural Hematoma from Real-World Head Impact Data

Abstract

Approximately 1,700,000 people sustain a traumatic brain injury (TBI) each year and motor vehicle crashes (MVCs) are a leading cause of hospitalization from TBI. Acute subdural hematoma (SDH) is a common intracranial injury that occurs in MVCs associated with high mortality and morbidity rates. In this study, SDH volume and midline shift have been analyzed in order to better understand occupant injury by correlating them to crash and occupant parameters. Fifty-seven head computed tomography (CT) scans were selected from the Crash Injury Research Engineering Network (CIREN) with Abbreviated Injury Scale (AIS) level 3 + SDH. Semi-automated methods were used to isolate the intracranial volume. SDH and additional occupant intracranial injuries were segmented across axial CT images, providing a total SDH injury volume. SDH volume was correlated to crash parameters and occupant characteristics. Results show a positive correlation between SDH volume and crash severity in near-side and frontal crashes. Additionally, the location of the resulting hemorrhage varied by crash type. Those with greater SDH volumes had significantly lower Glasgow Coma Scale (GCS) scores at the crash site in near-side crashes. Age and fracture type were found to be significant contributors to SDH volume. This study is a volumetric analysis of real world brain injuries and known MVC impacts. The results of this study demonstrate a relationship among SDH volume, crash mechanics, and occupant characteristics that provide a better understanding of the injury mechanisms of MVC-associated TBI.

Validation performance comparison for finite element models of the human brain

“…Models should be validated against additional displacement tests (Hardy et al 2001, Hardy 2007) in the future as well as against strain data from live humans obtained by magnetic resonance elastography (MRE) studies (Sabet et al 2008). Injury prediction capabilities will continue to increase as brain models are improved and validated against more experimental data and further correlated with real world injuries (Urban et al 2012, 2015). …”

Time‐dependent differences in cortical measures and their associations with behavioral measures following mild traumatic brain injury

“…Cortical thickening during initial scans following an mTBI and cortical thinning in later scans may reflect progressive normalization of CT, that is, physical recovery from brain lesions (Lewen et al, ; Wang et al, ). In addition, the brain areas, such as RMFG, which are more susceptible to direct impacts following a frontal–rear axis head injury, may result in the release of excitotoxins from damaged tissues causing inflammatory reactions, including microedema (Barkhoudarian, Hovda, & Giza, ; Lillie, Urban, Lynch, Whitlow, & Stitzel, ; Patterson and Holahan, ; Urban et al, ). These inflammatory reactions have been reported to elevate fractional anisotropy, thicken the cortical regions initially but cause cortical thinning over time with the reduction of microedema (Lewen et al, ; Ling et al, ).…”

Early Cortical Thickness Change after Mild Traumatic Brain Injury following Motor Vehicle Collision

“…21 In the current study, we identified cortical thickening in rMFG and precuneus areas that are vulnerable to direct impacts from coup/contrecoup injury in frontalrear axis head injury. 31,55 If the mTBI caused a local release of excitotoxins from damaged cells in these regions, 56 these in turn can contribute to inflammatory reactions, possibly including micro-edema. [57][58][59] Consistent with this possibility, a recent study reported elevated cortical fractional anisotropy in similar regions, 14 days to 4 months after mTBI, which could also be the consequence of cytotoxic edema.…”