Traumatic brain injury (TBI), a leading cause of death and disability across the United States, occurs when the brain experiences penetrating or blunt force impact. Cases are frequent, typically arising from falls, motor vehicle accidents, and assaults [1]. Despite this frequency, the field of emergency medicine (EM) has historically lacked consistency and quality in comprehensive TBI care–a grave concern for the condition’s complex biological consequences. The long-term adverse effects of TBI on individuals’ cognitive and neurological functioning are evident within clinical research; however, EM misses emphasis on the condition’s intricate pathophysiology and the necessity of tailored interventions.
Approx. sixty-nine million individuals worldwide sustain a TBI each year, with many visiting the emergency department (ED) [2]. In acute settings, care typically involves rapid imaging, such as CT scan, to eliminate the possibility of brain bleeding or swelling. In the absence of evident life-threatening conditions, a more minor TBI would be considered, and observation/potential discharge would follow. When the brain looks structurally sound on imaging, neurological interventions are more likely overlooked; invisible damage, however, may still exist. Brain damage occurs in two phases; the initial phase is the injury itself (irreversible yet manageable through preventative measures) and the secondary phase involves various physiological, cellular, and molecular responses that may cause further damage if not controlled [3]. Nerve fiber tears, nervous tissue inflammation, and blood-brain barrier disruption are all common impacts of TBI at this stage [4].
EM management of TBIs is over-reliant on the Glasgow Coma Scale (GCS) to assess severity, yet other aspects should carry higher priority. Though a score of 13-15 on the GCS is considered mild, a large portion of patients within this range develop persistent post-concussion symptoms–including cognitive deficits and emotional instability—indicating that impacts go beyond surface level [5]. Current EM protocols are limited in their guidance regarding these more complex implications. This has delayed proper diagnosis and neurorehabilitation, more powerfully impacting underserved populations for which post-discharge care is not as readily available. In addition, education regarding symptoms to expect and when/how to seek further checkups is often inadequate, leading to missed opportunities for early intervention [5].
Biologically, a cascade of secondary injuries occurs; this involves overstimulation of neurons resulting in cell damage (excitotoxicity), mitochondrial dysfunction, and neuroinflammation [6]. These molecular disruptions result in eventual damage of synapses, persistent neuropsychiatric deficits, and a reduction in hippocampal volume leading to memory impairment. Ultimately, these are exacerbated by the ED’s focus on broader triage efforts rather than biochemical roots. For example, a group of researchers has shone light on the excessive, unnecessary CT scans being performed when pediatric patients would otherwise benefit from more targeted strategies [7]. Their continuous research regarding blood-based brain biomarkers–glial fibrillar acidic protein (GFAP) and ubiquitin carboxy-terminal hydrolase-L1 (UCH-L1)–aims to emphasize the possibility of detecting neuronal injury by means other than standard imaging, ultimately aiding in TBI management efforts. These biomarkers have been approved for limited use, yet they have not fully been incorporated into EM due to cost and other barriers to access. Making these kinds of tests widely available could potentially aid in patient risk assessment, allowing for more personalized discharge plans and continued oversight [7].
In order to address these shortcomings, there must be a systemic shift in the field of EM, integrating scientific insights and social awareness into care. Protocols within the department must expand to involve comprehensive assessment of short and long-term neurological risk, especially for patients with TBIs initially deemed mild. This may involve scheduling follow-up neuropsychological assessments for as many patients as possible and honing in on those with risk factors such as prior TBIs or other psychiatric conditions. It could also include personally-tailored guidance. Another significant aspect is patient education about symptoms and deterioration that may stem from treatment delay; many are discharged without fully understanding the signs of worsening injury and the impact this may have on their lives as a whole. Finally, different kinds of tools should be implemented in the ED, such as biomarker assessment and more advanced digital tools to understand brain function and activity.
Socioeconomic disparities also must be addressed. They influence TBI prognoses due to discrepancies in treatment, post-discharge guidance, and access to rehabilitation. Community-based follow-up programs should be expanded and insurance coverage increased so that outcomes may improve. Overall, post-TBI survival and true recovery must be differentiated so invisible wounds may be accounted for and life-altering outcomes reduced.
Citations
- Cleveland Clinic. Traumatic Brain Injury. Cleveland Clinic. Published January 25, 2024. https://my.clevelandclinic.org/health/diseases/8874-traumatic-brain-injury
- Dewan MC, Rattani A, Gupta S, et al. Estimating the global incidence of traumatic brain injury. J Neurosurg. 2018;130(4):1080-1097. Published 2018 Apr 27. doi:10.3171/2017.10.JNS17352
- Ziebell JM, Morganti-Kossmann MC. Involvement of pro- and anti-inflammatory cytokines and chemokines in the pathophysiology of traumatic brain injury. Neurotherapeutics. 2010;7(1):22-30. doi:10.1016/j.nurt.2009.10.016
- Stahel PF, Shohami E, Younis F, et al. Experimental Closed Head Injury: Analysis of Neurological Outcome, Blood–Brain Barrier Dysfunction, Intracranial Neutrophil Infiltration, and Neuronal Cell Death in Mice Deficient in Genes for Pro-Inflammatory Cytokines. Journal of Cerebral Blood Flow and Metabolism. 2000;20(2):369-380. doi:https://doi.org/10.1097/00004647-200002000-00019
- Eagle SR, Barber J, Temkin N, et al. Follow up rates and patient interest in clinical care after mild traumatic brain injury presenting to a level 1 trauma center: a TRACK-TBI prospective cohort study. Front Neurol. 2025;16:1558204. Published 2025 Apr 2. doi:10.3389/fneur.2025.1558204
- 1.Aurelio M, Sousa G, Leonardo Oliveira Bittencourt, Falcao D, Rafael Rodrigues Lima, Lopes R. Cellular and Molecular Pathophysiology of Traumatic Brain Injury: What Have We Learned So Far? Biology. 2023;12(8):1139-1139. doi:https://doi.org/10.3390/biology12081139
- Lorton F, Lagares A, de la Cruz J, et al. Performance of glial fibrillary acidic protein (GFAP) and ubiquitin carboxy-terminal hydrolase L1 (UCH-L1) biomarkers in predicting CT scan results and neurological outcomes in children with traumatic brain injury (BRAINI-2 paediatric study): protocol of a European prospective multicentre study. BMJ Open. 2024;14(5):e083531. Published 2024 May 15. doi:10.1136/bmjopen-2023-083531