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Time To Expand The Term ‘Minor Head Injury’: Clinical Risk And Biomarker Research
*Corresponding author: Luis Rafael Moscote-Salazar, Department of Neurosurgery, University of Cartagena, Cartagena De Indias, Colombia. rafaelmoscote21@gmail.com
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Received: ,
Accepted: ,
How to cite this article: Moscote-salazar LR, Janjua T, Flórez Perdomo WA, Agrawal A. Time To Expand The Term ‘Minor Head Injury’: Clinical Risk And Biomarker Research. Ann Emerg Trauma Crit Care. doi: 10.25259/AETCC_1_2025
Dear Editor,
Mild head injury is responsible for more than 75% of presentations in the acute environment, exhibiting significant clinical heterogeneity—the wide variation in injury mechanisms and outcomes despite similar initial symptoms—yet most patients are under-examined or discharged prematurely. The prevalence is greatest in the elderly (≥65 years) who are at risk of late deterioration and young athletes with possible chronic cognitive dysfunction.1 Prognosis varies from complete recovery to permanent disability, especially where follow-up is not performed routinely. While often used interchangeably, “minor head injury” is a clinical descriptor for Glasgow Coma Scale (GCS) 13–15, whereas “mild traumatic brain injury (TBI)” is a specific diagnostic term.2 The phrase “minor head injury” has been common usage in clinical practice, research, and popular opinion to refer to awake and oriented patients with blunt head trauma, typically based on a GCS score of 13–15.1 This term does little more than downplay risk and obscure important variation in clinical course, radiologic presentation, and outcome.3
Even minor head trauma can induce remarkable pathophysiological alterations like axonal injury, breakdown of the blood–brain barrier, and neuroinflammation—without the development of imminent clinical manifestations.4 Delayed intracranial haemorrhage in the elderly or patients on anticoagulant or antiplatelet therapy can follow seemingly trivial trauma.2 Furthermore, glutamate excitotoxic cascades and mitochondrial damage contribute to secondary injury, emphasising the need for vigilant clinical monitoring and risk-stratification through biomarkers, even when GCS scores appear normal.2,5-7 Conversely, evolving advances in biomarker analysis have generated the potential for risk stratification of patients with seemingly “minor” head injury [Table 1]. GFAP (glial fibrillary acidic protein), UCH-L1 (ubiquitin C-terminal hydrolase-L1), S100B (S100 calcium-binding protein B), and NFL (neurofilament light chain) are biomarkers that have been shown to be of diagnostic and prognostic value in occult brain injury detection, prediction of intracranial pathology, and imaging decision-making—even in patients with 13–15 GCS scores.8 These molecular markers can assist physicians to transcend subjective judgment and enable accuracy in triage, monitoring, and follow-up care [Figure 1].
| Biomarker | Origin | Rise time (hrs) | Peak (hrs) | Decline (hrs) | Clinical relevance |
|---|---|---|---|---|---|
| S100B | Astrocytes | 0.5–1.5 | 1–3 | 24–48 (initial) | Early triage in mild TBI (high NPV for ruling out CT lesions), low specificity. |
| GFAP | Astrocytes | 1–4 | 6–24 | 48–72+ | Highly sensitive and specific for detecting intracranial lesions on CT scan. |
| NSE | Neurons | 6–12 | 12–24 | 72+ | An indicator of neuronal injury; less specific due to extracranial sources. |
| Tau | Axons | 6–12 | 12–24 | 72+ | A marker of axonal injury, particularly diffuse axonal injury, correlates with outcomes. |
| NF-L | Axons | 12–24 | 24–72 (to days-weeks) | Days–Weeks | Marker of persistent axonal damage; useful for long-term prognosis. |
| IL-6 | Immune cells | 1–3 | 3–6 | <24–48 | Acute neuroinflammation is associated with injury severity. |
TBI: Traumatic brain injury, GFAP: Glial fibrillary acidic protein, NPV: Negative predictive value, CT: Computed tomography, NF-L: Neuro filament light chain, IL-6: Interleukin-6, NSE: Neuron-specific enolase

Issues with the term “minor head injury"
This terminology lacks precision and significantly underestimates the clinical risk. Evidence shows that up to 15% of patients with GCS 13–15 head trauma demonstrate clinically relevant findings on computed tomography (CT) imaging.9 Delayed intracranial haemorrhage is seen, particularly in patients on anticoagulant or antiplatelet therapy.2 While the rates of mortality and neurosurgical intervention are lower than those associated with severe TBI, they remain clinically significant.1,2
This is important at all labels and can mask clinical heterogeneity, and is typically a euphemism. Furthermore, the term fails to differentiate between patients based on critical factors such as loss of consciousness, amnesia, emesis, advanced age, or high-risk mechanisms of injury. It also fails to account for findings on CT or advanced imaging.1 It can cause medico-legal and communication issues because patients or relatives can misinterpret the term as meaning no further concern or follow-up required.3 Worsening in the future can be complicated by previous use of the term “minor” in litigation or ongoing care.
Case vignettes illustrating the issue
We can mention that clinical recommendations are inconsistent across guidelines—such as NICE (UK) and ACEP (US)—and clinical decision rules like the Canadian CT Head Rule, which are discordant on thresholds of imaging and admission because they are inconsistent in defining “minor”.10 Some employ GCS 15 alone, others 13–14.
Case 1: 74-year-old on clopidogrel with GCS 15 following ground-level fall. CT shows a small subdural hematoma. Patient deteriorates within 12 hours and needs surgical evacuation. Originally referred to as “minor,” the prognosis is grave.
Case 2: A 19-year-old GCS 15 on presentation with a sport-related head injury. No imaging was taken. Three weeks later, he returns with headache, sleep disturbance, and cognitive impairment—classic post-concussion syndrome symptoms. The “minor” designation had ended the case too hastily.
A call for terminological reform and a proposed terminology framework
We propose substituting “minor head injury” with structured descriptors that are more specific: GCS Score: e.g., “Head injury with GCS 15” instead of “minor."; Imaging Results: “CT-negative mild head injury” vs. “CT-positive mild TBI."; Mechanism and Risk: “Low-risk closed head trauma,” “anticoagulated head injury,” or “mild TBI with high-risk features.” We believe it is essential to integrate risk-stratification instruments alongside biomarkers to optimise triage decisions and identify patients requiring specialised follow-up care. Validated clinical decision rules, such as the Canadian CT Head Rule, New Orleans Criteria, or National Emergency X-radiography utilization study (NEXUS) Head CT Rule , should be routinely applied.9,11 Combining these tools with the expanded use of biomarkers can introduce greater objectivity and a risk-stratified nomenclature [Table 1 and Figure 1].4-8, 12-17
In summary, the phrase “minor head injury” is an outdated descriptor. Once employed as a shorthand to prevent overresponse to low-risk trauma, the phrase now carries the danger of underestimating risk. With the uncertainty of outcome—even among patients with GCS 15—it is time to embrace terminology that appreciates the nuance of head trauma and emphasises clarity, safety, and specificity. Practically, this transition improves triage for high-risk groups (such as the elderly), provides clearer definitions for research cohorts, and ensures patients fully understand the necessity of follow-up care.
Ethical approval:
Institutional Review Board approval is not required.
Declaration of patient consent:
Patient's consent not required as there are no patients in this study.
Conflicts of interest:
There are no conflicts of interest.
Use of artificial intelligence (AI)-assisted technology for manuscript preparation:
The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript, and no images were manipulated using AI.
Financial support and sponsorship: Nil.
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