Traumatic brain injuries (TBIs) are caused by a hit to the head or a sudden acceleration/deceleration movement of the head. Mild TBIs (mTBIs) and concussions are difficult to diagnose. Imaging techniques often fail to find alterations in the brain, and computed tomography exposes the patient to radiation. Brain-specific biomolecules that are released upon cellular damage serve as another means of diagnosing TBI and assessing the severity of injury. These biomarkers can be detected from samples of body fluids using laboratory tests. Dozens of TBI biomarkers have been studied, and research related to them is increasing. We reviewed the recent literature and selected 12 biomarkers relevant to rapid and accurate diagnostics of TBI for further evaluation. The objective was especially to get a view of the temporal profiles of the biomarkers’ rise and decline after a TBI event. Most biomarkers are rapidly elevated after injury, and they serve as diagnostics tools for some days. Some biomarkers are elevated for months after injury, although the literature on long-term biomarkers is scarce. Clinical utilization of TBI biomarkers is still at a very early phase despite years of active research.

The diagnosis of mild traumatic brain injury (TBI) is challenging in the acute setting because the symptoms are nonspecific and often transient, or they develop with a delay. In these cases, the criteria for acute head imaging are frequently not fulfilled. This may lead to missed diagnoses in emergency care. There is a need for developing a rapid diagnostic test to verify the presence of TBI using body fluids. Blood, urine, and saliva samples from 11 adult patients (mean age 64 years, SD 24 years) with acute and clinically diagnosed TBI, and 12 healthy volunteers were collected at Turku University Hospital during a period of 5 months. The injuries necessitated hospitalization for at least one day. The TBIs were classified mild in nine cases and severe in two cases. The mean period between the trauma and the time for obtaining the samples was 27 h, SD 11 h. The samples were analyzed in an ISO-certified laboratory for the number of lectin-bound glycan molecules indicating destruction of nerve tissue. The screening was performed on several possible glycans for binding, and the measurement by degree of fluorescence. In the analysis, the group of patients with TBI was compared with healthy volunteers. The results showed a significant decrease (p < 0.05, Wilcoxon rank–sum two-sided test) in the level of two glycans in plasma, but no significant increase for any glycan; in saliva, one glycan showed a significant increase in the TBI group; in urine, three glycans were significantly different between the groups (one showed an increase, whereas two showed a decrease). The results support the idea of conducting more research on how diagnostic glycans could be detected in body fluids after TBI. As a proof-of-concept, significant changes in the concentration of five glycans were found in plasma, saliva, and urine between TBI patients and healthy controls. This may enable the development of a rapid body fluid-based point-of-care test to identify patients with TBI after a head injury.

Diagnosing mild traumatic brain injury (TBI) in the acute setting is challenging due to the nonspecific and often transient or delayed symptoms. Further, the criteria for acute head imaging are frequently not fulfilled, which may lead to a missed diagnosis. A rapid test to diagnose TBI using body fluids would be highly useful. Urine and saliva samples were collected from 28 pediatric patients (mean [SD] age, eight years two months [four years three months]) with acute, clinically diagnosed mild TBI and 30 healthy volunteers at Satasairaala Hospital, Pori, Finland, over 11 months. The mean (SD) time from trauma to first sampling was 3 h 56 min (1 h 14 min). Samples were analyzed to determine the number of lectin-binding glycan molecules, indicating nerve tissue damage. The relative levels of several lectin-bound glycans were measured by fluorescence. Compared with healthy controls, the TBI group showed significant increases (p < 0.05, Wilcoxon rank-sum two-sided test) in nine glycans in the saliva, one glycan in the urine, and a significant decrease in seven glycans in the urine. These findings of potentially diagnostic glycans in body fluids after TBI warrant further research and may enable the development of a rapid body fluid-based point-of-care test to identify pediatric patients with TBI after a head injury.