CSF-Biomarkers in Olympic Boxing: Diagnosis and Effects of Repetitive Head Trauma

Background Sports-related head trauma is common but still there is no established laboratory test used in the diagnostics of minimal or mild traumatic brain injuries. Further the effects of recurrent head trauma on brain injury markers are unknown. The purpose of this study was to investigate the relationship between Olympic (amateur) boxing and cerebrospinal fluid (CSF) brain injury biomarkers. Methods The study was designed as a prospective cohort study. Thirty Olympic boxers with a minimum of 45 bouts and 25 non-boxing matched controls were included in the study. CSF samples were collected by lumbar puncture 1–6 days after a bout and after a rest period for at least 14 days. The controls were tested once. Biomarkers for acute and chronic brain injury were analysed. Results NFL (mean ± SD, 532±553 vs 135±51 ng/L p = 0.001), GFAP (496±238 vs 247±147 ng/L p<0.001), T-tau (58±26 vs 49±21 ng/L p<0.025) and S-100B (0.76±0.29 vs 0.60±0.23 ng/L p = 0.03) concentrations were significantly increased after boxing compared to controls. NFL (402±434 ng/L p = 0.004) and GFAP (369±113 ng/L p = 0.001) concentrations remained elevated after the rest period. Conclusion Increased CSF levels of T-tau, NFL, GFAP, and S-100B in >80% of the boxers demonstrate that both the acute and the cumulative effect of head trauma in Olympic boxing may induce CSF biomarker changes that suggest minor central nervous injuries. The lack of normalization of NFL and GFAP after the rest period in a subgroup of boxers may indicate ongoing degeneration. The recurrent head trauma in boxing may be associated with increased risk of chronic traumatic brain injury

Early measurement of interleukin-10 predicts the absence of CT scan lesions in mild traumatic brain injury

Traumatic brain injury is a common event where 70%-90% will be classified as mild TBI (mTBI). Among these, only 10% will have a brain lesion visible via CT scan. A triage biomarker would help clinicians to identify patients with mTBI who are at risk of developing a brain lesion and require a CT scan. The brain cells damaged by the shearing, tearing and stretching of a TBI event set off inflammation cascades. These cause altered concentrations of a high number of both pro-inflammatory and anti-inflammatory proteins. This study aimed to discover a novel diagnostic biomarker of mTBI by investigating a broad panel of inflammation biomarkers and their capacity to correctly identify CT-positive and CT-negative patients. Patients enrolled in this study had been diagnosed with mTBI, had a GCS score of 15 and suffered from at least one clinical symptom. There were nine patients in the discovery group, 45 for verification, and 133 mTBI patients from two different European sites in the validation cohort. All patients gave blood samples, underwent a CT scan and were dichotomised into CT-positive and CT-negative groups for statistical analyses. The ability of each protein to classify patients was evaluated with sensitivity set at 100%. Three of the 92 inflammation proteins screened-MCP-1, MIP-1alpha and IL-10 -were further investigated in the verification group, and at 100% sensitivity their specificities reached 7%, 0% and 31%, respectively. IL-10 was validated on a larger cohort in comparison to the most studied mTBI diagnostic triage protein to date, S100B. Levels of both proteins were significantly higher in CT-positive than in CT-negative patients (p < 0.001). S100B's specificity at 100% sensitivity was 18% (95% CI 10.8-25.2), whereas IL-10 reached a specificity of 27% (95% CI 18.9-35.1). These results showed that IL-10 might be an interesting and clinically useful diagnostic tool, capable of differentiating between CT-positive and CT-negative mTBI patients