Article

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

Hangzhou Normal University, China
PLoS ONE (Impact Factor: 3.53). 04/2012; 7(4):e33606. DOI: 10.1371/journal.pone.0033606
Source: PubMed

ABSTRACT 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.
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.
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.
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.

1 Follower
 · 
111 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Despite substantial investments, traumatic brain injury (TBI) remains one of the major disorders that lack specific pharmacotherapy. To a substantial degree, this situation is due to lack of understanding of the pathophysiological process of the disease. Experimental TBI research offers controlled, rapid, and cost-effective means to identify the pathophysiology but translating experimental findings into clinical practice can be further improved by using the same or similar outcome measures and clinically relevant time points. The pathophysiology during the acute phase of severe TBI is especially poorly understood. In this Mini review, I discuss some of the incongruences between current clinical practices and needs versus information provided by experimental TBI research as well as the benefits of designing animal experiments with translation into clinical practice in mind.
    Frontiers in Neurology 03/2015; 6:47. DOI:10.3389/fneur.2015.00047
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Repeated exposure to low-level blast is a characteristic of a few select occupations and there is concern that such occupational exposures present risk for traumatic brain injury. These occupations include specialized military and law enforcement units that employ controlled detonation of explosive charges for the purpose of tactical entry into secured structures. The concern for negative effects from blast exposure is based on rates of operator self-reported headache, sleep disturbance, working memory impairment, and other concussion-like symptoms. A challenge in research on this topic has been the need for improved assessment tools to empirically evaluate the risk associated with repeated exposure to blast overpressure levels commonly considered to be too low in magnitude to cause acute injury. Evaluation of serum-based neurotrauma biomarkers provides an objective measure that is logistically feasible for use in field training environments. Among candidate biomarkers, ubiquitin carboxy-terminal hydrolase-L1 (UCH-L1) has some empirical support and was evaluated in this study. We used daily blood draws to examine acute change in UCH-L1 among 108 healthy military personnel who were exposed to repeated low-level blast across a 2-week period. These research volunteers also wore pressure sensors to record blast exposures, wrist actigraphs to monitor sleep patterns, and completed daily behavioral assessments of symptomology, postural stability, and neurocognitive function. UCH-L1 levels were elevated as a function of participating in the 2-week training with explosives, but the correlation of UCH-L1 elevation and blast magnitude was weak and inconsistent. Also, UCH-L1 elevations did not correlate with deficits in behavioral measures. These results provide some support for including UCH-L1 as a measure of central nervous system effects from exposure to low-level blast. However, the weak relation observed suggests that additional indicators of blast effect are needed.
    Frontiers in Neurology 03/2015; 6:49. DOI:10.3389/fneur.2015.00049
  • [Show abstract] [Hide abstract]
    ABSTRACT: Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disorder attributed to repetitive mild traumatic brain injury. The diagnosis in a living individual can be challenging and can be made definitively only at autopsy. The symptoms are often nonspecific and overlap with neurodegenerative disorders such as Alzheimer's disease (AD) and frontotemporal dementia (FTD). Higher exposure to repetitive head trauma increases the risk of CTE. Genetic risk factors such as presence of an apolipoprotein E ε4 allele may be important. Individuals have varying degrees of cognitive, behavioral, and motor decline. Limitations in the manner in which data have been obtained over the years have led to different clinical descriptions of CTE. At present, there are no biomarkers to assist in the diagnosis. Standard neuroimaging may show nonspecific atrophic changes; however, newer imaging modalities such as positron emission tomography (PET) and diffusion tensor imaging (DTI) show promise. Neuropsychological testing may be helpful in determining the pattern of cognitive or behavioral decline.
    Current Neurology and Neuroscience Reports 05/2015; 15(5):541. DOI:10.1007/s11910-015-0541-5 · 3.67 Impact Factor