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      Head Impact Exposure in Youth Football

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          Abstract

          The head impact exposure for athletes involved in football at the college and high school levels has been well documented; however, the head impact exposure of the youth population involved with football has yet to be investigated, despite its dramatically larger population. The objective of this study was to investigate the head impact exposure in youth football. Impacts were monitored using a custom 12 accelerometer array equipped inside the helmets of seven players aged 7–8 years old during each game and practice for an entire season. A total of 748 impacts were collected from the 7 participating players during the season, with an average of 107 impacts per player. Linear accelerations ranged from 10 to 100 g, and the rotational accelerations ranged from 52 to 7694 rad/s 2. The majority of the high level impacts occurred during practices, with 29 of the 38 impacts above 40 g occurring in practices. Although less frequent, youth football can produce high head accelerations in the range of concussion causing impacts measured in adults. In order to minimize these most severe head impacts, youth football practices should be modified to eliminate high impact drills that do not replicate the game situations.

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          The epidemiology and impact of traumatic brain injury: a brief overview.

          Traumatic brain injury (TBI) is an important public health problem in the United States and worldwide. The estimated 5.3 million Americans living with TBI-related disability face numerous challenges in their efforts to return to a full and productive life. This article presents an overview of the epidemiology and impact of TBI.
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            Chronic traumatic encephalopathy in a National Football League player.

            We present the results of the autopsy of a retired professional football player that revealed neuropathological changes consistent with long-term repetitive concussive brain injury. This case draws attention to the need for further studies in the cohort of retired National Football League players to elucidate the neuropathological sequelae of repeated mild traumatic brain injury in professional football. The patient's premortem medical history included symptoms of cognitive impairment, a mood disorder, and parkinsonian symptoms. There was no family history of Alzheimer's disease or any other head trauma outside football. A complete autopsy with a comprehensive neuropathological examination was performed on the retired National Football League player approximately 12 years after retirement. He died suddenly as a result of coronary atherosclerotic disease. Studies included determination of apolipoprotein E genotype. Autopsy confirmed the presence of coronary atherosclerotic disease with dilated cardiomyopathy. The brain demonstrated no cortical atrophy, cortical contusion, hemorrhage, or infarcts. The substantia nigra revealed mild pallor with mild dropout of pigmented neurons. There was mild neuronal dropout in the frontal, parietal, and temporal neocortex. Chronic traumatic encephalopathy was evident with many diffuse amyloid plaques as well as sparse neurofibrillary tangles and tau-positive neuritic threads in neocortical areas. There were no neurofibrillary tangles or neuropil threads in the hippocampus or entorhinal cortex. Lewy bodies were absent. The apolipoprotein E genotype was E3/E3. This case highlights potential long-term neurodegenerative outcomes in retired professional National Football League players subjected to repeated mild traumatic brain injury. The prevalence and pathoetiological mechanisms of these possible adverse long-term outcomes and their relation to duration of years of playing football have not been sufficiently studied. We recommend comprehensive clinical and forensic approaches to understand and further elucidate this emergent professional sport hazard.
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              Chronic traumatic encephalopathy in a national football league player: part II.

              We present the second reported case of autopsy-confirmed chronic traumatic encephalopathy in a retired professional football player, with neuropathological features that differ from those of the first reported case. These differing pathological features underscore the need for further empirical elucidation of the pathoetiology and pathological cascades of long-term neurodegenerative sequelae of professional football. A psychological autopsy was performed with the next-of-kin and wife. Medical and hospital records were reviewed. A complete autopsy was accompanied by a comprehensive forensic neuropathological examination. Restriction fragment length polymorphism analysis was performed to determine apolipoprotein-E genotype. Pertinent premortem history included a 14-year span of play in organized football starting from the age of 18 years. The subject was diagnosed with severe major depressive disorder without psychotic features after retirement, attempted suicide multiple times and finally committed suicide 12 years after retirement by ingestion of ethylene glycol. Autopsy revealed cardiomegaly, mild to moderate coronary artery disease, and evidence of acute ethylene glycol overdose. The brain showed no atrophy, a cavum septi pellucidi was present, and the substantia nigra showed mild pallor. The hippocampus and cerebellum were not atrophic. Amyloid plaques, cerebral amyloid angiopathy, and Lewy bodies were completely absent. Sparse to frequent tau-positive neurofibrillary tangles and neuropil threads were present in all regions of the brain. Tufted and thorn astrocytes, as well as astrocytic plaques, were absent. The apolipoprotein-E genotype was E3/E4. Our first and second cases both had long careers without multiple recorded concussions. Both manifested Major Depressive Disorder after retirement. Amyloid plaques were present in the first case and completely absent in the second case. Both cases exhibited neurofibrillary tangles, neuropil threads, and coronary atherosclerotic disease. Apolipoprotein-E4 genotypes were different. Reasons for the contrasting features in these two cases are not clear. Further studies are needed to identify and define the neuropathological cascades of chronic traumatic encephalopathy in football players, which may form the basis for prophylaxis and therapeutics.
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                Author and article information

                Contributors
                +1-856-9812512 , srowson@vt.edu
                Journal
                Ann Biomed Eng
                Ann Biomed Eng
                Annals of Biomedical Engineering
                Springer US (Boston )
                0090-6964
                1521-6047
                15 February 2012
                15 February 2012
                April 2012
                : 40
                : 4
                : 976-981
                Affiliations
                Center for Injury Biomechanics, Virginia Tech-Wake Forest University, 440 ICTAS Building, Stanger St., Blacksburg, VA 24061 USA
                Author notes

                Associate Editor K. A. Athanasiou oversaw the review of this article.

                Article
                530
                10.1007/s10439-012-0530-7
                3310979
                22350665
                9e399135-4986-4102-934a-bb8133ba3e4e
                © The Author(s) 2012
                History
                : 1 February 2012
                : 3 February 2012
                Categories
                Article
                Custom metadata
                © Biomedical Engineering Society 2012

                Biomedical engineering
                helmet,children,rotational,acceleration,brain injury,pediatric,linear,concussion,biomechanics

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