The aftermath of boxing

Corsellis, J. A. N.; Bruton, C. J.; Freeman-Browne, D L

doi:10.1017/s0033291700049588

Cited by 786 publications

(535 citation statements)

References 27 publications

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“…CTE was first described symptomatically in the late 1920s as 'punch-drunk' dementia in boxers, 69 was later described as 'dementia pugilistica' , 70 and was first described pathologically in 1973. 71 Since the identification of CTE in a former professional American football player in 2005, 72 and additional intensive pathological studies, this condition has gained widespread public attention, and has now been identified in brains of former ice hockey, baseball, rugby and soccer players, 73 wrestlers, 74 and military veterans. 75,76 The prevalence and incidence of CTE in amateur and professional athletes is still unknown, adding to difficulties in discussing its epidemiology and population risks for athletes.…”

Section: Subconcussive Blowsmentioning

confidence: 99%

Mind the gaps—advancing research into short-term and long-term neuropsychological outcomes of youth sports-related concussions

et al. 2015

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Section: Subconcussive Blowsmentioning

confidence: 99%

Mind the gaps—advancing research into short-term and long-term neuropsychological outcomes of youth sports-related concussions

et al. 2015

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“…9,10 This disease is associated primarily with the buildup of neurofibrillary tangles of hyperphosphorylated tau throughout the brain; however, 52% of cases also present with diffuse amyloid-b (Ab) deposits. 11 There has been difficulty reproducing tau pathology in rodents after rmTBI, and to date the only study that has seen a chronic (21 days after TBI) increase in hyperphosphorylated tau after rmTBI has required the use of aged tau transgenic mice to observe an effect.…”

mentioning

confidence: 99%

Dendritic Spine Loss and Chronic White Matter Inflammation in a Mouse Model of Highly Repetitive Head Trauma

Winston

Noël

Neustadtl

et al. 2016

The American Journal of Pathology

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Mild traumatic brain injury (mTBI) is an emerging risk for chronic behavioral, cognitive, and neurodegenerative conditions. Athletes absorb several hundred mTBIs each year; however, rodent models of repeat mTBI (rmTBI) are often limited to impacts in the single digits. Herein, we describe the effects of 30 rmTBIs, examining structural and pathological changes in mice up to 365 days after injury. We found that single mTBI causes a brief loss of consciousness and a transient reduction in dendritic spines, reflecting a loss of excitatory synapses. Single mTBI does not cause axonal injury, neuroinflammation, or cell death in the gray or white matter. Thirty rmTBIs with a 1-day interval between each mTBI do not cause dendritic spine loss; however, when the interinjury interval is increased to 7 days, dendritic spine loss is reinstated. Thirty rmTBIs cause white matter pathology characterized by positive silver and Fluoro-Jade B staining, and microglial proliferation and activation. This pathology continues to develop through 60 days, and is still apparent at 365 days, after injury. However, rmTBIs did not increase b-amyloid levels or tau phosphorylation in the 3xTg-AD mouse model of Alzheimer disease. Our data reveal that single mTBI causes a transient loss of synapses, but that rmTBIs habituate to repetitive injury within a short time period. rmTBI causes the development of progressive white matter pathology that continues for months after the final impact. (Am J Pathol 2016, 186: 552e567; http://dx.doi.org/ 10.1016/j.ajpath.2015 Athletes participating in contact sports are at high risk of exposure to large numbers of concussive and subconcussive mild traumatic brain injuries (mTBIs). Recent studies using head impact telemetry systems have begun to reveal how many head impacts an individual football player can receive in the process of playing his or her sport. In a study of high school football players, the number of helmet impacts >20 g recorded in a single season ranged from a low of 226 (average, 4.7 per session) to a high of 1855 (average, 38.6 per session). 1 Most of these impacts do not result in the clinical diagnosis of a concussion; however, it is not known if the cumulative effects of these impacts can result in increased damage to the brain. mTBI has been extensively modeled in mice and rats. 2 Most of these rodent models use fewer than five mTBIs, and report adverse events, including intracerebral bleeding, skull fractures, severe axonal injury, neuronal cell death, and increased mortality.

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“…The neuropathology of CTE was first described by Brandenburg, Hallevorden, and later Corsellis who found several characteristic areas of damage: septum pellucidum, adjacent periventricular gray, frontal and temporal lobes, substantia nigra, cerebellar scarring, and diffuse neuronal loss [7,[14][15]. Although originally described in boxers, CTE has since been found in other sports, including football, wrestling, and hockey as well as in individuals suffering repetitive brain trauma that were not athletes [7,14]. It more recently has also been found in military blast victims.…”

Section: Historical Backgroundmentioning

confidence: 99%

“…In severe cases there is a progressive slowing of movement, a propulsive gait, tremor, masked facies, deafness, dysarthria, dysphagia, ptosis and other ocular abnormalities [7]. Clinical deterioration in CTE typically occurs in three stages [7,14] :…”

Section: Review Clinical Presentationmentioning

confidence: 99%

Chronic Traumatic Encephalopathy as a Consequence of Repetitive Sports Head Injury: A Review

Galgano¹,

Cantu²,

Chin³

2014

Cureus

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Chronic traumatic encephalopathy (CTE) is a disabling condition seen most frequently in athletes involved in high-impact sports. Physical and emotional abnormalities begin to display themselves later on in an athlete's life. Routine neuroradiographic imaging generally does not show any significant findings; however, newer MRI-based techniques, such as DTI, fMRI, and MRS, have shown promise for earlier detection. Three stages of the clinical presentation of CTE have been described. CTE likely results from progressive neuronal loss. Once the cascades are started, the symptoms of CTE become progressive. Sport-specific preventive strategies and early detection in our athletes is of vital importance in the management of CTE.

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The aftermath of boxing

Cited by 786 publications

References 27 publications

Mind the gaps—advancing research into short-term and long-term neuropsychological outcomes of youth sports-related concussions

Mind the gaps—advancing research into short-term and long-term neuropsychological outcomes of youth sports-related concussions

Dendritic Spine Loss and Chronic White Matter Inflammation in a Mouse Model of Highly Repetitive Head Trauma

Chronic Traumatic Encephalopathy as a Consequence of Repetitive Sports Head Injury: A Review

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