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Results for “chronic traumatic encephalopathy”

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At least 19 recordsLinked to original sources
PubMed2006

Chronic traumatic encephalopathy in a national football league player: part II.

OBJECTIVE: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.

Brain↗
PubMed2005

Chronic traumatic encephalopathy in a National Football League player.

OBJECTIVE: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.

Amyloid beta-Peptides↗
PubMed2026

Regional ventricular enlargement as an in vivo biomarker of cumulative biomechanical neurodegeneration in former American football players.

INTRODUCTION: Repetitive head impacts (RHIs) have been linked to later life neurodegeneration, yet the in vivo structural correlates of cumulative biomechanical loading remain unclear. We examined whether regional ventricular morphology in former American football players reflects exposure burden and traumatic encephalopathy syndrome (TES) classification. METHODS: Participants included 170 male former football players and 54 age-matched asymptomatic male controls from the Diagnostics, Imaging, and Genetics Network for the Objective Study and Evaluation of Chronic Traumatic Encephalopathy Research Project. Subject-specific manual segmentation quantified lateral ventricle, inferior horn, third ventricle, and fourth ventricle volumes. Group and exposure associations were tested using generalized least squares models. RESULTS: Former players showed larger left inferior lateral ventricle volume than controls, with the largest effects among professional players. Greater cumulative linear and rotational acceleration exposure was associated with enlargement across lateral ventricular and inferior horn regions. DISCUSSION: Regional ventricular enlargement may represent an in vivo marker of cumulative biomechanical loading after RHI exposure.

Humans↗
PubMed1996

Controlled prospective neuropsychological assessment of active experienced amateur boxers.

OBJECTIVE: To use a practical battery of eight neuropsychological tests for the detection of an association between amateur boxing and chronic traumatic encephalopathy. DESIGN: A controlled prospective neuropsychological study over a 15-18-month period. SETTING: Dublin, Ireland. March 1992 to September 1993. PARTICIPANTS: Twenty experienced actively competing amateur boxers and 20 controls matched for age and socioeconomic status. INTERVENTIONS: Participation in competitive amateur boxing and training. MAIN OUTCOME MEASURES: Absolute scores, and changes in scores, in the neuropsychological tests. RESULTS: At the end of the study period, the boxers performed significantly better then the controls in both the Trail-Making Tests A and B (TMT-A, TMT-B), whereas the control group's scores for the Finger Tapping Tests (FTT) were significantly higher than those of the boxers. The boxer's scores for the dominant-hand FTT showed a significant deterioration, but there was no association between this change and boxing exposure. CONCLUSIONS: There was no evidence of neuropsychological impairment in the boxers as compared with socioeconomically, educationally and age-matched controls, and there was no association between boxing exposure and performances in any of the neuropsychological tests used. There is accumulating evidence that amateur boxing is not associated with chronic traumatic encephalopathy but longer term prospective studies are needed.

Adult↗
PubMed1995

The neuropsychiatric aspects of boxing.

OBJECTIVE: To review the neuropsychiatry of boxing. METHOD: This update considers the clinical, neuropsychological, diagnostic, neurobiological, and management aspects of boxing-related brain injury. RESULTS: Professional boxers with multiple bouts and repeated head blows are prone to chronic traumatic encephalopathy (CTE). Repeated head blows produce rotational acceleration of the brain, diffuse axonal injury, and other neuropathological features. CTE includes motor changes such as tremor, dysarthria, and parkinsonism; cognitive changes such as mental slowing and memory deficits; and psychiatric changes such as explosive behavior, morbid jealousy, pathological intoxication, and paranoia. Screening with neuropsychological tests and neuroimaging may help predict those boxers at risk for CTE. CONCLUSIONS: Boxing results in a spectrum of CTE ranging from mild, nonprogressive motor changes to dementia pugilistica. Recent emphasis on safety in the ring, rehabilitation techniques, and other interventions do not eliminate the risk for CTE. For this reason, there is an active movement to ban boxing.

Athletic Injuries↗
PubMed1990

Does Swedish amateur boxing lead to chronic brain damage? 2. A retrospective study with CT and MRI.

It is well known that professional boxers can develop chronic traumatic encephalopathy (dementia pugilistica) due to repeated head trauma. Beside CT findings indicating cerebral atrophy, the presence of a cavum septum pellucidum has been reported to indicate encephalopathy. CT findings in amateur boxers are not as well documented. The aim of this study was to find out if morphological changes could be demonstrated among former amateur boxers using CT and MRI. Two control groups of soccer players and track and field athletes in the same age-range were used for comparison. No significant differences in the width of the ventricular system, anterior horn index, width of cortical sulci, signs of vermian atrophy, or the occurrence of a cavum septum pellucidum were found between boxers and controls. A cavum septum pellucidum was found more often in the controls than in the boxers and is probably not a sign of earlier head trauma. MRI confirm no more findings than CT in this retrospective study.

Adult↗
PubMed1987

Neurologic aspects of boxing.

The assessment and prevention of potentially adverse neurologic consequences of boxing requires two important considerations. Acute neurologic injuries should be distinguished from chronic brain injuries and the level of competitive boxing (ie, amateur vs professional) must also be taken into account. Acute neurologic injuries such as concussion, post-concussion syndrome, intracranial hemorrhage, and brain contusion are more readily identified than chronic neurologic injuries because of their immediate devastation of the nervous system. In contrast, chronic neurologic injuries differ in their pathophysiologic mechanisms that are exemplified by an insidious onset and progression after the cessation of boxing. Accordingly, the chronic traumatic encephalopathy of boxing poses the most serious neurologic threat of boxing. Amateur boxing differs from professional boxing in the duration of fights, rules and regulatory policies, medical evaluation, and protective devices. These factors could produce a differential effect on the risk of injury to the brain. The prevention of neurologic injuries in boxing requires the integration of proper neurologic evaluation by qualified ring-side physicians, the design and utilization of effective protective devices, and the establishment of national regulatory agencies.

Athletic Injuries↗
PubMed2003

A 9-year controlled prospective neuropsychologic assessment of amateur boxing.

OBJECTIVE: To test the hypothesis that there is an association between amateur boxing and chronic traumatic encephalopathy using neuropsychologic assessments. DESIGN: A prospective, controlled, blinded, observational, neuropsychologic study. SETTING: Amateur boxing clubs in Dublin, Ireland, March 1992 to April 2001. PARTICIPANTS: Twenty randomly selected, actively competing, male amateur boxers and 20 age-matched, socio-economic controls. INTERVENTIONS: The boxers participated in amateur competition and sparring. MAIN OUTCOME MEASURES: Raw scores and changes in scores over time were recorded in the following neuropsychologic tests: Trail Making Tests A and B, Digit Symbol, Finger Tapping (dominant and nondominant hands), modified versions of the Finger Tapping Tests, Paired-Associate Learning, Digit Span, Rey-Osterrieth Complex Figure Tests A and B, and Serial Addition. Raw scores and changes in scores for the two groups were compared, and a regression analysis was performed to detect any association between these values and exposure to boxing. RESULTS: The boxers showed superior performance in the Trail Making Tests A and B at all time points and an inferior performance in both standard Finger Tapping Tests at all time points except baseline for the dominant hand. This inferior performance was not found in the modified versions of the tests. The controls showed significant deterioration in their performance in the Rey-Osterrieth Complex Figure Tests A and B. CONCLUSIONS: In this small controlled, prospective study of competitive amateur boxers, there was no evidence of neuropsychologic deterioration over 9 years. The amateur boxers demonstrated relative preservation and/or improvement of some neuropsychologic skills relative to the socioeconomic controls.

Adolescent↗
PubMed2004

A punch drunk jockey?

The case is reported of a retired professional jockey with progressive memory loss. The concern is that he may be suffering from chronic traumatic encephalopathy or the "punch drunk syndrome".

Accidental Falls↗
PubMed1996

[Minor head injuries in sport. Occurrence, management, sequelae and prevention].

Approximately 10% of all head injuries are caused during sport and about 10% of all sport-related injuries are head injuries. Most of these are minor head injuries. Many sports involve risk of repeated head injury. The classic punch-drunk syndrome in boxers reflects severe chronic traumatic encephalopathy. Recent research shows that repeated head injury can entail encephalopathy also in other types of athletes. They may experience symptoms such as headache, dizziness, irritability, memory deficit and concentration deficit. Neuropsychological testing reveals such cognitive deficits as impaired memory and attention, and reduced speed of information processing. Persistent sequelae can be prevented by correct management in the acute stage, appropriate follow-up, and prevention of repeated head injuries.

Athletic Injuries↗