| Key points |
What are the neuropathological and clinical findings in a convenience sample of young, deceased, symptomatic contact sport athletes? Findings In this case series of 152 contact sports athletes younger than 30 years at the time of death, chronic traumatic encephalopathy (CTE) was found in 63 (41.4%), and almost all had chronic traumatic encephalopathy (CTE). mild (stages I and II). Neuropathological abnormalities associated with chronic traumatic encephalopathy (CTE) included ventricular enlargement, cavum septum pellucidum , thalamic notching, and perivascular deposition of pigment-laden macrophages in the frontal white matter. Meaning These findings confirm that chronic traumatic encephalopathy (CTE) and other brain pathologies can be found in young, symptomatic contact sport athletes, but the clinical correlates of these pathological conditions are uncertain. |
Around the world, millions of people are exposed to repetitive head impacts (RHI) through participation in contact and collision sports, military service, physical violence, and many other activities.
Repetitive impacts to the head can lead to symptomatic concussions and much more common, non-concussive, asymptomatic injuries. Sustained exposure to repetitive head impacts (RHI) can produce persistent cognitive and neuropsychiatric symptoms and a progressive tau -based neurodegenerative disease , chronic traumatic encephalopathy (CTE).
Multiple studies link longer duration of RHI exposure in American soccer players with higher odds of CTE presence and greater CTE severity. In older American football players with pathologically diagnosed CTE, RHI exposure is also associated with white matter rarefaction, loss of myelin-associated proteins, and loss of oligodendrocytes.
Emerging data show white matter structural alterations on magnetic resonance imaging (MRI) in young, active, and recently retired contact sport players exposed to RHI, although the pathological condition underlying these changes is unclear.
A definitive diagnosis of chronic traumatic encephalopathy (CTE) requires neuropathological evidence of perivascular aggregates of hyperphosphorylated tau (p-tau) in neurons, with or without astrocytes, typically deep in the sulci of the cerebral cortex.
The clinical syndrome associated with CTE is known as traumatic encephalopathy syndrome (TES). Based on the National Institute of Neurological Disorders and Stroke (NINDS) consensus diagnostic criteria for TES, the main clinical features of TES include cognitive impairment, especially episodic memory and executive dysfunction, and neurobehavioral dysregulation, such as impulsivity, explosiveness, and emotional dysregulation.
Supporting features include delayed onset (i.e., core clinical features that begin years after exposure to repetitive head impacts (RHI) ends), parkinsonism, other motor signs (including amyotrophic lateral sclerosis), depression, anxiety, apathy and paranoia.
| Importance |
Young contact sport athletes may be at risk for long-term neuropathological disorders, including chronic traumatic encephalopathy (CTE).
| Objective |
To characterize the neuropathological and clinical symptoms of young brain donors who were contact sports athletes.
| Design , environment and participants |
This case series analyzes the findings of 152 of 156 brain donors under the age of 30 identified through the Understanding Neurologic Injury and Traumatic Encephalopathy (UNITE) Brain Bank who donated their brains from February 1, 2008 to September 31 2022. Neuropathological evaluations, retrospective telephone clinical evaluations, and online questionnaires with informants were performed in a blinded manner. Data analysis was carried out between August 2021 and June 2023.
| Exhibitions |
Repetitive impacts to the head from contact sports.
| Main results and measures |
Macroscopic and microscopic neuropathological evaluation, including diagnosis of chronic traumatic encephalopathy (CTE), according to defined diagnostic criteria; and informant-reported athletic history and informant-completed scales assessing cognitive symptoms, mood disorders, and neurobehavioral dysregulation.
| Results |
Among the 152 deceased contact sports participants (mean [SD] age, 22.97 [4.31] years; 141 [92.8%] men) included in the study, chronic traumatic encephalopathy (CTE) was diagnosed in 63 (41.4%; median [IQR] age, 26 [24]-27 years). Of the 63 brain donors diagnosed with chronic traumatic encephalopathy (CTE), 60 (95.2%) were diagnosed with mild CTE (stages I or II). Brain donors who had chronic traumatic encephalopathy (CTE) were more likely to be older (mean difference, 3.92 years; 95% CI, 2.74-5.10 years).
Of the 63 athletes with chronic traumatic encephalopathy (CTE), 45 (71.4%) were men who played amateur sports, including American football. ice hockey, soccer, rugby and wrestling; 1 woman with CTE played college soccer.
For those who played soccer, the length of playing career was significantly longer in those with CTE versus without CTE (mean difference, 2.81 years; 95% CI, 1.15-4.48 years ).
Athletes with chronic traumatic encephalopathy (CTE) had more ventricular dilation, cavum septum pellucidum, thalamic notches, and pigment-laden perivascular macrophages in the frontal white matter than those without CTE. Cognitive and neurobehavioral symptoms were common among all brain donors.
Suicide was the most common cause of death, followed by unintentional overdose; There were no differences in cause of death or clinical symptoms by chronic traumatic encephalopathy (CTE) status.
| Conclusions and relevance |
In a convenience brain bank sample of 152 young athletes exposed to repetitive head impacts (RHI) who were younger than 30 years at the time of death, 63 (41.4%) had neuropathological evidence of traumatic encephalopathy. chronic (CTE), including 1 athlete. Most young athletes with CTE played in high school and college, and sports included amateur soccer, ice hockey, rugby, soccer, and wrestling.
Young athletes with chronic traumatic encephalopathy (CTE) had significantly more ventricular dilation, cavum septum pellucidum , thalamic notching, p-tau pathological findings, and pigment-laden perivascular macrophages in the frontal white matter than those without CTE.
Young donors exposed to RHI were highly symptomatic regardless of CTE status, and the causes of symptoms in this sample, as reported by informants, are likely multifactorial and include RHI-related and non-RHI-related causes. Furthermore, although all donors were symptomatic, 58.6% had no pathological evidence of chronic traumatic encephalopathy (CTE).
Future studies including young brain donors not exposed to RHI are needed to clarify the association between RHI exposure, white matter and microvascular pathological findings, CTE, and clinical symptoms.
