Young contact sport athletes may be at risk for long-term neuropathological disorders, including chronic traumatic encephalopathy.
What are the neuropathological and clinical findings in a convenience sample of young, deceased, symptomatic contact sport athletes?
In this case series of 152 contact sport athletes under the age of 30 at the time of death, it was found chronic traumatic encephalopathy (CTE) in 63 (41.4%), and almost all had mild chronic traumatic encephalopathy (CTE) (stages I and II). Neuropathological abnormalities associated with chronic traumatic encephalopathy (CTE) include ventricular enlargement, cavum septum pellucidumPerivascular deposition of pigment-laden macrophages in the thalamic scar and frontal white matter.
These findings confirm that chronic traumatic encephalopathy (CTE) and other brain pathologies can be found in young, symptomatic contact sports athletes, but the clinical correlates of these pathological conditions are uncertain.
Millions of people around the world are exposed to it repeated impacts to the head (RHI) through participation in contact and collision sports, military service, physical violence and many other activities.
Repetitive blows to the head can cause symptomatic concussions and many more common, non-concussive, asymptomatic injuries. Chronic exposure to repeated head impacts (RHI) can lead to persistent cognitive and neuropsychiatric symptoms and progressive neurodegenerative disease. TauThe chronic traumatic encephalopathy (CTE).
Several studies link longer duration of RHI exposure to a higher likelihood of CTE presence and greater CTE severity in American football players. 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 changes on images magnetic resonance (MRI) have been associated with RHI in young, active and recently retired contact sport players, although the pathophysiological mechanisms underlying these changes are 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, usually deep in the sulci of the cerebral cortex.
The clinical syndrome associated with CTE is called traumatic encephalopathy syndrome (TES). Based on the National Institute of Neurological Disorders and Stroke (NINDS) consensus diagnostic criteria for TES, the core clinical features of TES include cognitive impairment, particularly episodic memory and executive dysfunction, and neurobehavioral dysregulation, Such as impulsivity, explosiveness and emotional dysregulation.
Concomitant features include delayed onset (ie, core clinical features that begin years after repetitive head impacts (RHI) have ended), parkinsonism, other motor signs (including amyotrophic lateral sclerosis), depression, anxiety , depression and paranoia.
Youth contact sport athletes may be at risk for long-term neuropathological disorders, including chronic traumatic encephalopathy (CTE).
To characterize the neuropathological and clinical characteristics of young brain donors who were exposed sports athletes.
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