New insights into the disease show head impact, not concussion, triggers CTE and pave way for early detection, prevention and treatment January 18, 2018 Boston University School of Medicine Researchers have identified evidence of early Chronic Traumatic Encephalopathy (CTE) brain pathology after head impact even in the absence of signs of concussion.
Early indicators of CTE pathology not only persisted long after injury but also spread through the brain, providing the best evidence to date that head impact, not concussion, causes CTE.
Researchers have identified evidence of early Chronic Traumatic Encephalopathy (CTE) brain pathology after head impact even in the absence of signs of concussion. Early indicators of CTE pathology not only persisted long after injury but also spread through the brain, providing the best evidence to date that head impact, not concussion, causes CTE.
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The findings, published online in the journal Brain, are based on analysis of human brains from teenagers with recent head injury and mouse models that recreate sportsrelated head impact and militaryrelated blast exposure. The investigators also performed laboratory experiments and computer modeling. Study results shed light on the origins of CTE and relationship to traumatic brain injury (TBI), concussion and subconcussive head injury. CTE is a neurodegenerative disease characterized by abnormal accumulation of tau protein around small blood vessels in the brain. CTE causes brain cell death, cognitive deficits, and dementia. The brain pathology of CTE has been observed in brains of teenagers and adults with exposure to repeated head injury, both concussive and subconcussive episodes. However, the mechanisms that cause CTE and relationship to concussion, subconcussive injury and TBI remain poorly understood. In the first part of their study, the researchers examined four postmortem brains from teenage athletes who had sustained closedhead impact injuries 1, 2, 10 and 128 days prior to death. Neuropathological analysis of these brains showed a spectrum of posttraumatic pathology, including one case of earlystage CTE and two cases with abnormal accumulation of tau protein. Brains from four agematched athletes without recent head injury did not show the pathological changes observed in the headinjury group.
To investigate causal mechanisms underlying these changes, the researchers conducted laboratory experiments using mouse models of two different injury mechanisms repeat closedhead impact and blast exposure both linked to CTE. The investigators compared brain responses to the experimental injuries and relationship to CTE pathology over time. Based on pathological findings in human cases, the researchers hypothesized that early CTE may result from damaged blood vessels in the brain that become leaky, resulting in blood proteins spilling into brain tissue and triggering brain inflammation. The researchers utilized a brain scan called dynamic contrastenhanced magnetic resonance imaging (DCEMRI) to detect leaky blood vessels in the brains of mice subjected to head impact.
The investigators also found that head impact caused persistent changes in brain electrical functions, which may explain cognitive difficulties experienced by some people after these injuries. "The same brain pathology that we observed in teenagers after head injury was also present in headinjured mice. We were surprised that the brain pathology was unrelated to signs of concussion, including altered arousal and impaired balance, among others. Our findings provide strong causal evidence linking head impact to TBI and early CTE, independent of concussion," explained corresponding author Lee E. Goldstein, MD, PhD, an associate professor at Boston University School of Medicine and College of Engineering. "The results may explain why approximately 20 percent of athletes with CTE never suffered a diagnosed concussion."
Source: ScienceDaily, Boston University