Chronic traumatic encephalopathy: a potential late and under recognized consequence of rugby union?

Abstract

The association between exposure to head injury and increased risk of neurodegenerative disease, specifically chronic traumatic encephalopathy (CTE), is widely recognized. Historically, this was largely considered a phenomenon restricted to boxers, with more recent case series identifying further 'high risk' individuals, such as former American footballers, or military personnel. However, in all cases thus far reported, it is clear that it is the exposure to head injury which is associated with increased dementia risk, and not the circumstances or environment of exposure. As such, there is considerable potential for under-recognition of CTE in patients presenting with neurodegenerative disease, particularly where head injury exposure might have been historical and through sport. This article reviews current understanding of CTE and, via an illustrative case in rugby union, highlights the value of a detailed history on head injury and also draws attention to imaging studies in assessing patients with neurodegenerative disease.

Chronic Traumatic Encephalopathy: The Neuropathological Legacy of Traumatic Brain Injury

“…To date, some 150 or so cases have been reported describing the neuropathology of those exposed to rTBI from a range of sports—including boxing (22, 46, 52), American football, ice hockey, wrestling, soccer, and rugby union (11, 13–20, 40, 41)—and former military personnel (12, 19, 20), together with sporadic cases exposed to rTBI in other circumstances, including domestic abuse (58, 69, 76). Approximately 40 further cases reporting the pathology of survival after an sTBI have been described (21, 23, 77).…”

“…Although the deposition of tau is a feature of a number of neurodegenerative pathologies and can be observed in normal aging, the pattern and distribution of tau pathology in CTE is sufficiently distinct to be proposed as pathognomonic. Specifically, whether in material from survivors of rTBI or an sTBI, this pathology is characterized by the accumulation of abnormal, hyperphosphorylated tau in both neurons and glia, showing a distinct perivascular accentuation and preferential involvement toward the depths of sulci in the neocortical gray matter (11, 17–19, 39, 40, 67, 82) (Figure 2). Typically, there is an irregular, patchy involvement within and between the involved cortical areas (17, 39, 40, 82).…”

“…Specifically, whether in material from survivors of rTBI or an sTBI, this pathology is characterized by the accumulation of abnormal, hyperphosphorylated tau in both neurons and glia, showing a distinct perivascular accentuation and preferential involvement toward the depths of sulci in the neocortical gray matter (11, 17–19, 39, 40, 67, 82) (Figure 2). Typically, there is an irregular, patchy involvement within and between the involved cortical areas (17, 39, 40, 82). This pattern, originally observed by Geddes and colleagues (67, 82) in their description of tau pathology in boxers, has since been confirmed and refined in subsequent case-series, both in rTBI and sTBI, such that its appearance might be considered as defining CTE, when observed in the correct clinical context.…”

Lifelong behavioral and neuropathological consequences of repetitive mild traumatic brain injury

“…However, a subset of this population demonstrates persisting neurocognitive dysfunction and non‐neurological disorders that cannot be considered mild 3. Notably, it is now well documented that the adverse effects of r‐mTBI in participants of contact sports and in former military personnel may continue for many years after the original event,4, 5, 6, 7, 8 with brain trauma being a risk factor for the development of neurodegenerative disease,9 in particular chronic traumatic encephalopathy (CTE); for review see Smith et al 10…”

Turning people into couch potatoes is not the cure for sports concussion

“…Originally thought exclusive to former boxers, hence formerly termed ‘dementia pugilistica’, more recently CTE has been reported in retired athletes from a range of sports,6 including a single case in a former rugby union player 7. To date, no clinical diagnostic criteria for CTE have been established; detailed neuropathological examination at autopsy remains the only means to confirm the diagnosis 6…”