The clinical spectrum of sport-related traumatic brain injury
ABSTRACT Acute and chronic sports-related traumatic brain injuries (TBIs) are a substantial public health concern. Various types of acute TBI can occur in sport, but detection and management of cerebral concussion is of greatest importance as mismanagement of this syndrome can lead to persistent or chronic postconcussion syndrome (CPCS) or diffuse cerebral swelling. Chronic TBI encompasses a spectrum of disorders that are associated with long-term consequences of brain injury, including chronic traumatic encephalopathy (CTE), dementia pugilistica, post-traumatic parkinsonism, post-traumatic dementia and CPCS. CTE is the prototype of chronic TBI, but can only be definitively diagnosed at autopsy as no reliable biomarkers of this disorder are available. Whether CTE shares neuropathological features with CPCS is unknown. Evidence suggests that participation in contact-collision sports may increase the risk of neurodegenerative disorders such as Alzheimer disease, but the data are conflicting. In this Review, the spectrum of acute and chronic sport-related TBI is discussed, highlighting how examination of athletes involved in high-impact sports has advanced our understanding of pathology of brain injury and enabled improvements in detection and diagnosis of sport-related TBI.
[Show abstract] [Hide abstract]
- "They reviewed these cases and documented their clinical features. They estimated that 29 would have possible CTE, 90 would have probable CTE, and 83 would have definite CTE based on Jordan's criteria (Jordan, 2013). "
ABSTRACT: Chronic traumatic encephalopathy (CTE) has been described in the literature as a neurodegenerative disease with: (i) localized neuronal and glial accumulations of phosphorylated tau (p-tau) involving perivascular areas of the cerebral cortex, sulcal depths, and with a preference for neurons within superficial cortical laminae; (ii) multifocal axonal varicosities and axonal loss involving deep cortex and subcortical white matter; (iii) relative absence of beta-amyloid deposits; (iv) TDP-43 immunoreactive inclusions and neurites; and (v) broad and diverse clinical features. Some of the pathological findings reported in the literature may be encountered with age and other neurodegenerative diseases. However, the focality of the p-tau cortical findings in particular, and the regional distribution, are believed to be unique to CTE. The described clinical features in recent cases are very similar to how depression manifests in middle-aged men and with frontotemporal dementia as the disease progresses. It has not been established that the described tau pathology, especially in small amounts, can cause complex changes in behavior such as depression, substance abuse, suicidality, personality changes, or cognitive impairment. Future studies will help determine the extent to which the neuropathology is causally related to the diverse clinical features. Copyright © 2015 Elsevier Ltd. All rights reserved.Neuroscience & Biobehavioral Reviews 07/2015; DOI:10.1016/j.neubiorev.2015.05.008 · 10.28 Impact Factor
[Show abstract] [Hide abstract]
- "c o m / l o c a t e / y n b d i signs (e.g., slurred speech, parkinsonism). Concurrently, autopsy studies of a limited number of athletes (including football players) who have suffered from TBI have led some researchers to diagnose chronic traumatic encephalopathy (CTE), a putative tauopathy characterized by global brain atrophy with a thinned corpus callosum, enlarged ventricles , and cavum septum pellucidum (Jordan, 2013). The prevalence of CTE among former athletes who have suffered from TBI is unknown, as is the prevalence of other injury-associated brain pathologies, for example those associated with Alzheimer's disease or frontotemporal degeneration . "
ABSTRACT: There are growing concerns about potential delayed, neuropsychiatric consequences (e.g, cognitive decline, mood or anxiety disorders) of sports-related traumatic brain injury (TBI). Autopsy studies of brains from a limited number of former athletes have described characteristic, pathologic changes of chronic traumatic encephalopathy (CTE) leading to questions about the relationship between these pathologic and the neuropsychiatric disturbances seen in former athletes. Research in this area will depend on in vivo methods that characterize molecular changes in the brain, linking CTE and other sports-related pathologies with delayed emergence of neuropsychiatric symptoms. In this pilot project we studied former National Football League (NFL) players using new neuroimaging techniques and clinical measures of cognitive functioning. We hypothesized that former NFL players would show molecular and structural changes in medial temporal and parietal lobe structures as well as specific cognitive deficits, namely those of verbal learning and memory. We observed a significant increase in binding of [(11)C]DPA-713 to the translocator protein (TSPO), a marker of brain injury and repair, in several brain regions, such as the supramarginal gyrus and right amygdala, in 9 former NFL players compared to 9 age-matched, healthy controls. We also observed significant atrophy of the right hippocampus. Finally, we report that these same former players had varied performance on a test of verbal learning and memory, suggesting that these molecular and pathologic changes may play a role in cognitive decline. These results suggest that localized brain injury and repair, indicated by increased [(11)C]DPA-713 binding to TSPO, may be linked to history of NFL play. [(11)C]DPA-713 PET is a promising new tool that can be used in future study design to examine further the relationship between TSPO expression in brain injury and repair, selective regional brain atrophy, and the potential link to deficits in verbal learning and memory after NFL play. Copyright © 2014 Elsevier Inc. All rights reserved.Neurobiology of Disease 11/2014; 74C:58-65. DOI:10.1016/j.nbd.2014.10.019 · 5.20 Impact Factor
[Show abstract] [Hide abstract]
- "In recent reviews, given urgency by the recognition of cumulative brain damage (chronic traumatic encephalopathy) in those who play hard-contact sports, head trauma is confirmed as a major 'environmental' cause of dementia , with many forms of pathology associated. These reports include hemorrhage as one of the sequelae of head trauma , but give more emphasis to 'Alzheimer'-like pathologies, such as amyloid deposition and the hyperphosphorylation of tau  . The degree to which hemorrhage generates these latter pathologies remains undefined in the literature on trauma-induced dementia. "
ABSTRACT: This review traces evidence that age-related dementia (Alzheimer's disease) results from the destructive impact of the pulse on cerebral vasculature. Evidence is reviewed that the neuropathology of the dementia is caused by the breakdown of small cerebral vessels (silent microbleeds), that the microbleeds result from pulse-induced damage to the cerebral vessels, and that pulse becomes increasingly destructive with age, because of the age-related stiffening of the aorta and great arteries, which causes an increase in the intensity of the pressure pulse. Implications for therapy are discussed, and evidence is reviewed that pulse-induced destruction of the brain, and of another highly vascular organ, the kidney, are becoming the default forms of death, the way we die if we survive the infections, cardiovascular disease, and malignancies, which still, for a decreasing minority, inflict the tragedy of early death.Journal of Alzheimer's disease: JAD 10/2014; 44(2). DOI:10.3233/JAD-141884 · 4.15 Impact Factor