In boxing, about ten deaths have occurred

annually during the 20th century; most were related to knockout or technical knockout (deaths due to boxing are registered in the Manuel Velazquez Boxing Fatality Collection, available at http://ejmas.com/jcs/jcsart_svinth_b_0700.htm). The most common cause Ibrutinib ic50 of death is subdural hematoma (Guterman and Smith, 1987; Unterharnscheidt, 1995). Most deaths (about 80%) are among professional boxers, and boxing-related deaths due to brain damage occur in all rounds and in all weight classes, but somewhat surprisingly, most deaths are in lower weight classes. Deaths declined since 1983, which might be related to lower exposure to repetitive head trauma among professional boxers with shorter careers and fewer fights (Baird et al., 2010). Catastrophic brain injury also occurs

in American Dasatinib supplier football. During the second half of the 20th century, more than 400 players died from brain or spinal cord injury in the United States while playing (McIntosh and McCrory, 2005). Repetitive brain trauma may cause chronic neurological problems. For example, in 1928, Martland (1928) described chronic brain damage in boxers, which was termed punch drunk syndrome. A few years later, Millspaugh (1937) called this syndrome dementia pugilistica, which is more commonly used. Forty years ago, Corsellis et al. (1973) described neuropathological changes in a series of professional boxers with dementia pugilistica. Their key findings included neurofibrillary tangles in cortical areas, cerebellar atrophy and gliosis, hypopigmentation of the substantia nigra, and cavum septum pellucidum. Many years after these early studies documenting the histopathological

Ketanserin changes in career boxers, it became evident that a similar chronic brain condition occurred in athletes who practiced other contact sports and had a history of repeated head trauma, and it was only recently that the first autopsy report from a football player was published (Omalu et al., 2005). Neuropathological changes were similar to those in boxers with dementia pugilistica, findings that have now been verified in larger studies (McKee et al., 2009). These authors introduced the more general term chronic traumatic encephalopathy (CTE), which has gained broader usage (Stern et al., 2011). CTE is regarded as a chronic brain syndrome due to effects of repetitive brain trauma, but there are no generally accepted guidelines for a clinical diagnosis of CTE or for how to distinguish neuropathological changes due to CTE from those due to aging and Alzheimer’s disease (AD). CTE is regarded as a neurodegenerative disorder that often occurs in midlife, years or decades after the sports career has ended (McKee et al., 2009). About one-third of CTE cases are progressive (Roberts, 1969), but clinical progression is not sequential or predictable.