4 December 2018
Recently, Zuckerman et al.  presented an interesting history of chronic traumatic encephalopathy (CTE), previously referred to as dementia pugilistica , beginning from Hippocrates up to recent publications, with emphasis on contact sports and American football. With regard to CTE in boxers, except for the first report of "punch drunk"  and a few others , they unfortunately did not refer to a number of other important contributions about brain damage in boxers, many of them having been mentioned previously . The term "dementia pugilistica" was introduced by Millspaugh in 1937 , referring to the observations in professional pugilists [6-8], later discussed by Critchley  and Roberts , most of them unaccompanied by autopsy records. In 1954, Brandenburg & Hallervorden  described the autopsy findings in a male aged 51 years who had boxed from age 18 to 29 and, at age 39, developed dementia. The most remarkable findings at autopsy were extensive Alzheimer-related pathology suggesting the presence of early-onset AD. Unfortunately, no family history nor genetic findings were available in this case. Another male aged 46, who had boxed between the ages 15 and 25 and developed progressive neurological decline at age 36, died from cerebral venous thrombosis and showed neurofibrillary changes in the brainstem and medial temporal lobe , while other cases of dementia pugilistica, at autopsy, showed cerebrovascular lesions  or nonspecific brain pathologies [13, 14]. The landmark study of CTE was published by Courville et al.  who emphasized neurofibrillary degeneration particularly in substantia nigra and medial temporal lobe but rather limited plaque pathology, thus separating CTE from typical AD. Although their sample showed heterotopic neuropathologies and numerous co-morbidities, they focussed on the importance of neurodegenerative pathology and, in particular, neurofibrillary degeneration in CTE in relation to boxing, the basis of which had been paved by Brandenburg & Hallervorden . Whereas in 2016, a consensus on thew preliminary neuropathologic diagnostic criteria for CTE, with pathognomonic lesions of hyperphosphorylated tau in both neurons and astrocytes at the basis of cortical sulci was reached , despite extensive research, neither the etiopathogenesis of CTE nor that of AD are fully understood yet [17, 18].
Kurt A. Jellinger
Institute of Clinical Neurobiology, Vienna, Austria
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