Abstract and Introduction
Chronic traumatic brain injury (CTBI) associated with boxing occurs in approximately 20% of professional boxers. Risk factors associated with CTBI include increased exposure (i.e., duration of career, age of retirement, total number of bouts), poor performance, increased sparring, and apolipoprotein (APOE) genotype. Clinically, boxers exhibiting CTBI will present with varying degrees of motor, cognitive, and/or behavioral impairments. The severe form of CTBI is referred to as dementia pugilistica. The diagnosis of CTBI is dependent upon documenting a progressive neurological condition that is consistent with the clinical symptomatology of CTBI attributable to brain trauma and unexplainable by an alternative pathophysiological process. Pathologically, CTBI shares many characteristics with Alzheimer's disease (i.e., neurofibrillary triangles, diffuse amyloid plaques, acetylcholine deficiency, and/or tau immunoreactivity). The mainstay of treatment of CTBI is prevention, however medications used in the treatment of Alzheimer's disease and/or parkinsonism may be utilized.
Chronic traumatic brain injury (CTBI) of boxing, also known as dementia pugilistica, chronic traumatic encephalopathy or the punch drunk syndrome, represents the cumulative, long-term neurological consequences of repetitive concussive and subconcussive blows to the brain.[1,2,3,4,5] CTBI is primarily a disorder of professional boxing that is infrequently encountered in amateur boxers unless they have excessive exposure to the sport. This article discusses the epidemiology, clinical presentation, diagnosis, pathology, pathophysiology, management, and prevention of this important public health concern.
Semin Neurol. 2000;20(2) © 2000 Thieme Medical Publishers
Comments