Neuropsychological deficits in active licensed professional boxers
✍ Scribed by Richard H. Drew; Bradley A. Schuyler; Donald I. Templer; Terry G. Newell; W. Gary Cannon
- Publisher
- John Wiley and Sons
- Year
- 1986
- Tongue
- English
- Weight
- 424 KB
- Volume
- 42
- Category
- Article
- ISSN
- 0021-9762
No coin nor oath required. For personal study only.
✦ Synopsis
Young, active, licensed professional boxers (N = 19) were found to display a pattern of neuropsychological deficits consistent with the more severe punch-drunk syndrome of years past. These deficits resulted in significantly lower test performance than that of control athletes (N = 10) matched for race, age, and level of education. Tests that showed significant differences between groups include subtests of the Quick Neurological Screening Test, subtests of the Halstead-Reitan Neuropsychological Test Battery, and the Randt Memory Test. Fifteen of the 19 boxers scored in the impaired range of the Reitan Impairment Index, as compared to 2 of the 10 controls.
Martland (1928) was the first to publish a description of the chronic "punch drunk" syndrome of boxers. Subsequent studies into the medical sequelae of boxing have resulted in a series of changes in the organization and regulation of this sport.
These changes, which include the organization of governing bodies; medical supervision; padding of gloves, rings, and posts; and forced layoff and retirement, have resulted in the reduction of observable chronic symptoms of brain damage. However, increasingly sensitive techniques of assessment, including EEG (Busse & Silverman, 1952), air encephalogram (Spillane, 1962), and CT scans , instituted in the 1950s, 1960s, and 1970s, respectively, have continued to evidence less obvious indications of brain damage in boxers than in the past.
Autopsies of the brains of older, retired boxers who suffered from boxers' chronic encephalopathy have revealed a pattern of structural damage consistent in part with the outward symptoms of this syndrome. found cerebellar damage that included cortical scarring, Peurkinje cell loss, and white matter demyelination consistent with ataxia, slowed movement, and awkward gait. They also found degeneration of the substantia nigra with loss of pigmented nerve cells consistent with Parkinson's-like symptoms. Both these authors and Payne (1968) found some