Mechanism
It is not well understood why this syndrome occurs. Loss of neurons, scarring of brain tissue, collection of proteinaceous, senile plaques, hydrocephalus, attenuation of corpus callosum, diffuse axonal injury, neurofibrillary tangles, and damage to the cerebellum are implicated in the syndrome. The condition may be etiologically related to Alzheimer's disease. Neurofibrillary tangles have been found in the brains of dementia pugilistica patients, but not in the same distribution as is usually found in people with Alzheimer's. One group examined slices of brain from patients having had multiple mild traumatic brain injuries and found changes in the cells' cytoskeletons, which they suggested might be due to damage to cerebral blood vessels.
Increased exposure to concussions and sub-concussive blows is regarded as the most important risk factor, which can depend on the total number of fights, number of knockout losses, the duration of career, fight frequency, age of retirement, and boxing style. One study found that the ApoE4 allele is associated (p < .001) with increased severity of chronic neurologic deficits in high-exposure boxers. Thirty professional boxers underwent neurological assessment and genetic testing for the ApoE4 allele, a known genetic risk factor for dementia, especially late-onset sporadic Alzheimer's disease. The severity of their cognitive, motor, and behavioral impairments was stratified using the Chronic Brain Injury scale, ranging from 0-9 with a score of greater than 0 identified as abnormal. Among 18 boxers with more than 12 professional bouts, those who possessed at least one ApoE4 allele had a higher CBI score (mean 3.9 ± 2.3) compared to boxers without the allele (mean 1.8 ± 1.2). The remaining boxers with less traumatic exposure had a mean score of 0.33, regardless of ApoE genotype.
Read more about this topic: Dementia Pugilistica
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