Dementia pugilistica

Dementia pugilistica (DP) is a type of chronic traumatic encephalopathy (CTE), a neurodegenerative disease with features of dementia. DP may affect amateur or professional boxers, wrestlers as well as athletes in other sports who suffer concussions. DP is also called chronic boxer's encephalopathy, traumatic boxer’s encephalopathy, boxer's dementia, chronic traumatic brain injury associated with boxing (CTBI-B), and punch-drunk syndrome. DP was historically considered equivalent to CTE but is now considered a subtype of CTE.

The condition is caused by repeated concussive and sub-concussive blows (blows that are below the threshold of force necessary to cause concussion), or both.^[1] Because of the concern that boxing may cause DP, there is a movement among medical professionals to ban the sport.^[2] Medical professionals have called for such a ban since as early as the 1950s.^[3]

Symptoms and signs of DP develop progressively over a long latent period sometimes amounting to decades, with the average time of onset being about 12 to 16 years after the start of a career in boxing. The condition is thought to affect around 15% to 20% of professional boxers.

Etymology

The word pugilistica comes from the Latin root pugil, for boxer (akin to pugnus fist, pugnāre to fight).^[4][5]

Symptoms

The condition, which occurs in athletes having suffered repetitive blows to the head, manifests as dementia, or declining mental ability, problems with memory, dizzy spells or lack of balance and Parkinsonism, or tremors and lack of coordination.^[2] It can also cause speech problems^[2] and an unsteady gait. Patients with DP may be prone to inappropriate or explosive behavior and may display pathological jealousy or paranoia.^[2] Individuals displaying these symptoms also can be characterized as "punchy", another term for a person suffering from DP.

Treatment

Sufferers may be treated with drugs used for Alzheimer's disease and Parkinsonism, although there is no known cure.^[6]

Mechanism

It is not well understood why this syndrome occurs.^[7] Loss of neurons, scarring of brain tissue, collection of proteinaceous, senile plaques, hydrocephalus, attenuation of the corpus callosum, diffuse axonal injury, neurofibrillary tangles, and damage to the cerebellum are implicated in the syndrome.^[8] The condition may be etiologically related to Alzheimer's disease.^[8] 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.^[9] 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.^[10]

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.^[11] 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.^[12]

An April 1983 article in Sports Illustrated titled “Too Many Punches, Too Little Concern” summarized what was then the state of the art in neurologic exams and diagnosis of “punch drunk” syndrome. The most common characteristics of boxers suffering obvious outward signs of dementia are enlarged brain ventricles and a cavum septi pellucidi. The article cites the results of CT scans on 8 former champions with 5 of them displaying evidence of a cavum septi pellucidi including Muhammad Ali and contender Jerry Quarry. Quarry, at that time displaying no obvious behavioral signs of brain atrophy or damage, would die of dementia pugilistica 16 years later, aged only 53 in 1999. The article cautiously advised of Quarry and Ali's results. Tex Cobb was noted had a shorter career and got a clear verdict on concerns. .^[13]

History

DP was first described in 1928 by a forensic pathologist, Dr. Harrison Stanford Martland, who was the chief medical examiner of Essex County in Newark, New Jersey in a Journal of the American Medical Association article, in which he noted the tremors, slowed movement, confusion, and speech problems typical of the condition.^[14] In 1973, a group led by J. A. Corsellis^[15] described the typical neuropathological findings of DP after post-mortem examinations of the brains of 15 former boxers.^[15]

See also

• Concussions in sport
• Traumatic brain injury
• Post-concussion syndrome
• Proteopathy
• Second-impact syndrome
• Chronic traumatic encephalopathy

References