|Boxers receive many blows involving rotational force, which is implicated in concussion. Repeat concussions can lead to dementia pugilistica.|
|Classification and external resources|
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. It 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. Because of the concern that boxing may cause DP, there is a movement among medical professionals to ban the sport. Medical professionals have called for such a ban since as early as the 1950s. 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.
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 to the point of not being able to walk under one's own power for a short time and or Parkinsonism, or tremors and lack of coordination. It can also cause speech problems and an unsteady gait. Patients with DP may be prone to inappropriate or explosive behavior and may display pathological jealousy or paranoia.
Sufferers may be treated with drugs used for Alzheimer's disease and Parkinsonism, although there is no known cure.
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. 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.
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 radiologic evidence by CT scan in boxers suffering obvious outward signs of dementia are cortical atrophy, enlarged brain ventricles and a cavum septi pellucidi. The article cites the results of CT scans on eight former champions with five of them displaying evidence of a cavum septi pellucidi including Muhammad Ali and contender Jerry Quarry. The article cautiously advised Quarry and Ali of the results.  Quarry, at that time displaying no obvious behavioral signs of brain atrophy or damage, would die of dementia pugilistica at age 53 in 1999. Tex Cobb, a heavyweight contender with far fewer fights on his professional record and no amateur fights in his career, performed well on cognitive tests and had a normal CT scan.
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. In 1973, a group led by J. A. Corsellis described the typical neuropathological findings of DP after post-mortem examinations of the brains of 15 former boxers.
- Concussions in sport
- Traumatic brain injury
- Post-concussion syndrome
- Second-impact syndrome
- Erlanger DM, Kutner KC, Barth JT, Barnes R (1999). "Neuropsychology of sports-related head injury: Dementia pugilistica to post concussion syndrome". The Clinical Neuropsychologist. 13 (2): 193–209. doi:10.1076/clin.188.8.131.523. PMID 10949160.
- Mendez MF (1995). "The neuropsychiatric aspects of boxing". International Journal of Psychiatry in Medicine. 25 (3): 249–262. doi:10.2190/CUMK-THT1-X98M-WB4C. PMID 8567192.
- Corsellis JA (1989). "Boxing and the Brain". BMJ. 298 (6666): 105–109. doi:10.1136/bmj.298.6666.105. PMC . PMID 2493277.
- Pugilism (origin), retrieved on 2013-2-2.
- NCERx. 2005. Brain Trauma, Subdural Hematoma and Dementia Pugilistica. About-dementia.com. Retrieved on 2007-12-19.
- Jordan BD (2000). "Chronic traumatic brain injury associated with boxing". Seminars in Neurology. 20 (2): 179–85. doi:10.1055/s-2000-9826. PMID 10946737.
- Graham DI and Gennareli TA. Chapter 5, "Pathology of Brain Damage After Head Injury" In, Cooper P and Golfinos G. 2000. Head Injury, 4th Ed. Morgan Hill, New York.
- Hof PR, Bouras C, Buée L, Delacourte A, Perl DP, Morrison JH (1992). "Differential Distribution of Neurofibrillary Tangles in the Cerebral Cortex of Dementia Pugilistica and Alzheimer's Disease Cases". Acta Neuropathologica. 85 (1): 23–30. doi:10.1007/BF00304630. PMID 1285493.
- Geddes JF, Vowles GH, Nicoll JA, Révész T (1999). "Neuronal Cytoskeletal Changes are an Early Consequence of Repetitive Head Injury". Acta Neuropathologica. 98 (2): 171–178. doi:10.1007/s004010051066. PMID 10442557.
- Jordan, B. D. (2009). Brain injury in boxing. Clinics in Sports Medicine, 28(4), 561-78, vi.
- Jordan, B. D., Relkin, N. R., Ravdin, L. D., Jacobs, A. R., Bennett, A., & Gandy, S. (1997). Apolipoprotein E epsilon4 associated with chronic traumatic brain injury in boxing. JAMA : The Journal of the American Medical Association, 278(2), 136-140.
- Boyle, Robert H. (April 11, 1983). "Too Many Punches, Too Little Concern". Sports Illustrated.
- Martland HS (1928). "Punch Drunk". Journal of the American Medical Association. 91 (15): 1103–1107. doi:10.1001/jama.1928.02700150029009.
- Corsellis JA, Bruton CJ, Freeman-Browne D (August 1973). "The aftermath of boxing". Psychological Medicine. 3 (3): 270–303. doi:10.1017/S0033291700049588. PMID 4729191.