Boxing & Parkinson’s
Boxing and Parkinson’s Disease
“Dementia Pugilistica” and “punch drunk.” These terms have been brought to the public’s attention and renewed interest in the long-term effects of boxing on the brain. Public statements by various experts, however, have clouded rather than clarified the issue. This article will review the literature on the topic. The term “chronic encephalopathy” or “chronic brain injury” of boxers encompasses a wide spectrum of disorders. At one end are boxers with minimal involvement and at the other end are severely affected boxers requiring institutional care. Along the spectrum are some boxers with varying degrees of speech difficulty, stiffness, unsteadiness, memory loss, and inappropriate behavior. The more severely affected boxers gave rise to labels such as “punch drunk”.
In different studies, 15-40% of ex-boxers have been found to have symptoms of chronic brain injury. Most of the boxers have mild symptoms. Recent work, employing detailed psychological testing and MRI scanning, has shown that most professional boxers (even those without symptoms) have some degree of brain damage. Although obviously symptomatic cases still occur, they are less common today probably because today’s boxers have fewer bouts and shorter careers, resulting in fewer blows to the head and less cumulative brain injury.
Onset of Symptoms:
Symptoms usually begin near or shortly after the end of a boxer’s career. On occasion they are first noticed after a particularly hard bout. Symptoms develop an average of 16 years after beginning the sport, although some cases have occurred as early as 6 years after becoming a boxer. Symptoms have been reported in boxers as young as 25 years of age. Although the disorder has been reported in amateurs, it is more common in professionals. It can occur in all weight classes but is seen most often in the heavier divisions, and champion boxers run as much risk of sustaining chronic brain injury as less skilled journeymen.
Recent work has demonstrated that MRI abnormalities and minimal memory deficits occur in many boxers who appear normal. These minimal deficits can begin after only a few years in the sport. While boxers with less than 20-30 professional bouts usually do not have any symptoms of brain injury those with 25-50 bouts often show MRI and psychological test abnormalities without obvious symptoms. Boxers with more than 50 professional bouts often have obvious symptoms of brain injury as well as MRI and psychological test abnormalities.
This continuum of symptoms strongly suggests that the chronic encephalopathy of boxers is a progressive illness. The older literature contains numerous case reports that document a progressive deterioration, even after the boxer had retired from the ring. The Parkinson-like disorder is as progressive as the other forms. As the damage accumulates, minimal symptoms merge gradually into more obvious symptoms. The boxer usually is not aware of his difficulties; his wife is often the first to notice subtle personality changes. Extreme intolerance of alcoholic beverages is a common symptom in the early stages. Confrontations with law enforcement authorities are often the result of lost social inhibitions or sudden changes in mood and behavior.
These difficulties usually are explained away as symptoms of depression, anxiety, or even the enthusiasm of an immature aging athlete. An example of such behavior is the ex-heavyweight champion Mike Tyson. Early motor symptoms usually are noticed first by the trainer. A mild lack of coordination, subtle loss of balance, or a generalized “slowing down” initially is attributed to the natural aging process. However, as these symptoms worsen, it may become apparent to the boxer’s companions that something is wrong, even while the boxer continues to insist that he is perfectly healthy.
Types of Disorders:
Critchley, the great English neurologist describe 4 types of disorder in former boxers: A disorder similar to general paresis (syphilis of the brain) but without syphilis A disorder similar to multiple sclerosis A disorder similar to Alzheimer disease A disorder similar to Parkinson disease
Martland first described a Parkinson disorder in a former boxer in 1928. During the next 40 years, 20 or more boxers showing Parkinson symptoms were described. In 1969, Roberts published a study of 250 British former boxers, of whom 224 were available for examination. The boxers received neurologic examinations and electroencephalograms (EEGs). 37 (17%) had evidence of brain damage that was attributed to boxing; 13 were severely affected.
Two major disorders were reported:
• A Parkinson disorder with tremor; rigidity; slowness of movements; stooped posture and masked faces
• A multiple sclerosis like disorder with an unsteady gait, tremor, and in-coordination Speech difficulty was characteristic of both disorder and was present in almost all cases. The slurred speech had characteristics of the speech of Parkinson, multiple sclerosis, and stroke victims. Roberts also showed a relationship between the length of the boxer’s career, the number of professional bouts, and the prevalence of brain injury. 47% of those whose careers exceeded 10 years were affected, compared with 13% of those who fought for less than five years. Half of the group who had more than 150 professional bouts showed symptoms of brain damage compared with 19% of those with 50 to 150 professional bouts and 7% of those who fought less than 50 times.
Roberts (unfortunately) did not focus on higher intellectual functioning or psychiatric disturbances. In the same year, however, Johnson reported 4 types of psychiatric disturbances in former boxers:
(1) A disorder with severe memory impairment
(2) A dementia
(3) A disorder with a progressive disorganization of personality and intellectual function
(4) A disorder with delusions, violent rage, and morbid jealousy including repeated accusations of infidelity Most boxers had more than one disorder.
Electroencephalography (EEG) is widely used as a screening test in the official boxing community. Unfortunately, it is not a highly sensitive test for evaluating chronic brain injury. Although some studies have reported EEG abnormalities in up to 50% of boxers, most of the evidence suggests that their EEGs are not different from those of non-boxers. Roberts reported abnormal EEGs in the same percentage of ex-boxers and a comparable group of non-boxer controls. He also noted that EEG abnormalities were present in the same percentage (approximately 15%) of boxers with obvious symptoms of brain damage and boxers without obvious symptoms of brain damage.
MRI scans of the brain, on the other hand, are often abnormal in boxers. These usually reveal an abnormality or absence of a specific membrane inside the brain. And an enlargement of the lateral and third ventricles (fluid cavities inside the brain). Half of the boxers who have been studied have been found to have abnormal scans. Brain atrophy shown by enlargement of the third and lateral ventricles and/or prominence of the brain’s folds are the most common abnormalities.
The number of professional bouts fought by a boxer is correlated with the presence of an abnormal MRI scan. We have demonstrated a significant correlation between an abnormal MRI scan and major psychological test battery impairment. Every boxer that I have found to be suffering from brain damage has also had an abnormal MRI scan.
Some state athletic commissions now use MRI scans of the brain as a periodic screening procedure in the evaluation of active boxers. Periodic administration of a battery of psychological tests, with special emphasis on those assessing recent memory are also performed.
The clinical and MRI disorders correlate well with the pattern of brain injury in boxers shown at autopsy. As reported by Corsellis, the brains of retired boxers demonstrate a characteristic pattern of abnormalities including changes similar to those of Alzheimer disease). Another feature of this syndrome is widespread neurofibrillary changes in neurons of the medial temporal gray matter in the absence of senile plaques. This pattern of damage indicates that the limbic regions bear the brunt of damage in boxing. These areas of the brain are involved integrally with recent memory, emotion, and personality.
Four boxers who had a Parkinson disorder during life were included examined. Microscopic study revealed marked loss of pigmented cells but without Lewy bodies. This pattern was similar to that seen in the Parkinson disorder that follows encephalitis.
The exact mechanism by which multiple and repeated blows to the head cause brain damage to boxers has not been fully established, although it appears that the deep mid-line areas of the brain are affected most severely. The major risk factors for development of brain damage are length of professional career and number of professional bouts, which obviously are measures of exposure to head blows. One can postulate that every blow to the head results in minute microscopic damage to the deep medial areas of the brain. As the exposure continues, this damage accumulates. However, while some boxers, Jack Dempsey, Joe Lewis, suffer brain damage, others, Gene Tunney, George Foreman, do not.
By Ira Casson
Suggested Reading: Casson I: Brain Damage in Modern Boxers. Journal of the American Medical Association year– 1984, volume–251, pages– 2663-2667.
Casson I Neurological and CT Evaluation of Knocked-out Boxers. Journal of Neurology Neurosurgery and Psychiatry 1982; 45: 170-174.
Corsellis J The Aftermath of Boxing. Psychological Medicine 1973; 3: 270-303.
Critchley M: Medical Aspects of Boxing Particularly From a Neurological Stand-Point. British Medical Journal 1957; 1: 357-362.
Johnson J: Organic Psycho-syndromes Due to Boxing. British Journal of Psychiatry 1969; 1 15:45-53.
Kaste M Is Chronic Brain Damage in Boxing a Hazard of the Past? Lancet 1982; 2:1186-1188.
Martland HS: Punch Drunk. JAMA 1928; 91: 1103-1107.
Mawdsley C Neurological Disease in Boxers. Lancet 1963 ;2 :799-801.
Roberts AH: Brain Damage in Boxers. London, Pitman Medical Scientific Publishing Co., 1969.
Spillane J: Five boxers. Br Med J 1962;2:1205-1210.