HomeEncylopedia Parkinson Disease: Boxing, Brain Injury, Muhammad Ali, Jack Dempsey
Parkinson Disease: Boxing, Brain Injury, Muhammad Ali, Jack Dempsey
Written by Abraham Lieberman
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or email al@liebermanparkinsonclinic _________________________________________________________________ Jack Dempsey, World Heavy Weight Champion 1920s Scoring a Knock-out
Head Injury, Boxing, as a Cause of PD, Boxing
Copyrighted by Abraham Lieberman MD 1 April 05
The brain, as an organ, a tissue is composed mainly of fat. Unlike muscle, or , joints, or ligaments, the brain is soft, gelatin like. The brain is enclosed, for protection, in the skull. Most brain injuries in civilian life result from closed head injuries: a blow to the head jars or fractures the skull, without opening it and injuries the brain. Most head injuries in the military result from open injuries: a bullet, a shell fragment, pierces or splinters the skull, exposing and injuring the brain.
A concussion, by definition, is a loss of consciousness. A blow to the head that frightens, or stuns a person but does NOT result in a loss of consciousness is NOT a concussion.
The severity of a closed head injury is measured by the duration of the loss of consciousness. There is period of amnesia for the period AFTER the loss of consciousness.
This is called retrograde amnesia and results from an inability of the brain to lay down permanent memories after a loss of consciousness. The duration of the retrograde amnesia is proportional to the loss of consciousness. There is a period of amnesia for the period BEFORE the loss of consciousness.
This is called anterograde amnesia and results from an erasure of those memories laid down before the loss of consciousness. The duration of the anterograde amnesia is proportional to the loss of consciousness.
Often, years later, when asking a person about the duration of his loss of consciousness, the person, having no memory of what went before, or came after, will merge the duration of his anterograde and retrograde amnesia and his loss of consciousness, and report a longer period of loss of consciousness than he had. This highlights the limits of trying to gauge, on the basis of a person’s memory, the severity of the injury he suffered.
A loss of consciousness of a few seconds or minutes is, a mild or minor injury. The word mild or minor when applied to head injuries often should be put in quotations (“mild” or “minor”), because the brain was not built to be injured.
Most people with such injuries are not admitted to the hospital. As a rule, with exceptions, a mild injury rarely results in permanent brain damage. The loss of the consciousness results from a pressure wave, from the force of the blow, and if the pressure of the wave is higher than the person’s blood pressure, blood flow to the brainstem is interrupted and the person blacks-out. As the pressure wave recedes, as blood flow to the brainstem returns, the person wakes-up. Although the person makes a full recovery, often, years later, at post-mortem examinations, minute, speck-like hemorrhages, called petechial hemorrhages, may be seen.
Their pattern depends on the force and direction of the original blow to the brain (Figure 1). In some people, in addition to the petechial hemorrhages, small tears are found in the fiber tracts, called white matter, that transmit messages from one region of nerve cells, called gray matter, to another region. Repeated mild injuries, however, may have a cumulative effect and may result in permanent brain damage. The tiny petechial hemorrhages and the tiny tears in the white matter add-up. The “punch-drunk” fighter who hears “bells”, who staggers and loses his balance (as though he were drunk), and who can’t remember what he did all day, may be an example of someone who has had multiple minor head injuries: multiple brief, 10 seconds or less, knock-outs. His speech, his walk, his memory does NOT resemble PD. Unless, some of the petechial hemorrhages and some of the tears in the white matter affect the substantia nigra, the putamen, and the globus pallidus: the anatomy, the geography, of PD.
A knock-down from a head injury is different from a knock-out. In a knock-down, the pressure wave from the blow temporarily shuts-down the inner ear, the balance control center. A knock-down, unlike a knock-out, does NOT injure the brain
A loss of consciousness of 1 – 24 hours is a moderate head injury. Most people with such injuries are admitted to the hospital. Moderate head injuries may or may not result in permanent brain damage. In a moderate, as in a mild head injury, the pressure wave recedes. However, in a moderate injury the person does NOT regain consciousness because of secondary complications.
The secondary complications include bleeding from a tear in an artery in the space between the skull and the outer covering of the brain (the dura): called an epidural hematoma. Bleeding from a tear in a vein between the dura and the brain: called a subdural hematoma. Bleeding into the substance of the brain: called an intra-cerebral hematoma. Or a combination of the above. Such complications can if NOT recognized and evacuated, removed, result in permanent brain injury or death.
A loss of consciousness of 24 hours or more is a severe head injury. Most people with such injuries are admitted to the hospital. Severe head injuries usually result in permanent damage. In a severe injury, as in a mild injury, the pressure wave recedes.
However, in a severe injury, as in a moderate injury, the person does NOT regain consciousness because of secondary complications In a severe head injury there are more complications. They may include epidural, subdural and intra-cerebral blood clots. They may include lacerations, from skull fragments), strokes, from occlusions of blood vessels, and tears in fiber tracts. Patients who recover from severe head injuries may have paralysis of one or both sides of the body, they may have difficulty thinking, speaking, and in seeing. Occasionally, less often than is thought, depending on the site of the injury, a person may develop parkinson features after a severe head injury.
In whiplash, or in a blow to the front of the head, the skull is propelled backward. The skull moves faster and further than the brain. After the skull stops moving, the brain catches up and injures itself on the bony skull.
A frontal blow, a coup, results in maximal brain damage to the back of the brain: a contre-coup. In a blow to the back of the head, the injury is maximal at the front of the brain: especially the tips of the frontal and temporal lobes.
A small number of people, about 1%, who sustain moderate or severe head injuries develop PD or a Parkinson-like disease.This includes boxers, professional or amateur who as a result of fight are knocked-out and are unconsciousness for 24 or more hours. A loss of consciousness of 1 to 24 hours is a moderate head injury, a loss of consciousness of 24 or more hours is a severe head injury.
Some boxers with moderate head injuries develop permanent brain damage. The degree of damage varies from barely recognizable and NOT incapacitating (with the boxer resuming boxing) to incapacitating. Most boxers with severe head injuries develop permanent brain damage. The degree of damage varies but tends to be incapacitating.
In a moderate or a severe injury, as the pressure wave from the injury recedes, the boxer does NOT regain consciousness because of secondary complications.
A SINGLE moderate or severe head injury, in the ABSENCE of prior head injuries, may lead to permanent brain damage, and about 1.0 % of such SINGLE injuries result in parkinson. For PD to begin approximately 60% of the cells in the substantia nigra must be lost. These cells are rarely lost because of a SINGLE moderate or severe injury.
A problem arises when there’s a lawsuit and a person claims a blow to his head, either an injury WITHOUT loss of consciousness, or a less than one hour loss of consciousness resulted in permanent brain damage including parkinson. The scientific evidence doesn’t support this. How a judge and jury decide may be different.
The issue of REPEATED mild head injuries with brief loses of consciousness is different. REPEATED brief episodes of loss of consciousness, usually more than two, have a cumulative effect on the brain. They may cause epileptic seizures, dizziness, ringing in the ears, unsteadiness, paralysis of an arm and/or a leg, speech and language difficulties, difficulty remembering, difficulty thinking, personality changes including violent behavior.
At post-mortem examination such symptoms are usually associated with Alzheimer-like changes in the brain. These changes include a loss of cells, neurons, in regions affected by Alzheimer disease. Under a microscope the regions affected are characterized by the appearance of amyloid plagues outside the cells. The plaques represent clumps of a protein called amyloid. The cells effected are characterized by the appearance of neurofibrillary tangles. The tangles represent clumps of a protein called tau.
The symptoms may develop after a boxer’s last knock-out or months or, even, years later. At one end of the spectrum are boxers with minimal symptoms and at the other end are those requiring institutional care. Along the spectrum are some boxers with varying degrees of speech difficulty, stiffness, unsteadiness, memory loss, and inappropriate behavior.
A H Roberts in his book Brain Damage in Boxer: A Study of Prevalence of Traumatic Encephalopathy Among Ex-Professional Boxers (London, Pitman, 1969) reported that 15-40% of former professional boxers had some symptoms of brain injury. That there was a relationship between the length of a boxer’s career, the number of professional bouts, and the prevalence of brain injury. He reported that 47 % of boxers whose careers exceeded 10 years were affected, compared with 13% who fought for 5 or less. Half of the boxers who had more than 150 professional matches had symptoms of brain damage compared with 19% of those with 50 - 150 professional matches and 7% of those who fought less than 50 times.
The Alzheimer-like symptoms usually begin near or shortly after the end of a boxer’s career. Occasionally they are first noticed after a particularly brutal match. Symptoms develop, on an average, 16 years after the boxer began ins his career. In some boxer’s symptoms develop as early as 6 years. Although boxers in all weight classes can develop Alzheimer-like symptoms, heavy weight boxers are more often affected. Champion boxers are as likely to be affected as less skilled boxers.
MRI abnormalities and mild memory changes occur in many boxers who appear normal. These mild changes can begin after only a few years in boxing. While boxers with less than 20-30 professional bouts usually do not have Alzheimer like symptoms those with 25-50 bouts often show MRI and psychological test abnormalities although they appear to be normal. That is the MRI and psychological test abnormalities are early changes.
Boxers with more than 50 professional bouts often have obvious Alzheimer like symptoms as well as MRI and psychological test abnormalities.
The spectrum of Alzheimer-like symptoms strongly suggests that the disorder called dementia pugilistica or chronic encephalopathy of boxers, a disorder resembling Alzheimer disease, is a progressive illness. As the damage accumulates, mild symptoms merge into more obvious symptoms.
The boxer usually is not aware of his symptoms: his wife is often the first to notice the personality changes. Early motor symptoms, slowness of movement, shuffling of gait, are usually are noticed first by the trainer. The slowness of movement, the shuffling gait, the lack of coordination, the loss of balance, are initially are attributed to the aging process. However, as the symptoms worsen, it becomes apparent to the boxer’s companions that something is wrong, even though the boxer continues to insist that he is healthy and is able to box. Speech difficulty is often a prominent feature of dementia pugilistica. The slurred, often difficult to distinguish speech of such boxes has characteristics of the speech of Parkinson, multiple sclerosis, and stroke victims.
When the issue of head injuries (minor, moderate or severe), boxing and parkinson is discussed, the question of Muhammad Ali’s Parkinson disease comes-up. Boxing when it causes brain damage results in an Alzheimer like changes in the brain: a loss of cells in the regions affected by Alzheimer disease with the appearance of amyloid plaques and neurofibrillary tangles (the hallmarks of Alzheimer disease). Boxing does not, to our present state of knowledge, result in the appearance of Lewy bodies (the hallmarks of PD). Ali does NOT have Alzheimer-like symptoms: his mind is sharp. The great boxer Joe Louis developed Alzheimer-like symptoms. Louis’s most famous opponent, Max Schmeling, the German boxer who Louis knocked out in 1938, died at age 90 with his mind intact
Conclusion The exact mechanism by which multiple and repeated blows to the head cause brain damage, especially to boxers, has not been fully established. The major risk factors for development of brain damage, in boxers, are length of professional career and number of professional matches, which are measures of exposure to head blows. One can postulate that every blow to the head results in microscopic damage, and that as they continue boxing the damage accumulates. However, while some boxers develop an Alzheimer like disorder (and rarely a parkinson like disorder), many boxers do not. Max Schmeling did not, and George Foreman who boxed as long as anyone did not.
CAT Scan of Brain: Showing Blood Clot, Subdural Hematoma, Left Side of Brain, with distortion of the Ventricles
Duration of cognitive impairment after sports concussion. Bleiberg J, Cernich AN, Cameron K et al National Rehabilitation Hospital, Washington, District of Columbia 20010, USA. t OBJECTIVE: We sought to determine the duration of cognitive impairment after sports concussion. METHODS: We conducted a study with a prospective design in which 729 athletes underwent preseason baseline testing by being administered a computerized neuropsychological test battery, followed by retesting at regular intervals after they sustained sports-related concussions. A control group consisting of non concussed athletes drawn from the same baseline population underwent testing at parallel intervals.
RESULTS: Cognitive impairment in this primarily American Academy of Neurology Grade II sample of boxing concussions was apparent on the day of injury and at 1 to 2 days post injury. Recovery of cognitive performance occurred during the 3- to 7-day interval. Comparison with control subjects showed that absent or attenuated practice effects, in addition to frank deterioration from baseline, were indications of recent concussion. CONCLUSION: The present findings of recovery during the 3- to 7-day interval post-injury are consistent with the American Academy of Neurology Grade II return-to-play practice parameters suggesting a 1-week time-out from participation in contact sports.
Clin J Sport Med. 2003 Jan volume 13 pages 21-7.
Assessment of cognitive recovery following sports related head trauma in boxers.
Ravdin LD, Barr WB, Jordan B, Lathan WE, et al Department of Neurology and Neurosciences, Weill Medical College of Cornell University and New York Presbyterian Hospital, New York, New York 10021,
OBJECTIVE: To prospectively examine recovery of cognitive function within one month following sub concussive sports related head trauma. DESIGN: A prospective study of New York State licensed professional boxers who underwent testing of cognitive functioning before and after (within days, one week, and one month) a professional bout. SETTING: Male professional athletes recruited from the New York State Athletic Commission and local boxing gyms. PARTICIPANTS: 26 licensed professional boxers were enrolled in the protocol. Data is presented on the 18 participants who completed testing on at least three of the four time points. INTERVENTIONS: : Serial neuropsychological assessment before and after the athletes engaged in competition. MAIN MEASURES: Neuropsychological measures of cognitive functioning, including new learning and memory, information processing speed, and mental flexibility.
RESULTS: A series of repeated measures revealed significant within subject differences across testing on complex information processing and verbal fluency. Post hoc analyses indicated significant differences between time 1 (baseline) and time 4 (one month post), with scores one month following the bout indicating significantly improved performance. Memory scores did not change significantly across testing; however, prior boxing exposure measured by total number of professional bouts was associated with poorer memory performance. CONCLUSIONS: Cognitive testing 1 month following participation in a professional boxing bout yielded scores suggestive of recovery to a level above the baseline. We conclude that baseline assessment taken during periods of intense training are likely confounded by other pre-bout conditions (i.e., sparring, rapid weight loss, pre-bout anxiety) and do not represent true baseline abilities.
Instability of performance associated with mild head injury may complicate the interpretation of post-injury assessments. Practice effects may also confound the interpretation of serial assessments, leading to underestimation of the effects of sports related head trauma.
Poorer cognitive performance was evident during the presumed recovery period in boxers with greater exposure to the sport (>12 professional bouts). This finding is consistent with reports of a cumulative effect of repetitive head trauma and the subsequent development of chronic traumatic brain injury. These data have implications for assessing recovery of function following head injury in players of other contact sports as well as determination of return-to-play following an injury.
Clin Neuropsychol. 1999 May volume 13 pages 193-209.
Neuropsychology of sports-related head injury: Dementia Pugilistica to Post Concussion Syndrome. Erlanger DM, Kutner KC, Barth JT et al Columbia University, New York, NY, USA.
This article reviews the existing literature on Dementia Pugilistica, concussion and Post Concussion Syndrome, Second Impact Syndrome, and the emerging role of the sports neuropsychologist regarding return to play decisions. Dementia Pugilistica is discussed as a condition that exists along a continuum: Although many boxers will develop mild neurocognitive deficits, it is not yet known what percent of these mild presentations will progress to Dementia Pugilistica.
Factors contributing to both increased and reduced risk are detailed. The role of neuropsychological assessment in research and management is reviewed. Existing studies of concussion incurred during contact sports provide evidence of an important role for such assessments in the management of mild head injuries. The importance of grading of concussions, monitoring of post-concussive symptom resolution, and the use of neuropsychological test results in return to play decisions is detailed. The Second Impact Syndrome is discussed with regard to return to play decisions. .
J Psychiatry Med. 1995 volume 25 pages 249-62.
The neuropsychiatric aspects of boxing. Mendez MF. UCLA School of Medicine, USA. OBJECTIVE: To review the neuropsychiatry of boxing. METHOD: This update considers the clinical, neuropsychological, diagnostic, neurobiological, and management aspects of boxing-related brain injury. RESULTS: Professional boxers with multiple bouts and repeated head blows are prone to chronic traumatic encephalopathy. Repeated head blows produce rotational acceleration of the brain, diffuse axonal injury, and other neuropathological features. Chronic traumatic encephalopathy includes motor changes such as tremor, dysarthria, and parkinsonism; cognitive changes such as mental slowing and memory deficits; and psychiatric changes such as explosive behavior, morbid jealousy, pathological intoxication, and paranoia. Screening with neuropsychological tests and neuroimaging may help predict those boxers at risk for chronic traumatic encephalopathy.
CONCLUSIONS: Boxing results in a spectrum of chronic traumatic encephalopathy ranging from mild, non-progressive motor changes to dementia pugilistica. Recent emphasis on safety in the ring, rehabilitation techniques, and other interventions do not eliminate the risk for chronic traumatic encephalopathy. For this reason, there is an active movement to ban boxing
American J Sports Med. 1993 Jan-Feb volume 21 pages 97-109.
Does amateur boxing lead to chronic brain damage? A review of some recent investigations. Haglund Y, Eriksson E. Department of Sports Orthopaedic Surgery, Karolinska Hospital, Stockholm, Sweden.
54 former amateur boxers were examined and compared with 2 control groups of soccer players and track and field athletes. All subjects were interviewed regarding their sports career, medical history, and social variables. They underwent a physical and a neurologic examination. Personality traits were investigated and related to the platelet monoamine oxidase activity.
Cerebral morphologic changes were evaluated using computed tomography and magnetic resonance imaging. Further, clinical neurophysiologic tests were made as well as neuro-psychological tests.
No significant differences were found between the groups in any of the physical or neurologic examinations or in platelet monoamine oxidase activity. Socially, the boxers had a lower degree of education and had chosen less intellectual professions, but they were less impulsive and more socialized.
The computed tomography images and magnetic resonance imaging studies showed no significant differences between the groups. There was a significantly higher incidence of slight or moderate electroencephalography deviations among the boxers.
The boxers had an inferior finger-tapping performance. Thus, no signs of serious chronic brain damage were found among any of the groups studied. However, the electroencephalography and finger-tapping differences between the groups might indicate slight brain dysfunction in some of the amateur boxers.
Neurology 1991 volume 41 pages 1554 – 1557 Brain Injury and Neurologic Sequelae: A cohort study of dementia, parkinsonism, and amyotrophic lateral sclerosis. Williams DB, Annegers JF, Kokmen E et al University of TexasSchool of Public Health, Mayo Clinic RochesterMN We reviewed the medical records of 821 Olmstead County residents who had suffered head trauma with presumed brain injury between 1935 – 1974 and were more than 40 years old.
These patients were followed over 15,000 person years for dementia and other degenerative diseases. The standardized morbidity ratio for dementia was 1.06 and for Alzheimer disease was 1.0 These values are not significantly elevated and are inconsistent with studies that suggest that head trauma is a risk factor for Alzheimer disease.
The standardized morbidity ratio for parkinson was 1.04, for Parkinson disease was 0.94 and for amyotrophic lateral sclerosis was .05 were. These are not significantly elevated and provide no evidence that head trauma is a risk for these disorders. However, these results are based on a smaller total number of cases.
Movement Disorders 1991 volume 6 pages 225 – 229 Prior History of Head Trauma in Parkinson Disease Factor SA, Weiner WJ
The purpose of this study was to evaluate the relationship between head trauma and PD. A questionnaire was completed by 97 PD patients (mean age 68.6 years, duration of disease 6.4 years) and 64 spouses acting as controls (mean age 63 years).
31 ]PD patients reported head trauma before onset of PD (mean 32.3 years earlier), whereas 11 controls reported head trauma before completing the survey (mean 26 years earlier).
This difference was significant (p < 0.05). 20 PD patients and 5 controls reported head trauma associated with alteration of consciousness (p < 0.05).
Trauma occurred a mean of 37.7 years before onset of PD and 37.2 years before survey completion in the two groups respectively.
When we adjusted frequencies to eliminate sex differences between the groups, the differences in reported head trauma was NOT significant.
However, a trend toward significance was observed when examining head injury with alteration of consciousness. Other observers have reported similar results indicating that previous head trauma may be a risk factor for PD. However, recall bias might have an effect on the outcome of these studies. The relationship between head trauma and PD is still tenuous.
Journal of Neurosurgery 1983 volume 58 pages 298 – 299 Parkinsonism due to Subdural Hematoma: Case Report Sandyk R, Kahn I
The authors describe the case of a 38 years old woman who presented with parkinson syndrome associated with a chronic subdural hematoma (a blood clot on the surface of the brain). Gradual disappearance of the symptoms followed removal of the hematoma.
Chronic subdural hematoma may in rare instances cause a parkinsonian syndrome probably by a pressure effect on the basal ganglia or by altering the function of neurotransmitters.
this article was written, edited, and updated 4/1/05
Dr Lieberman evaluated Jack Dempsey for his boxing injuries in the 1970s