American football injuries

 

American football injuries

American football injuries

The traumatism of American football.

The danger of American football has long been known. As of 1905, there were 19 deaths of College football players. After the public’s attention — grabbing beating of a player in the Pennsylvania-Swarthmore match, President Theodore Roosevelt gathered the leaders of Princeton, Harvard, and Yale to discuss the situation with the game. At that time, American football was almost not regulated by the rules — they were very free and did not provide protection for players. Shayler Matthew, Dean of the divinity Department at the University of Chicago, said of American football: “everyone, from the President of the United States to a humble College Professor, protests against this gladiatorial sport, which mutilates and kills young men, dishonors higher education and pursues only one goal — money.”6 However, Roosevelt was a staunch advocate of sports and healthy lifestyles, so despite calls to ban the game, he only recommended that schools establish stricter controls. The University of Pennsylvania was the first to introduce the new rules, and several colleges in new York followed suit. In 1906, to ensure the widespread introduction of new rules, the Intercollegiate athletic Association was established. In 1910, the organization was transformed into the National University athletic Association.

A century later, in April 2010, twenty-one-year-old Owen Thomas, captain of the University of Pennsylvania football team, committed suicide. An autopsy of the brain revealed chronic traumatic encephalopathy (CTE; I spoke about this disease in the section about Boxing).

It is a matter of concern that there was no single serious injury in Thomas’s case. According to his mother, she does not know that her son ever had a concussion. However, the same degenerative changes were found in his brain as in more than twenty deceased National football League players.

Since there were no obvious head injuries, this discovery suggests that minor but frequent blows to a player’s head, even if he is a Junior, can have a cumulative effect. Thomas ‘mother says:” in this game they are constantly bumping heads. A young midfielder can accumulate more than a thousand of such strikes. Each blow is like a teaspoon of water. But if you take a thousand teaspoons, the jug can overflow.”

In Thomas’s case, chronic traumatic encephalopathy was not recognized as a direct cause of suicide, or at least one of its causes. Meanwhile, it is known that CTE provokes the development of depression and impulsive behavior control disorder. Two former National football League players who also committed suicide (one of them, star midfielder Junior Seau, played twenty seasons in the League), the autopsy also showed the presence of chronic encephalopathy. The relationship between head trauma and suicide is currently only a hypothesis, but it has attracted the attention of researchers in the field of TBI, so I hope that we will soon learn much more about it.

Today, scientific evidence of the relationship between pathological changes in the brain and repeated concussions is just beginning to emerge. In April 2013, Mccrory and co-authors published an article on the subject in the British Journal of Sports Medicine. It provided a comprehensive overview of the accumulated knowledge of chronic traumatic encephalopathy in former professional athletes.

American football injuries

American football injuries

In a broad review of the existing literature, the authors identified four groups of concussions, mainly based on the following descriptive criteria:

– Long-term post-commotion symptoms that eventually disappear completely.
– Persistent, lasting more than three months post-commotion symptoms that eventually disappear completely. Neuroimaging studies show no changes in brain structure.
– Permanent post-commotion symptoms, constituting 10-20% of the group of persistent symptoms. Functional and psychological examinations can detect pathology, but the structure of the brain, as a rule, remains normal.

Identified neurological disorders characteristic of chronic traumatic encephalopathy. Postmortem examination shows the presence of neuropathological changes in the brain, neuroimaging study of the brain during life also often detects pathologies. With regard to the latter group, the authors note that there are cases when during life people showed all the signs of chronic traumatic encephalopathy, but the autopsy of the brain after death did not show any pathological changes. The authors also emphasize that the diagnosis of such conditions in life is usually complicated by the presence of accompanying neuropsychiatric problems (comorbidities), such as depression, personality disorders, anxiety, attention disorders. Since we know little about what physiological processes occur in the brain as a result of a concussion, we do not know where exactly in this organ the changes that give post-commotion symptoms are localized. We can not single out the specific damaged area, which would be the cause of headaches, fatigue, deterioration of attention, sleep disturbances and many other симптомов11. It is therefore not clear whether the four categories above describe deterioration within the same type of injury, known as mild traumatic brain injury, or four completely different types of injury. Most experts are inclined in favor of the first option.

Diffusion-tensor imaging (DTV), a form of magnetic resonance imaging, can effectively detect minute changes in the structure of white matter in the frontal lobes of the brain. In January 2013, an article by Virgie-Babool and colleagues at the University of calgary was published in the journal Pediatric Neurology. Using the DTV method, the researchers studied changes in the white matter in adolescents who had suffered concussions in sports during the previous two months. It is important to note that a control group of adolescents who did not have such traumas was also examined. Each subject was given a standard magnetic resonance imaging imaging of the structural anatomy of the brain and two diffuse tensor scans. Doctors who analyzed the scans were not aware of the presence or absence of injuries. In addition, the condition of each subject was assessed by the method of assessing concussions in sports (SCAT-2) – a standardized technique that includes a wide range of post-commotion symptoms, psychophysiological parameters and quality of coordination. According to this technique, the lower the scores, the more severe the injury.

Despite the limited number of subjects-12 in the main group and 10 in the control group-the results were statistically significant and very indicative. The authors found clear differences in the structure of white matter in adolescents with concussion compared to their healthy peers. And in most of the injured adolescents, the changes were bilateral. In addition, the results of the SCAT-2 assessment corresponded quite accurately to the data of the DTV survey. The lower the score (which reflected the severity of the injury), the more severe disorders in the structure of the white matter revealed diffusion-tensor brain scan.

White matter, formed by axons covered with myelin sheath (it is myelin that gives it a characteristic white color), is the most important component of the brain. Therefore, it is obvious to how serious consequences can lead to structural disorders of the white matter. One of the main theories describing the mechanics of concussions is that this injury causes stretching and sometimes even rupture of axons. This injury leads to improper functioning of the axons, which creates the characteristic symptoms of concussion.

This study is one of the first to show an unconditional relationship between mild TBI and changes in brain anatomy. We have no autopsy data to support this link, as concussions fortunately do not kill people. There is still a gap between the DTV data and the detected pathological changes in the brains of athletes who had multiple mild TBI and who subsequently developed severe symptoms of chronic traumatic encephalopathy. Although the existence of such a connection is very likely. In particular, the study of the brain in chronic traumatic encephalopathy reveals atrophy in the frontal and temporal lobes, which corresponds to the foci of concentration of white matter disorders, which were detected by diffusion-tensor imaging researchers from calgary.

In 1928, Dr. Harrison Martland coined the term “Boxing intoxication” to refer to the complex of symptoms encountered in professional boxers. Today, this condition is known as classical chronic traumatic encephalopathy, or “Boxing dementia”.14 Typical symptoms include impaired speech, movement, and memory. If memory is not affected, the symptoms are much like Parkinson’s disease and this condition is called Boxing Parkinson’s. As I have said, this was most evident in Muhammad Ali. Neuropathological changes that occur in the brain in such conditions are well known and include the death of nerve cells, scarring and the formation of neurofibrillary tangles, which is the result of repeated brain injury.