Chronic traumatic encephalopathy (CTE) is a neurodegenerative disorder characterised by neurological and psychological symptoms, its external cause generally being frequent trauma to the head. The question is not, however, one of severe traumatic brain injury with outcomes such as intracranial bleeding, but rather one of mild trauma – in the English-speaking world one also known as “concussion.” The definition describes concussion as traumatic brain injury caused by a sudden, direct or indirect trauma to the head, face or the neck.
The symptoms are very diverse, ranging from unconsciousness, dizziness, headaches and cognitive deficits to behavioral disorders, sleep disorders and depression. That frequent concussions may lead to chronic brain damage has long been suspected. Already in 1928, U.S. pathologist Harrison Martland from New Jersey writing in the JAMA described neurological disorders in boxers as “punch drunk”, in 1937 the concept of “dementia pugilistica” was introduced.
Sensational deaths among ex-athletes
The U.S. magazine Clinics in Sports Medicine has now devoted an entire issue to the topic. In Boston there has even been for three years now, in the Center for the Study of Traumatic Encephalopathy (CSTE), a special research center for the CTE. The backdrop for current interests of researchers on the subject includes illness and death among former professional athletes. Such a death, for example, in 2010 at the age of 45, took the Canadian former ice-hockey professional Bob Probert, who was regarded as a very rough player. Probert died of heart failure, but his autopsy at the CSTE revealed evidence of CTE.
And a few weeks ago, the 50-year-old, probably depressive ex-football player Dave Duerson took his own life. In a farewell letter, he asked that his brain be provided to the CSTE Brain Bank, which is funded by the U.S. Football League and is located at the Bedford VA Medical Center (Boston, Massachusetts). This tissue bank is under the care of scientist Dr. Ann McKee, co-director of CSTE, who has with colleagues for several years now studied the brain tissue of deceased athletes for signs of CTE. One reason for the increased interest is also that skull-brain trauma or concussions might have increased in the last two decades.
This could, according to Dr. Daniel H. Daneshvar from the Alzheimer Center of the Boston University School of Medicine be just an apparent increase as a result of improved diagnosis, but also a real one, as collisions between athletes do occur more frequently and the level of violent impact has increased. Women are, incidently, more often affected by such head injury and suffer effects from neurological and psychological impacts later and more often than men, explains Dr. Tracey Covassin of Michigan State University. The reason behind this is suggested as being different biomechanical proportions, but possibly also that men were more often concealing injuries, speculates Daneshvar.
Chronic damage only ascertained with professional boxers
Although chronic brain damage as a consequence of frequent traumatic brain injuries has been known or discussed for over 80 years, much is still unclear. According to Nashville registered neuropsychologist Dr. Gary S. Solomon, most existing studies up until now have been contradictory and, partly, limited in their diagnostic conclusiveness. It’s relatively clear that boxing can lead to permanent brain damage, neurological and psychological disorders. This is only so far scientifically backed in relation to professional boxers, but not for amateur boxers and other athletes, explains Solomon. In all likelihood, it is not only the frequent violence impact in boxing which brings about chronic brain damage. The threat of such permanent damage is increased, according to Solomon, in particular for the boxers who have a genetically increased risk (apolipoprotein E4 alleles) for Alzheimer’s disease. Overall, the risk in modern professional boxing is said to be less than at the beginning of the 20th century, since a boxer then was usually active for almost 20 years. Today, such a career averages only five years. In addition, medical care today is better.
Clinical diagnosis of CTE is very uncertain
In most cases, the symptoms of CTE appear only when the athletes are no longer active- by dependents or family members, such as a wife, who notices that her husband has changed, that he behaves differently. The symptoms include cognitive deficits and memory disorders, and with progression of the disease tremors and speech problems also occur. What’s more, it turns out again and again to be the case that massive behavioral problems emerge. However, the clinical diagnosis of CTE is uncertain since, for example, no consensus on the diagnostic criteria exists. A reasonably accurate diagnosis is therefore only possible by post-mortem neuropathological studies, such as those McKee and her colleagues carry out. But so far there is also no consensus on the neuropathological diagnostic criteria for CTE.
CTE findings: atrophy and clumped tau
Until now, the researchers led by McKee have published autopsy results on 46 athletes (39 boxers, five American football players, a wrestler and a football player). The average age of cases of alleged CTE confirmed by autopsy stands at almost 43 years, reports Dr. Brandon E. Gavett, a colleague of McKee. Neuropathological findings are, says Gavett,among others cerebral atrophy, shrunken mammillary bodies and clusters of clumped tau protein – like those in Alzheimer’s disease. In the CTE, however, the extensive amyloid plaques are lacking.
Only symptomatic therapy is possible
The scientists hope, of course, to make the diagnosis as early as possible at clinical level, using methods such as biomarkers in the CSF and imaging procedures, such as MRI spectroscopy. Nevertheless, just as is the case with Alzheimer’s disease and other neurodegenerative diseases, there is no causal therapy. Only symptomatic therapy is possible, such as treating insomnia with trazodone, post-traumatic headaches and depression with antidepressants. According to Dr. William P. Meehan from Children’s Hospital Boston, in instances of poor concentration methylphenidate comes into the picture, for memory disorders classic antidementia treatment such as rivastigmine and donepezil are also considered and beyond that, of course, natural and non-pharmacological therapies as well. However, according to Meehan, one must always weigh up whether or not the risks of therapy are greater than any possible benefits. In any case, what’s better than any therapy is prevention. Unfortunately, there is no sufficient evidence that helmets actually protect against the effects of frequent light craniocerebral trauma – against concussion as such – says Daniel H. Daneshvar.
Header game safe
However, there is also good news, at least for football players and their fans. Although a football can fly over 100 kilometres per hour through the air and so-called head-ball collisions are relatively common, foot-ball – or to be more exact football with the head – does not in the long term make one “stupid”, as is speculated again and again. Firstly, the impact of the ball is usually an anticipated one, the player is prepared for it, on the other hand the forces acting on the forehead are usually relatively low, rotational trauma such as a lateral temporal impact are rather an exception. More dangerous and more frequent causes of traumatic brain injury in codes of football, according to Daneshvar, are direct head-head collisions or contact with a goalpost. Evidence that football games are associated with an increased risk of neurodegenerative brain damage does not exist.