Chronic Traumatic Encephalopathy
We published recently a long article on ALS (Amyotrophic Lateral Sclerosis) in the newsletter of the AMHE. We did mention also chronic Traumatic encephalopathy (CTE) in the differential diagnosis. We decided to continue to extend on the subject especially after the recent publication of an article on National Football League players in the med-Page (April 2019).
Thinking about TCE, sport medicine specialists have initiated, years ago, rules on Concussion in different contact sports. Concussion was defined as a traumatic brain injury that affect temporary its function with headaches, memory loss (amnesia) and poor coordination and imbalance. A blow to the head is causing a shaking phenomenon to the upper body. Often, the player may lose consciousness. Most athletes will recover in time. Many researchers have voiced their concerns about contact sports especially in Football.
A study in which brain scans have been used to evaluate Football players in the American National league for cognitive and neuropsychiatric symptoms, has demonstrated that many areas in the brain were involved with chronic traumatic encephalopathy. The tomography (PET), called Flortaucipir positron-emission tomography showed a higher amount of tau in the bilateral superior frontal, bilateral medial temporal and left parietal lobes areas for 26 NFL players and these findings helped Robert Stern, PhD of Boston School of Medicine to conclude on the disease. The article can be found in its totality in the recent New England Journal of Medicine
It has always been suspicious that repeated head trauma eventually will present under the form of a chronic traumatic brain entity but this diagnosis was always asserted through a postmortem neuropathological examination. It is now suggested that we can detect the tau PET changes associated with CTE. Eric Reiman MD from the Banner Alzheimer’s institute in Phoenix AZ, is also a co-author of this paper and he believes in the capability of the PET Scan to pinpoint at suspicious areas of involvement with Chronic Traumatic Encephalopathy. He stated that he has not yet been able to show a relationship with cognitive or behavior symptom severity although he found only one of the NFL players with a positive amyloid PET scan, suggestive that the cognitive and behavioral symptoms were not attributable to Alzheimer ‘s disease.
As we discussed in the past, Chronic Traumatic Brain Encephalopathy (CTE) is a neurodegenerative disease associated with repetitive head injuries but pathologically defined by the deposition of paired helical filament tau in frontal, temporal and parietal cortices.
The events leading to Chronic Traumatic Encephalopathy as a result from injury while involved in contact sports, will lead to inflammation allowing an aggregation of tau protein to be able to degenerate the neurons and the supporting elements. Years after, behavior and cognitive disturbances may surface. So much have been said about “Concussion” and as sport medicine physicians, we have taken pride and courage in prohibiting a star player from returning during the game or weeks later after such injury.
Stern and co-authors used the flortaucipir PET to measure and assess amyloid–beta in those 26 football professional players with cognitive and neuropsychiatric symptoms as well as 31 asymptomatic men with no history of traumatic brain injury. The ratio of radioactivity (SUVR) in a cerebral region compared to the amount detected in the cerebellum was compared by the researchers to the symptoms and the amount of years passed playing football. The mean Flortaucipir SUVR was found higher among former players in both superior frontal, temporal and left parietal areas in relation to the years played.
No correlations were found between the tau deposition and the different scores obtained for any cognitive or neuropsychiatric tests except for one former NFL player who showed similar levels of amyloid-beta deposition to the one suffering from Alzheimer’s disease. Playing professional football for a long period did not necessarily correspond to the numbers of repeated concussions.
Ropper concludes that factors like player’s size, head-to-neck configuration, style of play or even the position played may influence the deposition of tau. Stern doubted that these criteria can allow us to diagnose Chronic Traumatic Encephalopathy(CTE) or any experimental test can be ready to support such diagnosis.
Reiman and others are working on a longitudinal study called “Diagnose CTE” to follow former college or NFL football players as well as others with no contact sport history with results expected to be published in the early 2020. This study is funded by a grant of Eli Lilly Cie, the National Institute of Health, the state of Arizona and the US government. All flortaucipir and florbetapir Pet radiotracers were provided by Avid Radiopharmaceuticals.
We hope to be able to diagnose such disease, at will on football players who have been involved in many concussions and demonstrated by scans a relation between their symptoms and multiple concussions as well as the deposition of tau protein in areas involved especially the parietal, frontal or temporal cortices. May we get some feedback from our neurologists in practice for the benefit of the reader of the AMHE Newsletter.
Maxime Coles MD
1- Stern R: “Tau Positron-Emission Tomography in Former National Football League Players”. NEJM 2019.
2- Ropper A: “Links in the chain of Chronic Traumatic Encephalopathy”. NEJM 2019