Introduction by Dominic A. Carone, PhD, ABPP-CN
These days, it is difficult for someone to turn on the television, open a newspaper, or surf the internet without coming across a story on the dangers of concussions, particularly repeat concussions. This has caused a great deal of concern among many athletes and their loved ones regarding participation in sports.
One of the greatest concerns that has emerged is the possibility of developing CTE (chronic traumatic encephalopathy) – which is described as a degenerative brain disorder caused by repeat brain trauma. But how much do we really know about CTE? Recently, Dr. Ann Mckee (neuropathologist) and colleagues published a review of CTE and other topics in a paper entitled “
The Neuropathology of Sport.” While McKee and colleagues discuss CTE as an established disease entity,
contrasting opinions exist in the literature on the associations between athletic head trauma and neurodegenerative disease.
A
neuropsychologist colleague of mine, Dr. Jim Andrikopoulos has been one of the most vocal critics of the existence of CTE. Below is a response by Dr. Andrikopoulos to the aforementioned article by Dr. McKee. Dr. McKee will be contacted and given a chance to respond. Presenting this material in blog format provides maximal exposure to the public, most of whom are not avid consumers of health care journals. Respectful comments are welcome.
Note: The views expressed by guest authors on this blog are not necessarily those of my own. For my own review of CTE and dementia pugilistica, see Carone, D., Bush, S. (2014). Dementia pugilistica and chronic traumatic encephalopathy. In R. Dean & C. Noggle (Eds.), The Neuropsychology of Cortical Dementias. New York: Springer, pp. 303-326.
The Neuropathology of CTE in the United States
Jim Andrikopoulos, Ph.D., ABPP-CN
This letter is in reference to a recent review by McKee et al. (1). To judge the validity of the core observation made in the review one needs an understanding, particularly non-Americans, of the current sociological context in the United States as it relates to contact sports. McKee begins by outlining the physical, emotional, cognitive and health benefits of sports. This can be contrasted with the current state of affairs in the United States, especially in American football. McKee reports that contact sports “rarely” results in the development of chronic traumatic encephalopathy (CTE). However, McKee found CTE in 34 of 35 professional football players, all nine college players, six high school athletes, and all four professional hockey players (reference 128 in [1]).
Despite McKee stating the incidence of CTE is unknown; her message to the American media is different: “I am really wondering, on some level, if every single football player doesn’t have this” (2). CTE in contact sports in the United States is now an “epidemic.”Since 2010, participation in youth football has dropped by 9.5% (3). What is the merit of the science that has created this concussion craze?
The symptoms outlined by McKee bear no clinical likeness to the CTE of the last century. CTE is now characterized as a mood and behavioral disorder. The clinical features of CTE are parkinsonian and speech symptoms at a relatively young age. McKee treats these hallmark features in her review as a historical footnote, mentioning them once. The observations of Martland (references 118 in [1]) defined the disease through the 20th century only for CTE to now to be morphed into an unrecognizable clinical entity.
While classic papers are cited, the parkinsonian clinical descriptions are ignored (references 38 and 44 in [1]). The seminal
epidemiological study that confirmed this parkinsonian phenotype and addresses prevalence is not cited at all (4). CTE is now artificially dichotomized. McKee proposes those with an early onset tend to have mood and behavior symptoms and later onset patients cognitive impairment. She states the earlier literature suggests this dichotomy. This is false based on my literature review and indirect proof is that no references are offered by McKee in support of this claim.
There is an observation that merits special comment because of its conspicuous absence. McKee has proposed four stages of CTE. There is no mention that the clinical features that accompany each progressive stage were not developed based on an examination of the patient. The clinical features were collected post-mortem. Alois Alzheimer was the first to give us a neuropsychiatric syndrome and a neuropathology to go with it. Remarkably, he did this in one patient.
As of today, McKee has conducted 85 neuropathological examinations and no clinical examination of a patient (reference 128 in [1]). Proposing a neuropathological entity in the
absence of a clinical syndrome is unprecedented in neurological medicine as is being told that a presumably degenerative disease, CTE, cannot be diagnosed in the living patient but instead requires an autopsy.
What remains to be addressed is the neuropathology of CTE. The classic description was given by Corsellis in boxers (reference 38 in [1]). CTE in football was first described by Omalu(5). The publication was so contentious that some, rightfully, called for the paper to be retracted. Among a number of shortcomings of the paper was that the neuropathological case description bore no resemblance to Corsellis (6). In turn, McKee’s original neuropathological observations appeared at odds with Omalu (reference 127 in [1]). McKee has made no effort in her published studies to reconcile these differences. It would stand to reason that a neuropathological "discovery" with dissimilar descriptions would result in a collegial scientific exchange to reconcile any discrepancies.
What are these disparate neuropathological differences? Omalu initially commented on the absence of tau in the medial temporal lobes while McKee reported it as a preferential location(reference 127 in [1]). McKee added two observations not reported by either Omalu or Corsellis. Citing Hof, McKee reported tau to be found disproportionately in the superficial cortical layer II and the upper layer of III versus Alzheimer’s disease where tau is preferentially in layers V and
VI (reference 91 and 92 in [1]). Second, citing Geddes, tau is observed in perivascular locations (reference 65 and 66 in [1]). In turn, Geddes who published her observations after Hof made no reference to the distribution of tau in the superficial layers but stated it was found in all cortical layers (reference 65 in [1]).
The last point is on what it means to be “encephalopathic,” a source of contention in the Omalu paper (6). Unlike Omalu and McKee, who consider a patient with tau to be
encephalopathic, Geddes does not suggest an encephalopathy, only that the tau present at autopsy may suggest repetitive trauma as the cause. The encephalopathy in CTE refers to the symptoms in a living patient not a neuropathological finding.
Braak has reported the presence of tau in patients under 30 years of age (reference 15 in [1]). McKee’s criticism of Braak was that the sample was not screened for head injury. If we accept McKee’s logic, does that obligate Braak to render a postmortem CTE diagnosis in those he can show had an antemortem head injury or two? This is how the neuropathology of CTE is currently practiced in the United
States.
References
1. McKee AC, Daneshvar DH, Alvarez VE, Stein TD. (2014).
The neuropathology of sport. Acta Neuropathol. 127(1):29-51.
2.
League of Denial: The NFL’s Concussion Crisis transcript. Frontline, PBS.
3.
Pop Warner participation dropping. Chicago Tribune, November 14, 2013.
4. Roberts AH (1969)
Brain damage in boxers: A study of prevalence of traumatic encephalopathy among ex-professional boxers. London: Pitman Royal College of Physicians.
5. Omalu BI, DeKosky ST, Minster RL, Kamboh MI, Hamilton RL, Wecht CH (2005).
Chronic traumatic encephalopathy in a national football league player. Neurosurgery, 57(1): 128-134.
6. Casson IR, Pellman EJ, Viano DC (2006).
Chronic traumatic encephalopathy in a NationalFootball League player. Neurosurgery,58(5): E1152.
Author Affiliations: Mercy Hospital Medical Center, Ruan Neurology Clinic, Des Moines, Iowa Corresponding Author: Jim Andrikopoulos, Ph.D. Ruan Neurology Clinic, 1111 6th Avenue, East Tower, Suite A100, Des Moines, Iowa 50314., Tel: 515 358-0020, Fax: 515 358-0099
neuroclinic@msn.com
Conflicts of Interest Disclosures: Dr. Andrikopoulos has provided expert testimony.
