2018 ANNUAL SPRING CONFERENCE
Joint meeting with the Psychology Section of the New York Academy of Sciences
Chronic Traumatic Encephalopathy:
Neuropathology, Knowledge Gaps, and Clinical Translation
Chronic traumatic encephalopathy (CTE) has been defined as a degenerative brain disease associated with multiple head injuries that leads to disabling changes in behavior, mood, and cognition. This definition is based on findings of tauopathy-like neuropathological changes in the brains of professional athletes who formerly played contact sports, many of whom reportedly showed severe neuropsychiatric changes later in life. These reports have raised serious questions in the minds of the public and scientific community alike about the long-term effects of contact sport play, military service, and other activities where repeated head injuries tend to occur and have alarmed some to the point of fearing disastrous neurological effects from a single concussion. However, some argue that many of the prevailing concepts about CTE are very far from settled science, citing methodological limitations of published studies, unexplored alternative explanations for the observed neuropathological and neuropsychiatric changes, and well-established scientific data unsupportive of the concept of CTE as a disease. This conference will bring together experts in the fields of neuropathology and clinical neuropsychology to discuss the neuropathological changes associated with CTE and review evidence both for and against the concept of CTE as a neurodegenerative disease causally linked to a history of head injuries. Suggestions for translating available scientific data about CTE and related issues, such as concussion management and return to play decisions, into the practice of clinical neuropsychology will also be discussed.
9:30am Registration and Breakfast
10:00am Welcome and Awards Presentation
Elise Caccappolo, PhD, ABPP
Past President’s Award to Christina Palmese, PhD, ABPP
Graduate Student Research Award to Melanie Lucas, MA
10:15am Conference Introduction
Jason Krellman, PhD, ABPP
10:20am Long-Term Effects of Warfare-Related TBI:
Is It Like Playing Football or Something Else?
Daniel Perl, MD
Introduction by Jason Krellman, PhD, ABPP
11:00am Coffee Break
11:20am Chronic Traumatic Encephalopathy is Not a Real Disease
Christopher Randolph, PhD
Introduction by Elise Caccappolo, PhD, ABPP
12:00pm Practicing Clinical Neuropsychology in the Age of ‘CTE’
Kenneth Perrine, PhD, ABPP
Introduction by Amy Weinstein, PhD
12:40pm Q&A (All Speakers)
Long-Term Effects of Warfare-Related
Traumatic Brain Injury:
Is It Like Playing Football or Something Else?
Daniel Perl, MD
Professor of Pathology (Neuropathology) Uniformed Services University
With increased use of improvised explosive devices (IEDs), traumatic brain injury (TBI) has become the “signature injury” of current warfare. With the protection of modern body armor and helmets, many military personnel who would have died in the past from equivalent explosive exposure are actually surviving -- with TBI. Following experiencing a mild TBI, service members often complain of persistent behavioral/neurologic symptoms including headaches, irritability, memory problems, difficulty concentrating and sleep disturbance, all suggesting that structural abnormalities can accompany TBI among military personnel. An additional very common disorder experienced by numerous returning service members has been post-traumatic stress disorder (PTSD).
With support from the US Department of Defense and the Congressionally-mandated Center for Neuroscience and Regenerative Medicine (CNRM), Dr. Daniel Perl has established a state-of-the-art laboratory dedicated to characterizing the nature of military TBI, especially following blast exposure. In this facility, Dr. Perl and colleagues are beginning to characterize the biologic nature of the acute and long-term effects of exposure to high explosives on the human brain. It has become clear that high explosives are capable of producing a specific pattern of damage to the brain that is consistent with our current understanding of biophysical principles (Lancet Neurol. 15:944-953, 2016). Furthermore, in some cases, these exposures also appear capable of triggering degenerative changes involving tau protein that are comparable to those seen in former contact sport athletes (chronic traumatic encephalopathy). The combination of these changes in brain structure and function results in a complex set of neurologic and psychiatric clinical features that have now forced us into discussions of the enigma between the nature of diseases of the brain and of the mind.
- 1. Learn the difference between the consequences of civilian TBIs and that seen in military personnel exposed to high-explosive blasts.
- 2. Understand how the history of the neurologic/behavioral effects of participation in warfare has molded our current approaches to this problem.
- 3. Understand the implications of new findings of the effects on the brain of blast TBI for explaining the long-term behavioral-neurologic sequelae of this form of injury.
Shively, SB, Perl, DP. Traumatic brain injury, shell shock and post-traumatic stress disorder in the military - past, present and future. J. Head Trauma Rehabil. 27: 234-239, 2012.
Shively, SB, Horkayne-Szakaly, I, Jones, RV, Kelly, JP, Armstrong, RC, Perl, DP. Characterisation of interface astroglial scarring in the human brain after blast exposure: a post-mortem case series. Lancet Neurol. 15: 944-953, 2016.
Shively, SB, Perl, DP. Viewing the invisible wound: novel lesions identified in postmortem brains of U.S. service members with military blast exposure. Mil. Med. 182: 1461-1463, 2017.
Cernak, I. Understanding blast-induced neurotrauma: how far have we come? Concussion, 2017.
Speaker bio-sketch: Dr. Daniel P. Perl was born and raised in New York City and received his BA and MD degrees from Columbia College and the State University of New York. He then took postgraduate training in anatomic pathology and neuropathology at Yale University, following which he served for two years as a pathologist in the US Public Health Service, stationed at the Centers for Disease Control in Atlanta, Georgia. In subsequent years he served on the faculty of the Brown University Medical School and then the University of Vermont College of Medicine. It was at Vermont that he began working on Alzheimer’s disease and other age-related neurodegenerative disorders. In 1986, Dr. Perl joined the Mount Sinai School of Medicine in New York, where for 24 years he served as Director of the Neuropathology Division and was Professor of Pathology, Psychiatry and Neurosciences.
Dr. Perl has authored over 290 peer-reviewed publications and book chapters and is co-author, with Professor Margaret Esiri, of the 3rd edition of Oppenheimer’s Diagnostic Neuropathology, a leading textbook in his field. He is highly regarded for his work on various aspects of the neuropathology of age-related neurodegenerative disorders, especially the role of environmental factors in their induction. He is a leading authority on the pathology of the fascinating complex of neurodegenerative disorders occurring among the native population living on Guam. In September, 2010, Dr. Perl left Mount Sinai to join the faculty of the Department of Defense’s Uniformed Services University of the Health Sciences, F. Edward Hébert School of Medicine, in Bethesda, MD. In conjunction with the congressionally mandated Center for Neuroscience and Regenerative Medicine, he has established a state-of-the-art neuropathology laboratory dedicated to research on the acute and long-term effects of traumatic brain injury (TBI) among military personnel. This culminated with his recent landmark publication in Lancet Neurology (15: 944-953, 2016) describing a distinctive and unique constellation of lesions in the brains of military personnel who had been exposed to blast TBI.
Chronic Traumatic Encephalopathy is Not a Real Disease
Christopher Randolph, PhD
Clinical Professor of Neurology
Loyola University Medical Center
There was a long-lasting debate during the first half of the 1900s about whether or not boxers suffered from a condition called “dementia pugilistica.” This included arguments as to whether there was such a distinct clinical condition, whether it was static or progressive, and whether or not boxers were actually at any increased risk of any neurological issues at all. The debate was never resolved, but was resuscitated in 2005 with the speculation that a similar condition, dubbed “chronic traumatic encephalopathy (CTE)” existed in retired National Football League (NFL) players. A specific pattern of p-tau deposition has been identified in the brains of NFL retirees, and also identifiable in the brains of at least a percentage of individuals exposed to contact sports in general. Advocates of CTE as a disease describe it as presenting with behavioral disturbance, increased suicidality, and neurodegeneration leading to dementia. The evidence to date, however, does not rise to the level of a verifiable disease, and remains at the level of case report. To assume that CTE pathology represents a neurodegenerative disease flies in the face of a number of facts, including that traumatic brain injury does not cause neurodegeneration, protein deposits in the brain are a poor predictor of behavioral symptoms, p-tau is not necessarily toxic or self-propagating, and retired NFL players are actually much physically and mentally healthier than men of their demographic background. They have an all-cause mortality rate that is 50% of that expected, and a suicide rate that is 40% of that expected. The most parsimonious explanation of the evidence to date is that repetitive head trauma may result in p-tau deposition, but that this isoform of p-tau is inert and has no toxic or self-propagating effects.
- Understand the current level of evidence, or lack thereof, for the existence of a clinical syndrome associated with repetitive head trauma.
- Understand the current level of evidence for a unique neuropathology associated with repetitive head trauma.
- Understand the relationship between protein deposition and behavioral symptoms in known neurodegenerative diseases.
- Consider alternative hypotheses for the recent series of case reports linking contact sports with neuropathological findings.
Baron SL, Hein MJ, Lehman E, Gersic CM. (2012). Body mass index, playing position, race, and the cardiovascular mortality of retired professional football players. American Journal of Cardiology, 109 (6), 889-896.
Bazarian JJ, McClung J, Shah MN, Cheng YT, Flesher W, Kraus J. (2005). Mild traumatic brain injury in the United States, 1998-2000. Brain Injury, 19 (2), 85-91.
Bennet DA, Schneider JA, Arvanitakis Z, Kelly JF, Aggarwal NT, Shah RC et al. (2006).
Neuropathology of older persons without cognitive impairment from two community-based studies. Neurology, 66 (12), 1837-1844.
Bieniek, KF, Ross, OA, Cormier, KA, Walton RL, Soto-Ortolaza, A, Johnson, AE, et al. (2015). Chronic traumatic encephalopathy pathology in a neurodegenerative disorders brain bank. Acta Neuropathology, 130, 877-899.
Corsellis, JA, Bruton CJ, Freeman-Brown D. (1973). The aftermath of boxing. Psychological Medicine 3 (3), 270-303.
Gao L, Tian S, Gao H, Xu Y. (2013). Hypoxia increases Abeta-induced tau phosphorylation by calpain and promotes behavioral consequences in AD transgenic mice. Journal of Molecular Neuroscience, 51, 138-147.
Genis L, Chen U, Shohami E, Michaelson DM. (2000). Tau hyperphosphorylation in apoliprotein E-deficient and control mice after closed head injury. Journal of Neuroscience Resarch, 60, 559-564.
Groot C, van Loenhoud AC, Barkhof F, Bart NM, van Berckel BNM, Koene T, Teunissen CC, Scheltens P, van der Flier WM, Ossenkoppele R (2017). Differential effects of cognitive reserve and brain reserve on cognition in Alzheimer disease. Neurology epub Dec 13.
Hart J, Kraut MA, Womack KB, Strain J, Didehbani N, Bartz E, et al. (2013). Neuroimaging of cognitive dysfunction and depression in aging retired National Football League players: A cross-sectional study. JAMA Neurology, 70 (3), 326-335.
Karantzoulis S, Randolph C. (2013). Modern chronic traumatic encephalopathy in retired athletes: What is the evidence? Neuropsychology Review, 23 (4), 350-360.
Lehman EJ, Hein MJ, Baron SL, Gersic CM (2012). Neurodegenerative causes of death among retired National Football League players. Neurology, 79 (19), 1970-1974.
Manley GT, Gardner AJ, Schneider KJ, Gukiewicz KM, Bailes J, Cantu RC, et al. (2017). A systematic review of the potential long-term effects of sport-related concussion. British Journal of Sports Medicine, 51 (12), 969-977.
McKee AC, Stein TD, Nowinski CJ, Stern RA, Daneshvar DH, Alvarez VE, et al. (2013). The spectrum of disease in chronic traumatic encephalopathy. Brain, 136 (1), 43-64.
Mez J, Daneshvar DH, Keiman PT, Abdolmohammadi B, Alvarex VE, Huber BR, Alosco ML et al. (2017). Clinicopathological evaluation of chronic traumatic encephalopathy in players of American football. Journal of the American Medical Association, 318 (4), 360-370.
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.
Omalu BI, DeKosky ST, Hamilton RL, Minster RL, Kamboh MI, Shakir AM et al. (2006). Chronic traumatic encephalopathy in a National Football League player: Part II. Neurosurgery, 59 (5), 1086-1092.
Randolph C, Karantzoulis S, Guskiewicz, KM. (2013). Prevalence and characterization of mild cognitive impairment in retired National Football League players. Journal of International Neuropsychological Society, 19 (8), 873-880.
Randolph C. (2014). Is chronic traumatic encephalopathy a real disease? Current Sports Medicine Reports, 13 (1), 33-37.
Schneider JA, Arvanitikas Z, Bang W, Bennett D. (2007). Mixed brain pathologies account for most dementia cases in community-dwelling older persons. Neurology, 69 (24), 197-204.
Webner, D & Iverson, G. (2016) Suicide in Professional American Football Players in the Past 95 Years. Brain Injury; 30 (13-14), 1718-1721.
Wen Y, Yang SH, Liu R, Perez EJ, Brun-Zinkernagel AM, Koulen P, et al. (2007). Cdk5 is involved in NFT-like tauopathy induced by transient cerebral ischemia in female rats. Biochimica et Biophysica Act, 1772 (4), 473-483.
Speaker bio-sketch: Dr. Christopher Randolph obtained his undergraduate degree from Vanderbilt University and his MS and PhD degrees from Rutgers/UMDNJ. He completed fellowships at the Clinical Brain Disorders Branch of the NIMH and the Experimental Therapeutics Branch of the NINDS. He served as the director of neuropsychology services at Northwestern and then Loyola University Medical Center for a total of over 20 years, prior to retiring from clinical practice in 2016. He is still Clinical Professor of Neurology at Loyola, and is the Chief Scientific Officer of MedAvante-Prophase. Dr. Randolph initially became involved in sports concussion research when he was asked to develop a concussion management program for the Chicago Bears in 1995, and he has published over 20 articles on the topic, including multiple articles on the short- and long-term risks of sports-related concussion and repetitive head trauma.
Practicing Clinical Neuropsychology in the Age of ‘CTE’
Kenneth Perrine, PhD, ABPP-CN
Associate Professor of Neuropsychology
Media attention to chronic traumatic encephalopathy (CTE) has developed heightened concern centering on the influence of concussion and sub-concussive blows both in athletic competition and everyday life leading to the development of a unique progressive neurodegenerative disorder. Despite the controversies in the scientific literature, the intricate pathology and clinical symptoms of CTE and TES are being accepted uncritically by the lay public. As a result, patients are self-educating themselves on concussions and the risks of developing CTE. Some are seeking out neuropsychological testing while harboring the fear of dying early from CTE. Clinical neuropsychologists are faced with the dilemma of how to approach these consultations. The proposed ideal consultation is a combination of brief neuropsychological testing and then reassurance that there is a highly unlikely possibility that the patient will develop CTE. The goal is to combat the fear brought on by media coverage of CTE through reassurance and understanding in addition to testing.
- Identify CTE and Traumatic Encephalopathy Syndrome (TES).
- Appreciate the difference between the scientific evidence and the media hype.
- Recognize the controversy surrounding CTE/TES and evidence for and against.
- Identify the overlap between TES and other neurodegenerative disorders.
- Apply the understanding that it is highly unlikely that a given patient will develop CTE/TES.
Iverson GL, Dirk Keene CD, Perry G, Castellani RJ. The Need to Separate Chronic Traumatic Encephalopathy Neuropathology from Clinical Features. J Alzheimer’s Dis 2017; 61:17–28.
McCrory P, Meeuwisse W, Dvorak J, et al. Consensus statement on concussion in sport—the 5th international conference on concussion in sport held in Berlin, October 2016. Br J Sports Med 2017; 51(11):838-847.
McKee AC, Stein TD, Nowinski CJ, et al. The spectrum of disease in chronic traumatic encephalopathy. Brain 2012; 136:43–64.
McKee AC, Cairns NJ, et al. The first NINDS/NIBIB consensus meeting to define neuropathological criteria for the diagnosis of chronic traumatic encephalopathy. Acta Neuropathol 2016; 131(1):75–86.
Stern RA, Daneshvar DH, Baugh CM, et al. Clinical presentation of chronic traumatic encephalopathy. Neurology 2013; 81:1122–1129.
Speaker bio-sketch: Dr. Kenneth Perrine is a board-certified clinical neuropsychologist affiliated with Weill-Cornell College of Medicine NY Presbyterian Hospital/Weill-Cornell since 1999. He received his undergraduate degree in Psychology from Cornell University and his Ph.D. in Clinical Psychology from the University of Kentucky. He completed an internship & later worked as the staff neuropsychologist at the VA Hospital in East Orange, NJ. He is currently a Clinical Neuropsychologist at NYP/Weill-Cornell Medical Center, and an Associate Professor of Neuropsychology in the Dept. of Neurological Surgery at Weill-Cornell College of Medicine. He sees patients for pre-surgical evaluations prior to surgery for epilepsy, Parkinson's disease, and tumor resection, as well as a variety of other disorders to determine the presence, breadth and extent of cerebral dysfunction for treatment planning. He is part of the Pediatric Concussion Clinic for which he sees children with mild TBI or concussions, and is also the consulting neuropsychologist for the NY Jets and the NY Islanders sports teams where he evaluates players with concussions. His clinical work and research interests include clinical neuropsychology, epilepsy, movement disorders, dementia, traumatic brain injury/concussion, brain tumors, and other conditions affecting cerebral functioning.
The mission of the New York Neuropsychology Group (NYNG) is to provide and foster educational opportunities for the study of brain-behavior relationships within the New York metropolitan region and to promote the general interests of scientists and clinicians in related disciplines at all stages of professional development. Toward this end, NYNG seeks to host academic seminars and conferences; sponsor informal activities that provide opportunities for professional networking; and establish a structure for the organization and dissemination of information regarding training and educational opportunities for both students and seasoned professionals.
Spring Conference Committee
Jason Krellman, PhD, ABPP, Chair
Elise Caccappolo, PhD, ABPP
Amy Weinstein, PhD
NYNG Board of Directors
Elise Caccappolo, PhD, ABPP, President
Ann DeSollar, PhD, Secretary
Peter Pramataris, PsyD, Treasurer
Bryan Freilich, PsyD, ABPP, Membership
Vanessa Guzman, MS, Student Rep
Heidi Bender, PhD, ABPP
Christopher Christodoulou, PhD
Chaya Gopin, PhD, ABPP
Dora Kanellopoulos, PhD
Jason Krellman, PhD, ABPP
Frank LeFever, PhD
Luba Nakhutina, PhD, ABPP
Christina Palmese, PhD, ABPP
Julia Rao, PhD
Stacey Snyder, PhD
Amy Weinstein, PhD