New York - In the legal equivalent of an all-out blitz, multiple lawsuits were recently filed against the National Football League (NFL) in Atlanta, Miami and New York federal courts.
Plaintiffs, all retired players, claim neuropsychological damages caused by head traumas sustained during their professional playing years. Part of the tort is alleged negligence: They assert that the NFL intentionally withheld knowledge of the long-term effects of concussion on cognition, personality and neurological health.
Those following this case should expect a prominent public display of a number of modern controversies in the clinical neurosciences, and in particular the focus of this piece: clinical neuropsychology.
This article is a game plan, intended to help understand and evaluate the general scientific issues and neuropsychological evidence likely to be presented by both sides. With an eye on the U.S. Supreme Court Daubert decision, which regulates the admission of scientific evidence in federal courts, the anticipated evidentiary pattern will be broken down into the known, the unknown and the dubious. But first, a working vocabulary.
Basic Definitions
The legal cause of action is a concussion, an injury from the mild end of the head trauma continuum. The term “concussion” is often misused as synonymous with “brain damage.” A concussion refers to a brief interruption of brain function after head trauma. Its Latin root means “violent shaking,” not destruction.
Head trauma becomes concussion if followed by one of two behavioral signs of altered consciousness: Either a brief period of unconsciousness, typically minutes in duration, or an interruption in the ability to form memories or recollect events even if awake with eyes open, typically of several minutes duration but most often less than one hour.
This brings us to the term mild traumatic brain injury, or “mTBI”, a term often casually interchanged with concussion. The U.S. Department of Defense Clinical Practice Guideline advocates for uniform use “concussion” over “mild TBI” to avoid misperception and lumping with more severe traumatic brain injuries.
Because TBI is closer to the layman’s understanding of “brain damage,” the use of “mild TBI” may leave the misimpression of permanent mild changes to brain matter. Concussion is preferred because it refers to a physiological injury to the brain, meaning reversible changes in the chemistry of brain cells, but without obvious damage to brain matter. Take the example of a player who is lying on the field, knocked out cold (unresponsive). He gets up after a few moments, and walks off the field. [1]
In contrast, more severe traumatic brain injuries involve longer interruptions of brain function after head trauma, but are usually accompanied by readily observable changes in brain structure. Sudden changes include bleeding, bruising and shearing of brain tissue that is best appreciated as visible lesions on a brain CT or MRI scan, but not in every case.
Such TBIs are associated with longer impairment of consciousness, a wider range of severities, from moderate to catastrophic, and longer periods of disability. Unlike concussion, active medical intervention is often necessary to reverse or limit the damage, such as neurosurgery, drugs to reduce brain swelling and sedation to control disorganized behavior.
The Damages Question: Tailor-Made for Neuropsychology?
Granting that professional football-related concussions are often well documented — games are televised, and and games and practices are filmed by a team’s coaching staff — the plaintiffs must prove two things: that they actually have life-altering cognitive problems, and that these are linked to the concussions sustained during their NFL careers.
These two issues are well-suited to be informed by neuropsychologists, the first more easily then the second.
Neuropsychological examinations and the test scores they yield provide an objective way of assessing a player’s cognitive functioning and emotional adjustment relative to persons of the same age, in a reasonably certain way. Cognitive domains of interest include memory, problem-solving, behavioral control and decision-making, processing tempo and language, and hand-eye coordination.
Age- or education-graded normative data (norms) provide context for the score in qualitative schemes such as superior, average, borderline, weak or abnormal. The characterization of score standing is crucial, as is the reminder that scores cannot be “impaired,” only people can.
This reminder segues to the more difficult problem: the interpretation of low scores.[2] While there are few potential explanations for high scores other than intact abilities, there can be numerous potential neuropsychological explanations for the appearance of low scores, much as physicians may present multiple explanations for any particular medical symptom.
For example, take an abnormally low memory score in an allegedly concussed player. Reasons for this low score could certainly include brain damage associated with individual or cumulative concussions as alleged.
The abnormal score might alternatively be caused by pre-existing intellectual limitations, learning disabilities, substance abuse, medication effects, mood disorders or daytime fatigue caused by sleep apnea, either alone or in combination. Dementia of nontraumatic origin also cannot be ruled out in older plaintiffs. Most persons who developed dementia, of course, never played football or other contact sports.
Test-taking effort could also be raised as a counterfactual to claims of brain damage due to football-related concussions. Low test scores can be caused by insufficient test-taking effort (not trying hard enough) or high effort to look impaired (malingering) in a context where there is clear financial gain.
The American Academy of Clinical Neuropsychology Consensus Statement considers it standard practice for neuropsychologists to evaluate effort and validity in clinical, disability and forensic matters.[3]
Questionable effort in athletes is not simply theoretical; quarterback Peyton Manning admitted tanking his baseline cognitive test battery, to ensure that postconcussion testing gave a good result, allowing return to play and pay.[4]
There are other reports of professional and amateur athletes intentionally suppressing performance on baseline testing to decrease the probability that they might be identified as brain injured if tested following a concussion sustained on the field of play.
Value of Self-Report
A symptom is a self-report of a private experience; it is subjective. Memory loss and other cognitive symptoms of players could be claimed as evidence of brain dysfunction.
Plaintiffs may point out that NFL players differ from everybody else only in their history of multiple traumatic injuries, thus their memory complaints must be attributable to those injuries. The defense may point out that football players differ in other ways from the general population, and not just in their concussion histories.
Clinical neuropsychologists view self-report of cognitive symptoms as ambiguous, a diagnostic clue only. This is termed the “nonspecific symptom” problem. Besides concussions, football players unarguably differ in other ways.
For example, thick necks, large chests and obesity increase risk for obstructive sleep apnea syndrome, a condition associated with daytime memory and concentration problems.
Further, particular player-plaintiffs may not be representative of the serially concussed population. Examples might include histories of brain-impairing lifestyles, such as drinking and drug abuse (see Boogaard example below), brawls and steroid use.
Next follows a description of what is generally accepted by neuropsychologists, what is uncertain and what is taken on faith but of dubious validity.
The Known: Single Concussions
The outcome of a single concussion is well-established and beyond reasonable dispute in the neuropsychology community. Single concussions resolve quickly and spontaneously. There is no proven medical or psychological method for speeding up the recovery process. There exist only old chestnuts like “rest and avoid mental activity for a while.” But such recommendations have not proven helpful, may actually be harmful and have no demonstrated clinical utility.
The neuropsychologist-run Three Center Study in the 1980s showed that concussions cause quantifiable memory and attention deficits that normalize with repeat testing between one to four weeks.[5] A World Health Organization meta-analysis was unable to identify neither any long-term cognitive deficits nor any neurological reason for persistent symptoms beyond a half year, but found litigation and personal problems more influential.[6]
A study of NFL players found no residual cognitive change after concussion from the 1996-2001 seasons.[7] Studies of collegiate football and hockey players have consistently supported the contention that single concussive injuries are relatively benign, resolving and self-limiting events.[8]
There is convergent evidence that the physiological and behavioral changes associated with concussions completely resolve in about seven days. There is also evidence that persistent complaints are overwhelmingly more closely linked to pain, sleep disturbance, psychiatric factors, negative expectation or secondary gain, as opposed to actual changes in brain structure or function.
The Unknown: Multiple Concussions
The key dispute in the NFL litigation will center on plaintiff’s argument in chief: Serial concussions leave subtle brain traces that slowly accumulate, cross a critical threshold and leave disabling cognitive deficits. In some of these complaints, the accumulation will be alleged to have led to dementia. On this issue, the research evidence is incomplete, albeit promising.
The brains of some deceased players are said to show distinct changes caused by cumulative traumas. Simple visual inspection of the brain shows large areas of brown discoloration, rather than grey-pink, reflective of widespread neural degeneration.
Chemistry shows the brown staining is due to excessive tau proteins, interpreted to result from the body’s failed efforts to repair brain damage. Researchers have coined chronic traumatic encephalopathy (CTE) as these findings have emerged in recent years. Plaintiff litigants are touting the power of an identified condition, CTE, to give momentum to their claims.
Whether trauma is a necessary or sufficient element of diagnosis is the legitimate question that defense efforts would raise in response, for no reliable signs of accumulated trauma nor other signs or symptoms appear to predict CTE prior to post-mortem study. Proposed clinical signs such as “aggression” are unhelpful because they occur so frequently in football players, are socially cultivated in training and may be reported in hindsight in the context of litigation or wrongful death claims.
To date, research on CTE by necessity encourages scientists to hunt down cases that confirm a theory, with less emphasis on cases that might falsify it. A Boston group advocating about awareness of CTE energetically pursues the brains of athletes whose unanticipated deaths occurred in dramatic circumstances or were heavily publicized, e.g., suicide.[9]
In scientific parlance, the cases may be “self-selected” rather than representative. Research has not yet resolved whether selection bias could inflate the link between sports concussion and brain damage, if in reality a weak or no link exists.
Unbiased research may turn the uncertain into the certain. A key development would be better proof of specificity: A landmark study showing CTE absent in athletes or nonathletes with histories of other pathology — drinking, drugs, steroid abuse or other medical conditions — but without serial concussions.
Only when other forms of causation are ruled out is the adjective “traumatic” in CTE truly applicable.
The Dubious: “Second Impact Syndrome”
Another concept expected to air during the litigation is Second Impact Syndrome (SIS). SIS describes rare sudden death shortly after a second concussion, typically separated by days from the first. SIS may be used at trial to prove that multiple concussions, in fact just two, are sufficient to cause long-term changes. There is nothing more long-term than death, so a jury could find believable a neurological condition short of that.
Fears of SIS have generated a cottage industry of computer-assisted cognitive screening tests, created for physicians, trainers and psychologists to test and retest concussed athletes and track mental recovery. The player returns when his/her score rises to a predetermined threshold.
Subscriptions to the software are expensive, but anxious parents and coaches pay, responding to the hook that SIS is preventable only with their particular product and return-to-play recommendations based upon same.
To date, there is little evidence that SIS exists, beyond bystander anecdotal accounts that make for interesting reads from investigatively minded news media. At the same time, slow brain swelling from a single minor trauma, causing death or impairment within days to a week, is a very rare but well-documented condition, typically seen in children. A second trauma, if it happens at all, could simply result from falls or other lapses caused by ongoing brain swelling.
Most problematic for SIS proponents is the huge gap in the epidemiological data pattern: no documented SIS deaths in the NFL or National Hockey League (NHL), ever. Additionally, deaths attributed to SIS are not reported in commonwealth countries, where helmetless rugby and other contact sports is the norm. It would literally take 18 million neuropsychology “concussion tests” to prevent just one case of SIS, assuming it exists.[10],[11]
Case Example
The case of Derek Boogaard illustrates some of the complexities to anticipate. A Minnesota hockey player known in the NHL as an “enforcer,” he sustained a number of concussions through fighting and hard play. He was only 28 when he died via drug overdose in May 2011.
A neuropathologist concluded that his brain showed CTE changes, and speculated further that middle-age dementia was inevitable were it not for his premature death. It was reasoned that because of young age, Boogaard’s brain problems were not caused by the aging process, proof that cumulative concussions are sufficient to cause damage.
However, Boogaard’s life history contained other brain-impairing factors. Boogaard consumed prodigious amounts of narcotics and alcohol. One news account described him as chewing eight Oxycontin at a time, and visiting many separate doctors for prescriptions.[12]
Conclusions
The neuroscience issues central to the NFL players’ suit — settled, unsettled and dubious alike — that will likely be raised at trial may include admissibility of neuropsychological opinions, outcome of single versus serial concussions, CTE and SIS. Additional battleground issues could be selection bias undermining the validity of CTE, and the interpretation of cognitive symptoms in plaintiffs with serial concussions but complex personal lives.
The fulcrum of the scientific discussion will center on (1) whether a cognitive score is normal and (2) the causal interpretation if abnormal. “Keeping score” requires rating the care and diligence with which the neuropsychologist places scores in a broad life-history context.
Both plaintiff- and defense-selected neuropsychologists should be judged by their balanced approach. That means identifying, detailing and weighing the factors that might reasonably explain abnormal findings. Those factors should include — by illustration, not exclusion — the number and severity of concussions from high school to the pros, test-taking effort, drug and alcohol use, sleep disorder, innate intelligence, vascular health and family neurological history.
A forensic science approach that reflects appropriate diligence and objectivity employs a causation analysis takes into account any factors known to have reasonable association with brain health.
The reader should find that neuropsychologists are as easy to rate as football players. Woe the receiver who drops an easy pass, the plaintiff neuropsychologist who views any squiggle in test data as evidence for brain damage and the defense neuropsychologist who treats anything short of total sobriety as a “gotcha moment.”
The best neuropsychology interpretation is not one that fits the facts, but fits the best facts.
[1] Department of Veterans Affairs, Department of Defense. April, 2009. VA/DoD clinical practice guidelines for management of concussion/mild trauma brain injury.
[2] M Lezak et al, 2004. Neuropsychological assessment, fourth edition. New York, Oxford.
[3] American Academy of Clinical Neuropsychology Consensus Conference Statement on the Neuropsychological Analysis of Effort, Response Bias, and Malingering, 2009. The Clinical Neuropsychologist, V23, 1093-1129.
[4] ESPN Archives, Interview of April 27, 2011. Manning said “[After a concussion] if you do worse on the second test than the first, you can’t play. So I just try to do badly on the first test”.
[5] H Levin et al, Neurobehavioral outcome after minor head injury: A three-center study. Journal of Neurosurgery, V66, 234-243, 1987.
[6] LJ Carroll, et al,, 2004, Methodological issues and research recommendations for mild traumatic brain injury: the WHO Collaborating Centre Task Force on Mild Traumatic Brain Injury. Journal of Rehabilitation Medicine, (Suppl. 43), 113–125.
[7] E Pellman et al, 2004, Concussion in professional football Part 6 – neuropsychological testing. Neurosurgery, V55, 1290-1305.
[8] M McCrea, 2008, Mild traumatic brain injury and postconcussion syndrome. New evidence base for diagnosis and treatment. Oxford Press AACN book series.
[9] www.bu.edu/cste/
[10] C Randolph, 2011, Baseline Neuropsychological Testing in Managing Sport-Related Concussion: Does It Modify Risk? Current Sports Medicine Reports, January/February 2011 - Volume 10 - Issue 1 - pp 21-26
[11] PR McCrory & SF Berkovic, 1998. Second impact syndrome. Neurology , V50, 677–83.
[12] J Branch, “Derek Boogaard: A brain gone bad”. New York Times, December 5th, 2011.
Dr. Manfred Greiffenstein is a neuropsychologist with The Forensic Panel and is board certified in clinical neuropsychology, forensic psychology and sleep disorders medicine.
Dr. Jack Spector is a neuropsychologist consultant to The Forensic Panel and is board certified in clinical neuropsychology.
Dr. Michael Welner, a forensic psychiatrist, is chairman of The Forensic Panel. He is board certified in forensic psychiatry and psychopharmacology.
