The recent death by suicide of Junior Seau of the San Diego Chargers is only one of many suicides in the NFL. O.J. Murdock, a 25-year-old wide receiver for the Tennessee Titans, died from a self-inflicted gunshot wound. These individuals showed no apparent signs of being unable to carry out their daily functions and responsibilities in their lives prior to these tragic events. Dave Duerson had committed suicide similar to Junior Seau by shooting himself in the chest. Seau wanted his brain donated to science as did Duerson.
In 1978 Lezak described alterations in personality after traumatic brain injury, including impaired self-control and regulation , emotional change and inability to learn from social experience. These deficits impair the ability of individuals to engage in acceptable social interactions and create a high potential for alienation from others. One wonders how much of the current and past epidemic of domestic violence in the NFL is linked to personality change in traumatic brain injury. Moreover, aside from traumatic brain injury is the phenomenon of posttraumatic stress disorder, which does not even seem to be addressed by the NFL, high school sports, or the NCAA. PTSD is the result of an individual being a victim of violence or witnessing violence that results in intrusive thoughts of the violent event or traumatic dreams. The structures in the brain regulating anger are changed. There is increased activity in the noradrenergic activating system, which increases arousal. Moreover, these individuals go around in a state of heightened arousal and vigilance in their surroundings. PTSD takes a chronic course. Thus, to view the suicides of the players in the NFL as solely the result or not the result of football is to ignore the facts of their being participants in an extremely violent sport.
Of relevance is the fact of where on the head is the impact of the trauma. For example, focal trauma to the tips of the frontotemporal lobes, inferior orbitofrontal regions, or frontal convexities may occur without neuroradiological evidence of injury and yet may have devastating clinical ramifications for the patient and the family (Jenkins et al. 1986; Langfitt et al. 1986; Wilson and Wyper 1992). Diffuse axonal injury is the underlying pathophysiological change accompanying traumatic brain injury (TBI) regardless of severity (Meythaler et al. 2001 ; Strich 1956, 1961). Diffuse axonal injury results in a "unplugging" of neural networks from one another with a decrease or loss of the associational matrix within the central nervous system. Thus, conversation and problem solving sequences are affected. Moreover, if a player is impacted and the point of force of the impact is in the frontal lobe of the brain , then reasoning , creativity, and impulse control are affected. The study involving Phineas Gage described by Harlow in 1868 describes Gage, who was a 19th century railroad worker experiencing a penetrating brain injury with a tamping rod had personality alteration described as apathy, disinhibition, lability, and loss of appropriate social behavior. There were profound personality changes in Phineas Gage. He became impulsive, irritable, and irresponsible as compared to being a responsible, compulsive individual in the past.
Agitation and confusion follow brain injury and can be present for years after the traumatic brain injury. Thus, a current event (for example, a player being injured in a game) the devastating effects of this are sometimes only evident years later, such as dementia, in players occurring many years after they are out of competition. A good example is John Mackey of the Baltimore Colts, who was on the offensive line of the Colts. He was asked to identify another individual who had played on the offensive line with him and was simply unable to even recognize the other individual. More recently Jim McMahon of the Chicago Bears complained of memory deficits, disorientation, and confusion. Why isn't the NFL providing supportive programs for he and people like him?
There are neurochemical changes in PTSD and TBI; namely, dysregulation of many neurotransmitter and neurochemical pathways in PTSD. In the setting of TBI there is a storm of neurotransmitter release, and the increase in serotonin is associated with depression of cerebral glucose utilization in areas damaged by TBI. The fallout is cognitive symptoms due to problems with declarative memory and the rhinal hippocampal function as well as executive function involving the frontal subcortical circuits. There is a resultant decreased synthesis as well as a loss of acetylcholine neurons (Schmidt and Grady 1995). Thus, in summary, PTSD is associated with a number of neurochemical changes and is a distinct neurobiological disorder with devastating biological consequences for the individual. TBI also involves damage to the prefrontal cortex and there may be impairment to the capacity to regulate the fear reaction .
The most compelling finding on structural and volumetric studies of PTSD patients related to us by Silver et al. (2010) is the observation of hippocampal atrophy. This was observed not only with volumetric studies but also magnetic-resonance spectroscopy studies in which reductions in N-acetylaspartate correlate with reduced density or viability of neurons. There have been many volumetric studies of hippocampal atrophy in PTSD. Again, this is one of the many neurological signs of neurological damage in an individual from participation in violent sports. The message is that individuals in violent sports such as the NFL are at risk for these devastating injuries. One wonders why the players are apparently not advised about the sequelae and the tremendously damaging effects in their future lives.
After brain injury, patients often experience agitation and confusion that may last for days to months. Characteristic features of aggression after brain injury are: reactive, wherein anger can be triggered by modest or trivial stimuli; nonreflective, involving no premeditation or planning; nonpurposeful, where aggression serves no obvious longterm aims or goals; explosive, where a buildup is not gradual; and, periodic, brief outbursts of rage and aggression punctuated by long periods of relative calm. These episodes of aggression are ego dystonic. Patients are upset and horrified at their behavior and embarrassed after these incidents. Outbursts of rage and violent behavior occur after damage to the inferior orbital surface of the frontal lobe and anterior temporal lobes. Thus, again, there is an overemphasis currently on discussion of "hits" on players and an underemphasis on the neurological damage from hits to particular areas of the brain and long-term consequences. In fact, damage to the amygdaloid area has resulted in violent behavior (Tonkonogy 1991). Injury to the anterior temporal lobe, which is a common site for contusions, has been associated with a dyscontrol syndrome wherein patients exhibit emotional lability, impairment of impulse control, and suspiciousness.
The key clinical points are that aggressive behavior and irritability are common after traumatic brain injury. Moreover, depression is the most common comorbid disorder. Depression is magnified after brain injury. This coupled with decreased emotional control due to the TBI and/or PTSD renders individuals more vulnerable to episodes of suicide.
Cognitive domains commonly impaired after closed TBI are attention, memory, executive function , language, and communication. Information processing speed is adversely affected as well as executive or supervisory control aspects and, in particular, short-term memory. TBI commonly disrupts working memory needed for day-to-day functions. This results in forgetting to take medications, attending appointments, making bill payments, and jeopardizes one's capacity for independent living. Jim McMahon currently is struggling with the impact on himself due to his football career and this impacting his independence in his life. Moreover, impairments of attention are the most prevalent findings after TBI, and the most robust finding is reduction in processing speed . Thus, an individual is unable to scan, interpret, and process information as he usually does.
There are a number of key clinical points which were made by Meyer et al. in traumatic brain injury (2011 ). These points are as follows:
Traumatic brain injury is a dynamic, unfolding, evolving process. It is much more than an "at the moment" event on the sideline after a play. Silver et al. (2011) report that even individuals who are asymptomatic several days after a mild concussion with no loss of consciousness can have impaired processing speed. This was also noted by Warden et al. (2001).
Postconcussive symptoms refer to common symptoms encountered that can be grouped into three categories: cognitive and somatic complaints and affective complaints (Le., depression, irritability, and anxiety). In the immediate post-injury period, 80-100% of mild brain injury patients describe one or more symptoms, as reported by Levin et al. (1987). Even at three months after injury, many studies suggest surprisingly high rates of symptoms, such as reported by Rimel et al. (1981). Even after one year several studies suggested a surprising rate of symptoms after moderate traumatic brain injury (MTBI). In some studies, almost one-third of the individuals had even moderate or severe disability measured by the Glasgow Outcome Scale and another third had some disability on the Edinburgh Rehabilitation Status Scale.
Psychotic symptoms can occur after brain injury even though rare, occurring within 0.07-9.8% of brain-injured patients (Davis and Bagley 1969; Kwentos et al. 1985).
Of relevance to the cases of Junior Seau and Duerson, depressive symptoms are a common complications of mild brain injury (see Busch and Alper 1998 for review). Fann et al. (1995) reported that 29 of 50 individuals who had an MTBI 26% of the sample met criteria for major depression. Moreover, TBI-related mania can occur after MTBI with racing thoughts, agitation, and heightened activity level. Moreover, there is an increasing awareness of the relationship between PTSD and mild or severe brain injury.
Functional imaging techniques, such as PET, SPEeT, and fMRI , show promising clarifying underlying pathophysiological physiology of the sequela of MTBI. fMRI capitalizes on the fact that oxygenated and deoxygenated hemoglobin differ in their magnetic properties. What we do know from brain studies is that clear evidence of brain injury can be seen in many patients with a history of mild brain injury. Moreover, Schoenhuber and Gentilini (1989) suggested that approximately 10% of patients with mild brain injury have persistent electroencephalogram (EEG) abnormalities.
In cases, such as with Junior Seau, individuals such as he have a lower lack of control over emotions and behavior than the average person. This is because of the nature of brain injuries and the effect on emotional control from neurological deficits in the brain. For example, the phenomenon of pseudobulbar affect can occur in which individuals can be tearful, depressed, and sad and yet have no reason why they are feeling this way. These symptoms are caused by neurologically driven phenomena. Thus even to the athlete, they are enigmatic and difficult to fathom .
It is hoped that this article sheds light on the horrific string of suicides as well as the spate of domestic violence in the NFL and professional sports, and, in particular, violent sports. It seems as though there is one tragedy after another, yet administrative bodies, such as the NFL and the NCAA, are only beginning to definitively address these areas. For example, even though the research has been around about the effects of brain injury since the '70s, the NFL's position is that it really didn't know about the effects of these brain injuries on players. This is difficult to believe because the literature is what it is and has existed for many years. Certainly, at the very least, players in competition have the right to know about the adverse impacts on their independence, their lives, their futures, their relationships, and their families. The players can then weigh the risk against these horrific and devastating impairments facing them in their futures. The NFL outlawing below-the-knee hits due to Brady and focusing more on safety is a step in the right direction.
It is hoped that the NFL and the NCAA would adopt gold-standard SLAM technology and adopt preseason and postseason cognitive testing such as at the Combine. If there is no baseline of neurological functioning with players, then how is one to gage their cognitive status down the line? The NCAA is only beginning to address this area. In the meantime, players deserve no less than a hard look at safety issues and the stepping up of the NFL and the NCAA to the findings of science, embracing these, and doing all they can to address these issues. This is particularly important in players' later lives when they are faced with tremendous disabling issues from TBI and PTSD associated with game violence. The real question is, "Can we do enough or have we done enough?" One must first see a robust neuropsychological assessment program for athletes as well as use of gold-standard technologies and relate these to decision-making and return-to-play paradigms. The players deserve no less than this!
Jenkins, A. , Hadley, M. D. M., Teasdale, G., et al. Brain lesions detected by magnetic resonance imaging in mild and severe head injuries. Lancet, 2:445-46, 1986.
Langfitt, T. W., Obrist, W. D., Alavi, A. , et al. Computerized tomography, magnetic resonance imaging and positron emission tomography in the study of brain trauma: Preliminary observations. J. Neurosurgery, 64:760-67, 1986.
Silver, Jonathan M. , et al. Textbook of Traumatic Brain Injury (2005). American Psychiatric Press.
Meyer, et al. Sports injuries in Silver, Jonathan M., et al. Textbook of Traumatic Brain Injury (2011). American Psychiatric Press.
Levin , H. S., High, W. M., Goethe, K. E., et al. The neurobehavioral rating scale: assessment of the behavioral sequelae of head injury by the clinician . J. Neurol Neurosurg Psychiatry, 50:183-93, 1987.
Dr. Perrotti received his PhD in Clinical Psychology from Alliant University in San Diego, CA. He is a licensed psychologist in California and Pennsylvania. Dr. Perrotti is a member of the National Register of Health Service Provider in psychology and the National Academy of Neuropsychology. He was an Assistant Professor of Psychiatry and Behavioral Sciences at the Keck School of Medicine, USC from 2005-2006. Dr. Perrotti is the author of numerous publications in forensic psychology and assessment, traumatic brain injury in college, professional sports and military populations, and child trauma and complex PTSD.
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