CTE and its violent underpining

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Google images – CTE
WESTBOROUGH, MA January 20, 2018 More is becoming known about Chronic Traumatic Encephalopathy or CTE.  It is now able to be diagnosed prior to the death of the patient by identifying unique protein markers in the blood of those who have sustained multiple brain injuries.  Former professional wrestler Chris Benoit was found to have CTE after killing his wife and son before killing himself in 2007. But murder or other violence against others has not typically been associated with CTE until recently.  As recently as summer, 2017, the brain of former N.E. Patriots star Aaron Hernandez was also found to have signs of severe CTE raising the specter of its possible impact on his violent life and eventual death by suicide. I have posted post-mortem photos of his brain first published on the Boston University site in a prior blog on my Concussion site (Sefton, 2017).  See that post by clicking here.  It is now understood that an athlete need not have sustained numerous concussions in his career to be found to have CTE at time of death.  More so, the accumulation of repeated blows to the head – subconcussive force – is being implicated in the etiology of this complex disease process. So contact sports like football, rugby and ice hockey are being closely scrutinized by experts in concussion, athletic training and sports medicine.  Researchers at BU School of Medicine have reported that a protein known as CLL11 may be elevated in the brain and spinal fluid of athletes with a history of brain injury.  It holds some promise of being able to diagnose athletes before death.  This protein leads to elevate Tau protein a known cause of progressive brain damage associated with dementia.
In 2014, The K.C. Star reported that analysis of Belcher’s brain after he’d been exhumed revealed a key signature of chronic traumatic encephalopathy, best known as CTE, a degenerative brain disease found to cause dementia, confusion, depression and aggression). “Belcher’s murder-suicide is the worst possible example of domestic violence, and these findings come as the NFL is under attack for its handling of domestic violence.” (Mellinger, 2014 Kansas City Star). 
“CTE has been found to cause erratic and sometimes tragic behavior by some NFL players, perhaps most notably Hall of Fame linebacker Junior Seau, who killed himself last year. The disease, only recently diagnosable before death, has often been found in former and longtime football players.” Mellinger, 2014 K.C. Star
 Riding a bicycle is a leading cause of brain injury in childhood. Recently, CTE has not been diagnosable before death. It has been found over and over in former and longtime football players. Domestic violence behaviors cut across all socioeconomic strata.  They germinate in an environment of secrecy often early in courtship.  During this time abusive spouse slowly isolates his intimate partner from her support – family, friends, finances.  “In doing so there is a subtle but undeniable manipulation of control – usually coupled with threats and intimidation.  There is growing awareness that red flag behaviors precede DV and domestic violence homicide.  Things like pathological jealousy, forced sexual contact, manipulating friendships, detachment from members of immediate family and others are the early signs of domestic violence.” (Sefton, 2012)  Some believe that the most significant pre-incident red flag is whether or not the victim truly believes she is going to be killed by her intimate partner one day and that these victims are at most risk of death.

Sefton, M (2012) Athletes and Celebrities Not Immuned: Kansas City Chief’s player kills wife and self in act of DVH, Blog post December 1, 2014, taken December 28, 2017. 
Sefton, M. (2017). Brain and Behavior: B.U. scientist says Aaron Hernandez had CTE. Blog post, Nov 19, 2017 Taken December 28, 2017
Read more here: http://www.kansascity.com/sports/nfl/kansas-city-chiefs/article2296030.html#storylink=cpy
Read more here: http://www.kansascity.com/sports/spt-columns-blogs/vahe-gregorian/article187534063.html#storylink=cpy
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CTE found in teenage brains by B.U. team

WESTBROUGH, MA January 18, 2018 The scientists studying the damaged brains of older athletes have had the opportunity to study brain damage in athletes who died from other causes.  In 4 such cases, there was evidence of chronic traumatic encephalopathy (CTE) that was not commensurate with the degree of brain trauma that was observed during their athletic careers according to Felice Freyer of the Boston Globe. This recent study was published in the journal Brain illustrates that the onset of CTE may be closer to onset of brain injury than first thought not much later in life.
“The report, published Thursday in the journal Brain, also provides what Goldstein called “the best evidence to date” supporting the theory that CTE is caused not just by concussions, but rather by any blow to the head, including mild impacts. Instead of diagnosing and responding to concussions, he said, coaches would do better to protect children from all hits to the head.” Felice Freyer – Boston Globe 1-8-18
The possibility of younger athletes developing CTE and the symptoms associated with this progressive disease is quite worrisome especially to parents.  It was always thought that CTE would develop later in life if at all. With the prospects of the disease having a much earlier onset the cost of CTE over a lifetime is incalculable in terms of medical costs and neuropsychological sequelae that may evolve in time. The true impact of this and the consequence for repeated, subclinical blows to the head is only now becoming clear.
Like dementia of the Alzheimer’s type the build up of tau protein underlies the changes associated with CTE. “Chronic traumatic encephalopathy is a condition bringing forth progressive tauopathy that occurs as a consequence of repetitive mild traumatic brain injury. We analysed post-mortem brains obtained from a cohort of 85 subjects with histories of repetitive mild traumatic brain injury and found evidence of chronic traumatic encephalopathy in 68 subjects: all males, ranging in age from 17 to 98 years (mean 59.5 years), including 64 athletes, 21 military veterans (86% of whom were also athletes) and one individual who engaged in self-injurious head banging behavior” according to the journal Brain. McKee, A. et. al. 2017

McKee, A. et. al. (2017) The spectrum of disease in chronic traumatic encephalopathy. Brain, Volume 136, Issue 1, 1 January 2013, Pages 43–64, https://doi.org/10.1093/brain/aws307

Neurological trauma and enduring change in survivors

Westborough, MA December 18, 2017 The British Medical Journal Lancet recently published a series of articles describing the long-term effects of brain trauma. The series is worth a serious read for those who are in the position to take care of trauma patients.

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There has been little change in our approach to handling the individual grind of caring for the TBI patient I must sadly admit.  Young and old it takes both patience and dedication to achieve the best outcomes with those we bring into our treatment continuum. “Survivors experience a substantial burden of physical, psychiatric, emotional, and cognitive disabilities, which disrupt the lives of individuals and their families, and pose huge costs to society” according the Lancet, 2017.  Many readers have read my post Updates in these pages where I have detailed well-known athletes like Formula 1 car driver Michael Schumacher and Mike Towell, the Irish boxer both of whom were seriously injured from TBI.  Towell died from injuries linked to second impact syndrome following a match in 2016.
Schumacher remains in a minimally conscious state in Switzerland.  He is conscious but does not speak or move about.  He requires 24 hour medical care and is living is a special suite adapted in his home that allows him to continue to receive the best care possible while being in his familiar setting surrounded by family and friends.  The cost of his care exceeds $ 100,000 per month.
Some reports suggest Mr. Trowell had sustained a brain injury in the early rounds of the fight.  “Essentially, “second impact syndrome” or SIS results from the brain’s inability to autoregulate cerebral perfusion pressure and swelling as a result of repeated cerebral trauma.” Sefton, 2016 on second impact syndrome and Mike Trowell
Autonomic regulation is the role of the brain stem that maintains the diurnal pattern of arousal for wakeful activity and sleep hygiene.  The brain stem regulates heart rate and respiratory drive as well.  These functions are vital to survival and comprise the autonomic nervous system.  The ANS functions as the brain and body’s alarm system signaling the need for fight-flight activation according to a Autonomic Storming post by Michael Sefton, Ph.D.
Lancet identifies the complexity of TBI and its multifactorial underpinning.  A growing number of patients are elderly that contribute to “heterogeneity of outcomes and consider ways forward for targeted management of severe TBI in the intensive care unit” as mentioned in the 2017 Lancet summary.  Improved management of TBI in the trauma centers and ICUs bring forth better rehabilitation candidates and better outcomes including return to home and eventually return to preinjury employment for many.  Surgical intervention crafted to decrease secondary injury to brain have been enhanced by improved diagnostic accumen, imaging and novel techniques such as radical craniectomy and cranioplasty for management of intracranial pressure and its associated edema.
The series also explains PSH or “autonomic storming” something that I have described in several posts and can be quite serious both in the trauma canter and later in the rehabilitation hospital   “Geert Meyfroidt and colleagues provide an overview of paroxysmal sympathetic hyperactivity, a consequence of acute brain injury, and discuss the promise of improved characterization and implications for management”. Damage to the system that regulates sympathetic and parasympathetic functioins due to traumatic brain injury can be unsettling for familiy members and clinicians alike. The recovering subject can have wild swings of autonomic arousal such as elevated heart rate – patients sometimes chug along at 140-160 while autonomic storming.  Paroxysmal changes in blood pressure may pose significant risk, respiratory rate may become tachypnic, patients frequent are febrile and may become excessively sweaty  as a consequence of autonomic dysfunction.  Patients in our rehabilitation frequently undergo repeated blood cultures and lab studies looking for a source of infection.  Many are returned to the trauma centers for additional brain imaging studies and cardiac monitoring that takes hours and is often unneccessary.  These procedures delay recovery and add confusion to the patient and his family.
The regulation of the secondary injuries such as paroxysmal sympathetic hyperactivity is essential for patient well-being and outcome measures including returning home and re-entering the work force. The Lancet series is a well written update on current brain injury treatment and management of this serious public health threat.

 Lancet Neuology (2017) Jun;16(6):452-464. doi: 10.1016/S1474-4422(17)30118-7. Traumatic Brain Injury. Taken 12-18-2017.

Brain and Behavior: B.U. scientist says Aaron Hernandez had CTE

Westborough, MA November 18, 2017 The NFL has some explaining to do. Why are former athletes killing themselves and in some cases other people? As students studying the brain it was something special when you could make a correlation between an identified brain lesion and the behavior you are seeing.  I was in China in early November 2017 at a conference on RNA targeted therapy for cancer.  As the non-scientist in the group I was referred to as the clinician who saw the phenotype rather than the genotype – referring to the innumerable genetic underpinnings of cellular biology and changing science of modified nucleotides.  I understood this to have some meaningful interest to the faculty that consisted of 3 prior Nobel laureates and leading scientists in RNA targeted therapy.  So after sitting through hours of presentations I realize the importance of not making a rush to judgment about the cause of some predicted outcome. As a neuropsychologist we are asked to make assumptions about brain integrity after CNS infarcts and make educated predictions about the functional implication of focal lesions in brain.
Recently the scientists at Boston University announced the results of the post-mortem analysis of the brain of Aaron Hernandez, former N.E. Patriots receiver and convicted murderer.  Hernandez had his conviction expunged after he died while his case was on appeal. The 27-year old brain was highly suggestive of having the tell tale signs of chronic traumatic encephalopathy or CTE thought to be the result of repeated concussions and now realized as the result of hundreds – perhaps thousands of sub-concussive blows to the head that accumulate over time.  Hernandez’s brain was the youngest of the donated brains to be identified with advanced CTE. Hernandez played football for 17 years starting when he was a young boy. The question remains did the brain damage that was identified in the post-mortem analysis cause behavior change in Hernandez and could the murder of Odin Lloyd be attributed to the build up of dangerous tau protein in his brain?
“While no one can prove a causal link between Hernandez’s brain damage and his actions, there is little dispute that he displayed CTE symptoms associated with behavioral problems, such as aggressiveness, explosiveness, impulsivity, and suicide.”
Boston Globe Bob Hohler November 9, 2017
By history Aaron Hernandez was an angry, impulsive and violent teenager that his mother reported began when his father died suddenly. Coupled with this was a biological proclivity toward degenerative brain disorders such as Alzheimer’s Disease and CTE.  Both are diagnosed only after the death of the victim. We know that brain-behavior relationships exist from research in stroke and traumatic brain injury where focal injuries result in specific and expected changes in behavior.  These often result from a disconnection between functional centers of the brain including limbic structures that link centers for emotional regulation and the frontal system that exerts inhibitory control over those emotions. The athlete’s who have donated their brain’s upon their death have almost universally exhibited changes in behavior including poor impulse control, depression, and anger.

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BU Medical School and WCVB images 2017

The state of knowledge and policy on concussion in Rugby Football Union

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Westborough, MA  August 15, 2017 Just as American’s have begun to understand the true impact of concussion and the risk associated with repeat concussion and other blows to the head, the Rugby Football Union has started to take a serious look at the problem with respect to the long-term consequence of brain injury.  According to the New York Times in April 2014 “a tidal wave of earnings” may confound the rightful medical response to concussion injuries and dominate the return to play decisions on behalf of athletes who are found to have concussion. The remove-from-competition protocol has not taken hold in European rugby where players are routinely returned to play after a 5 minute time out during which they are examined by team medical personnel. Most are back on the pitch within 5 minutes. I have seen college Rugby games where this precise “recovery” was the norm.  The NCAA has protocols for managing concussion but in some club sports these protocols are not followed.
In 2011, Ben Robinson, a 14-year old boy in Northern Ireland, died from second impact syndrome resulting from playing through a concussion. He returned to the game three times after first being injured in a high school rugby match.  Ultimately he died after collapsing on the rugby pitch. Second impact syndrome results from a repeat brain injury resulting in a metabolic “energy crisis” that interferes with brain function including maintaining homeostasis on a cellular level. I  have documented it in several published Word Press Human Behavior posts.
More recently Irish Boxer Mike Towell died from second impact syndrome hours after his fight much the same way as 14-year old Ben Robinson.  He was seriously injured early in the bout and knocked down.  His toughness and tenacity along with unacceptable referee decision making allowed him to return to the fight. “The assumption that rugby had a better handle on concussions than football, however, might have been flawed from the get-go. The most recent injury audit performed by England’s Rugby Football Union (RFU) established that concussions in elite-level professional games were occurring at a rate of 13.4 per 1,000 player hours.” Bandidi, 2016
The NCAA protocol is cited here.  “Medical personnel with training in the diagnosis, treatment and initial management of acute concussion must be “available” at all NCAA varsity practices in the following contact/collision sports: basketball; equestrian; field hockey; football; ice hockey; lacrosse; pole vault; rugby; skiing; soccer; wrestling.” Female athletes are particularly vulnerable to concussion and tend to have longer recover times. Concussion is sometimes considered an invisible injury largely due to the absence of frank signs of injury on the outside of the head.
According to the BBC, Towell was knocked to the mat in the first round of a 10 round bout.  He was given a standing 8 count and continued the fight.  Some said he dominated the next two rounds when finally in the fifth round he was again knocked down and the fight was ended.  Michael Sefton blog 2016

Burns, J. NY Times, In Europe, Echoes of America as Concussions Spur Debate, April 5, 2014. https://www.nytimes.com/2014/04/06/sports/in-europe-echoes-of-america-as-concussions-spur-debate.html?_r=0  Taken June 13, 2017
Sefton, M. (2016) Second Impact Syndrome. https://concussionassessment.wordpress.com/2016/10/03/second-impact-syndrome-rare-but-often-fatal/ Taken August 7, 2017
Bandidi, P. (2016) Rugby, like NFL, doesnt have the conussion-issue figured out.  http://www.espn.com/espn/story/_/id/16029747/rugby-nfl-concussion-issue-figured-out Taken August 7, 2017
NCAA Concussion Concussion Safety Protocol. Guidelines https://www.ncaa.org/sites/default/files/2017SSI_ConcussionSafetyProtocolChecklist_20170322.pdf Taken August 8, 2017

What is PCS? And why do I care?

ART1WESTBOROUGH, MA  September 28, 2016 Postconcussion Syndrome is a complex disorder that can stymie many physicians because of the abundance of both physical and emotional symptoms. There are about 3-25 percent of patients who are diagnosed with concussion that go on to have a longer duration of symptoms – sometimes a year or more . That is quite a discrepancy in the prevalence of cases.
The PCS cases with whom I have worked having prolonged symptoms from concussion often experience both physical and emotional symptoms that can be debilitating. “Post-concussion syndrome is a complex disorder in which various symptoms — such as headaches, light and sound sensitivity and dizziness — last for weeks and sometimes months after the injury that caused the concussion.” (Mayo Clinic)  If someone you know suffers from PCS the effects to a family system can be dramatic especially when the head of household can no longer go to work.  Whether it is a professional, elite student athlete or a salesman injured in a car crash there is an experience of stigma associated with the invisible injury of concussion. The emotional impact of this marginalizes patients often leaving them feeling alone and frustrated.
Sometimes vague physical symptoms create an overwhelming emotional response that comes from the lingering resentment patients feel when seeing doctors who seem unable to understand their needs. Sometimes the outward appearance of lingering concussion may appear to be solely a psychiatric condition rather than someone who is recovering from a brain injury. Some physicians unfairly believe prolonged symptoms may be linked to ongoing litigation.
In a blog published in December 2015, Concussion and PCS was discussed in some detail.  “Like concussion, it is an invisible injury that renders many people unable to work. Headaches, neck pain, fatigue, visual changes, irritability, sensitivity to sound and light, depression, and poor sleep hygiene were common” (Sefton, 2015).  The long-term impact negatively impacts both physical and emotional functioning by slowly increasing autonomic activation and impact sleep, appetite, and emotional well-being.
When I am working with someone who has been symptomatic for months or more it is quite apparent how frustrated they can become. It is important for the patient to feel they are believed in the story they are telling. Their symptoms are real and in many cases life changing.  I realize that they have never received the proper education from experts to understand their concussion and its potential recovery course.  Someone with prolonged PCS can be difficult to work with because symptoms can be refractory to traditional therapy. The last thing they may want is to sit with a neuropsychologist and retrace their steps all the way back to the beginning of their symptoms or personal injury. A multidisciplinary approach is best for all involved and should include physical exertion that does not exacerbate existing symptoms (Makdissi, et al, 2016).
Meanwhile, there is a growing body of literature that links prolonged symptoms of concussion to major life stress that can imprint psychologically – like PTSD when the timing is right.
References
Mayo Clinic Website, http://www.mayoclinic.org/diseases-conditions/post-concussion-syndrome/basics/definition/con-20032705. Taken September 28, 2016
Sefton, M. Concussion: physician’s once espoused a link to unresolved litigation. Blog post: https://wordpress.com/stats/insights/concussionassessment.wordpress.com Taken October 1, 2016.
Makdissi, et al. The difficult concussion patient. Br J Sports Med. 2013 Apr;47(5):308-13. doi: 10.1136/bjsports-2013-092255 Taken October 1, 2016