Chris Henry and TBI: Would Dr. House have Diagnosed Brain Injury in Time?

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Posted on 29th June 2010 by Gordon Johnson in Uncategorized

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Brain injury is a condition that involves microscopic damage to brain tissue that can only be seen in life through the lens of the patterns of the injured person’s life.  Chris Henry, the former NFL wide receiver whose autopsy results confirmed he was living with brain damage, may have finally made that clear.  See yesterday’s bloghttps://waiting.com/blog/2010/06/former-nfl-player-henrys-autopsy-reveals-evidence-of-brain-damage.html Mike Wilbon of Espn’s PTI (http://espn.go.com/espnradio/show?showId=pti) called the Henry story the most important sports story of the day and even went so far as to say that because of this story, his two year old child would never play football.  This story is important not just because it warns us of the dangers of playing football, but because it tells us we must think “brain injury” when looking at the patterns of troubled people’s lives.  This story also tells us that it is time that autopsy returned to head of the research class in understanding about all pathology, but especially that in the brain.

Since I posted yesterday’s blog, I have done some research on Chris Henry’s life, not just to see the pattern of behavior issues, but also to see if anyone had ever considered a diagnosis of “brain damage” at any time prior to his death. I could find no references to any physician, trainer, NFL official or commentator (including myself)  ever suggesting that Henry was suffering from Post Concussion Syndrome.  When doctors make a diagnosis, they should engage in something called a differential diagnosis, which involves a consideration of all the possible diseases.  I always think of this as a Doctor House (from the TV series) process of putting diseases on a whiteboard, then crossing out the ones that don’t fit.  I strongly suspect that no doctor had ever put TBI on Chris Henry’s whiteboard, or if they ever did, quickly dismissed it because there was no single concussion that he was treated for.

Here (with the easy job of Monday morning quarterbacking the diagnosis) is how I picture Dr. House and his cast approaching the problem.  It is the fall of 2009 and Henry is again asking Commissioner Goodell for reinstatement and Goodell orders a full assessment on Henry.  Because Henry is such a special case, Goodell enlists the services of Dr. House. (If you are not familiar with the show, the cast and plot is explained here: http://en.wikipedia.org/wiki/House_%28TV_series%29 ) House pulls his team together and starts writing on the whiteboard the following potential conditions:

  • Nutcase;
  • Jerk;
  • Spoiled jock; and
  • Bi-polar.

Dr.  “Thirteen” Hadley throws out “brain injury.”  He is a football player she says, a wide receiver, he does get hit often.  Dr. Chase states “it can’t be brain damage, the CT was clean.”  (He actually did say that in an episode in Season 6http://www.tv.com/house/moving-the-chains/episode/1320924/summary.html?tag=ep_guide;summary ).  Dr. Foreman, a neurologist, puzzled  by Thirteen’s suggestion, argues that Henry was never knocked out. Dr. Taub points out that according to the CDC you can have brain injury without ever losing consciousness and that CT’s show virtually no evidence of brain damage when done post-acutely.  House steps in and orders an MRI.

After the commercial, our cast reassembles, normal MRI in hand and now Dr. Foreman derisively dismisses the TBI theory, stating that this is all psychiatric and Henry should be shipped off for an inpatient evaluation at a psychiatric hospital.  House who has some experience with such places says to hold off on that until they have ruled out all “organic causes.”

Taub raises the possibility of Carbon Monoxide poisoning or toxins and House dispatches Chase and Foreman to search Henry’s apartment, where they find nothing.   Meanwhile, Thirteen has not abandoned her initial theory of TBI and pours over the history of Henry’s on the field and off the field problems in his NFL file (for a detailed history seehttp://en.wikipedia.org/wiki/Chris_Henry_%28wide_receiver%29 ).  Here is what she finds:

  • During Henry’s sophomore season in college at West Virginia , he was ejected from a game at Rutgers University due to multiple unsportsmanlike conduct penalties and was suspended for the season finale against the University of Pittsburgh. His former Mountaineers coach, Rich Rodriguez, stated that he was “an embarrassment to himself and the program” for his conduct.[6]
  • On December 15, 2005, Henry was pulled over in northern Kentucky for speeding. During a search, marijuana was found in his shoes. He was also driving without a valid driver’s license or valid insurance.[19] He pleaded guilty and avoided a jail sentence.
  • One month later, on January 30, 2006 he was arrested in Orlando, Florida for multiple gun charges including concealment and aggravated assault with a firearm.[20] He was reported to have been wearing his #15 Bengals jersey at the time of his arrest. He pleaded guilty to this charge and avoided jail time.
  • On April 29, Henry allowed three underage females (ages 18, 16 and 15) to consume alcohol at a hotel in Covington, Kentucky.[21] One of the three, an 18-year-old woman, accused Henry of sexually assaulting her; she later retracted her story and was charged with filing a false police report.[22] On January 25, 2007, Henry pleaded guilty to a misdemeanor violation of a city ordinance commonly referred to as a “keg law.” He was sentenced to 90 days in jail, with all but two of those days being suspended.[21]
  • He was pulled over on Interstate 275 in Ohio on June 3 at 1:18 A.M. by Ohio Highway Patrol trooper Michael Shimko for surmised drunk driving. He voluntarily submitted to a breathalyzer test at 2:06 A.M. at the Milford Police Department and registered a .092 blood-alcohol level, .012 above the level permitted in the state of Ohio.[23]
  • Henry allegedly assaulted a valet attendant at Newport on the Levee in Newport, Kentucky on November 6, 2007.[26] He was arrested for a second time in Orlando on December 3 for violating his probation he was on from a January 30, 2006 arrest. On February 21, 2008, he was found not guilty.
  • On March 31, 2008, Henry punched a man named Gregory Meyer, 18, and threw a beer bottle through the window of his car. Henry claimed it was a case of mistaken identity and also that he thought it was somebody else that owed him money. Henry was waived by the Bengals a day after this arrest and was then served a house arrest sentence.

What Thirteen concludes from this conduct history is that Henry never seems to grasp that there are rules or that there will be consequences to  his actions.  Even if he does, he doesn’t seem to be able to conform his actions.  The multiple unsportsmanlike conduct penalties in one game in college stands out as a precursor of all that followed.

Thirteen Googles “criminal behavior and tbi”.  What she finds is the articleAcquired Brain Injury and Criminal Behavior by Inés Monguió, Ph.D http://www.uninet.edu/union99/congress/confs/hi/03Monguio.html and our bloghttp://www.subtlebraininjury.com/blog/2010/04/more-on-roethlisberger-tbi-and-the-criminal-law.html

What she finds in Dr. Monguió’s paper:

Brain injury, particularly to the frontal lobes or to the connecting circuits of frontal areas to other brain centers, can affect the ability to form criminal intent. Deficits in executive function result in poor self monitoring, planning, judgment, and forethought. The rigidity or impulsivity often seen in traumatic brain injuries make the formation of criminal intent quite a challenge for the individual. Following are general areas to consider when evaluating a criminal defendant to provide information during the trial. The question of legal insanity will be explored in more detail as neuropsychological data may provide information to the courts regarding a defendant’s state of mind at the time of the commission of the crime.

She compares the paper to Henry’s behavior and finds poor self-monitoring, judgment, forethought, as well as impulsivity.   Thirteen renews her argument for TBI.  House points out that you need a traumatic event for a Traumatic Brain Injury.  Where was the event?  Thirteen, argues back that repeated sub-clinical blows, like boxers receive, can cause long term encephalopathy, without a specific concussion – Muhammad Ali was never knocked out.  She argues for a neuropsychological assessment.

This of course would be one of those episodes where House couldn’t walk in at the last instant with the miracle cure.  In the “fact is stranger than fiction” category, Henry actually dies of a traumatic brain injury when he falls from the back of his fiancé’s truck after another neurobehavioral event, a domestic squabble.  All of the circumstances leading up to his death point to brain injury – temper control, violence and judgment in getting into the back of the pickup.  We would hope that this would be one of those cases where House, haunted by the death he couldn’t solve. would order the autopsy.

Fortunately for the future of TBI research, the autopsy was ordered here.  The best thing that has come out of the NFL head injury awareness program is the move to enlist current and former players in this autopsy project.  What we don’t yet have and maybe never will is the answer as to what to do when the in vivo (during life) half of the diagnostic tree points to TBI in someone who makes his living getting hit.  Would treatment for TBI have saved Chris Henry’s career, his life?  Probably not the first, potentially the second.

 

Former NFL Player Henry’s Autopsy Reveals Evidence of Brain Damage

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Posted on 28th June 2010 by Gordon Johnson in Uncategorized

There are two litmus tests for determining whether there has been a traumatic brain injury: autopsy and behavioral changes.  Chris Henry, formerly of the Bengals, now deceased, has positive evidence of both.  An autopsy performed on the troubled former player who was killed last year when he fell out of the back of his girlfriend’s pickup has been reported to be positive for brain damage.  See http://www.nytimes.com/2010/06/29/sports/football/29henry.html?src=mv Henry’s brain has been found to have chronic traumatic encephalopathy (CTE), meaning that his brain shows damage which was caused by long term exposure to traumatic forces.  The subject of CTE has been swirling around the NFL since last winter’s Congressional hearing on the NFL and brain injury.  We have blogged on this topic often but see https://waiting.com/blog/2010/01/nfl-concussion-hearings-in-congress-moving-past-the-need-for-perfect-proof-of-brain-damage.html

Despite the calls for a litmus test for determining TBI in combat, sports and in accident cases, the only way to conclusively determine damage to the microscopic cells of the brain, has been through autopsy.  Most of what we have learned about brain injury pathology has been through autopsy and little has changed about that despite advances in neuroimaging, including PET, MRI, FMRI and CT.  In autopsy, you can examine damaged brain tissue under a microscope. In contrast, the best an MRI can do is see things the size of the point of a ball point pen.  Thousands of damaged brain cells can exist in close proximity to each other, yet such damage not reach be large enough to see on any neuroimaging technique.

Since autopsy is a  bit final what that leaves us in diagnosing brain injury  is the evaluating the way in which the brain is functioning.  While neuropsychology is a science based on the theory that such changes can be measured, the reality is that most brain injury disability is the result of the synergistic loading of cognitive emotional and behavioral challenges.  There is rarely a substantial pure  cognitive change in someone with less than a severe brain injury.  Only under real world stress (not a laboratory setting such as during a neuropsychological assessment) can the functional changes be fully appreciated. Thus, diagnosis must be made based upon the clinician’s evaluation of the patient’s behavioral change.   Listening to the patient and those who have interacted with him or her outside the doctor’s office are key to the diagnosis of TBI.

If the possibility of trauma had been considered with Chris Henry, the diagnosis of TBI would have been straightforward. If you know anything about Chris Henry, he has the precise behavioral telltales that would point to TBI.  One could even argue that his death, was the result of such a meltdown.  Where the surprise in the case arises is that he does not have either a long professional career or a documented history of concussion. This is not like Ben Roethlisberger where  you can pinpoint at least one significant TBI – the motor cycle accident.  At least according to current reports, Henry was never knocked out or taken out of play as a result of a concussion.

On the other hand, Henry played one of the two positions most vulnerable to concussive forces – wide receiver.  Like a quarterback, wide receivers put themselves in defenseless positions, where the torque on the head and neck from being “blindsided” can be extraordinary and the body has no counter momentum to absorb the force.  Also, like a quarterback, wide receivers concentration at the time of a hit has to be entirely away from the hit, but on the ball.

What is most disconcerting to the NFL about the discovery of CTE in Henry’s brain is the inference that even a partial career of routine hits, can not only result in microscopic residue in the brain, but materially alter behavior in such disturbing ways.  One suggestion last year (not adopted) to avoid TBI in football was to outlaw the three point stance.  While anything that reduces contact will help, it is the quarterbacks and the wide receivers that need the greatest protection.  In the twin tales of Henry and Roethlisberger, perhaps light as to the true danger of the blindsided hit can be shed.

Under Fire, Chief Of Military’s Mental Health Center Abruptly Quits

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Posted on 25th June 2010 by Gordon Johnson in Uncategorized

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I recently wrote several blogs that criticized the military’s approach to diagnosing and treating brain injury, and it looks like change is in the wind.

Earlier this week  Brig. Gen. Loree Sutton, director of the Defense Center of Excellence for Psychological Health and Traumatic Brain Injury, stepped down from her job. She is the one who has been blamed for flaws in the miliary’s attempt to detect brain injury and treat both it and post traumatic stress syndrome.

http://www.stripes.com/news/us/65m-tbi-center-opens-in-md-head-of-mental-health-research-resigns-1.108592

Despite her resignation, Loree was present for the dedicaiton of a new mental-health facility Thursday that was created after the military’s efforts came under fire. That new facility, the National Intrepid Center of Excellence, was contructed entirely with private funding. It’s located at the National Naval Medical Center in Bethesda, Md.   

The new 72,000-square-foot center, according to Stars and Stripes, cost $65 million to build, money that was donated by 125,000 private citizens.

The man behind the new center is Arnold Fisher, who told Stars and Stripes that he wanted to jumpstart better mental health-care services being provided for service members,  particularly soldiers returning from combat in Iraq and Afghanistan suffering from TBI and PTSD.

 The ceremony Thursday officially put control of the new facility into the hands of the the Defense Department.

Sutton is credited with helping to create the Defense Center for Excellence. But her abrupt resignation coincides with mounting  criticism of the military treatment of brain injury.

During a hearing this spring before the House Armed Services subcommittee, Rep. Susan Davis, D-Calif., was vocal in her complaints about the Defense Center,  saying it had  “not inspired much confidence,” and had made “some serious management missteps.”

Sutton’s replacement is Col. Robert  Saum, and Sutton has been switched to the army Surgeon General’s Office.

According to Stars and Stripes since 2000 more than 150,000 soldiers have been diagnosd with TBI, and it’s believed that many more go undiagnosed. 

 

 

Second Impact Syndrome – From CDC

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Posted on 24th June 2010 by Gordon Johnson in Uncategorized

The Massachusetts legislature is considering a new law, that among other things mandates an understanding of the second impact syndrome.  Very little is really known about it, but here is what the CDC has on its website at: http://www.cdc.gov/mmwr/preview/mmwrhtml/00046702.htm

Sports-Related Recurrent Brain Injuries — United States

An estimated 300,000 sports-related traumatic brain injuries (TBIs) of mild to moderate severity (1), most of which can be classified as concussions (i.e., conditions of temporarily altered mental status as a result of head trauma), occur in the United States each year. The proportion of these concussions that are repeat injuries is unknown; however, there is an increased risk for subsequent TBI among persons who have had at least one previous TBI (2,3). Repeated mild brain injuries occurring over an extended period (i.e., months or years) can result in cumulative neurologic and cognitive deficits (4,5), but repeated mild brain injuries occurring within a short period (i.e., hours, days, or weeks) can be catastrophic or fatal. The latter phenomenon, termed “second impact syndrome,” has been reported more frequently since it was first characterized in 1984 (6-8). This report describes two cases of second impact syndrome and presents recommendations developed by the American Academy of Neurology to prevent recurrent brain injuries in sports and their adverse consequences (9). Case Reports

Case 1. During October 1991, a 17-year-old high school football player was tackled on the last play of the first half of a varsity game and struck his head on the ground. During halftime intermission, he told a teammate that he felt ill and had a headache; he did not tell his coach. He played again during the third quarter and received several routine blows to his helmet during blocks and tackles. He then collapsed on the field and was taken to a local hospital in a coma. A computed tomography (CT) brain scan revealed diffuse swelling of the brain and a small subdural hematoma. He was transferred to a regional trauma center, where attempts to reduce elevated intracranial pressure were unsuccessful, and he was pronounced brain dead 4 days later. Autopsy revealed diffuse brain swelling, focal areas of subcortical ischemia, and a small subdural hematoma.

Case 2. During August 1993, a 19-year-old college football player reported headache to family members after a full-contact practice during summer training. During practice the following day, he collapsed on the field approximately 2 minutes after engaging in a tackle. He was transported to a nearby trauma center, where a CT scan of the head showed diffuse brain swelling and a thin subdural hematoma. Attempts to control the elevated intracranial pressure failed, and he was pronounced brain dead 3 days later. Autopsy revealed the brain to be diffusely swollen with evidence of cerebrovascular congestion and features of temporal lobe herniation.

Summary of Related Data

The true incidence of second impact syndrome is unknown. During 1984-1991, four cases were described, and during 1992-1995, a total of 17 cases were described; most cases have involved male adolescents or young adults and involved participation in boxing, football, ice hockey, and snow skiing (8). Combined data from four states (Colorado, Missouri, Oklahoma, and Utah) during 1990-1993 indicated an annual rate of 2.6 cases per 100,000 population of sports-related TBI that resulted in hospitalization or death; the proportion attributable to second impact syndrome is unknown.

Reported by: J Kelly, MD, Brain Injury Program, Rehabilitation Institute of Chicago, Illinois. Quality Standards Subcommittee and Task Force on Preventive Neurology, American Academy of Neurology, Minneapolis, Minnesota. Div of Acute Care, Rehabilitation Research, and Disability Prevention, and Div of Unintentional Injury Prevention, National Center for Injury Prevention and Control, CDC.

Editorial Note

Editorial Note: The two cases described in this report involved repeated head trauma with probable concussions that separately might be considered mild but in additive effect were fatal. The risk for catastrophic effects from successive, seemingly mild concussions sustained within a short period is not yet widely recognized. Second impact syndrome results from acute, usually fatal, brain swelling that occurs when a second concussion is sustained before complete recovery from a previous concussion. Brain swelling apparently results from a failure of autoregulation of cerebral circulation that causes vascular congestion and increased intracranial pressure, which may be difficult or impossible to control (7).

Population-based data are needed to define the incidence of this condition, describe causes, and identify populations at highest risk. CDC is developing a multi-state system for TBI surveillance (10). Based on this surveillance system, CDC, in collaboration with participating states, is developing methods to conduct surveillance for sports-related second impact syndrome.

The risk for second impact syndrome should be considered in a variety of sports associated with likelihood of blows to the head, including boxing, football, ice or roller hockey, soccer, baseball, basketball, and snow skiing. The American Academy of Neurology has proposed recommendations for the management of concussion in sports that are designed to prevent second impact syndrome and to reduce the frequency of other cumulative brain injuries related to sports (9) (see box (Table_1)). These recommendations define symptoms and signs of concussion of varying severity and indicate intervals during which athletes should refrain from sports activity following a concussion. Following head impact, athletes with any alteration of mental status, including transient confusion or amnesia with or without loss of consciousness, should not return to activity until examined by a health-care provider familiar with these guidelines.

The popularity of contact sports in the United States exposes a large number of participants to risk for brain injury. Recurrent brain injuries can be serious or fatal and may not respond to medical treatment. However, recurrent brain injuries and second impact syndrome are highly preventable. Physicians, health and physical education instructors, athletic coaches and trainers, parents of children participating in contact sports, and the general public should become familiar with these recommendations.

 

References

 

  1. Sosin DM, Sniezek JE, Thurman DJ. Incidence of mild and moderate brain injury in the United States, 1991. Brain Inj 1996;10:47-54.
  2. Salcido R, Costich JF. Recurrent traumatic brain injury. Brain Inj 1992;6:293-8.
  3. Annegers JF, Grabow JD, Kurland LT, Laws ER Jr. The incidence, causes, and secular trends of head trauma in Olmsted County, Minnesota, 1935-1974. Neurology 1980;30:912-9.
  4. Jordan BD, Zimmerman RD. Computed tomography and magnetic resonance imaging comparisons in boxers. JAMA 1990;263:1670-4.
  5. Gronwall D, Wrightson P. Cumulative effect of concussion. Lancet 1975;2:995-7.
  6. Saunders RL, Harbaugh RE. The second impact in catastrophic contact-sports head trauma. JAMA 1984;252:538-9.
  7. Kelly JP, Nichols JS, Filley CM, Lillehei KO, Rubinstein D, Kleinschmidt-DeMasters BK. Concussion in sports: guidelines for the prevention of catastrophic outcome. JAMA 1991;266: 2867-9.
  8. Cantu RC, Voy R. Second impact syndrome: a risk in any contact sport. Physician and Medicine 1995;23:27-34.
  9. Quality Standards Subcommittee, American Academy of Neurology. Practice parameter: the management of concussion in sports. Neurology 1997;48:581-5.
  10. CDC. Traumatic brain injuries — Colorado, Missouri, Oklahoma, and Utah, 1990-1993. MMWR 1997;46:8-11.

The Challenges Of Teaching Severely Brain-Damaged Kids, As Told Through Donovan’s Story

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Posted on 22nd June 2010 by Gordon Johnson in Uncategorized

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We no longer shut our severely disabled children, including those with traumatic brain injury, away in institutions 24/7, that’s true. But public school systems, mandated to teach the disabled by 1975 federal law, today struggle to find the best way to care for these students. 

The New York Times on Sunday did a masterful job of describing the difficulty of teaching kids with multiple disabilities, with 20-year-old Donovan Forde used as the case study to illustrate the issues and challenges. 

 http://www.nytimes.com/2010/06/20/education/20donovan.html?scp=1&sq=Dononvan%20Forde&st=cse

Donovan has spent 15 years in the New York City public school system. He is blind, wheelchair-bound and has cognitive problems, all the result of a traumatic brain injury he sustained when he was nearly six months old. 

Donovan is one of 132,000 students in the U.S. classified as having “multiple disabilities,”  at least two disabilities and special educational needs, according to The Times. They are part of a group of 6.5 million that now get some kind of special education at a cost of $74 billion annually.

 “Students with multiple disabilities, like Donovan and his schoolmates, can have a wide range of diagnoses, including cerebral palsy, rare genetic disorders and problems that stem from conditions in utero or at birth, some of which have no name,”  The Times wrote.

It is heart-breaking to hear about Donovan’s cognitive difficulties, how teachers shine a flashlight in front of his eyes to get his attention, how he can’t talk, how he can only see shapes and sometimes doesn’t even respond to being called by his name. His teachers, quite frankly, don’t know if they are ever getting through to him. 

“Donovan’s mother, Michelle Forde, likes his special education high school, Public School 79, the Horan School, in East Harlem, where she feels he is welcome and cared for,” The Times wrote. “But she wishes his teachers would spend more time working on his practical challenges, like his self-abusive habit of hitting himself in the face so hard that he has to wear thick white cotton mitts most of the time, even when he sleeps.”

Donovan was born with club feet, but was otherwise healthy. But in 1990, Donovan, nearly 6 months old, was being held by a family friend out on street in Brooklyn when a underaged drive in a stolen car hit them both. 

Donovan fell and hit his head on the pavement, and his heart stopped. A bystander administered CPR and revived him, but he was in a coma for  six weeks, long enough so that the swelling of his brain damaged his optic nerves, leaving him basically sightless.

Donovan’s mother never recovered a settlement for his life-changing accident, either. He  is living in a nursing facility, sharing a room with three other severely disabled youths, where he can get the constant care he needs.

One thing is clear about Donovan to his teachers: He loves music, and makes a pretty good effort to sing.

According to The Times, the trend in educating severely disabled children is to use emotion and human connection to reach them.

“As higher functioning areas of their brains are underdeveloped, emotion moves them at a deeper level, lighting up the same part of their brain, the limbic system, as meaningful music, and possibly creating a bridge to greater intellectual cognition,” The Times wrote.

But read the full story, which starts on Page One and jumps to a two-page spread.

Prior Combat Stressors Adds One More Trap for TBI

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Posted on 18th June 2010 by Gordon Johnson in Uncategorized

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In our last blog, we introduced the reader to the potentially disastrous combination of TBI and PTSD conditions in a combat survivor. But the problem in combat is not just the intersection of these two “co-morbidities”, but the likelihood that a third complicating factor- preexisting anxiety – will also be found in combat veterans.

As we outlined yesterday, the Limbic System is the part of the brain which regulates anxiety and memory. Just as the corpus callosum is the collection of axonal fibers that connects the two hemispheres of the brain, the uncinate fasciculous is the collection of axonal tracts that connect the principal memory and anxiety centers of the brain to the frontal lobes – the thinking and maturity parts of our brain.

See http://www.waiting.com/limbicsystem.html

The principal structures involved include the following;

Hippocampus. The brain’s save button is the hippocampus. It is the part of the brain most important to converting immediate memory to long term memory.

Amygdala. The brain’s anxiety center is the amygdala. It is the amygdala that protected us from predators in the pre-historic times. It triggers our startle reflex in modern times and is the principal culprit in anxiety disorders.

Frontal Lobes. The frontal lobes are where we learn to become adults, where all activity is initiated, decisions made, emotions modulated and judgment’s made. The orbital frontal part of the frontal lobe, on the underside, is essentially the conductor of the brain’s symphony, the part that tells the other instruments when to start and stop playing. The frontal lobes coordinate all activity.

Uncinate Fasciculous. Connecting the above critical structures is the uncinate fasciculous, the axonal tracts that run from one end of the lower brain structures to the underside of the frontal lobes.

A person with a pre-injury anxiety disorder is far more vulnerable to post concussional problems (PCS). In a person with an anxiety disorder, the amygdala is already overreacting to potential anxious moments. It runs “hot” so to speak. When, as a result of trauma, such as a blast, damage occurs to the hippocampus, frontal lobes and the uncinate fasciculous, the information that gets moved across this lower brain circuit gets garbled. When information between the limbic system and the frontal lobes gets garbled, anxiety can become panic, depression can become organic rather than just reactive and the person’s ability to modulate emotions and make decisions, seriously impaired. The combination of pathologies in these areas -coupled with inefficient communication between them – creates a synergistic pathology far more functionally impairing than any one of those impairments might have been alone.

As serious as this premorbid vulnerability is in a civilian, it is far more serious in a soldier. Think of it this way. The amygdala is there to get us to run, without stopping to think. Fortunately for peace time activities in the modern world, our socialization has taught us when not to panic. A civilian has few times when he or she needs to rely on the amygdala. There are few great predators, few brushes with real danger. Thus, our frontal lobes and other emotional centers have tamed our amygdala, in not so different of a way than we tame a pet.

Yet, the amygdala is needed for combat. To survive, a soldier must rely on his instincts and must put his mind into a hypervigilant state. One of the biggest problems that soldiers have reintegrating into civilian life is learning how to stop this hypervigilance. PTSD is primarily a disease where the traumatic emotional stress has so changed the amygdala that it never entirely goes back to its peace time role.

Thus even before a TBI, a combat veteran is likely to have a heightened anxiety. Without that anxiety- the hypervigilance – the soldier may not survive. Depending on the level of previous battle stresses, that anxiety may have elevated itself to PTSD levels prior to the TBI. Thus, the risk of emotional dysfunction is not only increased by the very battle in which the soldier is injured, but also by the pre-injury emotional state.

The irony of all of this is that this convergence of co-morbities is laid upon those we expect to be the toughest. “The Few, the Proud” are those at greatest risk of becoming the homeless, the disturbed, the arrested. Sadly, I can offer no solution other than peace.

 

D-Day and Second Impact Syndrome

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Posted on 16th June 2010 by Gordon Johnson in Uncategorized

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Yesterday, we talked about the practicalities of TBI and combat. Perhaps the best way to visualize those practical problems is to watch the opening scenes of the movie, Saving Private Ryan.  A clip of the first 10 minutes can be found at YouTube here: http://www.youtube.com/watch?v=kx7dFp0WhN4&feature=related At eight minutes into this clip, the lead character, Captain John Miller, played by Tom Hanks, is near a mortar or artillery shell which explodes upon the Allied troops as they land at Omaha Beach.  Captain Miller clearly suffers a concussion in this blast without any apparent loss of consciousness.

The next minute of this clip is the most honest treatment of concussion I have seen from Hollywood.  Captain Miller struggles to his knees, helmet in hand.  For the next minute he does nothing, seemingly unable to comprehend that he has been hurt, that he is in combat, that he should put his helmet back on.  In almost a childlike gaze, he takes in the horror that surrounds him. His hearing, his balance are impaired.  The viewer gets the sense of this because Director Steven Spielberg cuts all sound, the viewer, like the concussed soldier becomes deaf. Captain Miller, as we watch in horror,  does virtually nothing to defend himself, despite the cataclysm which surrounds him. After 90 seconds, his thinking clears and he regains his ability to command.  He is able to save his life, those of most of his troop and Private Ryan.

This portrayal of concussion by Hanks may be fictional, but it is a classic example of art showing us what is real.  Hanks and director Spielberg have gotten this just right, at least in the acute stage of the concussion.  What I believe is most important about this portrayal of concussion is that it demonstrates the combat challenges in avoiding second impact syndrome and simultaneous PCS and PTSD.

Second Impact Syndrome. The big impetus for the sport and concussion movement that has so changed how the world views concussion, was a 1991 description of the “second impact syndrome.  See Kelly, JP, JAMA.  1991 Nov 27;266(20):2867-9.  “Concussion in sports. Guidelines for the prevention of catastrophic outcome.” http://www.ncbi.nlm.nih.gov/pubmed/1942455 The concern in second impact syndrome is that a concussed brain is no better at defending against a catastrophic increase in brain blood pressure, than the Captain is in avoiding bullets.  For the sake of illustration, the brain becomes confused as to how to regulate its blood pressure by the first concussion.  When the second impact puts an added strain on such regulatory apparatus, the brain has no remaining defenses.  Death or severe injury results.

What makes second impact such a practical problem in combat is the increased risk of second concussion because of the disorientation and confusion from the first concussion.  While such is also true in sports, the risk factors of the second injury are so much greater in combat. No injury timeouts in combat. As you watch Saving Private Ryan, you realize how vulnerable a soldier with a 90 second disorientation is.  He is in the line of fire, without his helmet, completely confused as to what to do, what has happened. There is probably nothing we can practically do to reduce the risk of the contemporaneous second concussion in combat. But what me must do is make sure we don’t send the soldier back into a combat zone in the days and weeks afterwards. That is where battlefield screening would be so important.p>

Interplay Between Concussion and PTSD. While the science in this area is still evolving, I am completely convinced that Post Concussion Syndrome (PCS) has as its core problem, a compromised attentional capacity.  When compromised attentional resources are combined with emotional stressors (of which combat based PTSD would be among the worst) the likelihood of a disability multiplies.

The least understood but potentially most serious pathology after a mild traumatic brain injury  (MTBI) is compromised brain signaling between limbic structures like the amygdala and hippocampus and the frontal lobes.  Communication in the brain is electrical, with the electrical impulse being carried from one neuron to another down axons.  Fiber tracts are the bundles of axonal fibers that connect one part of the brain to other part of the brain or to the nervous system.  See http://www.subtlebraininjury.com/neuron.php One of the most exciting new developments in the last decade is the capacity to see damage axonal tracts on MRI through the use of Diffusion Tensor Imaging (DTI).   Even though axons are far too small to be seen on MRI, DTI can see the cumulative effect of axonal injury because of its ability to see an interruption in the fiber tracts.  See http://www.tbilaw.com/blog/tag/dti

Unfortunately, not enough DTI research is being done on what I believe to be the biggest culprit in PCS, the uncinate fasciculus. The uncinate fasciculus is a fiber tract that connects the limbic system to the frontal lobes. http://www.ajnr.org/cgi/content-nw/full/25/5/677/F11 Add structural injury to either the limbic or frontal lobes to damage to this fiber tract and the brain dysfunction can  hit critical mass.

One issue this week  has been what the Pentagon has done with the $1.5 billion that has been spent on TBI.  I can categorically say that if war is anything like Saving Private Ryan, the U.S. military owes it to its soldiers and Veterans to prioritize research into the limbic system, uncinate fasciculus and frontal lobe injury.  Lt. Col. Michael Russell, head of the Army’s ANAM program says there are too many “false positives” for TBI when administering the test mandated by Congress.  One of the reasons there are so many  is that the emotional stress of combat alone could impact the brain’s panic and emotional centers.  Add diminished attentional capacity and compromised axonal tracts which arise from MTBI and the risk of a catastrophic result will still be there when the bullets stop flying.

Too Many TBI’s, Not Enough Soldiers

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Posted on 15th June 2010 by Gordon Johnson in Uncategorized

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Our blog yesterday about the Pentagon’s failure to follow through on mandatory testing for brain injury raises numerous issues worth commenting on, including the military’s outright failure to follow orders, the superficial approach to the diagnosis of brain damage and the magnitude of the problem that is being pushed on down the road to the next generation.  Yesterday’s blog is here: https://waiting.com/blog/2010/06/611.html

The generals in essence are telling Congress that if they properly treated soldiers for TBI, there just wouldn’t be any soldiers left.  They use the term “false positives” but that is really short hand for saying that too many soldiers are showing symptoms to treat them all.  And frankly, the problem isn’t really the cost of treatment or even the availability of treatment facilities, although the second part of that could certainly get to be an issue.  The problem is that if they followed anything close to the protocols for treating athletes with concussions, there might not be anyone left to fight the wars.  You see, if we were talking athletes, we wouldn’t allow them to go back into the field until they were completely cleared of Post Concussion symptoms.  Our military is already scrambling to find enough soldiers to fight two wars.  Put any more on the sidelines and we would have to change our foreign policy.

While I may be one of the few civilians who fully understands the true implications of “no return to play” for soldiers, didn’t we promise to do better with this war?  I have been blogging about the Nightmare of War Time Brain Injuries since http://www.tbilaw.com/blog/2008/06 (read bottom up) and specifically since http://www.tbilaw.com/blog/2008/06/suicide-and-terror-continues-for-our-iraq-and-afghanistan-soldiers.html

This problem with combat TBI is not a new problem.  German, Japanese, Korean and Vietnamese artillery and mortars were far more potent than road side bombs.  And while it is true that we are saving more severely wounded TBI soldiers, the mild and moderate survival rates are likely unchanged since World War I.  What is different is that we have the capacity to diagnose MTBI now and we are supposed to care, because Congress and the American public says so.

The problem isn’t too many false positives.  It is too many positives, too many soldiers with brain damage.  It has always been true, since the day of the club and it will always be true – combat is hard on the brain. That is why  the helmet was invented.  What we as a society have to accept is that if we are truly to “be there” for our troups, we must pull them out of the field when they get a head injury.  That means we either have to have more soldiers or fewer military ambitions and then apply all of the best medicine to help them when they do suffer a TBI. If we don’t, the correlation between soldiers, homelessness and suicide will be the same in 2050 as it was in the 20th century.

Pentagon Failed To Abide By Order To Test Troops For Brain Injury Before And After Combat

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Posted on 14th June 2010 by Gordon Johnson in Uncategorized

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The U.S. military has failed to follow a Congressional directive that mandates that soldiers be tested before and after they serve in combat to gauge if they have suffered any brain injuries, according to a story in USA Today.

http://www.usatoday.com/news/military/2010-06-14-braintest_N.htm

The paper reported that more than 562,000 tests taken by soldiers before they were shippd out to fight weren’t readminstered when they came home by military health officials. 

According to one of the Congressmen who helped write the 2008 order on the testing, Rep. Bill Pascrell, D-N.J., now thousands of solidiers who may have brain damage will go undetected. Pascrell is co-chariman of the bi-partisan Congressional Brain Injury Task Force.

The Pentagon contends that the test, called the Automated Neuropsychological Assessment Metrics, or ANAM, used to check the soldiers isn’t accurate. Lt. General Eric Schoonmaker, the Army surgeon general, told USA Today that the test is “no better than a coin flip.”

 Another officer, Lt. Col. Michael Russell, chief of the army’s ANAM program, claimed the test comes out with too many false-positive results, and that such results could occur even by someone taking a medication such as Benadryl.

But defenders of the test said that it is just designed to indicate if a soldier’s cognitive processes have worsened, meaning that additional testing is necessary. In other words, the ANAM test is a good screening tool. 

Neuropsychologist Tresa Roebuck-Spencer, who is with the University of Oklahoma, told USA Today that when the post-combat test is compared to the first one, the false-positive test results drop out. The university developed and distributes the ANAM test for the army.

USA Today reported that 575,000 pre-deplolyment tests were collected at a price of about $30 each. But only 12,000 to 13,000 have been used for comparisons. 

Traditionally the military has expected soldiers to report their own head injuries. Somewhere in the range of 5 percent to 15 percent continue to have problems from their brain trauma, according to USA Today. 

   

 

    

Possible Connection Seen Between Vets’ Post Traumatic Stress Disorder And Alzheimer’s Disease

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Posted on 13th June 2010 by Gordon Johnson in Uncategorized

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A recent study has found an apparent link between post traumatic stess disorder, PTSD, and Alzheimer’s disease in older veterans.

 http://www.webmd.com/mental-health/news/20100607/posttraumatic-stress-disorder-linked-to-dementia

The research was described as the first to find a connection between combat-related PTSD and late-life dementia. It found  a significant increase in the likelihood of developing dementia — nearly  twice as high — for ex-solidiers who have PTSD compared to those who don’t.

Deborah Barnes at the University of California in San Francisco conducted the research, with her team keeping track of more than 180,000 veterans for seven years. Of that group, more than 53,000 had been diagnosed with PTSD.

Nobody in the group had dementia in late 2000, but by late 2007 about 31,000, or 17 percent, developed faulty memories and cognitive disorders.  As it turned out, the veterans with PTSD had roughly an 11 percent chance of getting dementia over the seven-year period of the study, compared with 7 percent for vets who don’t suffer from PTSD.

And after doing some adjustments of risk factors, the study determined that the veterans with PTSD were 77 percent more likely to get dementia than vets without PTSD.

Barnes’ study was financed by the Department of Defense and the National Institute on Aging, and was published in the June issue of the journal “Archives of General Psychiatry.” 

 http://archpsyc.ama-assn.org/cgi/content/abstract/67/6/608

 The study, however, is not definitive, according to Barnes. For example, it remains unclear if suffering from PTSD multiplies veterans’ risk for dementia as they  grow older, or if recurring PTSD is an early symptom of dementia in older veterans. 

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