Brain Injury Lawyer Blog

Autopsy is such a morbid concept, such a horrible invasion of privacy at a time when loved ones are dealing with the shock waves of grieving.  Yet, ironically it is the one good thing that can come out of death, especially the death of a young person.  The remarkable findings announced this week of former NFL player Chris Henry’s autopsy will contribute immeasurably to our understanding of brain injury and the risks of playing football.  Out of the tragedy of Chris Henry’s life and death, the lasting contribution he may make to our world is illuminating the connection between abnormal behavior and brain damage.

Mild Traumatic Brain Injury (MTBI) is one of the single most difficult things to diagnose and research in medicine. Its critical symptomotology, that momentary loss of consciousness or awareness, is almost never witnessed by the medical team.  The pathology is far too small to be seen on CT scan, and only in the most serious cases are conventional MRI’s showing clear cut evidence.  While it has a clear cut pattern of symptoms, other illnesses and conditions come with similar symptoms, making differentiating the condition harder.  This issue confounds the long thought gold standard for MTBI diagnosis, neuropsychology.  While in severe brain injury cases neuropsychology will demonstrate unequivocal patterns of  cognitive deficits, in MTBI or (Post Concussion Syndrome – PCS, a term used interchangeably) the deficits are subtle and could be dismissed as being caused by a myriad of other problems, including depression and poor motivation.  Adding to this problem is that depression and poor motivation are the symptoms of MTBI or PCS.  Further complicating the diagnostic puzzle is that those with premorbid histories of depression, anxiety, PTSD, or prior MTBI are far more likely to  be disabled by MTBI.  Finally, as many as half of the neuropsychologists practicing today are “non-believers” in PCS.

Now contrast an in vivo (during life) diagnosis of MTBI with an autopsy.  In autopsy there is no ambiguity.  The microscopic damage can be seen under a microscope.  The axonal tracts that may have been compromised, can be examined with the naked eye.  Actual residual blood stains can be seen on neural tissue.  The diagnosis can be made with a high certainty.  What value does it have to diagnose a non-life threatening condition after a person is already dead?  It moves the science of brain injury forward by leaps and bounds.  Were autopsy an integral part of mild traumatic brain injury research, the skeptics would have to play their sophistic (plausible but fallacious) games elsewhere.

But here is the problem with making autopsy a more integral part of MTBI research: Since MTBI is a non-fatal condition, it may be decades between the onset of the condition and the autopsy.  The movement to enlist NFL players to contribute their brains to a long term autopsy study is a true breakthrough, yet the research it will reveal will not become available for decades.  (As a side note, those autopsy’s done in the future generations, will be most illuminative if good records are kept of behavioral issues the players had after their careers ended and accurate records are kept of the concussions they suffered.)

Occasionally, medical science gets lucky on the misfortune of someone who dies young.  That is what happened with Chris Henry. This research was possible because someone with a documented MTBI, died seven months later from an unrelated cause.  Again, tragedy becomes fortuitous for medical science.  The autopsy revealed:

Gross inspection of the brain at autopsy was normal; however, microscopic analysis demonstrated what were considered trauma findings of hemosiderin-laden macrophages in the perivascular space and macrophages in the white matter, particularly the section taken from the frontal lobe.

All of the foregoing is important because this patient’s PCS was clearly documented.

The patient had partially returned to work at the time of death, but had encountered problems with diminished cognitive performance in his work as an appraiser. Neuropsychological studies were generally within normal limits although several tests of either speed of processing or short-term memory showed lower than expected performance. This case demonstrates the presence of subtle neuropathological changes in the brain of a patient who sustained a mild TBI and was still symptomatic for the residual effects of the injury 7 months post injury when he unexpectedly died.

As discussed above, neuropsychological testing showed issues, but nothing that a skeptic couldn’t dismiss as unrelated or feigned.  But you can’t fake the autopsy.

I have a narrow perspective on the neurosciences, devoting all of my time to representing those with traumatic brain injury. So take this with that bias in mind.

Nothing is more important to our medical science than to reach a greater understanding about the cause and nature of brain abnormalities, particularly those relating to trauma.

The U.S. government is now spending billions of dollars on TBI treatment for returning soldiers from Iraq and Afghanistan.  This hopefully will give us a tremendous data base to understand the nature of the forces, the acute period symptoms, the chronic problems that occur and neurobehavior abnormalities and disability that persist from TBI.  Some great data surveillance information could be available, with force sensors in helmets, pre-deployment and post-injury neuropsychological documentation, and long term treatment issues.  But as far as I can tell, there is one huge missing element in that focus: autopsy.

It would be a horrible invasion of privacy  and treading on the grieving process to make it autopsy mandatory, but all efforts and no expense should be spared to autopsy the brains of all American soldiers who die in combat.  This is imperative if the soldier suffered any head trauma or PTSD prior to death.  One of the wonders of autopsy is that it can sort out the chronic brain damage that existed prior to the fatal event from the brain damage which caused death, such as in Chris Henry’s case.

The fortuitous breakthrough from tragedy of a death from other causes with a documented prior TBI does not need to be a once in a generation opportunity.  Unfortunately, nearly every day an American soldier is being killed who had some previous MTBI.  Make those deaths mean something. Hundreds of such autopsies will advance our understanding not just about TBI in general.  Those autopsies could be of immeasurable value in treating other veterans who come home with TBI.

I give the NFL highest marks for its support of the give the brain to science program for its former players.  (A number of  ex-NFL players have agreed to donate their brains to the Boston School of Medicine, which is creating a bank of brains to examine as part of its research on head injury and future brain disease.) See http://www.tbilaw.com/blog/tag/nfl-and-brain-injury If veteran organizations, the VA, Congress or the Pentagon would show the same leadership, the dark cloud that shrouds the Post Concussion Syndrome could be lifted not in my lifetime, but in the next decade.  Let some good come out of war.

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.