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. 

Much-Needed Update Of Guidelines To Determine Brain Death Are Released

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Posted on 7th June 2010 by Gordon Johnson in Uncategorized

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There’s lots of injustice in this world, and declaring somone brain dead who isn’t would be high on the top of the list of such tragedies. 

 That’s why I think it’s a good idea that new guidelines for determining if a patient is brain dead have just been issued.  

Essentially saying it wants to take the guesswork out of the process, the American Academy of Neurology Monday released those new guidelines — the first update in 15 years. 

http://health.usnews.com/health-news/family-health/brain-and-behavior/articles/2010/06/07/experts-revise-guidelines-for-determining-brain-death.html

 The new guides tell physicians to do a extensive evaluation of a patient, with a check list of about 25 tests that must be performed and specific criteria that must be met.

The new guidelines were co-written by Dr. Panayiotis Varelas, director of the Neuro-Intensive Care Service at the Henry Ford Hospital in Detroit.

The U.S. Uniform Determination of Death Act does define when death takes place: When a person permanently stops breathing; the heart stops beating; and all brain functions, including those in the stem, stop.

The problem is that doctors differently determine who meets those criteria.

A 2008 study that included 41 of the country’s top hospitals, done by Varelas, found a lot of variability in how doctors and hospitals judged who fit the criteria. 

 Under the revised guidelines, the three signs of brain death are coma with a known cause; abscence of brain stem reflexes and the permanent cessation of breathing.  

Being in a vegetative state does not equate to being brain dead, according to the new rules.

Brain death is caused by severe traumatic brain injury, stroke or oxygen deprivation following cardiac arrest.         

Should Baseball Pitchers Wear Helmets?: Debate Renewed After Cleveland Pitcher Gets Beaned

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Posted on 3rd June 2010 by Gordon Johnson in Uncategorized

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 It hasn’t even been a week since New York Yankee slugger Alex Rodriguez hit Cleveland Indians pitcher David Huff in the head with a line drive. But Huff seems to have emerged magically uninjured by that heart-stopping accident.

http://www.nytimes.com/2010/05/30/sports/baseball/30yankees.html?ref=sports

 Huff, who had to be carried out of Yankee Stadium on a stretcher after getting beaned May 29, is back playing ball. The pitcher, who never lost consciousness after A-Rod’s hit struck him, didn’t sustain a concussion, or get so much as a headache, from being hit. His CT scan came back negative.

 http://bats.blogs.nytimes.com/2010/05/30/day-after-being-hit-in-head-huff-is-feeling-good/

 The evening of the day he was hit, Huff tweeted, “Everything is good. Was a little scary, but I’m out of the hospital and with my family.”

http://www.cleveland.com/tribe/index.ssf/2010/05/cleveland_indians_left-hander.html

 That’s all pretty remarkable, in that Rodriguez hit the ball with such force that it after it struck Huff’s head it flew and landed roughly 275 feet from home plate.

http://sports.yahoo.com/mlb/blog/big_league_stew/post/He-s-OK-folks-Indians-David-Huff-takes-A-Rod-?urn=mlb,244510

 Although the Huff case had a happy ending, the scary incident has some sports writer bringing up a question that’s been debated in baseball: Should pitchers be required to wear helmets for protection, like catchers?

 The knee-jerk reaction might be to say yes, pitchers should don helmets. After all, they face hardballs shooting back at race car-like speeds, more than 90 mph.

 And some players who have been hit in the head like Huff didn’t fare as well as him. The Cleveland Indians seem to be particularly jinxed. In 1920 Cleveland Indians shortstop Ray Chapman was killed by a pitched ball. And Indians pitcher Herb Score’s promising career ended when he was hit in the face with a line drive in 1957.

 But how far do you go to eliminate risk in sports? By their very nature, sports involve all kind of risks. You can’t eliminate them all.

 And if you believe baseball pitchers should wear helmets, then it follows that you would want to mandate that basketball players wear helmets, as well. In a recent week there were two concussions in just one basketball game. Basketball has a much higher frequency of concussions than baseball, except when it comes to batting.

 That said, the biggest risk of severe brain injury in baseball is not a pitcher taking a line drive in the head. It’s two outfielders going after the same ball and then colliding at a very high speed, head on head. Each year, some player dies as the result of such a collision.

 My answer to making baseball safer for pitchers isn’t a helmet, but rather a ban on aluminum bats. A player can swing an aluminum bat faster than a wooden bat, accelerating the speed the ball comes off the bat – and at the pitcher. That’s why for at least a decade the use of aluminum bats has been a controversial issue.

 Back in 2000, ESPN Magazine did a story headlined “Bat Controversy Lingers Over NCAA.”  In part, that article described how player stats soared as “hot” aluminum bats became more prevalent in the game. In the College World Series championship, from 1994 to 1998 there were 105 runs scored, versus only 33 in 1989 to 1993.  

http://espn.go.com/gen/s/2000/0329/453294.html

 Last year a Montana jury awarded a family $850,000 for the death of their son, who was killed in a 2003 baseball game where aluminum bats were used. The jury found that Louisville Slugger didn’t properly warn people about the potential dangers of the bat.

http://www.roundupnews.com/sports/aluminum-bats-still-safe-despite-lawsuit-against-bat-maker-1.861272

 But even that jury award didn’t convince people like New Mexico State University baseball coach Ricky Ward that aluminum bats were unsafe. In an interview, Ward said that deaths from batted baseballs were very uncommon.

 Ward suggested that instead of worrying about the aluminum bat, that the specifications on baseballs themselves be changed.

 That’s a new answer to an old problem, but we don’t know if it would work.

 

The Difference Between Life And Death: Bret Michaels’ And Gary Coleman’s Brain Hemorrhages

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Posted on 2nd June 2010 by Gordon Johnson in Uncategorized

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The New York Daily News Wednesday posed a question that may have crossed many people’s minds: Why did former child star Gary Coleman die last week of a brain hemorrhage, while rocker Bret Michaels lived?

http://www.nydailynews.com/lifestyle/health/2010/06/02/2010-06-02_brain_injuries_like_the_ones_suffered_by_bret_michaels_and_gary_coleman_can_have.html

Coleman, who had a lifelong history of health problems, suffered an intracranial brain hemorrhage when he slipped and fell in his Utah home last Wednesday after undergoing his usual dialysis treatment. Only 42 years old, Coleman went into a coma in the hospital on Thursday, and his family ended his life support on Friday.

Michaels, on the other hand, was at his Arizona home when he suddenly felt an incredible pain in his head. His wife rushed the singer to the hospital, where he was diagnosed with a subarachnoid brain hemorrhage. After some shakey moments, 47-year-old Michaels pulled through, and appeared on the finale of “Celebrity Apprentice,” which he won.

Reporter Rosemary Black explains the difference between the two brain hemorrhages. An intracranial hemorrhage takes place inside the brain, while a subarachnoid hemorrhage is bleeding into the lining around the brain.

Black interviewed physicians who said that the location of brain hemorrhage will determine if it will kill or not, if it will disable a patient in some way, or if they will fully recover. Of course, that’s just common sense: If the part of your brain that controls your breathing is damaged,  let’s face it, it’s unlikely you’re going to have a good outcome. 

One doctor added that Coleman’s poor health, he had two kidney transplants during his life and was on dialysis, likely made his prognosis grim after his brain injury. 

But then Michaels wasn’t a particularly well man. He had just had his appendix removed and he was a lifelong diabetic. And I believe that Michaels’ physician is jumping the gun by telling the press that the singer has fully recovered, that he is part of the small group of people — only 20 percent — who bounce back like new from this type of brain hemorrhage. 

I have written extensively on my blog, http://subtlebraininjury.com/, about apparent full recovery brain injury. Problems can develop later on with people who have sustained brain injury and appear to be back to normal. For example, those who have jobs that require their minds to have a high processing speed may find it harder to claim “full recovery” than those with less taxing jobs.  

And in a recent interview Michaels himself said, “I’m just not back to where I want to be just yet.” http://www.popeater.com/2010/06/04/bret-michaels-health-american-idol/?ncid=webmaildl2

 He performed Memorial Day weekend, and in the interview said, “On stage, normally, I go completely insane and kick ass. This time, I gave 100 percent of my 75 percent.” 

 

 

 

 

 

 

 

 

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