Traumatic brain injury on the front line

Traumatic brain injury (TBI) is said to be one of the “signature injuries” of the conflict in Iraq, and accounts for a larger proportion of troop casualties than it has in previous wars fought by the United States. According to the Defense and Veterans Brain Injury Center, the U. S. military formally diagnosed 2,121 cases of TBI between October 2001 and January 2007. But the incidence of TBI among troops may be much higher than these official statistics suggest, largely because of the increasing use of the signature weapon of the Iraq war: the improvised explosive device (IED). Neurologists say that the Pentagon’s figures are based on the number of recorded penetrative head wounds, and exclude the closed head wounds also caused by IEDs, which are much more difficult to diagnose, and which may far outnumber the other types of brain injuries. The actual numbers of troops with TBI may therefore be much greater than the official estimates.

An IED consisting of 155 mm shells, Semtex plastic explosive and canisters of butane or barrels of gasoline can completely destroy a Humvee or turn a 70 tonne tank upside-down. During the detonation of an IED, a solid or liquid is converted into a gas. This gas momentarily occupies the same volume as the “parent” solid or liquid, leading to an enormous increase in air pressure. As a result, the gases expand, heating and accelerating the air molecules and compressing the air surrounding the explosion. The high pressure blast waves generated by an IED travel at 1,600 feet per second, and can be propagated for several hundred yards from the site of the explosion. This initial blast wave is followed by what is called a “secondary wind” – a huge volume of displaced air that returns to the site of the explosion, also under extremely high pressure.

Detonation of an IED always propels fragments of shrapnel at a high velocity. These fragments can cause damage to the brain if they penetrate the skull. Such injuries (referred to as ballistic trauma) are “conventional” TBIs; they are easy to diagnose, because the shrapnel fragments leave entry wounds, and can be treated in a standard way: foreign bodies are removed from the brain, and the patient is given a type of drug called a calcium channel blocker, such as Amlodipine or Nifedipine, to prevent further damage to injured neurons. Diuretics may then be administered intravenously to prevent further swelling and, in extreme cases, a craniectomy can be performed. This surgical procedure, which involves the removal of a part of the skull, allows continued swelling while preventing the swollen region of the brain from coming into contact with the skull, which would otherwise cause more damage.

The symptoms of TBI can be mild, moderate or severe, depending on the extent of damage to the brain. The severity of injury is sometimes determined by the period of time it takes for a patient to regain consciousness following his or her injury. Patients with mild TBI often experience memory loss, sleep disturbances, confusion, dizziness and blurred vision. Those with moderate or severe TBI may also show these symptoms, as well as vomiting, nausea, loss of coordination, weakness or numbness of the extremities, convulsions and seizures.

Sergeant David Emme, a supply officer with a U. S. Army Stryker Brigade, sustained TBI while his armoured vehicle patrolled northen Iraq. The blast wave from the explosion had fractured his skull, injured his left eye, and burst his left eardrum (a ruptured tympanic membrane is the most frequent blast-related injury, because the parts of the body most vulnerable to changes in air pressure are those in which there is an interface between air and fluid, such as the lungs, bowels and inner ear). It had also caused a severe contusion in the frontal and temporal lobes; the swelling had damaged the brain’s speech centres, and in consequence, Sargeant Emme’s symptoms included two different types of aphasia – an inability to produce speech and an inability to understand it.

Here, Sergeant Emme describes his symptoms:

I remember waking up and wondering who the hell I was, where the hell Iwas, and why can’t I see or hear? My soldier was screaming for me to get out of the truck and I told him no, because it hurttoo much. So he literally threw me out of the truck and guided me to a Stryker [a lightweight armoured vehicle]. The next time I came to, I’m at Walter Reed [Army Medical Center] — like, 10 days later. I called for the nurse…I kept on just trying to say something, but I couldn’t really say anything. Basically, I had to learn what things were again. I knew what they were — I just didn’t know what the names of them were.

Because he had a penetrative head wound, Sergeant Emme was evacuated almost immediately to a nearby combat support hospital, where neurosurgeons performed a craniectomy. The large piece of skull removed from over his left temporal lobe was implanted under the subcutaneous tissue in his abdomen, so that it could be replaced once he had recovered. Subsequently, Sergeant Emme received months of speech therapy and other forms of rehabilitation. But for every veteran whose brain injury is diagnosed and treated, there may be ten whose injuries have not yet been recognized, because IEDs can also cause closed head injuries that are more difficult to diagnose. These occur as a result of the shock waves generated by a blast, which subject all the organs in the body to displacement, shearing and tearing forces. The brain is especially vulnerable to these forces – the fronts of compressed air waves cause rapid forward or backward movements of the head, so that the brain rattles against the inside of the skull. This jarring of the brain against the skull can cause subdural hemorrhage (bleeding in the cavity between two of the collagenous linings around the brain) and contusions (bruises). Most often, these contusions are to be found in the anterior (front), lateral (side) and inferior (lower) aspects of the frontal and temporal lobes, and, less frequently, in the occipital lobe and cerebellum.

Troops with closed head injuries show no external signs of injury, and appear to be normal. And, if they have sustained other obvious external injuries, the medics treating them may neglect to test for neurological damage. Subtle personality changes that may occur as a result of such injuries would only be noticed by relatives or close friends who know the patient well, and other symptoms could take years to develop. The effects of such injuries may therefore go unnoticed for years or even decades. The difficulty in diagnosis is further compounded by the fact that many of the symptoms of closed head injuries overlap with, or sound similar to, those of post-traumatic stress disorder (PTSD).

The forces exerted on the brain by shock waves are known to damage axons in the affected areas. This axonal damage begins within minutes of injury, and can continue for hours or days following the injury. The subsequent impairment of axonal transport causes swelling of the damaged processes. At least some TBI symptoms are believed to be the result of this axonal damage, and the subsequent loss of synapses. The exact cause of axon damage is unknown, but excitotoxicity (death of neurons by over-excitation) and oxidative stress (death of neurons by exposure to free radicals) have been suggested.

Shock waves are now known to damage the brain at the subcellular level, but exactly how remains unclear. As the compressed sound waves travel through the brain, they seem to lead to the formation of small air bubbles, which leave small cavities in the brain tissue when they burst. If these bubbles form within blood vessels, they can form emboli (blood vessel blockages) that travel to the brain, causing parts of the brain to die due to lack of oxygen. A study by Japanese researchers, published last month, described the effects of a small controlled explosion on rats’ brain tissue. It was found that very brief exposure to high pressure shock waves (i. e. for fractions of a second), of the type that would be experienced upon detonation of an IED, led to contusions and hemorrhage in both cortical and subcortical brain regions. The shock waves also induced programmed cell death throughout the tissue surrounding areas of hemorrhage. It is also clear that shock waves lead to activation of microglia, cells of the immune system that are recruited at sites of brain injury. Such injuries are, however, poorly understood by neurologists, and are therefore difficult to treat.

Neurologists affiliated with the U. S. military now estimate that up to 30% of troops who have been on active duty for 4 months or longer (in both Iraq and Afghanistan) are at risk of some form of disabling neurological damage. This is partly based on the knowledge that closed head injuries far outnumber the penetrative head injuries on which official statistics are based. So, while official figures put the number of U. S. troop casualties in Iraq and Afghanistan at 22,600 (as of November 2006), there may be up to 150,000 already suffering from TBI.

These same neurologists are among those who have highlighted the Bush administration’s neglect of its injured troops. They emphasise the need for prompt diagnosis and evaluation of troops who have sustained TBI, as well as improved methods for screening returning troops for brain damage and better monitoring of injured troops’ progress during treatment and rehabilitation. With a U. S. presidential election looming, the subject has now been picked up by politicians: at last month’s hearing of the Veterans Affairs and Armed Services Committee, for example, Senators Susan Collins (R-Maine) and Hilary Clinton (D-N. Y.) proposed to Defense Secretary Robert Gates that he set aside $3.75 million for the creation of a computer-based system for the measurement of cognitive functions in troops before and after deployment to war zones. And the legislators have started putting plans into motion: Congress recently authorized $450 million from the Iraq spending bill for research into TBI.

References:

Kato, K., et al (2007). Pressure-dependent effect of shock waves on rat brain: induction of neuronal apoptosis mediated by a caspase-dependent pathway. J. Neurosurg. 106: 667-676. [Abstract]

Kaber, K. H., et al. (2006). Blast-related traumatic brain injury: What is known? J. Neuropsychiatry Clin. Neurosci. 18:141-145. [Full text]

Okie, S. Traumatic brain injury in the war zone. NEJM 352: 2043-2047. [Full text]

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9 thoughts on “Traumatic brain injury on the front line

  1. This is a great post highlighting a critical problem for the U.S. military that we will be dealing with for decades to come. Between TBI, PTSD, and injured or lost limbs, hardly any of our soldiers and marines are returning from deployment unscathed. Those who appear whole and healthy are likely still suffering an injury of some kind.

  2. In the late 1980′s I suffered a concussion. Upon seeing the company doctor, within hours after the injury, I felt intense anger. The doctor wrote it off as “my fellow employees seeing the cut on my head”. Within a year I had horrible panic attacks/depression and became housebound. For years I had doctors who misdiagnosed my illness as everything from Bipolar to depression and agoraphobia. I thank God that this is finally getting the attention it deserves. TBI and post-concussion syndrome are horrible illnesses that will destroy your life. And the lives of your family.

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  4. I worked as a non-union movie extra on a union made movie in 1990 and was assaulted and battered and blasted with
    concealed military high explosives PETN (plastic explosive), Lead Azide and Lead Styphnate. Now, in 2007 I still have head pain. In 1994 the first federal judge ruled that I had no private right of action to charge the movie people with a crime and dismissed the case, 94-4630(RMT) U.S.D.C. Central California (Los Angeles). The next federal judge wrote an opinion full of error or fraud, and dismissed the case. He apparently regarded these concealed military high explosives as “special effects” and seemed to consider it normal workers comp. jurisdiction to assault and batter and blast unsuspecting non-union movie extras. 97Civ3081(TPG) U.S.D.C. Southern District of New York. I have never had a brain scan. The F.B.I. sent me a Freedom of Information Act Report in 1999 and apparently they expunged and destroyed material in my case. God Bless America! It’s not safe at home or abroad!

  5. Contrary to what the article states, this is NOT a new problem, nor is it confined to the Bush Administration. I was nearly fatally injured in a military parachute training accident in 1982. I was scalped on the left side of my head and left for dead by medics as part of the triage process. I woke, was able to finally get help and had apparently recovered from my injuries enough so that eight months later I was put back on Jump Status as a fully fit paratrooper, rising rapidly through the ranks and seeing combat service in Grenada in 1983.

    However, after my injuries I began experience weight gain which in the post-Vietnam Army is one of the unforgivable sins. Five years after being declared a “water walker” for coming back from my injuries I found myself facing discharge under the terms of AR 600-9, the Army weight control program. It was only an alert physician who noted my head injuries and subsequent weight gain and linked the two.

    I was medically discharged with 10% disability for having post-traumatic hypothalamic obesity secondary to my head injuries. That was in 1987. It didn’t take long to realize my injuries and condition were much more severe than I had orginally been led to believe (or perhaps anyone knew) and I have been fighting the VA for years to get a proper rating for my condition – there is none, the VA only has a rating for hypothyroidism – which is a secondary condition to the damage to my hypothalamus. I had just about given up when I began reading articles such as this one.

    I would hate to see another generation of soldiers go through the same hell as I. So I thank you for bringing attention to this situation. It goes much farther than even psychological damage. I, for all outward appearances have suffered no psychological damage (what I do have I handle), however, physically, the hypothalamus, which sits at the base of your brain, controls the entire endocrine system. Since my injuries I have not only experienced massive weight gain (from 170 to 300+ pounds), but severe allergies, asthma, hypopituitarism, hypogonadism, hypothyroidism, and other endocrine related maladies. This doesn’t take into account the stress my added weight has placed on my joints. What is the VA’s answer? 10% for hypothyroidism, 10% for each knee, 0% for my other maladies, and 50% for -get this- Sleep Apnea caused my obeisty.

    So I thank you for articles such as these. Knowledge is power.

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  7. Hello Friend,

    I am interested in providing encouragement to our veterans and the soldiers who have been wounded while protecting our great country. Additionally, I am interested in providing practical information and insight to assist their families. My name is Craig J. Phillips. I am an alumnus of Oral Robert’s University Class of 1985, an alumnus of the University of Kentucky, graduate program in Rehabilitation Counseling Class of 1990, and a traumatic brain injury survivor. I sustained an open skull fracture with right frontal lobe damage and remained in a coma for 3 weeks at the age of 10 in August of 1967. I underwent brain and skull surgery after waking from the coma. Follow-up cognitive and psyche / social testing revealed that I would not be able to succeed academically beyond high school. In 1967 Neurological Rehabilitation was not available to me, so I had to teach myself how to walk, talk, read, write and speak in complete sentences. I completed high school on time and went on to obtain both my undergraduate and graduate degrees. For an in depth view of my process please read my post, http://secondchancetolive.wordpress.com/2007/02/18/my-journey-thus-far/

    Through out my lifetime I developed strategies to overcome many obstacles and in so doing I have achieved far beyond all reasonable expectations. On February 6, 2007 at the encouragement of a friend I created Second Chance to Live. Second Chance to Live, which is located at http://secondchancetolive.wordpress.com presents topics in such a way to encourage, motivate and empower the reader to live life on life’s terms. I believe our circumstances are not meant to keep us down, but to build us up. As a traumatic brain injury survivor, I speak from my experience, strength and hope. As a professional, I provide information to encourage, motivate and empower both disabled and non-disabled individuals to not give up on their process. Please read my post, http://secondchancetolive.wordpress.com/2007/04/18/the-power-of-identification/

    My interest is to provide encouragement, hope, motivation and empowerment to survivors and their families. Please encourage your readers to visit Second Chance to Live at http://secondchancetolive.wordpress.com and consider adding Second Chance to Live to your web site as a useful resource and placing a notice in your newsletter.
    Thank you for your time and kindness.

    Have a simply phenomenal day!
    Craig J. Phillips MRC, BA
    Second Chance to Live

    Our circumstances are not meant to keep us down, but to build us up!

    Note: I recently found out that Second Chance to Live has been published by the European Brain Injury Society E.B.I.S. with in their Autumn 2007 Newsletter http://www.ebissociety.org/automn/newsletter-angl.htm in both French and English. Specifically, My Journey thus Far has been printed. I am encouraged by the growing global interest of the material presented in Second Chance to Live and wanted to share the good news with you.

    My article, Traumatic Brain Injury and Displaced Energy has been published by the Brain Injury Association of Niagara, Newsletter January 2008 http://www.niagara.com/bian/

    Virginia Commonwealth University’s Department of Physical Medicine & Rehabilitation Neuropsychology http://www.tbi.pmr.vcu.edu/ My Journey thus Far, TBI Today Volume 6 Issue I — winter 2008 issue News, Ideas and Resources from the Virginia TBI Model System

    As of Thursday, February 21, Second Chance to Live started receiving ongoing visits from the Department of Veteran’s Administration via their offices located throughout the United States.

    I am available for speaking engagements, conferences and seminars. My message is to encourage the faint hearted, to hold up the arms of the weary and to empower people to dream again. In the event that you know of groups, churches or organizations that could benefit from my experience, strength and hope please let them know about Second Chance to Live.

    Thank you!

  8. In response to Wayne Wood’s posting. I am 2 years out from a head injury and am having to buy new pants each season. Prior to my injury I was one of those that had to work to keep the weight on & now….it’s quite different. I have just recently thought that it has got to be connected to my head injury. So, thank you for your posting. I will investigate the hypothalamus theory. Seems possible, in that my brain stem was also injured & I think they may be located quite close. Thank you!

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