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.
The incidence of TBI among troops may actually 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 I was, 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 hurt too 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.
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]