As a combat engineer in Iraq, Jeremy was supposed to find roadside bombs. They found him instead. Within 72 hours of each other, two improvised explosive devices (IEDs) went off within 15 feet of this father in his late 20s. The first set of blast waves, a moving wall of highly compressed air that emanates from an explosion, knocked him out briefly. The second left him dazed for about 30 minutes and produced ringing in his ears that disappeared within a week. These detonations did not visibly injure Jeremy (not his real name)—but he was never the same.
After his tour in Iraq, Jeremy became more irritable with his spouse and child. At his job as a manager of a national firm, he would get very frustrated when customers were abrupt or business was brisk. Jeremy’s memory had deteriorated, too, and he had to use a daily planner to remind himself of even the most basic tasks. He also had incapacitating headaches, spells of panic or confusion, mood swings, and sensory illusions such as a metallic taste or ringing in his ears. Neuropsychological tests revealed that Jeremy had real deficits in mental processing, attention and short-term verbal memory.
Jeremy was diagnosed with a “mild” traumatic brain injury (TBI), in which trauma to the head produces only a brief loss of consciousness or a transient disturbance of mental or sensory function. Such trauma is deemed mild, moderate or severe based on its immediate consequences rather than its long-term effects. Thus, some patients diagnosed with severe TBI—because they spent four days in a coma, for example—eventually return to work without incident, whereas some 10 to 15 percent of civilian patients who sustained mild TBI never fully recover from its effects.
According to the Centers for Disease Control and Prevention, 1.4 million American civilians sustain a TBI every year, three quarters of them mild. Indeed, mild TBI is the most common neurological condition in the U.S. other than headache, a category that includes migraines. In addition, as many as 320,000 U.S. service members have experienced a probable TBI of any severity in Iraq or Afghanistan, according to a 2008 report from RAND Corporation.
A blast strong enough to cause TBI is also powerful enough to produce emotional trauma and the psychiatric condition post-traumatic stress disorder (PTSD). Thus, many veterans, Jeremy included, experience both ailments. In particular, the combination of mild TBI and PTSD is considered the signature injury of the Iraq War. Responding to this emerging problem, the U.S. Congress allocated $300 million in 2007 to investigations into mild TBI and PTSD.
Meanwhile scientists have identified a number of ways in which blunt-force trauma (being hit in the head) damages the brain, including the creation of bruises, stretched or torn nerve cells, and electrical misfiring. They have also built a case for brain injury resulting directly from the pressure waves unleashed by explosions, even in cases where a soldier’s head did not strike any solid object. The new knowledge is spawning research into treatments for mild TBI, which may include antiepilepsy medications and various forms of psychotherapy.
By far the most common type of brain trauma in ordinary life is closed head injury—in which no bullet, knife or other object actually penetrates—resulting from the skull hitting a surface in a car crash, fall, sports activity, assault, or other incident or pursuit. Physician Claudia Osborn, now at the Michigan State University College of Osteopathic Medicine, sustained a mild TBI from a bicycle accident that permanently diminished her ability to practice medicine and cope with daily life. She describes her struggle to overcome her disability in Over My Head: A Doctor’s Own Story of Head Injury from the Inside Looking Out (Andrews McMeel Publishing, 1998).
About 300,000 mild TBIs (also referred to as concussions) result from sports every year in the U.S. Former professional wrestler and Harvard University defensive tackle Chris Nowinski has been knocked out, seen double and become disoriented many times after blows to the head. Most of the time he kept playing, but after six concussions Nowinski had to stop wrestling professionally. Repeated concussions have also ended the careers of a number of professional football players. Long-term consequences include a heightened risk of dementia and epilepsy.
Our brains are encased in a bony skull and a triplet of membranes called meninges. In addition, the brain floats in a clear liquid called cerebrospinal fluid (CSF), which provides a modest cushion against the effects of blunt-force trauma to the skull. These protective pieces prevent damage from minor falls or being hit in the head by wooden clubs and small rocks—the kinds of injuries typically experienced during the evolutionary history of humans. But because the brain’s biological barriers have not had time to respond to selective pressures from recent technological advances, they do little to shield the brain from a blast wave from a roadside bomb or a high-speed collision with a telephone pole. Even impacts from contact sports such as boxing, football and wrestling or from falls from riding horseback or skiing can inflict serious brain damage.
Concussions typically result from blows to the head or from the head hitting a hard surface or being shaken or spun. In response to such forces, the brain may smash against the skull, popping blood vessels and bruising brain tissue. Sometimes the impact causes the brain to bounce off one side of the skull and back into the other, producing a coup contrecoup injury in which the brain is injured at the site of the impact and on the opposite side. This type of injury may also occur without blunt-force trauma, say, when a soldier’s head is displaced a short distance extremely rapidly by an IED blast.
When brain structures move relative to one another and to the skull, tissue may stretch or even shear. In particular, the force can distend nerve axons, the long, slender fibers that extend from the main cell bodies and transmit messages among neurons. Axons are normally elastic, but when rapidly elongated they become brittle and weak. Often an axon swells and tears, killing the neuron.
Such cellular disintegration can also cause a neuron to release toxic levels of neurotransmitters (chemical messengers), damaging other neurons. This process sparks further degeneration of axons as well as apoptosis, or programmed cell death, throughout the cerebrum. Such diffuse axonal injury may underlie many of the persistent cognitive problems experienced by victims of mild TBI. In addition, mechanical forces can set off other problematic chemical cascades that can lead to latent symptoms, which may not appear until days after the initial assault.
Concussions may alter the firing patterns of nerve cells. Neurons damaged by trauma can become electronically unstable and thereby induce a type of neuronal static in small brain regions that, though too small to show up on an electroencephalogram (EEG), can spawn illusions, memory gaps and mood swings.
Although victims of mild TBI rarely display conventional epilepsy, many of their symptoms resemble an epileptic syndrome called simple partial seizures, in which an abnormal burst of cellular electrical activity in a restricted part of the brain produces brief motor, sensory, or even cognitive or emotional oddities while a person is conscious. (Which type of peculiarity—experiencing a memory gap, hearing an imaginary voice or feeling a burst of anxiety—depends on the part of the brain affected.)
Concussion patients typically have a wider spectrum of complaints than patients with simple partial seizures do. In this regard, they may even more closely resemble people diagnosed with epilepsy spectrum disorder, which is characterized by a variety of sensory, cognitive and emotional symptoms similar to those Jeremy experienced.
Aside from blunt-force trauma, soldiers on the battlefield may experience brain damage from penetrating missiles such as bullets and shrapnel—the dominant brain injury in past wars such as Vietnam—and the blast waves from IEDs, bombs, mortars and the like. The blast-wave brain injuries are appearing in record numbers among veterans of the wars in Iraq and Afghanistan. Hundreds, if not thousands, of U.S. soldiers are returning from Iraq with symptoms similar to Jeremy’s.
Such blast-related problems are not new to these wars. As early as World War I, soldiers reported psychiatric symptoms as well as sensory and cognitive impairments that appeared after explosions that caused no external visible injury. British army physician Fred Mott ascribed most such cases of “shell shock” to psychic trauma or emotional distress. Other doctors believed that the condition arose from an organic injury to the brain, citing changes on an EEG similar to those seen from closed head injuries.
But nobody seriously followed up on the brain damage theory until the 1990s, when neurologist Ibolja Cernak, now at the Johns Hopkins University Applied Physics Laboratory, noticed the effects of blast exposure in her medical practice at the Military Hospital in Belgrade during the war in the Balkans. Cernak repeatedly observed soldiers with memory lapses, dizziness and speech problems—clear signs of brain damage—who had never experienced any direct, blunt-force trauma to their heads. In brain-imaging studies, Cernak saw signs of injury: bleeding or enlarged ventricles (spaces in the brain filled with CSF).
Since then, studies by Cernak and others have hinted that blast concussions may indeed lead to brain damage directly and not just through psychological trauma. In 1998, for example, psychiatrist David Trudeau, then at the Minneapolis Veterans Affairs Medical Center, and his colleagues reported that 27 of 43 war veterans diagnosed with PTSD who had also been briefly knocked out or dazed by nearby explosions showed abnormal brain activity, as assessed by quantitative electroencephalography. Their quantitative EEG patterns differed from those of the 16 PTSD patients who had not had a history of mild TBI. In addition, 88 percent of the veterans who had experienced concussion blasts had significant problems related to attention and impulsivity as compared with 60 percent of the control group, indicating that the blasts had effects above and beyond stress.
Cernak reported similar findings in a 1999 study of 1,300 patients who had sustained wounds to their lower bodies but not their heads. She found that 30 percent of those who had been injured in a blast showed abnormal brain activity a year later as compared with only 4 percent of patients who had been wounded by projectiles.
But how could a roadside explosion affect the brain? Of course, brain damage could occur from blunt-force trauma associated with the explosion. A person may be hit in the head by an object—shrapnel, say, or debris from surrounding buildings—propelled by the blast. Similarly, an individual may be blown out of a vehicle or up against some solid structure, sustaining an injury similar to one that would occur from a head striking a car’s windshield.
Too Much Pressure
In addition—or in the absence of any impact with a solid object—rapid changes in atmospheric pressure produced by the explosions could cause brain damage, according to a 2006 paper by neurologist Deborah L. Warden of Walter Reed Army Medical Center and two of her colleagues.
During an explosion, the researchers explain, a solid or liquid is almost instantaneously converted into gases. These gases temporarily occupy the same volume as the solid or liquid and are thus under extremely high pressure. The gases then expand, compressing the surrounding air and forming a pulse of pressure called blast overpressure. As the gases continue to spread out behind the high-pressure region, they create a huge pressure drop.
Brain tissue itself has the consistency of firm custard—but custard of differing densities. As the shock wave reaches a soldier, the high- and then low-pressure air accelerates body tissues of differing densities at different rates. Inside the brain, the varied accelerations could shear and stretch axons just as blunt-force trauma does.
Yet a compression wave may also initiate brain damage in ways distinct from blunt-force trauma. According to neurologist P. Steven Macedo of the Washington Medical Group, shock waves can cause cavitations, or gas bubbles, in brain tissue. These bubbles can then pop, leaving holes.
Cernak, however, favors a different explanation. She speculates that blast waves pushing against the body’s surface create oscillating pressure waves in major blood vessels, similar to the rippling of open water in stormy weather. These ripples then travel up a person’s torso through his or her neck and into the brain, which is extremely sensitive to mechanical perturbation. Thus, the kinetic energy (energy of motion) of this blood could damage neurons, which may lead to neurological deficits. If such an indirect mechanism is involved in mild TBI, Cernak suggests, prevention of these injuries in soldiers must extend beyond better helmets or other measures that protect only the head.
Whatever the exact physical mechanism, animal research bolsters the notion that compression waves alone—in the absence of blunt-force trauma—can hurt the brain. In a 2007 study researchers at Tohoku University in Japan exposed adult male rats to shock waves of differing magnitudes from experimental explosions after removing a section of their skull to expose their brain. The scientists found that high-pressure shock waves, those similar in magnitude to explosions at close range, cause cerebral bruising and bleeding that induce neurons to commit cell suicide.
Lower-pressure waves, such as those that might arise from a tire blowing out near your face, can distort the shape of neurons. The findings suggest, the authors write, “that the threshold for shock-wave induced brain injury may be lower than 1 MPa [megapascal], which is a lower level than that reported for other organs.” (One MPa is about 10 times normal atmospheric pressure.) Moreover, they say, the damage from these shock waves resembles that from other types of traumatic brain injury.
On top of these physical forces, the psychological stress of being near a detonation may cause brain damage or dysfunction through excessive secretion and action of stress hormones in the brain. Brain injury often co-occurs with PTSD, and elevated levels of stress hormones such as cortisol associated with PTSD may exacerbate or slow the healing of any blast-induced brain damage. Jeremy’s symptoms may have, in fact, arisen from both disorders, given that he shows clear signs of PTSD: he experiences flashbacks, avoids war reminders and is easily startled.
What is more, some researchers such as Harvard neurologist Michael P. Alexander still maintain that emotional and psychiatric issues are the main if not sole cause of the problems experienced by veterans like Jeremy. In a 1995 paper in the journal Neurology, Alexander suggested that telling patients they have hurt their brain could stall their recovery by making them perceive their problems as more intractable than they are.
And when psychiatrist Charles W. Hoge of Walter Reed Army Institute of Research and his colleagues surveyed 2,525 U.S. Army infantry soldiers three to four months after their return from a year of duty in Iraq, they found that PTSD was strongly associated with mild TBI. The researchers conclude in their 2008 paper in the New England Journal of Medicine that PTSD and depression—rather than the physical impact to the brain—were the probable causes of the veterans’ neurological complaints, which included irritability and concentration lapses, because these psychiatric disorders have been linked to a wide range of physical health problems.
No matter the relative roles of emotional fallout versus organic brain damage after an explosion, fall, car accident or sports injury, both psychiatric issues and brain injury are part of the medical equation in many patients. When a patient suffers from PTSD or depression, doctors often prescribe an antidepressant and psychotherapy, including individual and group counseling, both of which Jeremy received for his PTSD.
In particular, patients with PTSD often respond to cognitive-behavior therapy, in which practitioners try to dismantle distorted thought patterns and correct maladaptive behaviors. One behavior-modification technique is exposure therapy, in which a counselor uses experiences similar to those that gave rise to the traumatic stress to help a patient get used to these situations, reducing their emotional impact. Patients may sometimes receive such exposure through virtual-reality computer programs that reenact war zones, the 9/11 attacks on the World Trade Center or other harrowing scenarios [see “Fantasy Therapy,” by Nikolas Westerhoff; Scientific American Mind, October/November 2007].
When a patient is also likely to have sustained a bona fide brain injury, he or she often improves with a class of drugs known as anticonvulsant mood stabilizers, which include valproic acid and carbamazepine, most often used to treat classic epilepsy and bipolar disorder. In 1997 neuropsychiatrist Bruno Wroblewski, then at the Greenery Rehabilitation Center in Boston, and his colleagues reported that treatment with valproic acid markedly reduced destructive and aggressive behaviors in patients who had experienced blunt-force TBI. Jeremy took the same drug and found that it helped reduce his memory lapses, sensory illusions and mood swings.
In a similar vein, in 2000 psychologist Michael A. Persinger of Laurentian University in Ontario reported that 12 of 14 patients who took carbamazepine after blunt-force brain trauma resulting from motor vehicle accidents “experienced marked reductions in the incidence of sudden confusion and depression, increased attention and focus, and either elimination or reduction of an aversive sensed presence” (the last is an illusion of movement in peripheral vision). No one is sure why such agents might be effective, because mild TBI patients rarely have classic epilepsy, but perhaps the drugs help to alleviate some of the electrical instability among neurons that brain injuries can induce.
The brain also tries to repair itself after injury, and scientists are trying to learn more about those repair processes in hopes of boosting them with medications. They are developing treatments to be given during the first hours after a TBI designed to limit any ongoing injury [see “Duct Tape for the Brain,” by Lucas Laursen]. A more futuristic approach might involve the implantation of neural stem cells, immature cells that can give rise to different types of mature cells in the central nervous system, to repair or replace damaged brain tissue.
But for now, patients must make do with more symptomatic relief from antidepressants, sleep medications and, in some cases, anticonvulsants. Many also receive cognitive rehabilitation in which they learn strategies that enable them to circumvent their deficits. For instance, when introduced to someone new, the patient might rehearse his or her name several times or use visual imagery as a memory cue.
Becoming better organized is another useful skill for the cognitively enfeebled. Some tricks include using a weekly pillbox or finding one place for key items such as a wallet and cell phone. Technology can also help patients manage daily life. Jeremy, for instance, now uses a PalmPilot to serve as an electronic prosthesis for his inconsistent memory functioning. “Smart” phones and tape recorders can also serve as backups for fragile human memory, enabling the brain-injured (not to mention the rest of us) to record key information as soon as they receive it.
Sometimes patients must alter their way of life to accommodate their decreased ability to function. They may, for example, have to avoid social situations that are too stimulating, radically adjust their work hours, leave a risky or stressful job, or even enter a residential program for the brain-injured. Jeremy decided to resign from his demanding managerial position and is now interviewing for another job. He hopes to find work assisting fellow veterans who are, like him, looking for a new career in civilian life.
Note: This article was originally printed with the title, "Impact on the Brain".