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IMPACT AND THE BRAIN: MILD TRAUMATIC
BRAIN INJURY
A PLAGUE AMONG COMBAT VETS -- VA
neuropsychologist
Richard J. Roberts, writing for Scientific
American,
brings the issue of MTBI to the forefront.
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http://www.sciam.com/ar
ticle.cfm?id=impact-and-the-brain
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-------------------------
Impact and the Brain
Mild traumatic brain injury
represents a silent but brutal plague among combat veterans and a hidden
threat to the health of civilians
By Richard J. Roberts
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.
Blunt Force
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.
Shell Shock
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.
Treating Trauma
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".
ABOUT THE AUTHOR
Richard J. Roberts is a neuropsychologist at the Iowa City Department of
Veterans Affairs Medical Center. He received his Ph.D. from the University
of Iowa, where he is currently clinical adjunct associate professor. The
author wishes to express appreciation to numerous professional colleagues
with whom he discussed aspects of this article and to Kathryn Elizabeth
Roberts for fact-checking and reference work.
-------------------------
posted by Larry Scott
Founder and Editor
VA Watchdog dot Org
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