Traumatic brain injury (TBI) is “an
alteration in brain function, or other evidence of brain pathology, caused by
an external force” (Bagalman, 2013, p. 2). There are two major forms of TBI;
closed head and penetrating head. Closed head TBI is a result of the head
coming to a rapid standstill while the brain, suspended in fluid, continues to
strike the skull; also termed the “bobble head” effect (Goldstein, McKee, &
Stanton, 2014). The severity of closed head TBI is classified as: mild, moderate
or severe (Graner, Oakes, French et al., 2013). Penetrating head TBI is a
result of an object entering the skull and into the brain (Kovacs, Leonessa,
Grimes et al., 2014). Blast-induced TBI (bTBI) is argued to be a third type,
although this is not universally accepted (Kovacs et al., 2014).
In war
settings, the majority of military-related TBI is the result of exposure to
explosive blasts (McKee & Robinson, 2014). Bombings have become an
increasingly effective terrorism tool and in the current
conflicts in Iraq and Afghanistan, bTBI has become frequently common among
service members. Explosive related injury
is not a new phenomenon, but an increasing use of bombings in modern warfare
has created further attention.
In World War I (1914-1918),
military exposed to bomb blasts often experienced what became known as shell
shock or “commotio cerebri”. The condition often
left soldiers unable to fight, but the pathology was unclear. In modern times, it is now known that blast-related brain
injury can leave no external marks of damage (Suh et al.,
2007).
Improvised explosive devices (IEDs) are regularly encountered in the
Iraq and Afghanistan wars. Explosives are categorized as either
high-order explosives (HE) or low-order explosives (LE). Briefly, HE detonate quickly and produce an
over-pressurization blast wave that rapidly expands from the detonation point. In contrast, LE produce a subsonic explosion without an
over-pressurization wave, and are regarded as less destructive. Soldiers in the proximity of an explosion can receive four types of
blast injury; primary, secondary, tertiary, and quarternary.
Primary injuries result from the physical forces generated by the blast wave,
secondary injuries are inflicted from flying debris, tertiary can occur from a
body being thrown and striking an object and quarternary relate to all other
injuries not covered by the first three types; such as burns (Kovacs et al.,
2014).
All
body parts can be affected from secondary, tertiary, and quarternary blast
injuries (Lemonick, 2011); however the current post focuses on blast-wave
associated primary injuries. As well as neurotrauma, a
number of injuries are associated with primary blast effects. The most
vulnerable regions of the body are the air-fluid components found in the lungs,
bowel, and middle ear.
Barotrauma (injuries sustained from blast-wave induced changes in atmospheric
pressure) can lead to organs and tissues being damaged from stretching and
shearing forces (Kocsis & Tessler, 2009). Pulmonary barotrauma, or “blast
lung”, is the most commonly fatal primary blast injury (Scott, Vanderploeg,
Belanger et al., 2005). Other injuries include ruptures to the tympanic
membrane of the ear and gastrointestinal tract, and damage to the eye globe (Fuse,
Okumura, Tokuno et al, 2011).
Brain
injuries from primary blast can include: concussion (Lemonick, 2011); systemic
acute gas embolism induced by pulmonary barotrauma can cause the blood vessels
to the brain to become obstructed, and this can cause
damage such as edema, diffuse axonal injury and hemorrhage (Fuse et al., 2011);
vasospasm, the constriction of blood vessels, can occur in cerebral regions and
last for as long as one month (Levine & Kumar, 2013); contusions can also
appear on the frontotemporal regions and occipital lobes as a result of brain shift
(Elder, Mitsis, Ahlers et al., 2010). Blast-related mild TBI has been
associated with neurodegeneration and large disruptions to white matter tracts,
and this damage is compounded if the person had experienced previous bTBI (Davenport,
Lim, Armstrong et al., 2011). Symptoms of concussion and mild TBI often subside
over a few weeks, however some people may develop chronic symptoms or
postconcussive syndrome; including symptoms of sleep disturbances and prolonged
psychological distress (McKee & Robinson, 2014). The pathological effects
on the brain from a blast-wave are still not fully understood; the two most prominent theories are presented below.
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| Coup-Contre-Coup Injury |
The leading
theory on how explosive blast causes TBI is the
pressure wave mechanism. This theory posits that shock
waves generated from an explosion travel through the air, impacting the head,
which then passes through the brain causing its acceleration and deformation
(Kovacs et al., 2014). In addition to the shock waves impacting the victim’s
head, further damage can be inflicted to the brain by what is known as a
‘coup-contre-coup’ injury. When an explosion detonates close to a soldier, the
pressure-wave impacts the blast-facing surface of the skull; this ‘coup’ injury
causes the brain to knock against the skull that creates neurotrauma at the
point of contact. Following the initial
impact, the brain is violently shifted to the opposite side of the skull
leading to the ‘contre-coup’ injury (Goodrich et al., 2013).
Since the Balkan
Wars in the 1990s, Dr. Ibolja Cernak has become a leading researcher in
blast-induced neurotrauma. Interest in this form of TBI was
inspired when she examined soldiers presenting with memory deficits, speech
problems, dizziness, and decision-making difficulties after exposure to
explosions. Unusually, the majority of these soldiers did
not have any external signs of injury, but MRI scans showed much internal
damage to the brain; including enlarged ventricles and minor internal bleeding
(Bhattacharjee, 2008). Later, soldiers returning from the Iraq war complained
of cognitive and behavioural problems; many of whom had suffered blast exposure
and loss of consciousness without noticeable head injuries. This resulted in Cernak
devising her theory for the pathology of this TBI; the vascular transmission theory. The theory
argues that once a blast-wave strikes a soldier, kinetic energy travels through
the blood vessels towards the brain. Specifically, the blast
that impacts the torso area compresses organs and forces blood into the skull
(Dennis & Kochanek, 2007). The pulse oscillates rapidly through the neck
and enters the brain, damaging axons and neurons in the hippocampus, brainstem,
and structures around the cerebral vessels (Bhattacharjee, 2008). This theory
is debated more than the pressure wave mechanism but both theories are likely
valid in the pathogenesis of bTBI (Kovacs et al., 2014). Moreover, whichever
theory is accepted, what is certain is that brain injuries are the result.
A
neurodegenerative disease that can develop in military exposed to bomb blast is
chronic traumatic encephalopathy (CTE); which is caused, in part, by repetitive
brain trauma (Baugh et al., 2012; Goldstein et al, 2012). Previously only
associated with boxers, the symptoms of CTE often appear years after a
trauma-producing event which can make it difficult to diagnose. Symptoms of CTE can include cognitive deficits, mood disorders, and
behavioural problems (Baugh et al., 2012). Frequently observed gross pathologic
features of CTE are generalized cerebral atrophy, thalamic and hypothalamic
atrophy, enlargement of the lateral and third ventricles, shrinkage of the
mammillary bodies, and thinning of the corpus callosum (McKee & Robinson,
2014). Injuries associated with bTBI are not only confined to neurological
damage, as psychological issues can also develop.
A
psychological problem encountered by some victims of bTBI is post-traumatic
stress disorder (PTSD) (Warden, 2006). PTSD is an anxiety disorder stemming
from “a delayed and protracted response after experiencing or witnessing a
traumatic event involving actual or threatened death or serious injury to self
or others”. Warden (2006) notes soldiers with mild TBI
have a higher risk of developing PTSD. Mild bTBI shares much similarity with
the clinical features of PTSD, such as difficulties with concentration (Kanter,
2007), sleep disturbances, and mood alteration (Ling et al., 2009). Due
to the similar characteristics of both, a problem arises here with the
potential for misdiagnosis (Ling et al., 2009). As soldiers may present with
co-occurring symptoms, Warden (2006) advises that clinicians should be mindful
of each diagnosis during assessments. This helps to avoid the wrong forms of
therapy being offered to soldiers. Soldiers who suffer TBI
are also more susceptible to depression. Depression after TBI is estimated to be three times more likely
than the rates for the general population. Further, as with PTSD, overlapping
symptoms of depression and TBI can make TBI diagnosis difficult. This again highlights a need for
clinicians to adequately assess military personnel exposed to bomb blast.
Treating
TBI victims from the Iraq and Afghanistan wars could be astronomical, with some
estimating that 14 billion dollars could be spent over the next 20 years
(Bhattacharjee, 2008). Due to the economic burden and the physical and
psychological consequences of bTBI, there is a growing interest in research of
animal models of trauma. The most common experimental models of explosive blast
are open field blasts, blast tubes, and shock tubes. A detailed description of
each was discussed by Kovacs and colleagues (2014) and is summarized here. Open
field blasts are regarded as the most accurate representation of blast-injury
in humans. They utilize an explosive device that is detonated in an outdoor
location. The instrument can be placed on the ground or suspended, with animal
subjects placed at specific distances. It is a valid blast model; as real-life
combat explosions involve shock wave reflections from surfaces such as the
ground or walls.
The second model, the blast tube, creates a shock wave and
blast wind once detonated. It ensures animal subjects are exposed to a “pure”
blast without reflected shocks, and prevents secondary, tertiary, and quarternary
injuries.
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| Typical Shock Tube Experimental Setup |
Lastly, shock tubes use compressed gas and are an alternative to the
blast tube. Regarded as safer and more economical, they have the added benefit
of being easily used in lab settings. Furthermore, shock tubes can mimic
primary blast injuries to isolated body parts, such as the head or abdomen.
Kovacs et al. (2014) also highlight some problematic elements of the models,
such as weather conditions when using open field blasts, or the possibility of
shock tube fragments impacting the subject, making comparison to human injury
difficult to extrapolate.
Exposing
animals to primary blast effects show that neurological impairments can occur
due to structural changes in the brain (Kocsis & Tessler, 2009). For
example, rodent brains examined after a primary blast exposure in concrete
bunkers showed evidence of widespread microglial activation (Kaur, Singh, Lim
et al., 1995), suggesting cell damage
after the blast. Although studies often employ using rodents because of expense
factors, numerous physiological responses can be different in smaller animals. Therefore, a larger animal would be more suitable to replicate
blast-induced trauma, with swine becoming the preferred choice.
The key reason for using swine is that they closely match some human anatomy
and physiology (Swindle, 2010). As well as having anatomical similarities with
abdominal organs such as the liver, kidney, and pancreas; similarities also
exist with the skin and subcutaneous tissues. Swindle (2010) adds that they
have a large gyrencephalic brain and similar cardiothoracic anatomy and
physiology.
Blast
models use anesthetized swine suspended in slings or in fixed supports. The
animal is exposed to altering degrees of explosives that are situated at
various proximities. Injuries incurred are mainly due to the blast wave that
follows the explosion. Specifically researching neurotrauma in
the animal, Swindle (2010) discovered that neuropathology was most evident in
the white matter with fiber degeneration and astrocytosis; while short and
long-term movement disruptions were also observed. Again, drawbacks exist with
these animal models. As a general anesthesia is required for ethical purposes,
experimenters regard it to complicate factors when later examining
physiological outcomes on the animal (Swindle, 2010). Further, experimental
difficulties have been acknowledged when comparing low level blasts on animal
subjects to how they may affect a human (Elder, Stone, & Ahlers, 2014);
with some authors arguing that blast experiments need to start incorporating
phantoms and human (cadaver) heads to fully validate the results in these blast
models (Gupta & Przekwas, 2013).
Bombings have
increased dramatically in modern warfare. Blast-induced TBI
can have neurological (Baugh et al., 2012; Davenport et al., 2011; Fuse et al.,
2011), psychological (Warden, 2006) and economic implications (Bhattacharjee,
2008), consequently much interest focuses on soldier protection. Due to
advancements in improving the effectiveness of body armor, more and more
soldiers are surviving explosions that may have resulted in death during
previous wars (Warden, 2006). Subsequently, this has led to an increased
prevalence of TBI. Research on protective head gear in sport has
shown that impact forces to the brain are reduced; however they do not lessen
incidences of concussion (McCrory et al., 2009; Zafonte & Discussant, 2011).
Difficulties developing the most optimal forms of head protection (and armor)
in the military also exist. For example, Cernak (2010) conducted experiments
with mice examining protective blast measures. Using shock tubes, the animal
model had three conditions; whole body blasts without protection, torso
protected, and head protected.
Cernak discovered that; head
protection did not prevent chronic inflammation and neurological deficits in
the mice; the same damage was seen in both the head protected condition as well
as full body exposure; and the torso protection reduced blast-induced
morphological changes in the brain. Cernak (2010) believes that this research
further supports the vascular transmission theory of bTBI. In military settings,
blast pressure waves can be more than 1,000 times that of atmospheric pressure,
which can make the most modern helmets ineffective. Resultantly,
combat soldiers wearing helmets beside explosions often display neurological impairments
(Bhattacharjee, 2008). Therefore, Cernak suggests that to prevent bTBI,
there should not only be a focus on developing optimal head protection, but a
strong emphasis on body armor.
Although
physical protection from explosions is paramount, other authors have examined neurological protection post blast
(Giovanni et al, 2005). After initial blast exposure, neural activity can be
weakened, and as a brain injury evolves; subsequent excitotoxicity exacerbates
neuronal damage (Dennis & Kochanek, 2007). Giovanni and colleagues
(2005) researched treatment on cell cycle inhibition after TBI. They found that
neural degeneration may be halted with the use of cell-cycle inhibitors.
Reductions in lesion volume and a near complete recovery were observed in rats,
with the experimenters proposing that cell-cycle inhibitors be incorporated as
a TBI clinical treatment. If researchers continue to
struggle with developing blast protection, techniques to assess and diagnose
bTBI will be increasingly required. Neuroimaging techniques have become vital
tools in this regard.
Soldiers are often exposed to blasts but fail to report it due to not perceiving any injury. Therefore a number of neuroimaging techniques are used to improve diagnosis and treatment of bTBI. The first of these is computerized tomography (CT) scanning which is presently the standard equipment used for examining soldiers with head injuries (Benzinger et al., 2009). Readily available in most military hospitals, it has the ability to identify contusions, hematomas, penetrating injuries and fractures; although it is limited in distinguishing normal from mild blast injury (Benzinger et al., 2009). As noted, vasospasm is regularly identified in soldiers exposed to blast (Levine & Kumar, 2013), and transcranial doppler (TCD) is a vital screening tool for this bTBI symptom. The equipment is also highly portable which makes it ideal for battlefield implementation.
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| MRI Scan |
Magnetic Resonance Imaging
(MRI) has recently become a preferred imaging tool for identifying brain
lesions in people with mild TBI. Although it can
identify up to 50% more lesions than CT, precaution must be taken for embedded
shrapnel which could lead to further injury from the equipment’s magnet. Positron emission tomography (PET) has also added
understanding to the underlying pathophysiology in TBI, but it requires
significant equipment that makes it logistically unfeasible for military field
screenings (Benzinger et al., 2009).
In cases of
mild TBI, technology such as MRI and CT regularly fail to detect focal lesions
(Graner et al., 2013). However, neuroimaging that shows increasing promise with
bTBI is Diffusion-tensor imaging (DTI). DTI is an MRI technique used to examine microstructural
properties of white matter (Davenport et al., 2011). DTI can identify lesions
on specific axonal pathways, which may improve future diagnoses of cognitive
dysfunction in mild TBI (Benzinger et al., 2009). Hayes and colleagues (2011)
reported a case study of a soldier exposed to multiple blast injuries. Using
DTI, analysis revealed changes in white matter integrity that had led to
cognitive decline in the subject; further supporting the theory of neurotrauma
from blast exposure. Unfortunately, there is little
research on the usefulness of DTI in assessing CTE (Baugh et al., 2012) and
debate surrounds its effectiveness for evaluating acute concussion (Ianof et
al, 2014).
An additional
suggestion for bTBI diagnoses is the possible implementation of oculomotor
testing. Neural connections in eye movements and higher
cognitive functions are similar and eyetracking could offer a sensitive tool
for diagnosing certain cognitive impairments (Suh et al, 2007). The
researchers add that the mobile equipment makes it simple to administer on the
injury site. Alternatively, as some neuroimaging may not detect certain forms
of neurological damage associated with bTBI (Graner et al., 2013), a new device
has been introduced that may help decide what form of neuroimaging should be used.
“Blast badges” use specialized colour-changing crystals that break apart when
exposed to a blast shockwave. Attached to the soldiers
uniform, the colour change corresponds with the level of blast intensity and
potential harm to the brain (Cullen et al., 2011). The researchers expect this
novel device to become a key instrument in the future, that will compliment
neuroimaging techniques, help decide what medical care to provide, and when the
soldier should return to duty.
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| Colour changing Blast Badges |
In the Iraq and Afghanistan conflicts, TBI has become the ‘signature injury’
akin to that of shell shock in the 1st World War. In civilian populations, TBI is regularly experienced (Goodrich et
al., 2013); however bTBI is more confined to combat settings (Ling et al.,
2009; McKee & Robinson, 2014). Blast-induced TBI can have psychological and
neurological consequences. Kovacs et al. (2014) remark that “knowing the
pathology is necessary to fully understand a disease” (p. 5). In this regard,
research with animals shows promise in producing a reliable model that can
replicate blast injuries to the human brain. Although difficulties surround
creating the ideal protective equipment for soldiers, neuroimaging techniques
and novel technology such as “blast badges” may help in future guidance of the
appropriate treatments for blast-induced neurotrauma.
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Only the dead have seen the end of war ~ Plato
