Download Bomb blast, mild traumatic brain injury and psychiatric morbidity: A

Injury, Int. J. Care Injured 41 (2010) 437–443
Contents lists available at ScienceDirect
Injury
journal homepage: www.elsevier.com/locate/injury
Review
Bomb blast, mild traumatic brain injury and psychiatric morbidity: A review
Jeffrey V. Rosenfeld a,b,*, Nick L. Ford c
a
Dept of Surgery, Monash University, Australia
Department of Neurosurgery, The Alfred Hospital, Melbourne, Australia
c
Discipline of Psychiatry, University of Adelaide, Australia
b
A R T I C L E I N F O
A B S T R A C T
Article history:
Accepted 30 November 2009
Traumatic brain injury (TBI) arising from blast exposure during war is common, and frequently
complicated by psychiatric morbidity. There is controversy as to whether mild TBI from blast is different
from other causes of mild TBI. Anxiety and affective disorders such as Post-traumatic Stress Disorder
(PTSD) and depression are common accompaniments of blast injury with a significant overlap in the
diagnostic features of PTSD with post-concussive syndrome (PCS). This review focuses on this overlap
and the effects of mild TBI due to bomb blast. Mild TBI may have been over diagnosed by late
retrospective review of returned servicemen and women using imprecise criteria. There is therefore a
requirement for clear and careful documentation by health professionals of a TBI due to bomb blast
shortly after the event so that the diagnosis of TBI can be made with confidence. There is a need for the
early recognition of symptoms of PCS, PTSD and depression and early multi-disciplinary interventions
focussed on expected return to duties. There also needs to be a continued emphasis on the destigmatisation of psychological conditions in military personnel returning from deployment.
ß 2009 Elsevier Ltd. All rights reserved.
Keywords:
Blast injury
Traumatic brain injury
Post-traumatic Stress Disorder
Contents
Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Scope of the problem. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Mechanisms of injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Direct effects of the pressure wave. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Air embolism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Acceleration/deceleration . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Animal studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Blast injuries and human studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Emotional disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Evaluation of patients with blast-related TBI . . . . . . . . . . . . . . . . . . . . . . . . .
Treatment of mild TBI including emotional disorders following bomb blast
Long-term effects of mild TBI following bomb blast . . . . . . . . . . . . . . . . . . .
Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Disclosure statement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Conflict of interest statement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Introduction
The rate of survival of soldiers in war has increased from 2:1,
injured to dead in WWII, to 7.4:1 in Operation Iraqi Freedom
* Corresponding author at: Dept of Surgery, Monash University, The Alfred
Hospital, Commercial Rd, Melbourne, Australia 3004. Tel.: +61 3 9866 6688.
E-mail address: [email protected] (J.V. Rosenfeld).
0020–1383/$ – see front matter ß 2009 Elsevier Ltd. All rights reserved.
doi:10.1016/j.injury.2009.11.018
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(OIF)28 and with it more complex rehabilitation needs to improve
the level of function of those who survive their wounds.58 The use
of improved body armour, tourniquets, advances in resuscitation
and trauma systems, early damage control surgery, and critical
care air transport teams account for the increased rates of survival
for those injured at proximity to point sources of explosions that
previously might have caused death.54,58
Traumatic brain injury (TBI) caused by bomb blast has been
described as the ‘signature wound of the war on terror’6 and its
438
J.V. Rosenfeld, N.L. Ford / Injury, Int. J. Care Injured 41 (2010) 437–443
identification and management a source of interest and controversy.12,71 Survivors of blast injury frequently suffer a TBI of
variable severity ranging from a mild concussion to severe ‘blast
brain’ with cerebral swelling, with or without penetrating injury
and burns. Is the brain susceptible to injury from explosions in the
absence of penetrating injury? What might be the mechanisms of
such injury, and are the current acute markers of brain injury
adequate for the assessment and what is the longer term outcome?
Few studies have provided long-term observations on the effect of
blast injury to the brain.5,15,29,42,63,72
Scope of the problem
An extensive non-governmental study by the Rand Corporation
noted that 2726 cases of TBI were diagnosed in returned personnel
between 2001 and 2007, with an estimated societal cost of $590–
910 million dollars.70 The 1-year estimate of societal cost
associated with treated cases of mild TBI is up to USD $32,000
per case, while estimates for moderate to severe TBI range from
USD $268,000 to more than USD $408,000.70 The authors estimate
that about 320,000 service members may have experienced a TBI,
ranging from mild concussion to severe penetrating TBI, during
deployment up to October 2007, with only 43% reporting being
evaluated by a physician.70
The treatment of military personnel from the USA with PTSD
and depression post-combat exposure estimated by the Rand
Corporation to cost as much as USD $6.2 billion in the 2 years
following deployment which includes both direct medical care and
costs for lost productivity and suicide.70
A number of epidemiological studies of personnel returned
home from the current conflicts have linked impairment postdeployment, with or without blast exposure, primarily to
depression or anxiety related disorders such as PTSD.27,35,61,74
The experience of field hospitals is that blast-related brain injury
occurs, often in conjunction with other physical injuries and that
wounds to the face, head and neck are common.30,32,53,80
Studies of personnel who have returned home have defined
traumatic brain injury (TBI) as any disturbance of consciousness;
including being dazed or seeing stars, or not remembering the
injury.35,61,74 Population estimates of total TBI in these studies35,61,74
are between 10 and 15% of deployed samples, noting that 4% of nondeployed soldiers also experience a TBI during the same time
period.74 Xydakis et al.79 have suggested that delay, in surveying
soldiers may have lead to under-reporting of the extent or
occurrence of head injury. In the heat of battle lack of documentation
of a head injury or exposure to bomb blast will exacerbate this
problem. In practice the US Department of Veterans Affairs uses
historical data as a screen for blast exposure and then proceeds with
physical, radiological and neuropsychological screening.56
Over half the veterans reported by Schneiderman et al.61 had
more than one mechanism of injury, suggesting multiple concussions. Schneiderman et al.61 stratified the severity of mild TBI in
their sample of veterans from Iraq and Afghanistan and found an
association of persistent symptoms with more severe TBI, multiple
injury mechanisms and the presence of PTSD, and noted that the
findings of association between TBI and PTSD could relate to the
stress of wounding and deployment or brain injury manifesting as
PTSD.61
In support of this observation Chen et al.18 showed that there is
neuroimaging evidence of neural dysfunction, in concussed
depressed compared to non-depressed athletes with and without
concussion. Concussed athletes as a group showed reduced insula
gray matter, and those athletes who were also depressed showed
reduced gray matter in the medial frontal and temporal areas. Chen
et al.18 suggest that the changes causing depression were related to
the concussion itself.
A survey of UK armed forces personnel found post-concussional
syndrome (PCS) symptoms such as memory and concentration
problems, tinnitus, visual disturbance, irritability and affective
disturbance were related to blast exposure, but the same
symptoms were related to other in theatre exposures.27 In this
study participants were asked if they had been under attack at any
time from explosive munitions. The authors suggest PCS symptoms may be a non-specific marker of psychological distress and
there is overlap between the symptoms of PCS, and stress for
example irritability and concentration problems.27
There is some data concerning more severely injured soldiers
who were admitted to hospital.76 Of 433 patients received
between January 2003 and April 2005 at the Defence and Veterans
Brain Injury Centre (DVBRC) at Walter Reed Army Medical Centre
(WRAMC) 68% received their injury from blast, 88.8% had a closed
TBI and 43% had a post-traumatic amnesia (PTA) of less than
24 h.76 Post-concussive symptoms were almost universal.76 A
further 183 brain injured patients were admitted to four polytrauma rehabilitation centres (PRC) between September 2001 and
January 2006, of whom approximately 20% had closed head injury
due to blast, a slightly smaller proportion than those with closed
brain injury from other causes, most commonly vehicle trauma.58
Vasterling et al.74 described a pattern of increased reaction time,
poor concentration and short-term memory problems in soldiers
returned from Iraq, independent of the effects of TBI. They
suggested that this may represent both an adaptive mechanism
and the effects of a prolonged stressful environment.74
Mechanisms of injury
The types of injury arising from blast are described as primary
through to quaternary, being the effect of a blast pressure wave,
penetrating trauma from fragments, the direct concussive and
contre-coup effects of collapsing structures and of being thrown by
the blast wind and striking the head against fixed structures, and
injuries due to burns, asphyxia and exposure to toxins respectively.25,43,48,55 The blast pressure wave or primary blast injury is
unique to explosions.25,48,55 Individuals are likley to be affected by
some or all of these mechanisms sustaining multiple injuries.30,32,43,63,77
Direct effects of the pressure wave
An explosion causes a high pressure wave to sweep across the
immediate surrounds at about the speed of sound.25,26 The
intensity of the blast wave declining as a function of distance to
the third power from its source.77 Enhanced explosive devices,
with secondary ignition of disseminated explosive, spread the
point source from which the explosion radiates causing more
damage from the primary blast effect.25 Possible mechanisms of
brain injury from the primary blast are the primary pressure wave
transiting the skull and body43,25, air embolism14,19 and acceleration/deceleration of the head.3,43 Where the wave meets tissues of
different density there will be further turbulence.
Animal research has demonstrated transcranial transmission of
pressure waves17 resulting in skull fractures and structural and
ultra-structural damage to the brain.16,39–41 Transmission of an
intravascular pressure wave up the neck may also contribute.16,40,43 Protective devices provide limited protection.16,30
Air embolism
In the lung, the air gas interface creates the phenomenon of
spalling where air enters the pulmonary circulation by blasting
though the alveoli creating the phenomenon of blast lung.77 Air
embolism is unlikely to be a factor in mild TBI following blast
J.V. Rosenfeld, N.L. Ford / Injury, Int. J. Care Injured 41 (2010) 437–443
439
exposure because the pulmonary blast injury is also likely to be
mild.
et al.61 reported multiple mechanisms of injury and concussions in
their group of deployed personnel.
Acceleration/deceleration
Emotional disorders
A solid object in the way of a rapidly moving pressure front will
be accelerated. Body parts able to move such as the limbs and head
will be subject to acceleration and deceleration, particularly if the
pressure wave reverses its direction due to reflection which occurs
in blast waves in closed environments such as vehicles and
buildings.24,26 This would give rise to a similar pattern of brain
injury which occurs in a high speed motor vehicle accident, i.e.
diffuse axonal injury (DAI).
The epidemiological data emerging from Iraq and Afghanistan
link the occurrence of blast exposure, mild TBI and affective
disturbance such as depressive or PTSD symptomatology.28,36,61,75
This data should be viewed with caution because the definitions of
mild TBI are more liberal than the agreed WHO definitions and the
samples although large were not complete. The occurence of PTSD in
a head-injured population has been considered problematic due to
amnesia for the event and an inability to encode traumatic
memories.59 However PTSD has been demonstrated in civilians
following TBI49 and it has been suggested that encoding may occur at
an implicit level21, amnesic survivors of accidents may show
physiological reactivity in response to reminders of their accident.13
Physiological derangement due to the impact itself has also been
suggested as a contributor to depression in brain injured athletes18
and it may be that causality between psychiatric disorder and brain
injury is due to both emotional and physical factors.67
Hoge et al.35 surveyed 2525 US Army infantry soldiers 3–4 months
after their return from a 1-year deployment to Iraq. Psychiatric
diagnoses of major depression and PTSD were made according to
DSM IV criteria.2 124 (4.9%) reported head injuries with loss of
consciousness (LOC), 260 (10.3%) reported injuries with altered
mental status, and 435 (17.2%) reported other injuries during
deployment. Of those reporting LOC, 43.9% met criteria for PTSD,
compared to 27.3% of those reporting altered mental status, 16.2%
with other injuries and 9.1% with no injury.35 Those soldiers with
mild TBI, especially if there was a LOC, were significantly more likely
to report poor general health than were soldiers with other injuries.35
After adjustment for PTSD and depression, mild TBI was no
longer significantly associated with these physical health outcomes
except for headache.35 Hoge et al.34 have more recently argued
against the non-discriminate use of diagnoses such as TBI/concussion and ‘signature injury’, and that this has resulted in excessive
diagnoses of ‘mild TBI’ following bomb blast exposure in US soldiers
returning from the Middle East. They argue that this has in turn
resulted in an increase in persistent PCS and compensation claims.34
The linkage between mood disorders, PTSD and cognitive
dysfunction is strong with studies demonstrating hippocampal
atrophy9,47 and neuropsychological impairment44 in the absence
of TBI and substance misuse. There are abnormal patterns of neural
activation in PTSD. Functional neuroimaging shows a reversal of
the normal inhibition of the amygdala by the medial prefrontal
cortex in human subjects in both basal and threat conditions.64 In
traumatic brain injury due to acceleration/deceleration and
contre-coup injuries the areas affected (basal frontal lobes and
temporal poles) tend to be those involved in the regulation of
emotions, judgment and memory and may mimic psychological
illness or complicate the course of such illness.18,22
Jones et al.37 argue that it is unwise to label TBI as a unique
signature injury and that symptoms that cross the divide between
physical and psychological require a nuanced view of their
interpretation and treatment.
Animal studies
Microscopic damage is seen in the brain of blast exposed
animals.16,39,41 There appears a generalised inflammatory response with microglia and astrocyte proliferation and cytoskeletal
disruption, primarily affecting not only the cortex but also subcortical structures, including the hippocampus.16,39,41 There is
some suggestion that repeated blasts may lead to a decreased
threshold for damage, although the duration of the window of
increased vulnerability is not clear.41 In cell cultures exposed to
blast there is an increase in membrane permeability, persisting for
some hours after blast exposure.41 Cernak et al.16 demonstrated
cognitive and histological changes in rats exposed to blast with and
without head protection, finding the latter more severely affected,
although with a trend to improvement over the 5-day duration of
the study. Similarly, Kaur et al.39 showed histological changes
normalising 28 days after exposure to blast injury in rats.
Blast injuries and human studies
Studies from WWI attempted to distinguish ‘shell shock’ related
to emotional impact, from concussion, related to nearby blast
exposure, a physically based syndrome.37 That there were fatalities
from a nearby explosion, without visible wounding and due to
brain injury was accepted at the time.
Bomb blast results in a range of TBI severity from mild TBI with
subtle disabilities which may severely limit performance69 to
severe brain swelling, intracranial haemorrhage and penetrating
injury with metal fragments and other foreign bodies which are
often heavily contaminated.54 Post-traumatic vasospasm, particularly where there has been subarachnoid haemorrhage, and later
pseudo-aneurysm formation is likely in those who have experienced intracranial bleeding with penetrating injury.3,43,63
In blast affected humans subarachnoid haemorrhage, subdural
hematoma, cerebral venous congestion, leptomeningeal haemorrhage and hyperaemia of the brain and meninges are seen in
individuals dying from blast injury.1,4,20,43
In studies of military personnel, the mechanism of brain injury
of blast compared to other causes such as motor vehicle accidents,
does not appear predictive of outcome.58 However there is wide
variability in the outcomes of personnel injured by blast which
may reflect the multiple mechanisms involved.5,58
At the milder end of the spectrum of TBI, the recent literature on
concussion in athletes suggests there is metabolic brain vulnerability following concussion, the time course of which may not
correspond to the clinical recovery.73 Recovery in athletes is
significantly slower after a second concussion65 and sports related
concussions have adverse cumulative effects on intracortical
inhibitory systems and visuo-motor coordination.23 A similar
lowering of threshold to injury may occur in repeated blast injury
in animals.41 It is unknown how much this corresponds to
concussion due to human blast injury, although Schneiderman
Evaluation of patients with blast-related TBI
It is very difficult to reliably differentiate between symptoms
caused by severe stress and mild TBI which is made more difficult
by retrospective accounts of injury.12,79 As much information
should be recorded at an early stage after blast exposure as
possible so that the TBI component can be verified at subsequent
asessments. This will assist with therapy but also the evaluation of
compensation claims.
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J.V. Rosenfeld, N.L. Ford / Injury, Int. J. Care Injured 41 (2010) 437–443
Clinical markers at the time of injury for TBI are the history or
observation of head impact and signs of cranial trauma, GCS,
duration of coma and post-traumatic amnesia, ongoing headache
and focal neurological deficit (which is uncommon). The symptoms of being dazed, seeing stars, being confused and disorientated
and brief amnesia for the event are not necessarily due to blast
trauma and may be due to the emotional shock of the event.34 Skull
fracture, including of the base of the skull (28) may be present if the
head has been impacted. In deployed situations computed
tomography (CT) or magnetic resonance (MR) scanning may be
unavailable and clinical markers of skull fracture should be
specifically examined. Rupture of the tympanic membrane should
arouse suspicion of brain injury78 and damage to the auditory and
vestibular apparatus may occur51 and cause persisting disability.60,69 Damage to the eyes may occur30,77 although the likelihood
is diminished where eye protection is worn.32
The circumstances of the explosion are relevant; in particular
the type of explosive, where known, the distance from the centre of
the explosion, the presence or absence of armour and head
protection and whether the patient was in a confined space.
In the acute recovery phase serial measures of brain function
such as the abbreviated Westmead scale are very useful measure of
post-traumatic amnesia and can be administered by nurses.52 It is
preferable to use measures of post-traumatic amnesia (PTA) to
validate whether mild TBI has occurred.12 Comparisons of pre- and
post-deployment cognitive screens would be helpful in the
investigation of cognitive deficits following blast injury. Assessment of balance and coordination is also useful.69,79
Plain skull X-ray may show skull fractures especially following
head impact. The availability of CT scans in field hospitals is useful
to document pathology and plan management. Although CT is
usually normal in mild concussion there is a greater likelihood of
skull fractures, cerebral contusions or small haemorrhages
following blast exposure particularly if the head has been
impacted.63 In civilians, 7–20% of apparent mild TBI patients have
CT or MR abnormalities.8 In a civilian setting 36% of patients with
blast head injury and a GCS of 15 were subsequently shown to have
brain injury either by CT scan on admission or by CT scan later in
the course of hospitalisation, ordered due to a deteriorating mental
state.7 In some cases the intake CT was normal with deterioration
over the next 48 h.7 These findings suggest a need for a high index
of suspicion for TBI in blast-injured patients. MR is more sensitive
than CT for detecting lesions in the brain following traumatic brain
injury but is not available in remote military hospitals. Hence there
are no reported MR studies in the early phase following blast
injury. MR T2 Gradient Echo (T2GE) is sensitive for detecting the
lesions of diffuse axonal injury.31 Brenner et al. studied veterans
with traumatic brain injury and/or PTSD and found that those with
moderate or severe TBI were more likely to have traumatic brain
lesions than mild TBI patients and those with PTSD had negative
neuroimaging.10 MR diffusion tractography imaging (DTI) may
demonstrate subtle structural brain abnormalities after primary
blast injury which are not seen on routine MR. An instructive case
was reported recently and indicates that DTI should be used more
often in patients with a mild TBI following bomb blast.75
Biochemical markers may also provide objective evidence of
concussion and this can be done using 1H-Magnetic Resonance
Spectroscopy.73 The serum level of S100B protein has been
evaluated in mild TBI but its specificity has been questioned
and the levels increase following exercise.68
Treatment of mild TBI including emotional disorders following
bomb blast
Mild TBI has not been reported as a cause of psychiatric
evacuation during Operation Enduring Freedom (OEF) and OIF,
although emotional disorders, in particular anxiety disorders have
been.57 However 35% of physically injured evacuees required
neurosurgical consultation and management.3 The subtle deficits
in performance that occur from blast-related concussion may
impair performance in a highly demanding occupation and put
individuals, and others, at risk unless adequately assessed and
managed in the acute and rehabilitation phases.69 There is a
likelihood that affective symptoms will synergise with the
concussion and physical symptomatology to potentially worsen
outcome. Civilian patients with TBI are at high risk of developing
acute stress disorders,11 and the co-morbid presence of PTSD
significantly worsens cognitive performance in military patients
with mild TBI.46
There is still reluctance by military personnel to self-report
mental health problems. Mental health professionals must
continue to address this problem and reduce the stigma attached
to mental health. This might occur by increased efforts to liaise
with commanders who should be well briefed and supportive of
mental health strategies. It is important that personnel understand
that seeking treatment is confidential and that seeking help is a
sign of interest in getting better, not a weakness and that treatment
will minimise stress related conditions.33,70
An expectant approach to mild TBI is recommended with
education about likely resolution of emotional and cognitive
dysfunction over the first year. Attribution of injury source may
affect outcome36 and the term ‘‘concussion’’ may be more familiar
and less frightening to patients than the label of TBI. Coordination
of rehabilitation efforts, with the setting of benchmarks, duties,
review dates, and liaison with parent units is likely to have the
most impact on functional recovery. Comprehensive rehabilitation, social support and a younger age of victims is associated with
a better outcome for survivors in survivors of terrorist incidents in
Israel63 and has been recommended in the RAND review.70 In more
severe blast injuries disfigurement, chronic pain, limb damage or
loss, damage to the ear and vestibular apparatus, and psychiatric
illness will complicate recovery.
Physical and mental rest is also an important treatment strategy
for PCS. Poorly adapted cognitive strategies after trauma, including
concussion and are a predictor of PTSD and may hinder the
outcome.12 The PCS is associated with PTSD45 similarly PTSD and
depression worsen disability after physical injury.50 The diagnosis
and early management of psychological disorders arising from
trauma exposure have been extensively covered in the literature.47,66
Long-term effects of mild TBI following bomb blast
Outcome studies of TBI are largely from civilian data, sports and
motor vehicle accidents with acceleration/deceleration as the
usual injury mechanism.36 Mild TBI (defined as a GCS of 13–15, PTA
of less than 24 h and loss of consciousness of less than 30 min) in a
meta-analysis showed complete recovery after 1 year62, however
post-concussional symptoms may persist. Mild TBI is commonly
complicated by mood and anxiety disorders with premorbid
factors contributing significantly to the outcome.38
There have been few long-term studies of the effects of blastrelated TBI, other than assessing the prevalence of PTSD. Cernak
et al.15 reported on 665 casualties admitted to a military hospital
with blast injury and external wounds confined to the lower limbs.
At 1 year 30% showed electroencephalographic (EEG) abnormalities.15 During the wars in Lebanon one-third of head-injured
patients had closed injuries, with one-third of these due to blast
exposure. They were described as making progress over the
subsequent years but a proportion had ongoing cognitive
problems, the extent of which is unknown.42 The significance of
the prolonged EEG abnormalities reported by Cernak et al.15 and
J.V. Rosenfeld, N.L. Ford / Injury, Int. J. Care Injured 41 (2010) 437–443
mentioned by Trudeau et al.72 is unknown. Most casualties had comorbid PTSD15,72 which might account for the attentional
problems described, although the EEG changes reported are
unexpected.
Belanger et al.5 reported on a sample of blast-injured soldiers,
and compared them to TBI cases with other mechanical forms of
injury. There was no difference in neuropsychological performance
at 2 years between the two groups. At admission to a PRC there is a
trend for blast-injured patients to be more likely to have cognitive
impairment than those from other mechanisms of injury.58 Blastinjured patients had a greater likelihood of psychological
symptomatology, which was attributed to the likely circumstances
of the original injury, terrifying at the time, but preceded and
followed by extreme stressors in a hostile environment5,58,63
Belanger et al.5 concluded that blast injury although more likely to
be severe showed similar behavioural manifestations to other
types of injury.
Schwartz et al.63 reviewed survivors of terrorist bombings with
TBI in Israel finding that despite severe injuries at intake, in
particular intracerebral lesions, and high rates of PTSD, the longer
term outcome was similar to a non-blast TBI group, with the
exception of a higher rate of post-traumatic epilepsy in the blast
TBI group.
Conclusions
Blast injury to the human brain may cause the whole spectrum
of TBI from mild TBI to severe brain injury with brain swelling,
intracranial haemorrhage and penetrating injury. The circumstances of the blast exposure and premorbid personality will
determine the mix of psychological and physical injury. The
pathological mechanisms of blast injury to the brain are well
understood from animal and human research. Mild TBI (concussion) in soldiers deployed to Iraq and Afghanistan is strongly
associated with affective symptoms such as depression and PTSD,
and physical health problems.
It cannot be concluded that bomb blast causes PTSD and
depression by psychogenic means alone. The emotional shock of
the blast and the circumstances surrounding it may be enough in
some cases to explain the PTSD and depression. However, there is
emerging evidence that parts of the brain injured in blast TBI are
concerned with regulation of emotions and judgement and this
organic component of brain injury may contribute to the onset of
PTSD and depression.
In assessing the contribution of TBI to PTSD, affective disorders
and cognitive impairment following blast exposure, contemporaneous history, examination and imaging data (where available) is
essential. Duration of coma, persistent headache and posttraumatic amnesia are particular features of TBI concussion which
should be documented. It is difficult to differentiate the symptoms
of severe stress from those of mild TBI and PCS as there is a great
overlap. This is also made more challenging by retrospective
accounts of injury. Having a record of the circumstances of the
blast, and the immediate clinical and performance picture after
blast is important in identifying a TBI. Persistent symptoms are
more likely in the patients diagnosed with mild TBI following blast
injury compared with the civilian population of mild TBI and
compensation claims and litigation are also higher in patients with
persistent concussional symptoms.34
The relationship between mild TBI and blast injury awaits
further elucidation, but there is evidence that a concussion has
both physical and psychological components, the former possibly
diminishing in contribution to the overall pattern of disability as
time passes. There is likely a synergistic interaction between the
physical and psychological components of blast injury in promoting disability.
441
Disclosure statement
The views expressed in this article are solely those of the
authors and do not represent the policy or views of the
Commonwealth of Australia Department of Defence or the
Australian Defence Force.
Conflict of interest statement
There is no conflict of interest by either author.
Appendix A. Diagnostic criteria for Post-traumatic Stress
Disorder and major depression [DSMIV]2
A.1. Criteria for major depressive episode
A. Five (or more) of the following symptoms have been present
during the same 2-week period and represent a change from
previous functioning; at least one of the symptoms is either (1)
depressed mood or (2) loss of interest or pleasure.
Note: Do not include symptoms that are clearly due to a
general medical condition, or mood-incongruent delusions or
hallucinations.
(1) depressed mood most of the day, nearly every day, as
indicated by either subjective report (e.g., feels sad or
empty) or observation made by others (e.g., appears tearful).
(2) markedly diminished interest or pleasure in all, or almost
all, activities most of the day, nearly every day (as indicated
by either subjective account or observation made by others).
(3) significant weight loss when not dieting or weight gain (e.g.,
a change of more than 5% of body weight in a month), or
decrease or increase in appetite nearly every day.
(4) insomnia or hypersomnia nearly every day.
(5) psychomotor agitation or retardation nearly every day
(observable by others, not merely subjective feelings of
restlessness or being slowed down).
(6) fatigue or loss of energy nearly every day.
(7) feelings of worthlessness or excessive or inappropriate guilt
(which may be delusional) nearly every day (not merely
self-reproach or guilt about being sick).
(8) diminished ability to think or concentrate, or indecisiveness,
nearly every day (either by subjective account or as
observed by others).
(9) recurrent thoughts of death (not just fear of dying),
recurrent suicidal ideation without a specific plan, or a
suicide attempt or a specific plan for committing suicide.
B. The symptoms do not meet criteria for a mixed episode.
C. The symptoms cause clinically significant distress or impairment
in social, occupational, or other important areas of functioning.
D. The symptoms are not due to the direct physiological effects of a
substance (e.g., a drug of abuse, a medication) or a general
medical condition (e.g., hypothyroidism).
E. The symptoms are not better accounted for by Bereavement, i.e.
after the loss of a loved one, the symptoms persist for longer
than 2 months or are characterised by marked functional
impairment, morbid preoccupation with worthlessness, suicidal ideation, psychotic symptoms, or psychomotor retardation.
A.2. Diagnostic criteria for 309.81 Post-traumatic Stress Disorder
A. The person has been exposed to a traumatic event in which both
of the following were present:
(1) the person experienced, witnessed, or was confronted with
an event or events that involved actual or threatened death
or serious injury, or a threat to the physical integrity of self
or others.
J.V. Rosenfeld, N.L. Ford / Injury, Int. J. Care Injured 41 (2010) 437–443
442
B.
C.
D.
E.
F.
(2) the person’s response involved intense fear, helplessness, or
horror.
The traumatic event is persistently re-experienced in one (or
more) of the following ways:
(1) recurrent and intrusive distressing recollections of the
event, including images, thoughts, or perceptions.
(2) recurrent distressing dreams of the event.
(3) acting or feeling as if the traumatic event were recurring
(includes a sense of reliving the experience, illusions,
hallucinations, and dissociative flashback episodes, including those that occur on awakening or when intoxicated).
(4) intense psychological distress at exposure to internal or
external cues that symbolise or resemble an aspect of the
traumatic event.
(5) physiological reactivity on exposure to internal or external
cues that symbolise or resemble an aspect of the traumatic
event.
Persistent avoidance of stimuli associated with the trauma and
numbing of general responsiveness (not present before the
trauma), as indicated by three (or more) of the following:
(1) efforts to avoid thoughts, feelings, or conversations associated with the trauma.
(2) efforts to avoid activities, places, or people that arouse
recollections of the trauma.
(3) inability to recall an important aspect of the trauma.
(4) markedly diminished interest or participation in significant
activities.
(5) feeling of detachment or estrangement from others.
(6) restricted range of affect (e.g., unable to have loving
feelings).
(7) sense of a foreshortened future (e.g., does not expect to have
a career, marriage, children, or a normal life span).
Persistent symptoms of increased arousal (not present before
the trauma), as indicated by two (or more) of the following:
(1) difficulty falling or staying asleep.
(2) irritability or outbursts of anger.
(3) difficulty concentrating.
(4) hypervigilance.
(5) exaggerated startle response.
Duration of the disturbance (symptoms in Criteria B, C, and D) is
more than 1 month.
The disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of
functioning.
Specify if:
Acute: if duration of symptoms is less than 3 months.
Chronic: if duration of symptoms is 3 months or more.
Specify if:
With delayed onset: if onset of symptoms is at least 6 months
after the stressor.
Note: Paediatric aspects have been removed from these criteria.
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