Bomb blast, mild traumatic brain injury and psychiatric morbidity: A review
Authors: Jeffrey V. Rosenfeld a, b and Nick L. Ford c
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 de-stigmatisation of psychological conditions in military personnel returning from deployment.
a Dept of Surgery, Monash University, Australia
b Department of Neurosurgery, The Alfred Hospital, Melbourne, Australia
c Discipline of Psychiatry, University of Adelaide, Australia
Injury. 2010 May;41(5):437-43. Epub 2010 Feb 26.
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 (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. and
Traumatic brain injury (TBI) caused by bomb blast has been described as the ‘signature wound of the war on terror’6 and its identification and management a source of interest and controversy. and 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., , , , and .
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 post-deployment, with or without blast exposure, primarily to depression or anxiety related disorders such as PTSD., , and 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., , and
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., and Population estimates of total TBI in these studies, and are between 10 and 15% of deployed samples, noting that 4% of non-deployed 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 poly-trauma 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., , and The blast pressure wave or primary blast injury is unique to explosions., and Individuals are likley to be affected by some or all of these mechanisms sustaining multiple injuries., , , and
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. and 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 body and , air embolism and and acceleration/deceleration of the head. and 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., , and Transmission of an intravascular pressure wave up the neck may also contribute., and Protective devices provide limited protection. and
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 exposure because the pulmonary blast injury is also likely to be mild.
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. and 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).
Microscopic damage is seen in the brain of blast exposed animals., and There appears a generalised inflammatory response with microglia and astrocyte proliferation and cytoskeletal disruption, primarily affecting not only the cortex but also sub-cortical structures, including the hippocampus., and 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., and
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., , and
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. and
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 et al.61 reported multiple mechanisms of injury and concussions in their group of deployed personnel.
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., , and 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 atrophy and 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. and
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.
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. and 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.
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. and Damage to the eyes may occur and 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. and .
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. and
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. and
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 blast-related 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 mentioned by Trudeau et al.72 is unknown. Most casualties had co-morbid PTSD and 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 Blast-injured 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 environment, and 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.
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 post-traumatic 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.
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.
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Source: Science Direct