Blast exposure, body armor, and TBI
Injury risk from blast exposure has been studied for nearly 100 years and has mostly focused on pulmonary injury and fatalities from the blast.8 For much of this time, it has been generally accepted that the lungs are much more vulnerable than the brain for blast fatalities.9,10 Indeed, our findings suggest that the pressure levels needed to cause fatalities from blast brain trauma are about twice the levels needed to cause fatalities from pulmonary injury.11 However, substantial questions remain about whether sublethal brain injury can occur at levels of blast that do not result in pulmonary fatality.
Emerging results suggest that the apparent brain injury associated with a blast exposure in recent military conflicts likely results from 2 sources. First, unpublished research by our group has shown that current military body armor, especially systems with a hard armor plate, is highly protective against pulmonary blast. This protection substantially decreases the risk of pulmonary injuries at a given distance from the explosion. So, service members can now survive much closer to blasts than is possible without body armor, saving many lives that would have been lost previously, but resulting in a greater risk of mild and moderate head injuries.
Second, our findings from recent studies of large animal models suggest that organic neurotrauma may occur at levels of blast that are near or below the level of pulmonary threshold injury.11 This compelling finding suggests that even civilians exposed to blast may be at risk for organic brain injury in addition to the risk of PTSD. These 2 sources, increased protection of the body relative to the brain and previously unsuspected vulnerability to blast brain trauma, are the likely sources of much of the blast-associated traumatic brain injury anecdotally reported in military hospitals and Veterans Affairs (VA) medical centers.
Neuropsychiatric symptoms, comorbidities, and diagnostic dilemmas
TBI can present with many different affective, anxiety, or cognitive symptoms. In the combat veteran, TBI is also seen with comorbid conditions, with the most common diagnoses being PTSD, major depression, panic disorder, and substance use disorders. Until the associated pathophysiology is better understood, there is not a single coherent scientific model of TBI. These facts lead to the present diagnostic model for TBI and its similarity to the criteria-based diagnostic system in DSM-IV. Although the DSM-IV authors were careful to create exclusionary criteria for similar conditions (eg, schizophrenia diagnosis requires the exclusion of mood disorders), there are no such exclusionary criteria for PTSD and TBI. This situation leads to the possibility of arbitrary assumptions for diagnosing PTSD and/or TBI in blast-exposed combat veterans.
Reexperiencing symptoms can suggest the presence of PTSD; if it is present, it should be treated following established guidelines, such as the 2010 VA/Department of Defense Clinical Practice Guidelines for PTSD. The presence of specific neurological abnormalities can indicate TBI. An experienced neuropsychologist can look for relative deficits that are atypical for PTSD. An extended, multidisciplinary evaluation is often required for diagnostic accuracy; without an accurate diagnosis, the psychiatrist will be challenged in prescribing appropriate treatment.
Standardized tests can help clarify the diagnosis of suspected TBI and can complement the clinical assessment. These tests include bedside tests, also useful in the outpatient psychiatry office, and more involved tests up to and including a complete neuropsychological test battery. Tests can be useful for detecting and tracking psychiatric symptoms. We like the Beck Depression Inventory and the PTSD Checklist (PCL) for quick assessment of veteran outpatients. The PCL is an excellent instrument for capturing PTSD symptoms, but it can lead to false-positive diagnoses when TBI might contribute to or cause irritability, insomnia, impaired concentration, and apathy.
Cognitive difficulties are a common complaint after TBI and thus should be evaluated. Our institution uses a panel of tests to capture several different cognitive domains. Including a neuropsychologist on the interdisciplinary TBI team is highly recommended. These subspecialty psychologists can assist with difficult diagnostic situations, such as the influence of premorbid attention-deficit/hyperactivity disorder on cognitive complaints in a combat veteran with suspected TBI and/or PTSD; determination of any regional specificity to neuropsychological testing results; evaluation of personality tests; and administration of tests of effort, motivation, and malingering.
Psychiatrists may consider bedside tests for patients with cognitive disorders, but evidence supporting the use of such tests is inconsistent. The Mini Mental State Examination (MMSE) is not recommended as a TBI evaluation instrument, and while the Montreal Cognitive Assessment (MoCA) may be better than the MMSE for detecting subtle abnormalities, there are no published trials of the MoCA in patients with TBI.12 Another brief clinical evaluation tool is the Military Acute Concussion Evaluation (MACE). The MACE was developed by the Defense and Veterans Brain Injury Center and can be ordered from their Web site (www.dvbic.org). The MACE appears to be a reliable instrument for TBI assessment, but according to a recent military medical study, the MACE is only effective if it is administered within 12 hours of a head injury.13
Until better brief diagnostic tests are shown to be effective, our recommendations for TBI diagnosis include paying careful attention to physical signs and symptoms, noting the presence of cognitive disturbances that cannot be explained by known psychiatric or neurological comorbidity, and noting the presence of psychiatric symptoms that do not respond to usual care.
Among the possible comorbid diagnoses and shared symptoms, one significant diagnostic challenge is impaired motivation.14 The patient with subcortical damage may appear to be depressed. The clinical picture may include apathy, cognitive slowing, motor slowing, and a blunted emotional response. Consultation-liaison psychiatrists may note a similarity to other conditions, such as HIV encephalopathy and a subcortical dementia.
