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Cognitive Sequelae of Blast-Induced Traumatic Brain Injury: Recovery and Rehabilitation

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Cognitive Sequelae of Blast-Induced Traumatic Brain Injury: Recovery and Rehabilitation Neuropsychol Rev (2012) 22:4–20 DOI 10.1007/s11065-012-9192-3 REVIEW Cognitive Sequelae of Blast-Induced Traumatic Brain Injury: Recovery and Rehabilitation Yelena Bogdanova & Mieke Verfaellie Received: 30 December 2011 /Accepted: 1 February 2012 /Published online: 17 February 2012 # Springer Science+Business Media, LLC (outside the USA) 2012 Abstract Blast-related traumatic brain injury (bTBI) poses increased the risk of physical and psychological injuries in a significant concern for military personnel engaged in military personnel. Multiple tours of duty and high rates of Operation Enduring Freedom and Operation Iraqi Freedom exposure to blasts, as well as higher survival rates due to (OEF/OIF). Given the highly stressful context in which such enhanced body armor, have likely contributed to elevated injury occurs, psychiatric comorbidities are common. This rates of traumatic brain injury (TBI) and stress-related health paper provides an overview of mild bTBI and discusses the problems, such as posttraumatic stress disorder (PTSD) cognitive sequelae and course of recovery typical of mild (Bruner 2006; King et al. 2008; Otis et al. 2011). Blast- TBI (mTBI). Complicating factors that arise in the context related traumatic brain injury (bTBI) is one of the most of co-morbid posttraumatic stress disorder (PTSD) are con- common injuries in OEF/OIF, and according to statistics sidered with regard to diagnosis and treatment. Relatively from Walter Reed Medical Center, an estimated 60% of all few studies have evaluated the efficacy of cognitive reha- blast injuries result in TBI (Warden et al. 2005). Large bilitation in civilian mTBI, but we discuss cognitive training surveys suggest that an estimated 15% to 23% of OEF/ approaches that hold promise for addressing mild impair- OIF personnel have experienced a TBI, with the majority ments in executive function and memory, akin to those seen being mild TBI (mTBI) (Terrio et al. 2009; Warden 2006). in OEF/OIF veterans with bTBI and PTSD. Further research In one survey (Hoge et al. 2008), 15% of Army infantry is needed to address the patient and environmental charac- soldiers reported mTBI after their return from a year-long teristics associated with optimal treatment outcome. deployment in Iraq. Another study (RAND 2008) estimated the incidence of TBI at 19.5%, with the likelihood of TBI Keywords Neurorehabilitation . Executive function . directly linked to length of deployment. Memory. OEF/OIF. TBI . PTSD There are other deployment-related factors that may com- plicate and extend the course of natural recovery in OEF/ OIF returning veterans, such as prolonged stress exposure Introduction and related psychiatric sequelae (Hoge et al. 2004). The RAND study reported that of the 1.64 million individuals Thenatureofthecurrentconflicts (Operation Enduring deployed in Afghanistan and Iraq, an estimated 300,000 Freedom and Operation Iraqi Freedom; OEF/OIF) has veterans suffer from PTSD or depression (RAND 2008). A : recent systematic review reported that estimated rates of Y. Bogdanova M. Verfaellie PTSD among Iraq War veterans vary across studies from VA Boston Healthcare System, Memory Disorders Research 1.4% to 31% (Sundin et al. 2010). Heterogeneity of study Center, Boston University School of Medicine, Boston, MA, USA samples and methodological differences may account for the wide range of reported PTSD rates. In general, studies that use Y. Bogdanova (*) anonymous surveys report higher rates of PTSD than those Psychology Research (151-A), VA Boston Healthcare System, that use on-the-record screening, reflecting possible concerns 150 South Huntington Avenue, Boston, MA 02130, USA about stigmatization and confidentiality (see Sundin et al. e-mail: [email protected] 2010 for discussion). Prevalence rates also tend to increase Neuropsychol Rev (2012) 22:4–20 5 in the 12 months following deployment. Among combat- Blast Injury deployed troops, a relatively consistent prevalence in the range of 10–17% is reported. The rate of PTSD in OEF/OIF According to the Department of Defense, more than 73% of veterans receiving health care at the Department of Veterans OEF/OIF military casualties are caused by explosive weap- Affairs (VA), however, is higher (B. E. Cohen et al. 2010), and onry, with the majority of deployment-related TBI resulting the highest rates of PTSD (33% to 39%) are reported among from IEDs (Galarneau et al. 2008). Although enhanced body OEF/OIF soldiers with a history of mTBI (Carlson et al. armor has done much to protect service members from 2011). There is emerging evidence that a history of mTBI penetrating injuries, it does not protect against the damaging increases the risk for PTSD in both civilian (Bryant et al. effects of explosions. Explosions generate a powerful blast 2010;Fannetal.2004) and military populations (Hoge et al. wave of high pressure with associated blast wind, followed 2008). As we discuss below, the neuroanatomical overlap in by reversal of wind back toward the blast and under- neural circuits involved in mTBI and PTSD may mediate the pressurization (DePalma et al. 2005; Wightman and Gladish interaction between mTBI and PTSD, as the same brain 2001). These rapid pressure shifts affect air-filled organs (e.g. regions that are commonly affected in TBI are also involved lungs) and air-fluid interfaces (e.g. eardrum), and can also in PTSD. While neurobiological mechanisms underlying the affect the brain (Taber et al. 2006). In addition to these primary expression of PTSD in mTBI remain a subject of ongoing brain injuries, secondary injuries may occur, caused by objects investigation, the increased risk for PTSD in association with accelerated by the blast wind that strike the victim; tertiary mTBI is attributed to TBI-related neural damage that compro- injuries occur when a victim’s body is displaced by explosive mises the neural circuitry critical for regulation of fear follow- forces, resulting in contusions or other blunt trauma; and ing the trauma (Bryant 2008, 2011). Identification and early quaternary injuries result from radiation, burns, and toxin treatment of TBI-related symptoms and PTSD are critical for exposure from fires, explosions, or noxious fumes (DePalma successful recovery in returning veterans (Kessler 2000). et al. 2005; Wightman and Gladish 2001). There is a need for empirically based treatment protocols Evidence from animal studies indicates that explosions to address the multiple impairments in returning veterans can exert detrimental effects on the brain, depending on the with bTBI and PTSD. The VA Polytrauma System of Care, intensity and proximity of the blast and characteristics of the which includes Polytrauma Network Sites and Polytrauma blast-wave (Bhattacharjee 2008; Cernak and Noble- Rehabilitation Centers, was developed to identify, diagnose Haeusslein 2010; Cernak et al. 2001a; Chafi et al. 2010; and treat patients with multiple injuries. Local VAs and Taber et al. 2006). At least two mechanisms have been community-based Veteran Centers are equipped with mental identified by which a blast wave can lead to neural injury: health personnel trained to identify and manage mTBI and (1) when passing through the head, the blast wave and PTSD symptoms using current “standard of care” treatments subsequent blast wind can directly interact with the head specific for TBI or PTSD. However, it is unknown if and cause acceleration and/or rotation of the head; and (2) evidence-based interventions specific for mTBI and PTSD kinetic energy from the blast wave can be transmitted to the are effective in comorbid mTBI/PTSD, as each condition nervous system through large blood vessels in the chest. The may exacerbate symptoms and complicate treatment, ulti- resulting blood surge dramatically increases cerebral perfu- mately affecting the course of the recovery. In a recent survey, sion pressure and causes damage to both tiny cerebral blood providers treating patients with mTBI and co-occurring PTSD vessels and the blood–brain barrier (Chen and Huang 2011). reported that each condition interfered with traditionally pre- These complex mechanisms of injury result in a cascade of scribed TBI or PTSD-specific treatment, with treatment ad- responses at the level of the vascular system, autonomic herence and symptom management among the most common nervous system, and local tissue (Cernak and Noble- problems (Sayer et al. 2009). Thus, there may be a need to Haeusslein 2010). While the pathobiology of blast-TBI is adapt current approaches or to develop novel interventions unique, secondary injury cascades are thought to be similar specifically geared towards patients with mTBI/PTSD. to those seen in non-blast TBI. In this paper, we review the effects of bTBI on cognitive Animal studies suggest that damage to the brain caused function and identify factors that may affect recovery of by primary blast forces can lead to impairments on tests of OEF/OIF military personnel. Next, we discuss current cog- coordination and balance, and can lead to persistent memory nitive rehabilitation treatment options and provide updated deficits (Cernak et al. 2001a; Moochhala et al. 2004; Saljo et practice guidelines and recommendations for this popula- al. 2008). There is evidence of neural injury (neuronal tion. We also highlight current developments and ongoing swelling, astroglial response, and myelin fragments) in the research efforts in the field of cognitive rehabilitation, and hippocampus and brainstem reticular formation (Cernak et discuss key issues to address
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