C
Workshop Speakers’ Papers

Overview of Traumatic Brain Injury Within the Department of Defense

Kimberly S. Meyer1 and Michael S. Jaffee2

INTRODUCTION

Traumatic brain injury (TBI) has been declared by the media as the signature injury of the current conflicts in Iraq and Afghanistan. The Department of Defense (DoD) defines TBI as a traumatic blow or jolt to the head resulting in an alteration or loss of consciousness (DoD, 2007).

TBI surveillance efforts within DoD began in 2000 and, through the fourth quarter of 2010, 202,281 service members have been diagnosed with TBI.3 The majority of these injuries (77 percent) are classified as mild TBI (mTBI) or concussion. The severity of injury for the remainder of cases is as follows: moderate (16.8 percent), severe (1 percent), and penetrating (1.7 percent). A small proportion (3.5 percent) is of undetermined severity, likely because of coding incongruencies. Since 2000, the frequency of diagnosis has increased each year (Table C-1), which is likely a result of the aggressive pursuit of increased screening efforts instituted by DoD in 2006.

SCREENING

Screening of TBI occurs at various time points following combat activities. During the acute stages, screening takes place in theater. Early efforts regarding TBI screening required

1

Defense & Veterans Brain Injury Center.

2

San Antonio Uniformed Services Health Education Consortium.

3

Available online: http://www.dvbic.org/TBI-Numbers.aspx (accessed March 25, 2011).



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C Workshop Speakers’ Papers Overview of Traumatic Brain Injury Within the Department of Defense Kimberly S. Meyer1 and Michael S. Jaffee2 INTRODUCTION Traumatic brain injury (TBI) has been declared by the media as the signature injury of the current conflicts in Iraq and Afghanistan. The Department of Defense (DoD) defines TBI as a traumatic blow or jolt to the head resulting in an alteration or loss of consciousness (DoD, 2007). TBI surveillance efforts within DoD began in 2000 and, through the fourth quarter of 2010, 202,281 service members have been diagnosed with TBI.3 The majority of these injuries (77 percent) are classified as mild TBI (mTBI) or concussion. The severity of injury for the remainder of cases is as follows: moderate (16.8 percent), severe (1 percent), and penetrating (1.7 percent). A small proportion (3.5 percent) is of undetermined severity, likely because of coding incongruencies. Since 2000, the frequency of diagnosis has increased each year (Table C-1), which is likely a result of the aggressive pursuit of increased screening ef- forts instituted by DoD in 2006. SCREENING Screening of TBI occurs at various time points following combat activities. During the acute stages, screening takes place in theater. Early efforts regarding TBI screening required 1 Defense & Veterans Brain Injury Center. 2 San Antonio Uniformed Services Health Education Consortium. 3 Available online: http://www.dvbic.org/TBI-Numbers.aspx (accessed March 25, 2011). 286

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287 APPENDIX C TABLE C-1 The Number of DoD Service Members (All Armed Forces) Diagnosed with TBI, 2000–2010a Year Number of Service Members 2000 10,963 2001 11,830 2002 12,470 2003 12,898 2004 13,312 2005 12,192 2006 16,946 2007 23,160 2008 28,555 2009 29,252 2010b 30,703 Total 202,281 aAvailable online: http://www.dvbic.org/TBI-Numbers.aspx (ac- cessed March 25, 2011). bAs of quarter 4 of 2010, as of February 17, 2011. evaluation when an individual presented to medical care with symptoms concerning for TBI. An in-theater assessment of TBI care sponsored by the Joint Chiefs of Staff, however, found that individuals at risk for TBI failed to seek medical evaluation; consequently, mandatory event-based screening protocols were implemented in July 2010. These protocols include obligatory medical evaluations for all individuals within 50 meters of a blast, those who were located in a building or vehicle damaged by a blast, and those with certain other indi- cations like blunt trauma to the head. The Military Acute Concussion Evaluation (MACE) is the tool used in acute TBI screening (Figure C-1). The MACE tool was instituted in 2006 and assesses the following four domains: history of the traumatic event, including presence or absence of changes in consciousness; current symptoms; neurological exam; and, if indicated, a brief cognitive appraisal. The MACE tool is based on the Standardized Assessment of Concussion used for sports-related injuries where scores of 25 or less are indicative of cognitive impairment (McCrea et al., 2000). A validation study of MACE use in an austere environment is cur- rently under way. Preliminary evidence suggests cognitive scores slightly less than 25 in a deployed setting may be normal because simple orientation may be affected by lack of dif- ferentiation during daily routines. Further validation testing is ongoing to optimize the use of this cognitive evaluation in theater. Initially, the only documentation required when utilizing MACE was the numeric score associated with the cognitive assessment, which led to incomplete capture of the TBI exposure and an immediate written record in a member’s medical history. Subsequently, documentation requirements were modified and the following were added: cognitive score, neurological assessment, and current symptoms (CNS). Using this additional documenta- tion facilitates the identification of a temporal relationship between the traumatic event and symptom onset in addition to changes in symptom profiles over time. Although MACE is not a definitive diagnostic tool for TBI, positive screens trigger a detailed clinical exam to confirm the diagnosis or determine the differential diagnosis for ongoing symptoms. Service members evacuated to Landstuhl Regional Medical Center (LRMC) for any injury or illness undergo additional screening using the MACE tool. From May 2006 to October 2008, approximately 18,000 patients (approximately 12,200 inpatients and 5,800

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288 NUTRITION AND TRAUMATIC BRAIN INJURY FIGURE C-1 An example of a MACE form. SOURCE: Available online: http://www.dvbic.org/Providers/TBI-Screening.aspx (accessed April 5, 2011). FIGURE C-1 bitmap outpatients) completed the initial MACE screening at LRMC. Sixteen percent of outpatients screened positively as being at risk for TBI. Additional screening revealed that 78 percent of the positive screens described symptoms associated with TBI. Thirty-one percent of inpa- tients screened positively as being at risk for TBI. Of those inpatients screening positive, 66 percent reported associated symptoms (Dempsey et al., 2009). Those with significant find- ings are triaged to a stateside military medical facility with appropriate resources to further evaluate and treat TBI. Increased funding has led to allocation of resources at most military installations, thereby allowing those with mTBI to be treated at their home base. The U.S. Army has credentialed its hospitals based on resources available (Figure C-2). Similarly, the U.S. Navy and U.S. Air Force have declared certain facilities as TBI centers. Those deter-

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bitmap FIGURE C-2 289 FIGURE C-2 U.S. Army TBI medical assets.

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290 NUTRITION AND TRAUMATIC BRAIN INJURY mined to need specialized services (i.e., severe and penetrating TBI patients), however, are directed to Walter Reed Army Medical Center (WRAMC) or National Naval Medical Center (NNMC) for additional acute and subacute care. Active-duty service members undergo a final screening during mandatory Post- Deployment Health Assessment (PDHA, DD-Form 2796). This assessment is not limited to TBI and covers symptoms associated with a variety of other medical and psychological conditions. The TBI component consists of the following four questions, which are based on the Brief Traumatic Brain Injury Screen (Schwab et al., 2006): 1. During this deployment, did you experience any of the following events? • Blast or explosion • Vehicular accident • Fragment wound or bullet wound above the shoulders • Fall • Other event causing injury to the head 2. Did any of the following happen to you, or were you told happened to you, IMME- DIATELY after any of the event(s)? • Lost consciousness or got “knocked out” • Felt dazed, confused, or “saw stars” • Didn’t remember the event • Had a concussion • Had a head injury 3. Did any of the following problems begin or get worse after the event(s)? • Memory problems or lapses • Balance problems or dizziness • Ringing in the ears • Sensitivity to bright light • Irritability • Headaches • Sleep problems 4. In the past week, have you had any of the symptoms you indicated? • Memory problems or lapses • Balance problems or dizziness • Ringing in the ears • Sensitivity to bright light • Irritability • Headaches • Sleep problems One study of a returning U.S. Army Combat Brigade Team revealed that 22.8 percent of soldiers who reported injury during assessment with PDHA sustained a clinician-confirmed TBI (Terrio et al., 2009). The majority were mTBIs (i.e., concussions). Although 33.4 per- cent of this sample reported multiple symptoms immediately following the injury, symptom reporting decreased to 7.5 percent in the postdeployment period. These results suggest that most individuals recover within weeks to months of concussion injury, which is consistent with findings among the civilian population. Further screening occurs for those entering the Veterans Health Administration (VHA) for care. Affirmative responses on all questions are required to be a positive screen. This

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291 APPENDIX C serves to identify those still in need of medical care for TBI-related symptoms but does not enhance current TBI surveillance methods. NEUROCOGNITIVE ASSESSMENT TESTING In accordance with the congresional National Defense Authorization Act of 2007, predeployment neurocognitive testing was implemented in 2008. To date, 723,981 service members have completed this testing, which currently uses the Automated Neurocognitive Assessment Metrics (ANAM). This is a brief computerized battery that is designed to detect speed and accuracy of attention, memory, and thinking ability. By completing the ANAM within 12 months of deployment, each service member establishes an individual preinjury baseline; thus, if a TBI is sustained in theater, the ANAM can be repeated to allow for pre- and postinjury comparison and to better inform return-to-duty determinations. Pend- ing inclusion in the electronic medical record, test results are stored in a central repository. Health-care providers can obtain these results from the helpdesk by emailing pertinent de- mographic information to anam.baselines@amedd.army.mil. To date, there have been 5,820 requests for baseline scores with 1,826 from Afghanistan, 202 from Iraq, and 3,792 from the Continental United States. TREATMENT Clinical practice guidelines have been developed to guide the evaluation and manage- ment of TBI in both the acute and chronic settings. These guidelines incorporate available evidence and expert consensus. Acute care begins on the battlefield with theater-based guide- lines, which incorporate the tactical requirements of the combat setting. Previous guidelines were only useful if the service member sought a medical evaluation. Recent revisions, sup- ported by the Joint Chiefs of Staff, require all service members involved in a traumatic event to undergo screening and a mandatory 24-hour rest period. Those with serious neurologic injury are evacuated to facilities with imaging capabilities. Those with symptoms of con- cussion, such as headache or dizziness, are managed aggressively with local medical assets. Once symptoms resolve, exertional testing is performed prior to return to duty to ensure that symptoms do not return with physiologic stress. Those with persistent symptoms undergo combat stress evaluations and more detailed medical examinations. Because of concerns that multiple concussions may result in slower recovery or, in more severe cases, chronic traumatic encephalopathy (Guskiewicz et al., 2003; McKee et al., 2009), service members sustaining three or more concussions in a 12-month period are required to undergo a com- plete neurological and psychological evaluation. The result of this exam may lead to one of the three following dispositions: stateside evacuation, restricted duty, or return to full duty. Subacute and chronic TBI care is guided by the Department of Veterans Affairs (VA) and DoD Evidence-Based Clinical Practice Guideline for the Management of Concussion/ Mild Traumatic Brain Injury (2009). This document was developed under the auspices of the VHA and DoD with the intent of providing evidence-based recommendations to patients and their providers, reduce practice variability, and provide structure for measurement of patient outcomes. The guidelines include three algorithms: initial presentation, symptom management, and follow-up of persistent symptoms. More detailed guidance is included for the use of pharmacotherapy and management of common physical symptoms associated with concussion.

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292 NUTRITION AND TRAUMATIC BRAIN INJURY TELEMEDICINE Various telemedicine modalities are currently used in the care of TBI patients within the Military Health System (MHS). For example, TBI.consult is an electronic consult service available to deployed providers, and it is staffed by neurologists, neurosurgeons, and nurse practitioners with expertise in TBI. A confidential history and physical record are transmit- ted to the consult team via email. The team considers local resources and within two to three hours of consult receipt an initial response is provided. The team makes individualized recommendations based on the patient’s medical condition. Resources such as the theater clinical practice guidelines (Brain Trauma Foundation, 2005) and MACE are provided when needed as well as in-theater contacts for specialty care. In some cases, collaboration occurs with other specialty services (i.e., ear, nose, and throat services for hearing loss associated with TBI), with TBI staff in theater, or with LRMC staff to facilitate necessary evacuations. Stateside TBI care in more remote locations is supported by the virtual TBI (vTBI) clinic. The vTBI clinic currently provides symptom management and neuropsychological screening via videoconferencing. Plans are in process to increase capabilities to include mass screening and some components of neurorehabilitation. The Defense Centers of Excellence for Psychological Health and Traumatic Brain Injury (DCoE) has established a 24/7 Outreach Center. Service members can contact the center via email, live online chat, or telephone for immediate assistance. After immediate concerns are addressed by trained operators, callers are connected with appropriate TBI resources, most often through the Defense and Veterans Brain Injury Center (DVBIC). CARE COORDINATION In the acute care phase, service members sustaining severe or penetrating TBI are as- signed a federal recovery coordinator to facilitate coordination of care across the health-care continuum. Those with mTBI may also require coordination of services during their recov- ery. This is accomplished by the DVBIC Care Coordination Program. Once identified with TBI, service members are contacted by a regional care coordinator (RCC), who conducts assessments and identifies patient needs. The RCC works with the individual’s case manag- ers to identify ongoing needs and local TBI resources for up to two years. Data from this program indicate that physical symptom reporting decreases with time while psychological symptom reporting increases. Further work is needed to determine the cause and implica- tions of these findings. EDUCATION TBI-related educational efforts within DoD are aimed at two main consumers: provid- ers and patients/families. Three websites have been developed to assist patients and their families with their understanding of TBI. • www.traumaticbraininjuryatoz.org Sponsored by the U.S. Air Force Center of Excellence for Medical Multimedia, this award-winning site provides an overview of TBI by severity, expected courses of recovery, and personal stories of service members with TBI. In addition, there are

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293 APPENDIX C downloadable components to the congressionally mandated DoD/VA TBI Family Caregiver Curriculum. • www.afterdeployment.org (mTBI) Developed by the DCoE’s National Center for Telehealth and Technology, this web- site provides an overview of mTBI. Self-assessments are available for many common symptoms or conditions associated with mTBI. A resource library is also included. • www.brainline.org A service of WETA4 public communications with funding by DVBIC, this website provides information about TBI for patients, families, and providers. Various research topics, TBI experts, and other headlines are presented. The National Defense Authorization Act of 2007 established a 15-member panel to develop a curriculum to train family caregivers of service members and veterans with TBI. Panel members were appointed by the DoD and the Department of Health and Human Services on March 6, 2008. The members of the panel include professionals from DoD and the VA specializing in TBI, family caregivers, and experts in the development of curricula. The curricula were approved for distribution in April 2010. The curricula are presently be- ing disseminated by recovery coordinators at WRAMC and NNMC to family members of patients with significant TBI. They are also available to the public for download at www. dvbic.org, in addition to other currently approved patient and provider materials. Many modalities are used to ensure that DoD providers have an adequate understand- ing of TBI. Since 2007, DVBIC has hosted the annual TBI military training conference. The 2010 event registered more than 850 participants from all branches of service for the two-day conference. Experts from across the country contributed to education through case studies, panel discussions, and podium presentations. The DCoE and DVBIC host regularly scheduled webinars to further facilitate provider education. TBI education is also provided at deployment platforms. The U.S. Army Proponency Office for Rehabilitation and Reinte- gration convened a panel of subject-matter experts—both military and civilian—to develop a series of TBI materials ranging from a public service announcement (101) to treatment paradigms. • TBI 101: Introduction and Awareness—Army • TBI 101: Introduction and Awareness—Joint • TBI 201: TBI Overview for Healthcare Personnel • TBI 401: Primary Care Assessment and Management for Concussion This program is available for use at deployment platforms and, most recently, has been included on the MHS Learning Portal (MHS Learn), accompanied by appropriate continu- ing medical education credits. Thirteen other TBI-related lessons are also available on MHS Learn. RESEARCH In 2009, more than $40 million were allocated for TBI and psychological health re- search through the Congressionally Directed Medical Research Program (CDMRP). Fund- ing priorities included cellular regeneration and interconnection strategies for the central 4 WETA is the flagship, not-for-profit public broadcasting station serving Washington, DC; Virginia; and Maryland.

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294 NUTRITION AND TRAUMATIC BRAIN INJURY nervous system, evidence-based prevention and rehabilitation strategies, three-dimensional models of blast injury, and advanced diagnostic modalities (e.g., neuroimaging, biomarkers). Figure C-3 depicts an overview of current CDMRP-funded studies. Key collaborations with academia and industry are likely to provide high-yield informa- tion in the upcoming years. A partnership between DVBIC and the Armed Forces Institute of Pathology established a state-of-the-art research lab. This alliance also introduced an organizational structure for the development of a “brain bank” allowing for detailed neuro- pathological examinations. In addition, the lab has a small animal imaging facility featuring a 7 Tesla horizontal bore imager used in various preclinical research protocols. In conjunc- tion with Massachusetts Institute of Technology and the Institute of Soldier Nanotechnology, DoD scientists have developed the most comprehensive computerized simulation model of the interactions between blast and brain. It is anticipated that this initial effort will lead to further work on the utilization of nanotechnology to protect and improve survivability of wounded service members. Findings from the U.S. Army Medical Research and Materiel Command Blast Sympo- sium reveal pathological differences in blast and blunt trauma seen on diffusion tensor imag- ing. Data presented at the symposium from functional Magnetic Resonance Imaging (fMRI) showed statistically significant differences between breacher instructors and students. During their training to be breachers, students are exposed to 50 to 70 blasts of weapons-grade explosives. Finally, animal models suggest axonal, neuronal, and glial damage following blast injury as well as physiologic, histologic, and behavioral differences between blunt and blast injury. Proceedings from this symposium are scheduled to be published in an upcoming special issue of the journal Neuroimage. Other studies still in progress include helmet sensor studies, a 15-year longitudinal study of TBI, and the Head to Head Study of computerized neurocognitive tools. All of these studies will greatly enhance the understanding of TBI and its consequences. TBI Drugs Funded TBI Investigators PI Funded TBI Other Interventions in Hawaii Awards range from $150K over 18 months to $4M over 4 years 201 Proposals selected from a pool of 2110 applicants TBI Research Gaps Treatment and Clinical Management Neuroprotection and Repair Rehabilitation/Reintegration Field Epidemiology Physics of Blast FIGURE C-3 CDMRP-funded studies and their locations. SOURCE: Jaffee, 2010. FIGURE C-3 bitmap

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295 APPENDIX C TABLE C-2 Key Combat-Related TBI Scholarly Papers, 2003–2009 Category Reference Title Screening Ivins et al., 2009 Performance on the Automated Neuropsychological Assessment Metrics in a nonclinical sample of soldiers screened for mTBI after return returning from Iraq and Afghanistan: A descriptive analysis Terrio et al., Traumatic brain injury screening: Preliminary findings in a U.S. Army 2009 Brigade Combat Team Ivins et al., 2003 Traumatic brain injury in U.S. Army paratroopers: Prevalence and character Clinical Bell et al., 2009 Military traumatic brain and spinal column injury: A 5-year study of the Findings impact blast and other military grade weaponry on the central nervous system Brahm et al., Visual impairment and dysfunction in combat-injured service members with 2009 traumatic brain injury Hoge et al., Mild traumatic brain injury in U.S. soldiers returning from Iraq 2008 Blast Ling et al., 2009 Explosive blast neurotrauma Neurotrauma Moore et al., Computational biology—Modeling of primary blast effects on the central 2009 nervous system Dewitt et al., Blast-induced brain injury and posttraumatic hypotension and hypoxemia 2009 TBI & Post- Stein and Exploring the convergence of posttraumatic stress disorder and mild Traumatic McAllister, 2009 traumatic brain injury Stress Nelson et al., Relationship between processing speed and executive functioning Disorder 2009 performance among OEF/OIF veterans: Implications for post deployment rehabilitation Kennedy et al., Posttraumatic stress disorder and posttraumatic stress disorder-like 2007 symptoms and mild traumatic brain injury Imaging Moore et al., Diffusion tensor imaging and mTBI—A case-control study of blast (+) in 2009 returning service members following OIF and OEF Huang et al., Integrated imaging approach with MEG and DTI to detect mild traumatic 2009 brain injury in military and civilian patients Outcomes Bjork and Does traumatic brain injury increase risk for substance abuse? Grant, 2009 Han et al., 2009 Clinical, cognitive, and genetic predictors of change in job status following traumatic brain injury in a military population Gottshall et al., Objective vestibular tests as outcome measures in head injury patients 2003 Drake et al., Factors predicting return to work following mild traumatic brain injury: A 2000 discriminant analysis continued

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296 NUTRITION AND TRAUMATIC BRAIN INJURY TABLE C-2 Continued Category Reference Title Rehabilitation Lew et al., 2009 The potential utility of driving simulators in the cognitive rehabilitation of combat-returnees with traumatic brain injury Vanderploeg Rehabilitation of traumatic brain injury in active-duty military personnel and et al., 2008 veterans: Defense and Veterans Brain Injury Center randomized controlled trial of two rehabilitation approaches Trudel et al., Community-integrated brain injury rehabilitation: Treatment models and 2007 challenges for civilian, military, and veteran populations Walker et al., Motor impairment after severe traumatic brain injury: A longitudinal 2007 multicenter study Miscellaneous Cote et al., 2007 A mixed integer programming model to locate traumatic brain injury treatment units in the Department of Veterans Affairs: A case study Warden, 2006 Military TBI during the Iraq and Afghanistan wars Ivins et al., 2006 Hospital admissions associated with traumatic brain injury in the U.S. Army during peacetime: 1990s trends Clinicians continue to contribute to the understanding of combat-related TBI. Table C-2 summarizes recent observations of providers involved in the day-to-day care of those with TBI. These efforts identify some of the consequences associated with TBI and lead to ad- ditional scientific inquiry. SUMMARY Much work remains to be done in order to fully understand TBI and its long-term consequences. Efforts within DoD to rapidly transform bench science and observed best practice to clinical practice continue. This is most readily evident by the annual revisions of educational materials, clinical practice guidelines, and screening techniques. REFERENCES Brain Trauma Foundation. 2005. Guidelines for field management of combat-related head trauma. New York, NY: Brain Trauma Foundation. Dempsey, K. E., W. C. Dorlac, K. Martin, R. Fang, C. Fox, B. Bennett, K. Williams, and S. Flaherty. 2009. Landstuhl Regional Medical Center: Traumatic brain injury screening program. Journal of Trauma Nursing 16(1):6–12. DoD (Department of Defense). 2007. Traumatic brain injury: Definition and reporting. Memorandum. HA Policy 07-030. Dated October 1, 2007. Available online at http://mhs.osd.mil/content/docs/pdfs/policies/2007/07-030. pdf (accessed March 25, 2011). Guskiewicz, K. M., M. McCrea, S. W. Marshall, R. C. Cantu, C. Randolph, W. Barr, J. A. Onate, and J. P. Kelly. 2003. Cumulative effects associated with recurrent concussion in collegiate football players: The NCAA Concussion Study. The Journal of the American Medical Association 290(19):2549–2555. Jaffee, M. S. 2010. Overview of Combat Related Traumatic Brain Injury and DoD TBI Initiatives. Presented at Institute of Medicine’s Workshop on Nutrition and Neuroprotection in Military Personnel, Washington, DC, June 23, 2010. McKee, A. C. M., R. C. M. Cantu, C. J. A. Nowinski, E. T. M. Hedley-Whyte, B. E. P. Gavett, A. E. M. Budson, V. E. M. Santini, H.-S. M. Lee, C. A. Kubilus, and R. A. P. Stern. 2009. Chronic traumatic encephalopathy in athletes: Progressive tauopathy after repetitive head injury. Journal of Neuropathology & Experimental Neurology 68(7):709–735.

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402 NUTRITION AND TRAUMATIC BRAIN INJURY Trudeau, D. L., J. Anderson, L. M. Hansen, D. N. Shagalov, J. Schmoller, S. Nugent, and S. Barton. 1998. Findings of mild traumatic brain injury in combat veterans with PTSD and a history of blast concussion. Journal of Neuropsychiatry and Clinical Neurosciences 10(3):308–313. Nutritional Care of Active Duty Patients with TBI Stephanie Sands27 INTRODUCTION Traumatic brain injury (TBI) is a leading cause of death and disability in the United States. Among military personnel serving in Operation Enduring Freedom/Operation Iraqi Freedom (OEF/OIF), the likelihood of traumatic brain and other polytrauma injuries is significantly elevated. As defined by the U.S. Veterans Health Administration, polytrauma is “two or more injuries to physical regions or organ systems, one of which may be life threatening, resulting in physical, cognitive, psychological, or psychosocial impairments and functional disability” (United States Department of Veterans Affairs, 2009). Such inju- ries are often a result of rocket-propelled grenades, improvised explosive devises, gunshot wounds, and landmines. In 2005, the United States Congress established four Polytrauma Rehabilitation Centers, one of which is the James A. Haley Veterans’ Hospital (JAHVH) in Tampa, Florida (Scott et al., 2006). This report is largely based on nutritional management and monitoring of complex variables of patients who have suffered TBI and polytrauma in the sub-acute and long-term setting at JAHVH. SUB-ACUTE NUTRITIONAL MANAGEMENT Following severe trauma and acute TBI, striking metabolic changes involving an ac- celerated catabolic rate and extensive nitrogen losses proportional to the severity of injury are common (Cook and Hatton, 2007). The hypermetabolic response is related to increases in energy expenditure, oxygen consumption, carbon dioxide production as well as primary mediators such as catecholamines, corticosteroids, and inflammatory cytokines (Berry, 2009; Esper, 2004). Because the brain functions as a regulator for metabolic activity, disruptions caused by TBI result in a cascade of hormonal modifications, irregular cellular metabolism, and dynamic cerebral and systemic inflammatory response as an effort to circulate substrate required at the cellular level. The end result of these alterations involves systemic catabolism causing an increase in basal metabolism, oxygen consumption, glycogenolysis, hyperglyce- mia, proteolysis, muscle wasting, and energy requirements (Cook et al., 2008). Optimal tim- ing of nutrition, fluid, and electrolyte management may improve the overall clinical course in TBI patients. The fundamental goal of nutritional intervention is to provide adequate calories and protein sufficient to meet the demands of hypermetabolism and increased pro- tein breakdown as a means of preserving lean body mass while maintaining skin integrity, immune function, gastrointestinal mucosal integrity, wound healing, and nitrogen balance during rehabilitation. While providing nutritional care of polytrauma patients during the months following injury, one of the most challenging decisions is the accurate assessment and provision of essential calories as the complications related to under- or overfeeding can compromise rehabilitation prognosis. Nutrition support should be aimed toward current physiologic 27 James A. Haley Veteran’s Hospital.

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403 APPENDIX C reactions and should not exacerbate complications of the current phase (stress, catabolic, anabolic). Underfeeding can result in decreased respiratory muscle strength, decreased ventilator drive, failure to wean from mechanical ventilation, impaired organ function, immunosuppression, poor wound healing, increased risk of nosocomial infection, and low transport protein levels. This cachexia (i.e. wasting syndrome or loss of weight, muscle atro- phy, fatigue, weakness, and significant loss of appetite in someone who is not actively trying to lose weight) can impact mobility, functional rehabilitation and overall length of stay as well as the development of complications such as decubitus ulcers, pneumonia, urinary tract infections, and venous thromboembolism. Among the complications of overfeeding include the risk of refeeding syndrome,28 hyperglycemia, azotemia, hypertriglyceridemia, electrolyte imbalance, immunosuppression, alterations in hydration status, hepatic steatosis, and failure to wean from mechanical ventilation (Cook et al., 2008; Esper, 2004). Calorie Provision Energy expenditure has been investigated extensively and has been shown to be elevated following acute TBI (Cook and Hatton, 2007; Rajpal and Johnston, 2009). Two methods for determining energy requirements involve measurement of resting metabolic rate using indirect calorimetry (IC), or estimating energy needs with the use of predictive equations and clinical judgment. Although IC is considered the “gold standard” for determining energy expenditure in TBI, many clinicians do not have access to resources necessary to measure metabolic rate. Additionally, calorie requirements may vary day to day in this population secondary to symptoms such as sympathetic storming, fevers, or muscle contractions. More commonly, clinicians use one of more than 200 predictive equations that have been devel- oped for estimating energy expenditure (McCarthy et al., 2008). For example, the Brain Trauma Foundation (BTF) recommends use of the Harris Benedict Equation multiplied by a stress factor of 1.4 with an observed variance of 1.2–2.5 (Bratton et al., 2007), and the American Society of Enteral and Parenteral Nutrition recommends 25–30 kcal/kg in criti- cally ill patients. However, it should be noted that there is a limited amount of literature available following the critical care setting or for patients with further polytrauma injuries in addition to TBI. Because utilizing the above methods to determine energy expenditure can be imprecise considering the complexity of this patient population, the following variables have been observed or proven to alter metabolic rate (Berry, 2009; Cook et al., 2008; Dickerson and Roth-Yousey, 2005; Esper, 2004; Frankenfield, 2006; Rajpal and Johnston, 2009): • Severity of trauma and additional injuries, burns, or wounds • Time since injury, depending on the ongoing stress response and degree of healing • Physiologic effects—blood pressure, heart rate, respiratory rate, sympathetic storm- ing such as seen in Paroxysmal Autonomic Instability with Dystonia (Blackman et al., 2004), body temperature (diaphoresis, hyperthermia, and medically induced hypothermia) • Physical activity (restlessness, agitation) or muscular dysfunction (posturing, dystonia) • Level of consciousness (Glasgow Coma Score) • Cognitive Functioning (Rancho Los Amigos Scale) • Neuroendocrine disruption • Sepsis and inflammatory response 28 Abnormalities in fluid balance, glucose metabolism, vitamin deficiency, hypophosphatemia, hypomagnesemia, and hypokalemia in patients exposed to enteral or parenteral nutrition after a period of starvation.

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404 NUTRITION AND TRAUMATIC BRAIN INJURY • Medications: Central nervous system agents—sedatives, anticonvulsants, analgesics, narcotics, hypnotics, barbiturates; autonomic neuromuscular blocking agents; cardio- vascular agents—beta-adrenergic blockers; steroids, inotropic agents. • Ventilator support • Thermic effect of food generated by caloric intake • Preinjury nutritional status and/or malnutrition Protein Requirements Protein requirements following TBI are grossly elevated. Protein catabolism peaks 8 to 14 days after injury with documented nitrogen losses up to 30 grams per day. This extreme protein breakdown can cause a 10 percent loss of lean body mass during the first seven days of injury (Cook and Hatton, 2007; Gleghorn et al., 2005; Rajpal and Johnston, 2009). Uri- nary urea nitrogen (UUN) values can be monitored to determine a state of nitrogen balance. Although it is often unrealistic to obtain nitrogen balance during the first week after injury regardless of nutritional provision, nitrogen balance is an important way to measure the adequacy of caloric intake and metabolism in the weeks that follow (Esper, 2004; Rajpal and Johnston, 2009). The BTF recommends protein provision of 1.5–2.0 g/kg of body weight in TBI patients (Cook and Hatton, 2007; Cook et al., 2008). Although hepatic production of transport proteins (albumin, prealbumin, transferring) is reduced during states of inflam- mation regardless of nutrition, monitoring their trends can be helpful to determine recovery from the inflammatory process along with overall clinical improvement such as wound healing, infection resolution, and weaning from ventilator support. Some facilities also in- corporate specific amino acids into their nutritional programs such as glutamine, arginine, or branched chain amino acids (Esper, 2004; Rajpal and Johnston, 2009). Method of Feeding Another area of consideration during nutritional care of TBI patients is the method of feeding. Initially, it has to be determined whether to use parenteral (PN) or enteral (EN) nutrition. It is generally accepted that EN is preferable over PN, with the exception of cases such as barbiturate coma, multiple vasopressors (risk of bowel necrosis), or prolonged pe- riods of being supine. When it is determined that EN is desirable, many clinicians debate whether to obtain small bowel or gastric access given that there is limited consensus that postpyloric feedings have demonstrated improved outcomes. TBI patients often exhibit gastrointestinal dysfunction with increased incidences of aspiration pneumonia, diarrhea, vomiting, abdominal distention, and increased gastric residuals. Impaired gastric emptying is often present secondary to decreased lower esophageal sphincter tone, vagus nerve damage, elevated levels of endogenous opioids/endorphins, elevated intracranial pressure, or medi- cation side effects (Cook et al., 2008; Esper, 2004; Ott et al., 1991; Rajpal and Johnston, 2009). Often nasogastric or nasoenteral tubes are placed until it is determined that longer term EN access is needed. The placement of longer term EN access via percutaneous endo- scopic gastrostomy (PEG) tubes often proves successful in establishing well-tolerated feeding access (Cook and Hatton, 2007). Despite the potential feeding difficulties in many TBI pa- tients, the majority of these patients are able to receive safe and adequate nutrition through EN. Approaches to improve EN tolerance include head of bed elevation (30–45 degrees), continuous tube feeding at low infusion rates advanced per tolerance, the use of pro-motility agents, using concentrated enteral formulas to decrease total volume, and consideration of small bowel versus gastric feeds (Cook et al., 2008).

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405 APPENDIX C TABLE C-11 Sample of Drug-Nutrition Interactions Common in TBI Medical Management Medication Examples of Nutrition Implications Antipsychotics (Ziprasidone, Linked to weight gain Olanzapine, Risperidone) Barbiturates May lower metabolic rate or cause constipation Bisacodyl Risk of hypocalcemia and decreased fat absorption Bromocriptine Potential of nausea/vomiting/constipation, elevated residuals Carbamazepine Increased risk of hyponatremia, can cause formation of orange rubbery precipitate when combined with water/dilatants Corticosteroids Risk of hyperglycemia; osteoporosis and gastric ulcer risk with chronic use Mannitol Monitor for hypokalemia, hypomagnesemia, hypovolemia Metoclopramide Possible for changes in mental status/cognition Mirtazapine Related to increased appetite and weight gain Narcotic analgesics Delayed emptying/constipation (especially in opioid usage) Linked to elevated liver enzymes and/or lipid panela Oxandrolone Phenytoin Absorption may be impaired with provided with enteral nutrition, possible decline in folate, vitamin D Propofol Provides lipid calories (pro-inflammatory fat source) Stimulants (Methylphenidate, May cause decreased appetite and weight loss Dextroamphetamine amphetamine) Vasopressors Decreases gut perfusion May cause appetite changes, binge eating, nocturnal eatinga Zolpidem aAnecdotal observations noted at JAHVH; UpToDate Online 18.3. SOURCE: Cook and Hatton, 2007. Medication Interactions Drug-nutrient interactions require consideration when providing medical nutrition ther- apy to TBI patients. Registered dietitians review patient medications as a part of nutritional assessment to identify nutritional implications. For example, enteral nutrition is typically held one to two hours before and after the administration of phenytoin to prevent absorptive changes and chelation. Other medications may lower electrolyte and micronutrient levels, or increase the risk of weight gain or loss. Table C-11 provides examples of some interactions encountered in the clinical setting. Sample of 12 Polytrauma Patients As discussed previously, there is a limited amount of research evaluating nutritional needs of TBI patients following the acute critical period or with multiple polytrauma injuries in addition to TBI. Figures C-23 through C-28 represent a snapshot of 12 patients in acute rehabilitation at JAHVH. The categories illustrated include patient age, time since injury, method of feeding, percent of usual body weight lost and caloric provision required to fa- cilitate weight maintenance of weight gain of one to two pounds per week. The illustrations depict at typical distribution of patients which changes from day to day.

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406 NUTRITION AND TRAUMATIC BRAIN INJURY FIGURE C-23 Distribution of 12 polytrauma patients according to age (captured 9/15/2010 at JAHVH). Figure C-23.eps bitmap FIGURE C-24 Distribution of 12 polytrauma patients according to the number of months since injury (captured 9/15/2010 at JAHVH). Figure C-24.eps bitmap FIGURE C-25 Distribution of 12 polytrauma patients according to the method of feeding (captured 9/15/2010 at JAHVH). Figure C-25.eps bitmap FIGURE C-26 Distribution of 12 polytrauma patients according to the percent of pre-injury weight loss since injury (captured 9/15/2010 at JAHVH). Figure C-26.eps bitmap

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407 APPENDIX C FIGURE C-27 Distribution of 12 polytrauma patients according to number of calories per kilogram to attain weight maintenance or gain (1–2 lbs per week) (cap- tured 9/15/2010 at JAHVH). Figure C-27.eps bitmap FIGURE C-28 Distribution of 12 polytrauma patients according to percent of estimated resting metabolic rate using the Harris Benedict Equation to attain weight maintenance or gain (1–2 lbs per week) (captured 9/15/2010 at JAHVH) Figure C-28.eps bitmap LONG TERM NUTRITIONAL CONSIDERATIONS While the concerns of severe weight loss following TBI in active duty service members are significant, the opposing issue regarding unintentional weight gain has scarcely been discussed in the literature. Following TBI, changes such as alterations in the brain’s regula- tion of hunger and satiety, neuroendocrine dysfunction, brain injury-induced hyperphagia, medication related side effects, cognitive impairments, or emotional coping may impact the ability to maintain a healthy weight. In the post-acute rehabilitation setting at JAHVH, a number of polytrauma patients experience detrimental weight gain and dyslipidemia. Under normal conditions, the brain functions to regulate energy homeostasis by constant transmission of signals that influence energy intake and ultimately body weight (Woods and D’Alessio, 2008). Satiation signals such as cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), peptide tyrosine-tyrosine (PYY) and apolipoprotein A-IV (apo A-IV) are secreted in response to specific macronutrient stimuli. These peptides, many of which are synthesized in the brain in addition to the gastrointestinal tract, are released in response to food ingestion and act to reduce meal size. Adiposity signals, insulin and leptin, are secreted relative to the amount of body fat and are transported across the blood-brain barrier to interact with neuronal receptors predominately in the hypothalamus. Because TBI may impair the trans- mission of these signals, many patients experience an altered sensation of hunger and satiety.

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408 NUTRITION AND TRAUMATIC BRAIN INJURY TABLE C-12 Nutritional Implications of Post Traumatic Hypopituitarism Hormone Insufficiency/Deficiency Nutritional Implications Adrenocorticotrophic hormone (ACTH) (0–19 Nausea/vomiting, abdominal pain, anorexia, weight percent of TBI patients with deficiencies) loss, hypotension, tachycardia, hyponatremia, hypoglycemia, normocytic anemia Growth hormone (GH) Osteoporosis, dyslipidemia, atherosclerosis, visceral (6–33 percent of TBI patients with deficiencies) obesity, reduced lean body mass Hypothyroidism-Thyroid stimulating hormone (TSH) Weight gain, hypotension, myopathy, dyspnea, (1–10 percent of TBI patients with deficiencies) periorbital edema, bradycardia, normocytic anemia, mild hyponatremia Luteinizing hormone (LH)/Follicle-stimulating Reduced muscle mass and exercise tolerance (men), hormone (FSH) (2–20 percent of TBI patients with decreased breast tissue and bone mineral density deficiencies) (women) SOURCE: Compiled from Schneider et al., 2007. Disturbances of the neuroendocrine system following TBI have nutritional implications that should be considered. Schneider et al (2007) identified 19 clinical studies that report the prevalence of endocrine dysfunction ranges from 15–68 percent in TBI patients. Most researchers agree upon the association of neuroendocrine changes and the severity of brain injury, however variables such as secondary brain damage and medical complications make analysis and prediction more complicated (Rothman et al., 2007). Klose and associates (2007) reported that TBI patients with posttraumatic hypopituitarism display symptoms such as adverse lipid profiles, unfavorable body composition, and worsened perceived health-related quality of life (lowered energy, sleep, increased social isolation) compared to those with preserved pituitary function. Table C-12 reflects sample nutritional implications of post-traumatic hypopituitarism. Although there is a paucity of information regarding brain injury-induced hyperphagia, clinicians working in TBI are likely to encounter patients with an abnormally increased appetite for and consumption of food. This can be especially problematic in a significantly impaired patient with limited self-awareness. Rao and Lyketsos (2000) describe a complex syndrome they refer to as Behavioral Dyscontrol Disorder, Major Variant. This syndrome has mood, cognitive, and behavioral manifestations in both acute and chronic stages of 5–70 percent of TBI. The behaviors reported in this report include impulsivity, aggression, hyper- activity, hyperphagia, and pica. One such scenario at JAHVH resulted in the removal of a patient-accessible family refrigerator secondary to a patient with an insatiable appetite and weight gain. This patient experienced weight gain at a rate of 15 pounds per month, with a total gain of 110 pounds over seven months. He required constant nursing supervision to prevent further instances of excessive eating and consumption of non-food substances like coffee grounds. Instances of rapid and nearly uncontrollable weight gain as described are not uncommon among this population. A multidisciplinary approach should be utilized to treat such conditions by developing environmental modification strategies, behavioral therapy, psychotherapy, and family therapy. Another contributing factor to the weight gain experienced in the postacute setting following TBI is medication side effects. Common medications prescribed following brain injury such as antidepressants, anxiolytics, anticonvulsants, and antipsychotics may promote increased appetite and unintentional weight gain. Healthcare providers should be aware of these side effects and consider weight-neutral alternatives.

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409 APPENDIX C Cognitive impairments among service members who have suffered TBI greatly impact the successfulness of nutrition counseling to a degree that cannot be overstated. For example, consider how executive dysfunction may inhibit the ability to make healthful choices sec- ondary to difficulties in planning, problem solving, organizing, sequencing, self-regulation and monitoring, judgment, set-shifting, impulse control, initiation, and motivation (Rao and Lyketsos, 2000). Tasks such as grocery shopping, reading a recipe, preparing a meal, or understanding and applying healthful eating guidelines can be nearly impossible for some patients. Furthermore, among patients with varying levels of memory impairment, the ability to remember nutritional recommendations may be compromised in addition to recalling and identifying problematic eating behaviors. The combination of impaired hunger and satiety cues as well as short-term memory loss often results in patients who cannot remember hav- ing eaten just minutes after mealtime and are likely to overeat as well. Lastly, the emotional strain of suffering from TBI can play a significant role in the ability to make smart choices and maintain a healthy weight. Coping with symptoms such as depression, boredom, demoralization, anxiety, irritability, anger, the feeling of loss, dis- couragement, and posttraumatic stress disorder can lead to uncontrolled emotional eating. Additionally, families of those who have experienced a TBI are susceptible to encourage the use of food as a coping and comforting mechanism. These patients greatly benefit from a team approach to identify coping strategies and alternatives to eating as well as nutrition education to encourage healthy choices. COMPLEMENTARY AND ALTERNATIVE MEDICINE Incorporation of complementary and alternative medicine (CAM) into treatment regi- mens has become more prevalent among both acute and chronically ill patients. Many researchers are investigating the role of CAM in providing resilience to brain injury or as a treatment modality following an injury. A large portion of posttraumatic neurodegenera- tion is a result of secondary damage from a pathochemical and pathophysiological cascade during the first minutes, hours, and days following an injury (Hall et al., 2010). Many investigators seek to discover the optimal timing of neuroprotective substances to prevent exacerbation of damage caused by the primary injury. However, there are many challenges that come with both performing and interpreting research relating to CAM. As described by Mullin (2009): • The majority of CAM providers are non-physician based, utilizing techniques and tools that are more experiential than evidence-based. • CAM often focuses on treatment of symptoms, which can be subjective, rather than the underlying diagnosis of Western-based medicine. • Blinding is often compromised and many publications labeled as randomized control trials are actually not blinded. • Publication biases are created when investigators, reviewers, and editors submit or accept manuscripts based on the strength or direction of the findings. Access to CAM literature is incomplete; one such example includes mainstream databases such as MEDLINE, which indexes only 10 percent of CAM journal worldwide. Negative CAM findings are more likely to be published in mainstream medical journals, whereas most studies published in leading CAM journals have positive results.

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410 NUTRITION AND TRAUMATIC BRAIN INJURY Studies outside of the United States are more likely to be positive than those in the United States. For example, while completing a PubMed literature review on supplements and TBI over the past five years, Table C-13 depicts the number of articles referenced with various supplements. It is important to note that the majority of these references utilize animal studies to answer their research question. While understanding the possibility of publica- tion bias, one may wonder how to identify the CAM articles being published and indexed in other locations. Clinicians attempting to provide evidence-based guidelines to patients and families are likely to encounter difficulties interpreting the literature and making recommendations. Reasons for this include the publication bias as described above, the lack of clear data, and the number of supplements being promoted. There is a copious amount of marketing which targets TBI patients anywhere along the spectrum of severity and time since injury. Patients and their families are likely to encounter or trial a number of supplements which are promoted to treat side effects of TBI or improve brain health and functioning. Table C-14 reflects a list of supplements being taken among different levels of TBI severity as disclosed by patients and families over one month at JAHVH. An especially susceptible population includes the caregivers of emerging conscious patients. Some programs seek to discover a beneficial cocktail of nutraceuticals which may assist in promoting consciousness. Incidences of patients receiving 45 different nutraceuticals, some of which are administered two or three times a day, as an effort to cause the patient to emerge have been encountered. While assisting patients in making informed decisions regarding supplements, factors should be evaluated such as the risk of causing harm if taken in excessive doses, decreasing medication side effects or modifying the action, lowering seizure threshold, instigating other deficiencies, or mislabeling or adulterating supplements. TABLE C-13 Depiction of PubMed Literature Review of TBI and Various Supplements Over the Past 5 Years (2005–2010) Number of Hits Supplements Being Investigated 137 TBI and Antioxidants 53 TBI and Arginine 43 TBI and Fiber 40 TBI and Vitamins (6-B vitamins, 4-vitamin D) 36 TBI and Choline 28 TBI and Tyrosine 24 TBI and Melatonin 23 TBI and Zinc 23 TBI and CoEnzyme 10 15 TBI and Glutamine 8 TBI and Curcumin 8 TBI and Ketogenic Diet 5 TBI and Omega 3 4 TBI and Caffeine 3 TBI and Branched Chain Amino Acids 2 TBI and Lipoic acid NOTE: The majority of TBI and CAM articles are animal studies, very few of these studies represent human research.

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411 APPENDIX C TABLE C-14 Illustration of Supplements Encountered Among TBI patients, Ranging from Mild to Severe Injuries (JAHVH from 8/20/2010–9/20/2010) Antioxidant vitamins Cinnamon Ginseng Omega-6 fatty acids Apigenin Citric Acid Green tea Resveratrol B Vitamins (mega-doses) CoEnzyme Q10 Huperzine RNA Baicalein Cognitex (a-glyceryl Individual amino acids or Rutin Butcher’s Broom phosphoryl choline, blends (most commonly: ginger, rosemary, branched chain, tyrosine, phosphatidylserine, glutamine, arginine) pregnolone, vinpocentine, leucoselect phytosome, wild blueberry, sensoril ashwagandha, perluxan) Caffeine Corella Lipoic acid Spirulina Capsaicin Creatine Luteolin St. John’s wart Carnitine Curcumin Magnesium Tocopherol (L-configuration) Carnosine D-Ribose Milk thistle Valarian root (L-configuration) Catechin Feverfew Mycelia extract Vinpoceti Choline Ginkgo biloba n-3 fatty acids Zinc CONCLUSION Nutritional assessment, monitoring, and evaluation should be a priority throughout the course of TBI and polytrauma injuries among active-duty service members. Registered dietitians have the educational background to coordinate acute nutritional support and subacute nutritional management based on the variety of nutritional conditions prevalent following TBI. Furthermore, a multidisciplinary team approach is critical to discuss progress, treatment plans, and goals for overall best outcomes. REFERENCES Berry, A. 2009. Neurocritical Care 101: Learning the lingo for effective nutrition management. Support Line 31(6):3–11. Blackman, J. A., P. D. Patrick, M. L. Buck, and R. S. Rust Jr. 2004. Paroxysmal autonomic instability with dystonia after brain injury. Archives of Neurology 61(3):321–328. Bratton, S., D. Chestnut, J. Ghajar, F. Hammond, O. Harris, R. Hartl, J. Schouten, L. Shutter, S. Timmons, J. Ullman, W. Videtta, J. Wilberger, and D. Wright. 2007. Nutrition. Journal of Neurotrauma 24(1 Suppl.):S77–S82. Cook, A., and J. Hatton. 2007. Neurological impairment. In The A.S.P.E.N. Nutrition support core curriculum: A case-based approach-the adult patient. 2nd ed., edited by M. Gottschlich, M. DeLegge, T. Mattox, C. Mueller and P. Worthingon. Silver Spring, MD: American Society for Parenteral and Enteral Nutrition. Pp. 424–439. Cook, A. M., A. Peppard, and B. Magnuson. 2008. Nutrition considerations in traumatic brain injury. Nutrition in Clinical Practice 23(6):608–620. Dickerson, R. N., and L. Roth-Yousey. 2005. Medication effects on metabolic rate: A systematic review (part 1). Journal of the American Dietetic Association 105(5):835–843. Esper, D. 2004. Metabolic response and nutrition management in patients with severe head injury. Support Line 26(2):9–13.

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