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WINDOWSTOTHEBRAIN   |    
PTSD and Combat-Related Injuries: Functional Neuroanatomy
Katherine H. Taber, Ph.D.; Robin A. Hurley, M.D.
The Journal of Neuropsychiatry and Clinical Neurosciences 2009;21:iv-4.
View Author and Article Information

Drs. Taber and Hurley are affiliated with the Veterans Affairs Mid-Atlantic Mental Illness Research, Education, and Clinical Center, and the Mental Health Service Line at the W.G. Hefner Veterans Affairs Medical Center in Salisbury, N.C. Dr. Taber is affiliated with the Division of Biomedical Sciences at the Virginia College of Osteopathic Medicine in Blacksburg, Va., and the Department of Physical Medicine and Rehabilitation at Baylor College of Medicine in Houston, Tex.; Dr. Hurley is affiliated with the Departments of Psychiatry and Radiology at Wake Forest University School of Medicine in Winston-Salem, N.C., and the Menninger Department of Psychiatry and Behavioral Sciences at Baylor College of Medicine in Houston. Address correspondence to Dr. Robin Hurley, Hefner VA Medical Center, 1601 Brenner Ave., Salisbury, NC 28144; Robin.Hurley@va.gov (e-mail).

There is growing evidence that physical injury during deployment is associated with a higher prevalence of mental health issues post-deployment.7 Military personnel are returning from combat with different levels and types of injury than in previous wars. This is partially due to more rapid and sophisticated medical response on the battlefield and to improved protective equipment such as Kevlar vests.8,9 These protect soldiers from mortal internal injuries but not from extremity trauma or concussive brain injuries. Recent studies detailing the most common injuries have found that approximately one-half involved the head or neck.10,11 The great majority of injuries were due to explosions, and many involve more than one area of the body (polytrauma).9 Several studies from the Defense and Veterans Brain Injury Center (DVBIC) of soldiers returning from Afghanistan or Iraq document the occurrence of traumatic brain injury (TBI) in many soldiers.1215

A history of experiencing physical injury during deployment is associated with a higher prevalence of post traumatic stress disorder (PTSD) post-deployment.7 A recent survey study of soldiers following return from deployment reported that ∼9% of military personnel who had not been injured while deployed screened positive for PTSD.1 The rate was almost doubled (∼16%) in those reporting bodily injury during deployment. This rate is very similar to an earlier study assessing the increased risk for PTSD due to combat-related injury.16 Another post-deployment survey study reported an increased incidence of PTSD with number of injury mechanisms: ∼14% for one, ∼29% for two, and ∼51% for three or more.2 These results are consistent with the incidence of PTSD symptoms following significant orthopedic trauma in civilians.17,18

Although at one time it was believed that the loss of consciousness and memory deficits that frequently result from TBI made it unlikely that PTSD would develop, recent studies have found that PTSD can develop even when the patient has no conscious memory of the traumatic event.1922 Studies in military personnel indicate that higher rates of PTSD are associated with having experienced potentially brain-injuring conditions (Figure 1 ).7 In a group who reported experiencing a concussion while deployed (as indicated by altered mental status, n=260), ∼27% screened positive for PTSD.1 The rate was ∼44% in those who reported a loss of consciousness (n=124). In another survey study the rate of PTSD was ∼7% in those without evidence of brain injury (n=1,960), ∼34% with level 1 mild TBI (altered mental status, n=163), and ∼47% with level 2 mild TBI (loss of consciousness, amnesia, or head injury, n=112).2 Similarly, an inpatient study of service members who had experienced both a burn and blast injury (n=76) found that 32% were positive for PTSD.23 The rate of PTSD was 22% in the group without and 45% in the group with mild TBI. A retrospective study in combat veterans found that head injury was associated with increased frequency of PTSD, and combat-related head injury was associated with increased severity of PTSD.24 There is also evidence that veterans with combat-related PTSD have more severe symptoms than veterans with PTSD due to noncombat-related events.25 Increased incidence of PTSD in military personnel experiencing TBI is consistent with research studies in other populations. These have concluded that development of psychiatric symptoms following TBI is relatively common, with 13%—27% exhibiting PTSD.26,27

Recent reviews provide an excellent summary of what is presently known about the functional neuroanatomy of PTSD.2831 In brief, symptom provocation studies have implicated anterior limbic-related areas in PTSD including regions in the medial prefrontal, anterior cingulate, orbitofrontal, insular, and medial temporal cortices as well as the amygdala. Cognitive activation studies indicate increased amygdalar and decreased medial prefrontal cortical responding to threat, and impaired responding in rostral anterior cingulate cortex to emotional tasks. Some morphometric studies have reported decreased volume in several limbic-related areas, including hippocampus, rostral anterior cingulate, dorsal anterior cingulate, and subcallosal cortices.

A critical issue is determining whether particular anatomic or functional differences that have been associated with PTSD preexisted the trauma exposure or arose afterward.32 Preexisting differences may indicate risk or vulnerability factors, whereas differences that arise after exposure are more likely to be consequences of the traumatic event and/or the development of PTSD. A series of case-control studies utilizing Vietnam Era veterans and their identical twins have shed light on this key question.3,33,34 Overall, these studies support increased incidence of neurological soft signs, presence of cavum septum pellucidum and perhaps smaller hippocampal volume as preexisting factors. Interestingly, average neurological soft signs score correlated with total gray matter but not with total white matter volume. As noted by the authors of these studies, the findings may be indicative of subtle neurological compromise as a risk factor for PTSD. Increased reactivity to sudden loud sounds (as indicated by heart rate) and decreased gray matter volume in the hippocampus and several limbic-related areas of the cortex (Figure 2 ), on the other hand, were more likely to have arisen subsequent to trauma exposure and the development of PTSD. These findings indicate that longitudinal changes may occur, supporting the concept that early intervention has the potential to change the trajectory of the illness.

Achieving a better understanding of the possible interactions between TBI and PTSD is of great clinical importance. If areas implicated in PTSD or their interconnecting pathways have been injured, symptom severity and/or response to treatment may be altered. A recent series of studies of pediatric (ages 4—19 years) severe (Glasgow Coma Scale 3—8) closed head injury provides some insight into the interaction between focal brain injury and the development of psychiatric symptoms (Figure3 ).5,6,35 One study examined the correlations between injury locations and both the formal diagnosis of PTSD and probability of satisfying the specific diagnostic criteria (reexperiencing, hyperarousal, avoidance).5 Meeting all three diagnostic criteria (9/94, 10%) was associated with a higher lesion burden in the middle temporal gyrus and a lower lesion burden in the medial frontal gyrus. Satisfying the reexperiencing criterion (41/94, 44%) was associated with a lower lesion burden in the cingulum, medial frontal gyrus, and hippocampus. Satisfying the hyperarousal criterion (55/94, 59%) was associated with a lower lesion burden in the subcallosal gyrus. Satisfying the avoidance criterion (12/94, 13%) was associated with a higher lesion burden in the middle temporal gyrus and a lower lesion burden in the medial frontal and inferior temporal gyri. A later analysis reported a higher lesion burden in the orbitofrontal cortex was associated with a lower probability of developing PTSD (Figure 3 ), whereas a higher lesion burden in the temporal lobe was associated with a higher probability of developing PTSD.6 Higher lesion burden in orbitofrontal cortex was also associated with decreased probability of developing obsessive-compulsive disorder.35 Similarly, a study of Vietnam veterans with combat-related penetrating head injuries reported that injury to ventromedial prefrontal and anterior temporal cortices was associated with a lower probability of developing PTSD (Figure 3 ).4 PTSD was present in 40% of veterans with TBI, but without injury to either of these areas (n=133). This was similar to the incidence of PTSD in veterans without TBI (48%, n=52). Only 18% of veterans with injury to the ventromedial prefrontal cortex had PTSD (n=40). Of particular importance, PTSD was not found in any veteran with injuries that included the amygdala (n=15). This was a very specific association, as 32% of veterans with injury to anterior temporal and/or medial temporal areas, but no injury to the amygdala (n=28), had PTSD, as did 44% of veterans with injury to the hippocampus but not the amygdala (n=9).

Another factor that complicates both diagnosis and clinical management is the widely acknowledged overlap between the symptoms common following TBI and those of PTSD.7 This is likely a contributing factor to the underrecognition of mild TBI, as has been reported in a study of combat veterans diagnosed with PTSD.36 The need for measures that can reliably differentiate these conditions was recognized more than a decade ago.37 The overlap of symptoms also suggests the possibilities of symptom aggravation due to additive effects and/or alterations in resilience/coping. Several studies support the idea that presence of TBI can influence the expression of symptoms in PTSD.6,3840 At minimum, presence of TBI requires alterations of PTSD treatment approaches to adjust for common cognitive and emotional deficits (e.g., concentration, memory, emotional control).41,42

Recent studies have begun to provide insight into the influence of specific symptoms or cognitive/emotional deficits on response to particular treatment approaches. Exposure therapy presumably works by promoting habituation/extinction of the overly fearful response to a stimulus that is no longer threatening.43 This is an effective approach for many, but not all, patients with PTSD. A study utilizing a group of patients with PTSD who had not responded to prolonged exposure therapy found that most (18/23) achieved recovery following imagery rescripting and reprocessing therapy (a form of cognitive restructuring therapy).44 The authors of the study suggest that cognitive restructuring therapy may be more efficacious in patients whose predominant PTSD-related emotions are guilt, shame, or anger rather than fear. Another study measured multiple aspects of memory and attention in a group of female patients with PTSD prior to initiation of cognitive behavior therapy (CBT).45 PTSD symptom severity was assessed prior to and following eight sessions of CBT. Seventy percent of the group (16/22) had symptom reduction sufficient to no longer meet DSM-IV criteria for PTSD. Response to treatment, as measured by the Clinician Administered PTSD Scale (CAPS), was not related to measures of attention or digit span. Response to treatment was predicted by performance on story recall (immediate) even after controlling for differences in initial symptom severity and attention performance.

Other neuropsychiatric issues may also arise following TBI, including depression, personality changes, substance use disorders, aggression, and impulsivity.27,46,47 These conditions complicate clinical management and can impair recovery and psychosocial outcome. To date, when patients have both diagnoses, there is no clearly defined way to distinguish which condition is responsible for symptoms that cross both domains (e.g., decreased focus and concentration, decreased sleep, agitation, irritability, inability to maintain employment or schooling). Therefore, establishing a clear symptom delineation, prognosis, and long-term treatment planning is extremely challenging.46 There are no currently FDA-approved medications for the long term treatment of psychiatric symptoms due to brain injury.4851 The few studies on rehabilitative approaches are promising but inconclusive.5254

 
Figure 1. Two recent survey studies of military personnel following deployment indicate that combat-related traumatic brain injury (TBI) is associated with increased incidence of PTSD.
 
Figure 2. A recent study in identical twins discordant for PTSD reported PTSD-related reductions in gray matter density in the hippocampus (not shown) and several areas of the cortex (pink).
Both pregenual anterior cingulate cortex (left) and insula (middle) contribute to limbic-related functions.
 
Cover and Figure 3. The influence of TBI location on the development of PTSD is a relatively unexplored area. Interestingly, the few studies that are available agree that TBI involving areas within prefrontal cortex are associated with decreased probability of developing PTSD for both children and adults. A recent study of Vietnam veterans with combat-related penetrating head injuries reported that injury to ventromedial prefrontal and anterior temporal cortices was associated with a lower probability of developing PTSD (left panel).
The color-code at the bottom indicates the likelihood of developing PTSD if there is injury to the areas, with larger negative numbers (blue) associated with lower occurrence of PTSD. Note that PTSD was unlikely to develop in veterans with injury to the central white matter of the prefrontal cortex. The studies in children followed a cohort after severe closed head injury.
One study reported an inverse relationship between lesion burden in the medial frontal gyrus (right, blue) and meeting diagnostic criteria for PTSD.
The other reported an inverse relationship between lesion burden in the orbitofrontal cortex (right, purple) and probability of developing PTSD.
.
Hoge CW, McGurk D, Thomas JL, et al: Mild traumatic brain injury in U.S. soldiers returning from Iraq. N Engl J Med 2008; 358:453—463
 
.
Schneiderman AI, Braver ER, Kang HK: Understanding sequelae of injury mechanisms and mild traumatic brain injury incurred during the conflicts in Iraq and Afghanistan: Persistent postconcussive symptoms and posttraumatic stress disorder. Am J Epidemiol 2008; 167:1446—1452
 
.
Kasai K, Yamasue H, Gilbertson MW, et al: Evidence for acquired pre-genual anterior cingulate gray matter loss from a twin study of combat-related posttraumatic stress disorder. Biol Psychiatry 2008; 63:550—556
 
.
Koenigs M, Huey ED, Raymont V, et al: Focal brain damage protects against post-traumatic stress disorder in combat veterans. Nature Neuroscience 2008; 11:232—237
 
.
Herskovits EH, Gerring JP, Davatzikos C, et al: Is the spatial distribution of brain lesions associated with closed-head injury in children predictive of subsequent development of posttraumatic stress disorder? Radiology 2002; 224:345—351
 
.
Vasa RA, Grados M, Slomine B, et al: Neuroimaging correlates of anxiety after pediatric traumatic brain injury. Biol Psychiatry 2004; 55:208—216
 
.
Kennedy JE, Jaffee MS, Leskin GA, et al: Posttraumatic stress disorder and posttraumatic stress disorder-like symptoms and mild traumatic brain injury. J Rehabil Res Dev 2007; 44:895—920
 
.
Warden D: Military TBI during the Iraq and Afghanistan wars. J Head Trauma Rehabil 2006; 21:398—402
 
.
Sayer NA, Chiros CE, Sigford B, et al: Characteristics and rehabilitation outcomes among patients with blast and other injuries sustained during the Global War on Terror. Arch Phys Med Rehabil 2008; 89:163—170
 
.
Murray CK, Reynolds JC, Schroeder JM, et al: Spectrum of care provided at an Echelon II medical unit during Operation Iraqi Freedom. Mil Med 2005; 170:516—520
 
.
Gondusky JS, Reiter MP: Protecting military convoys in Iraq: an examination of battle injuries sustained by a mechanized battalion during Operation Iraqi Freedom II. Mil Med 2005; 170:546—549
 
.
Okie S: Traumatic Brain Injury in the War Zone. N Engl J Med 2005; 352:2043—2047
 
.
Warden DL, Ryan LM, Helmick KM, et al: War neurotrauma: the Defense and Veterans Brain Injury Center (DVBIC) experience at Walter Reed Army Medical Center (WRAMC). J Neurotrauma 2005; 22:1178—1178
 
.
Schwab KA, Baker G, Ivins BJ, et al: The Brief Traumatic Brain Injury Screen (BTBIS): investigating the validity of a self-report instrument for detecting traumatic brain injury (TBI) in troops returning from deployment in Afghanistan and Iraq. Neurology 2006; 66:A235
 
.
Warden D: Military TBI during the Iraq and Afghanistan wars. J Head Trauma Rehabil 2006; 21:398—402
 
.
Koren D, Norman D, Cohen A, et al: Increased PTSD risk with combat-related injury: a matched comparison study of injured and uninjured soldiers experiencing the same combat events. Am J Psychiatry 2005; 162:276—282
 
.
McCarthy ML, MacKenzie EJ, Edwin D, et al, the LEAP study group: Psychological distress associated with severe lower-limb injury. J Bone Joint Surg Am 2003; 85-A:1689—1697
 
.
Starr AJ, Smith WR, Frawley WH, et al: Symptoms of posttraumatic stress disorder after orthopaedic trauma. J Bone Joint Surg Am 2004; 86-A:1115—1121
 
.
Warden DL, Labbate LA, Salazar AM, et al: Posttraumatic stress disorder in patients with traumatic brain injury and amnesia for the event? J Neuropsychiatry Clin Neurosci 1997; 9:18—22
 
.
Harvey AG, Brewin CR, Jones C, et al: Coexistence of posttraumatic stress disorder and traumatic brain injury: Towards a resolution of the paradox. J Int Neuropsychol Soc 2003; 9:663—676
 
.
Klein E, Caspi Y, Gil S: The relation between memory of the traumatic event and PTSD: Evidence from studies of traumatic brain injury. Can J Psychiatry 2003; 48:28—33
 
.
Gil S, Caspi Y, Ben-Ari IZ, et al: Does memory of a traumatic event increase the risk for posttraumatic stress disorder in patients with traumatic brain injury? A prospective study. Am J Psychiatry 2005; 162:963—969
 
.
Gaylord KM, Cooper DB, Mercado JM, et al: Incidence of posttraumatic stress disorder and mild traumatic brain injury in burned service members: preliminary report. J Trauma 2008; 64:S200—S206
 
.
Chemtob CM, Muraoka MY, Wu-Holt P, et al: Head injury and combat-related posttraumatic stress disorder. J Nerv Ment Dis 1998; 186:701—708
 
.
Brinker M, Westermeyer J, Thuras P, et al: Severity of combat-related posttraumatic stress disorder versus non-combat-related posttraumatic stress disorder: a community-based study in American Indian and Hispanic veterans. J Nerv Ment Dis 2007; 195:655—661
 
.
Kim E, Lauterbach EC, Reeve A, et al: Neuropsychiatric complications of traumatic brain injury: a critical review of the literature (a report by the ANPA committee on research). J Neuropsychiatry Clin Neurosci 2007; 19:106—127
 
.
Rogers JM, Read CA: Psychiatric comorbidity following traumatic brain injury. Brain Inj 2007; 21:1321—1333
 
.
Rauch SL, Shin LM, Phelps EA: Neurocircuitry models of posttraumatic stress disorder and extinction: Human neuroimaging research: past, present, and future. Biol Psychiatry 2006; 60:376—382
 
.
Yehuda R, LeDoux J: Response variation following trauma: A translational neuroscience approach to understanding PTSD. Neuron 2007; 56:19—32
 
.
Liberzon I, Sripada CS: The functional neuroanatomy of PTSD: a critical review. Prog Brain Res 2008; 167:151—169
 
.
Bremner JD, Elzinga B, Schmahl C, et al: Structural and functional plasticity of the human brain in posttraumatic stress disorder. Prog Brain Res 2008; 167:171—186
 
.
Botteron KN: Regional specificity of traumatic stress-related cortical reduction: further evidence from a twin study of post-traumatic stress disorder. Biol Psychiatry 2008; 63:539—541
 
.
Pitman RK, Gilbertson MW, Gurvits TV, et al: Clarifying the origin of biological abnormalities in PTSD through the study of identical twins discordant for combat exposure. Ann NY Acad Sci 2006; 1071:242—254
 
.
Gurvits TV, Metzger LJ, Lasko NB, et al: Subtle neurologic compromise as a vulnerability factor for combat-related posttraumatic stress disorder. Arch Gen Psychiatry 2006; 63:571—576
 
.
Grados MA, Vasa RA, Riddle MA, et al: New onset obsessive-compulsive symptoms in children and adolescents with severe traumatic brain injury. Depress Anxiety 2008; 25:398—407
 
.
Trudeau DL, Anderson J, Hansen LM, et al: Findings of mild traumatic brain injury in combat veterans with PTSD and a history of blast concussion. J Neuropsychiatry Clin Neurosci 1998; 10:308—313
 
.
Ohry A, Rattok J, Solomon Z: Post-traumatic stress disorder in brain injury patients. Brain Injury 1996; 10:687—695
 
.
Bryant RA, Marosszeky JE, Crooks J, et al: Posttraumatic stress disorder after severe traumatic brain injury. Am J Psychiat 2000; 157:629—631
 
.
Turnbull SJ, Campbell EA, Swann IJ: Post-traumatic stress disorder symptoms following a head injury: does amnesia for the event influence development of symptoms? Brain Inj 2001; 15:775—785
 
.
Feinstein A, Hershkop S, Ouchterlony D, et al: Posttraumatic amnesia and recall of a traumatic event following traumatic brain injury. J Neuropsychiatry Clin Neurosci 2002; 14:25—30
 
.
Warden DL, Labbate LA: Postraumatic stress disorder and other anxiety disorders, in Textbook of Traumatic Brain Injury. Edited by Silver JM, McAllister TW, Yudofsky SC. Arlington, Va, American Psychiatric Publishing, 2005, pp 231—243
 
.
Pollack IW: Psychotherapy, in Textbook of Traumatic Brain Injury. Edited by Silver JM, McAllister TW, Yudofsky SC. Arlington, Va, American Psychiatric Publishing, 2005, pp 641—654
 
.
McNally RJ: Mechanisms of exposure therapy: How neuroscience can improve psychological treatments for anxiety disorders. Clin Psychol Rev 2007; 7:750—759
 
.
Grunert BK, Weis JM, Smucker MR, et al: Imagery rescripting and reprocessing therapy after failed prolonged exposure for post-traumatic stress disorder following industrial injury. J Behav Ther Exp Psychiatry 2007; 38:317—328
 
.
Wild J, Gur RC: Verbal memory and treatment response in post-traumatic stress disorder. Brit J Psychiatry 2008; 193:254—255
 
.
McAllister TW: Neurobehavioral sequelae of traumatic brain injury: evaluation and management. World Psychiatry 2008; 7:3—10
 
.
Corrigan JD, Cole TB: Substance use disorders and clinical management of traumatic brain injury and posttraumatic stress disorder. JAMA 2008; 300:720—721
 
.
Warden DL, Gordon B, McAllister TW, et al: Guidelines for the pharmacologic treatment of neurobehavioral sequelae of traumatic brain injury. J Neurotrauma 2006; 23:1468—1501
 
.
Francisco GE, Walker WC, Zasler ND, et al: Pharmacological management of neurobehavioral sequelae of traumatic brain injury: a survey of current physiatric practice. Brain Inj 2007; 21:1007—1014
 
.
Lombari F: Pharmacological treatment of neurobehavioral sequelae of traumatic brain injury. Eur J Anaesth 2008; 25:131—136
 
.
Bernardo CG, Singh V, Thompson PM: Safety and efficacy of psychopharmacolgical agents used to treat the psychiatric sequelae of common neurological disorders. Expert Opin Drug Saf 2008; 7:435—445
 
.
Ylvisaker M, Turkstra L, Coehlo C, et al: Behavioral interventions for children and adults with behavior disorders after TBI: a systematic review of the evidence. Brain Inj 2007; 21:769—805
 
.
Soo C, Tate R: Psychological treatment for anxiety in people with traumatic brain injury (review). Cochrane Database Syst Rev 2007; 3:CD005239
 
.
Snell DL, Surgenor LJ, Hay-Smith EJC, et al: A systematic review of psychological treatments for mild traumatic brain injury: an update on the evidence. J Clin Exp Neuropsychol 2009; 31:20—38
 

Figure 1. Two recent survey studies of military personnel following deployment indicate that combat-related traumatic brain injury (TBI) is associated with increased incidence of PTSD.

Figure 2. A recent study in identical twins discordant for PTSD reported PTSD-related reductions in gray matter density in the hippocampus (not shown) and several areas of the cortex (pink). Both pregenual anterior cingulate cortex (left) and insula (middle) contribute to limbic-related functions.

Cover and Figure 3. The influence of TBI location on the development of PTSD is a relatively unexplored area. Interestingly, the few studies that are available agree that TBI involving areas within prefrontal cortex are associated with decreased probability of developing PTSD for both children and adults. A recent study of Vietnam veterans with combat-related penetrating head injuries reported that injury to ventromedial prefrontal and anterior temporal cortices was associated with a lower probability of developing PTSD (left panel). The color-code at the bottom indicates the likelihood of developing PTSD if there is injury to the areas, with larger negative numbers (blue) associated with lower occurrence of PTSD. Note that PTSD was unlikely to develop in veterans with injury to the central white matter of the prefrontal cortex. The studies in children followed a cohort after severe closed head injury. One study reported an inverse relationship between lesion burden in the medial frontal gyrus (right, blue) and meeting diagnostic criteria for PTSD. The other reported an inverse relationship between lesion burden in the orbitofrontal cortex (right, purple) and probability of developing PTSD.
+

References

.
Hoge CW, McGurk D, Thomas JL, et al: Mild traumatic brain injury in U.S. soldiers returning from Iraq. N Engl J Med 2008; 358:453—463
 
.
Schneiderman AI, Braver ER, Kang HK: Understanding sequelae of injury mechanisms and mild traumatic brain injury incurred during the conflicts in Iraq and Afghanistan: Persistent postconcussive symptoms and posttraumatic stress disorder. Am J Epidemiol 2008; 167:1446—1452
 
.
Kasai K, Yamasue H, Gilbertson MW, et al: Evidence for acquired pre-genual anterior cingulate gray matter loss from a twin study of combat-related posttraumatic stress disorder. Biol Psychiatry 2008; 63:550—556
 
.
Koenigs M, Huey ED, Raymont V, et al: Focal brain damage protects against post-traumatic stress disorder in combat veterans. Nature Neuroscience 2008; 11:232—237
 
.
Herskovits EH, Gerring JP, Davatzikos C, et al: Is the spatial distribution of brain lesions associated with closed-head injury in children predictive of subsequent development of posttraumatic stress disorder? Radiology 2002; 224:345—351
 
.
Vasa RA, Grados M, Slomine B, et al: Neuroimaging correlates of anxiety after pediatric traumatic brain injury. Biol Psychiatry 2004; 55:208—216
 
.
Kennedy JE, Jaffee MS, Leskin GA, et al: Posttraumatic stress disorder and posttraumatic stress disorder-like symptoms and mild traumatic brain injury. J Rehabil Res Dev 2007; 44:895—920
 
.
Warden D: Military TBI during the Iraq and Afghanistan wars. J Head Trauma Rehabil 2006; 21:398—402
 
.
Sayer NA, Chiros CE, Sigford B, et al: Characteristics and rehabilitation outcomes among patients with blast and other injuries sustained during the Global War on Terror. Arch Phys Med Rehabil 2008; 89:163—170
 
.
Murray CK, Reynolds JC, Schroeder JM, et al: Spectrum of care provided at an Echelon II medical unit during Operation Iraqi Freedom. Mil Med 2005; 170:516—520
 
.
Gondusky JS, Reiter MP: Protecting military convoys in Iraq: an examination of battle injuries sustained by a mechanized battalion during Operation Iraqi Freedom II. Mil Med 2005; 170:546—549
 
.
Okie S: Traumatic Brain Injury in the War Zone. N Engl J Med 2005; 352:2043—2047
 
.
Warden DL, Ryan LM, Helmick KM, et al: War neurotrauma: the Defense and Veterans Brain Injury Center (DVBIC) experience at Walter Reed Army Medical Center (WRAMC). J Neurotrauma 2005; 22:1178—1178
 
.
Schwab KA, Baker G, Ivins BJ, et al: The Brief Traumatic Brain Injury Screen (BTBIS): investigating the validity of a self-report instrument for detecting traumatic brain injury (TBI) in troops returning from deployment in Afghanistan and Iraq. Neurology 2006; 66:A235
 
.
Warden D: Military TBI during the Iraq and Afghanistan wars. J Head Trauma Rehabil 2006; 21:398—402
 
.
Koren D, Norman D, Cohen A, et al: Increased PTSD risk with combat-related injury: a matched comparison study of injured and uninjured soldiers experiencing the same combat events. Am J Psychiatry 2005; 162:276—282
 
.
McCarthy ML, MacKenzie EJ, Edwin D, et al, the LEAP study group: Psychological distress associated with severe lower-limb injury. J Bone Joint Surg Am 2003; 85-A:1689—1697
 
.
Starr AJ, Smith WR, Frawley WH, et al: Symptoms of posttraumatic stress disorder after orthopaedic trauma. J Bone Joint Surg Am 2004; 86-A:1115—1121
 
.
Warden DL, Labbate LA, Salazar AM, et al: Posttraumatic stress disorder in patients with traumatic brain injury and amnesia for the event? J Neuropsychiatry Clin Neurosci 1997; 9:18—22
 
.
Harvey AG, Brewin CR, Jones C, et al: Coexistence of posttraumatic stress disorder and traumatic brain injury: Towards a resolution of the paradox. J Int Neuropsychol Soc 2003; 9:663—676
 
.
Klein E, Caspi Y, Gil S: The relation between memory of the traumatic event and PTSD: Evidence from studies of traumatic brain injury. Can J Psychiatry 2003; 48:28—33
 
.
Gil S, Caspi Y, Ben-Ari IZ, et al: Does memory of a traumatic event increase the risk for posttraumatic stress disorder in patients with traumatic brain injury? A prospective study. Am J Psychiatry 2005; 162:963—969
 
.
Gaylord KM, Cooper DB, Mercado JM, et al: Incidence of posttraumatic stress disorder and mild traumatic brain injury in burned service members: preliminary report. J Trauma 2008; 64:S200—S206
 
.
Chemtob CM, Muraoka MY, Wu-Holt P, et al: Head injury and combat-related posttraumatic stress disorder. J Nerv Ment Dis 1998; 186:701—708
 
.
Brinker M, Westermeyer J, Thuras P, et al: Severity of combat-related posttraumatic stress disorder versus non-combat-related posttraumatic stress disorder: a community-based study in American Indian and Hispanic veterans. J Nerv Ment Dis 2007; 195:655—661
 
.
Kim E, Lauterbach EC, Reeve A, et al: Neuropsychiatric complications of traumatic brain injury: a critical review of the literature (a report by the ANPA committee on research). J Neuropsychiatry Clin Neurosci 2007; 19:106—127
 
.
Rogers JM, Read CA: Psychiatric comorbidity following traumatic brain injury. Brain Inj 2007; 21:1321—1333
 
.
Rauch SL, Shin LM, Phelps EA: Neurocircuitry models of posttraumatic stress disorder and extinction: Human neuroimaging research: past, present, and future. Biol Psychiatry 2006; 60:376—382
 
.
Yehuda R, LeDoux J: Response variation following trauma: A translational neuroscience approach to understanding PTSD. Neuron 2007; 56:19—32
 
.
Liberzon I, Sripada CS: The functional neuroanatomy of PTSD: a critical review. Prog Brain Res 2008; 167:151—169
 
.
Bremner JD, Elzinga B, Schmahl C, et al: Structural and functional plasticity of the human brain in posttraumatic stress disorder. Prog Brain Res 2008; 167:171—186
 
.
Botteron KN: Regional specificity of traumatic stress-related cortical reduction: further evidence from a twin study of post-traumatic stress disorder. Biol Psychiatry 2008; 63:539—541
 
.
Pitman RK, Gilbertson MW, Gurvits TV, et al: Clarifying the origin of biological abnormalities in PTSD through the study of identical twins discordant for combat exposure. Ann NY Acad Sci 2006; 1071:242—254
 
.
Gurvits TV, Metzger LJ, Lasko NB, et al: Subtle neurologic compromise as a vulnerability factor for combat-related posttraumatic stress disorder. Arch Gen Psychiatry 2006; 63:571—576
 
.
Grados MA, Vasa RA, Riddle MA, et al: New onset obsessive-compulsive symptoms in children and adolescents with severe traumatic brain injury. Depress Anxiety 2008; 25:398—407
 
.
Trudeau DL, Anderson J, Hansen LM, et al: Findings of mild traumatic brain injury in combat veterans with PTSD and a history of blast concussion. J Neuropsychiatry Clin Neurosci 1998; 10:308—313
 
.
Ohry A, Rattok J, Solomon Z: Post-traumatic stress disorder in brain injury patients. Brain Injury 1996; 10:687—695
 
.
Bryant RA, Marosszeky JE, Crooks J, et al: Posttraumatic stress disorder after severe traumatic brain injury. Am J Psychiat 2000; 157:629—631
 
.
Turnbull SJ, Campbell EA, Swann IJ: Post-traumatic stress disorder symptoms following a head injury: does amnesia for the event influence development of symptoms? Brain Inj 2001; 15:775—785
 
.
Feinstein A, Hershkop S, Ouchterlony D, et al: Posttraumatic amnesia and recall of a traumatic event following traumatic brain injury. J Neuropsychiatry Clin Neurosci 2002; 14:25—30
 
.
Warden DL, Labbate LA: Postraumatic stress disorder and other anxiety disorders, in Textbook of Traumatic Brain Injury. Edited by Silver JM, McAllister TW, Yudofsky SC. Arlington, Va, American Psychiatric Publishing, 2005, pp 231—243
 
.
Pollack IW: Psychotherapy, in Textbook of Traumatic Brain Injury. Edited by Silver JM, McAllister TW, Yudofsky SC. Arlington, Va, American Psychiatric Publishing, 2005, pp 641—654
 
.
McNally RJ: Mechanisms of exposure therapy: How neuroscience can improve psychological treatments for anxiety disorders. Clin Psychol Rev 2007; 7:750—759
 
.
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