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Post-traumatic stress disorder vs traumatic brain injury Richard Bryant, PhD

Overview

The intersection between traumatic brain injury (TBI) and post-traumatic stress disorder (PTSD) has become a major focus of attention in recent years. Stimulated largely by injuries sustained in the Iraq and Afghanistan wars, this issue has been debated widely Post-traumatic stress disorder (PTSD) and traumatic brain because these conditions, both independently and addi- injury (TBI) often coexist because brain injuries are often tively, are regarded as being responsible for much sustained in traumatic experiences. This review outlines impairment following deployments. This review will the significant overlap between PTSD and TBI by com- commence with defining these conditions, explain poten- mencing with a critical outline of the overlapping symp- tial overlaps between them, and discuss the differential toms and problems of differential diagnosis. The impact diagnosis challenges of determining the extent to which of TBI on PTSD is then described, with increasing evidence presenting symptoms can be attributed to organic or psy- suggesting that mild TBI can increase risk for PTSD. Several chological factors. The review then discusses evidence of explanations are offered for this enhanced risk. Recent PTSD following TBI, and possible mechanisms that may evidence suggests that impairment secondary to mild TBI impact on the nature of PTSD following TBI. The is largely attributable to stress reactions after TBI, which respective roles of PTSD and TBI in impairment after challenges the long-held belief that postconcussive symp- TBI are then addressed, with specific focus on the under- toms are a function of neurological insult. This recent evi- standing of postconcussive symptoms. Finally, the impli- dence is pointing to new directions for treatment of post- cations for managing the effects of TBI and PTSD are concussive symptoms that acknowledge that treating discussed in terms of recent developments in how each stress factors following TBI may be the optimal means to condition can affect the other. manage the effects of many TBIs. © 2011, LLS SAS Definitional issues Dialogues Clin Neurosci. 2011;13:251-262. TBI Keywords: post-traumatic stress disorder; traumatic brain injury; trauma; postconcussive syndrome TBI involves damage to the brain from an external force. Author affiliations: School of Psychology, University of New South Wales, Sydney, New South Wales, Australia Brain injuries can involve contusion, brain laceration, intracranial hematoma, contrecoup injury, shearing of Address for correspondence: Richard Bryant, School of Psychology, University of New South Wales, NSW 2052, Australia nerve fibers, intracranial hypertension, hypoxia, anemia, (e-mail: [email protected]) metabolic anomalies, hydrocephalus, and subarachnoid

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hemorrhage. Severity of TBI is typically described in occur in the initial month following a trauma. As PTSD terms of mild or moderate/severe; however, the exact is only diagnosed 1 month after trauma, it was decided definitions vary. Mild traumatic brain injury (MTBI) is that there was a need to fill the nosological gap between usually defined as: (i) an external injury to the brain; (ii) the traumatic event and PTSD, in part to facilitate diag- confusion, disorientation, or loss of consciousness for 30 nosis and access to health care. A second major goal of minutes or less; (iii) Glasgow Coma Scale score of 13 to the ASD diagnosis was to describe acute stress responses 15; and (iv) post-traumatic amnesia for less than 24 that precede longer-term PTSD, and therefore could be hours.1-3 Moderate TBI often involves loss of conscious- used to identify people who were at high risk for subse- ness between 30 minutes and 24 hours, Glasgow Coma quent disorder and could benefit from early interven- Scale score of 9 to 12, and post-traumatic amnesia tion. ASD is conceptually similar to PTSD and shares between 1 and 7 days. Severe TBI involves more many of the same symptoms.5 A key difference between extended loss of consciousness and post-traumatic ASD and PTSD is the former’s emphasis on dissociative amnesia, which typically results in more severe cognitive symptoms. Specifically, ASD requires the individual to impairment. These differences in TBI severity are impor- experience at least three of the following: emotional tant because they appear to interact differentially with numbing, reduced awareness of one's surroundings, PTSD. derealization, depersonalization, and dissociative amnesia. These symptoms may occur either at the time of the PTSD trauma or during the subsequent month. The dissociative symptoms were included in ASD on the premise It is important to distinguish between immediate and that dissociative responses following trauma are predic- longer-term PTSD reactions. Most diagnostic systems tive of subsequent PTSD, presumably because they limit have distinguished between these two types of trauma emotional processing of the traumatic experience.5 response because acute stress reactions are frequent, Support for the inclusion of dissociative symptoms in the but often transient, and they need to be distinguished ASD diagnosis to predict subsequent PTSD came from from the less common persistent PTSD responses. In evidence demonstrating an association between peri- terms of the persistent responses, PTSD is described in traumatic dissociation and subsequent levels of PTSD, a the American Psychiatric Association’s DSM-IV as an finding that has been replicated across several longitu- anxiety disorder that comprises five major criteria.4 dinal studies.6-10 Across many longitudinal studies, the First, one must have been exposed to or witness an ASD diagnosis has been shown to be a flawed predictor event that is threatening to safety, and one must of subsequent PTSD.11 Nonetheless, ASD is being respond to this event with fear, horror, or helplessness. retained in DSM-5 as a descriptor of acute stress reac- Second, one must report a re-experiencing symptom, tions.12 which may include intrusive memories, nightmares, a sense of reliving the trauma, or psychological or phys- Differential diagnosis iological distress when reminded of the trauma. Third, there need to be at least three avoidance symptoms, A key issue in this discussion is the overlap between which can include active avoidance of thoughts, feel- symptoms accompanying each condition. In terms of the ings, or reminders of the trauma, inability to recall dissociative symptoms often observed in PTSD, and some aspect of the trauma, withdrawal from others, or especially in the acute phase in ASD, there is much evi- emotional numbing. Fourth, one must suffer marked dence that TBI can result in emotional numbing, dere- arousal, which can include insomnia, irritability, diffi- alization, reduced awareness of surroundings, deper- culty concentrating, hypervigilence, or heightened star- sonalization, and amnesia.13-15 The issue of amnesia is tle response. These symptoms must cause marked particularly important in cases of TBI and PTSD impairment to one’s functioning, and can only be diag- because of the difficulty in differentiating between nosed when they are present at least 1 month after the organic and psychogenic amnesia.16 Some commentators trauma. have adopted the approach of excluding dissociative DSM-IV also introduced a new diagnosis, acute stress amnesia as a possible symptom of ASD and PTSD fol- disorder (ASD), to describe acute trauma reactions that lowing TBI to reduce the likelihood of falsely increasing

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diagnostic rates.17,18 In diagnosing PTSD, it is probably exposure may result in a rather general state of distress safer to not include dissociative amnesia as a potential that can include many emotional responses that cannot symptom. be readily classified into different responses.28 This con- Relevant to the interplay with TBI is the proposed revi- struct has particular relevance for the acute phase of sion of PTSD in the upcoming revision of DSM-5, which TBI, especially more severe TBI, when many of the suggests several changes to the PTSD criteria.19 The sub- symptoms described as acute stress reactions may be a jective response to the trauma at the time of the event function of impaired consciousness. (Criterion A2) is to be deleted because it does not A further complicating issue in the differential diagnosis enhance accuracy of identifying people with PTSD. This between PTSD and TBI is the range of other comorbid is important for patients with TBI because many patients, problems that commonly coexist with both TBI and especially those with more severe TBI, do not initially PTSD. For example, depression is highly prevalent with respond with a sense of fear or helplessness because of both conditions. Numerous studies have suggested that their impaired consciousness. Avoidance is being rede- TBI increases the risk for developing depression,29,30 eg, fined to only include active avoidance of thoughts and refs 31,32,33. Some of the core symptoms noted across situations, in recognition of the fact that numerous factor TBI and PTSD are also seen in depression, especially the analytic studies have identified four factors of PTSD: re- more severe forms of TBI, including concentration prob- experiencing, active avoidance, numbing/passive avoid- lems, memory problems, irritability, reduced motivation, ance, and arousal.20-24 Most of these studies have found and fatigue. Highlighting this problem in one study was that emotional numbing and social withdrawal are dis- a finding that more than 50% of depressed patients met tinct from more active avoidance strategies. This is rele- symptom criteria for moderate/severe postconcussive vant because numbing and withdrawal can often be syndrome.34 This contributes to the conclusion that some observed in more severe TBI; by separating these passive of the symptoms attributed to TBI may in fact be generic responses into a separate requisite cluster, it raises the symptoms of psychological malaise, which are observed possibility of differential diagnosis problems for more across anxiety and depressive responses. Complicating severe TBI patients, many of whom will display these the issue of comorbidity is compounded by the fact that symptoms. This cluster also includes alterations in mood TBI, PTSD, and depression commonly occur in the con- and cognition, and comprises a range of symptoms that text of chronic pain, which also results in symptoms that may include a range of emotional responses beyond fear overlap with each of these conditions.35-41 and anxiety.25 This may also be problematic in terms of differential diagnosis because of the frequent depressive Prevalence and generalized anxiety seen in more severe TBI patients. Although the arousal cluster is retained, there is PTSD and TBI are not uncommon. Epidemiological the expansion of several symptoms, including aggressive studies indicate that most people in the community have behavior and self-destructive/reckless behavior. These been exposed to traumatic stressors,42,43 although anly a latter symptoms can be observed in the context of minority develop PTSD. For example, the National reduced inhibition in more severe TBI patients, thereby Comorbidity Survey found that 21% of the women and raising further differential diagnosis problems in distin- 8% of the men had developed PTSD.42 Similarly, a guishing between symptoms of severe TBI and PTSD. Detroit study found that 13% of the women and 6% of In contrast to ASD, the International Classification of the men had developed PTSD.43 That is, although men Diseases26 conceptualizes acute stress reaction as a tran- are more likely to be exposed to trauma than women, sient reaction that can be evident immediately after the women have at least a twofold risk of developing PTSD traumatic event and usually resolves within 2 to 3 days compared with men.44 More severe traumas tend to after trauma exposure. The ICD description of acute result in more severe PTSD. Interpersonal violence leads stress reaction includes dissociative (daze, stupor, amne- to more PTSD than impersonal trauma; for example, sia), anxiety (tachycardia, sweating, flushing), anger, or whereas 55% of rape victims develop PTSD, only 7.5% depressive reactions, which may have more utility for of accident victims develop PTSD.42,45 clinicians than the more focused ASD criteria.27 This In terms of TBI, there are between 1.5 and 2 million peo- position presumes that the initial period after trauma ple in the USA alone who sustain a TBI, with approxi-

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mately 70 000 to 90 000 experiencing persistent func- sympathetic nervous system activation, including resting tional difficulties.46 The Centers for Disease Control and heart rate. Indirect support for this hypothesis comes Prevention estimates that approximately 5.3 million peo- from multiple longitudinal studies that indicate that ele- ple in the USA are living with a disability due to TBI.47 vated heart rate in the acute post-trauma phase is asso- Certain populations appear to be more at risk of sus- ciated with subsequent development of PTSD72; elevated taining TBIs. For example, military estimates of mild TBI heart rate in the initial days after trauma may reflect of deployed (non-medically evacuated) personnel indi- stronger conditioning, which can then translate into cate that between 10% and 20% may have suffered a longer-term PTSD. Although conditioning occurs opti- mild TBI during deployment.48 One study reported a mally when one is aware of the contingency between the rate as high as 23% in personnel assessed after return- unconditioned and conditioned stimuli,73 conditioning ing to the USA.49 may occur with varying levels of awareness of the contingency between the trauma and the consequences, Can PTSD develop following TBI? which may allow for some fear conditioning following TBI. Consistent with this proposal, there is evidence that Some earlier commentators argued that PTSD could not people can develop PTSD following severe TBI, even develop following TBI because the impaired conscious- though these patients do not recall the trauma and do ness at the time of trauma precluded encoding of the not suffer intrusive memories of the event.17 These traumatic experience, and this prevented trauma mem- patients display reactivity to reminders of the trauma in ories that are necessary for PTSD development.50,51 In the absence of recall of the event; this observation is contrast, evidence has accumulated that PTSD can consistent with fear conditioning explanations of TBI- develop following mild TBI.52-60 Intriguingly, both case related PTSD. Further support for the possibility of fear studies61-66 and cohort studies17 have noted the existence conditioning leading to PTSD after severe TBI patients of PTSD developing following severe TBI. In many of is evidence of higher heart rates immediately after the the latter cases, these individuals suffer very significant trauma in severe TBI patients who develop PTSD (even periods of retrograde and anterograde amnesia, such during dense post-traumatic amnesia) than those who that they do not recall any episodes of the traumatic do not develop PTSD.74 experience. Memory reconstruction Fear conditioning An alternate mechanism is that TBI patients reconstruct Several mechanisms have been put forward to explain trauma memories in ways that result in a traumatic rep- how PTSD can develop following TBI. Fear condition- resentation of what occurred during impaired conscious- ing models posit that the fear elicited during a traumatic ness. A prospective study of mild TBI patients assessed event results in conditioning in which subsequent motor vehicle accident survivors immediately after the reminders of the trauma elicit anxiety in response to accident, and subsequently reassessed for their memory trauma reminders (conditioned stimuli).67 This model of the event 2 years later; this study found that although proposes that extreme sympathetic arousal at the time all patients initially reported amnesia of some aspect of of a traumatic event may result in the release of stress the accident, 40% reported 2 years later that they had neurochemicals (including norepinephrine and epi- subsequently achieved full recall of the experience.75 nephrine), mediating an overconsolidation of trauma Supporting this view, case reports describe severe TBI memories. This proposal is consistent with animal stud- patients developing images of the traumatic event based ies that indicate that epinephrine administration after an on police reports, dreams, and other secondary sources.61,65 aversive experience enhances fear conditioning.68 Fear For example, Bryant76 reported a man who developed conditioning models are also supported by considerable PTSD 12 months after his injury, which involved an evidence that people with chronic PTSD are hyperre- extended period of anterograde and retrograde amnesia. sponsive to trauma reminders.69-71 The adrenergic When this man was directed to resume driving he devel- increase occurring after trauma exposure that may con- oped distressing and intrusive images of his accident that tribute to fear conditioning may be reflected in increased were based on a newspaper photograph of his wrecked

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car. Although he was densely amnesic of the accident, he study of 939 health plan members that patients with a developed a series of images that were founded on his history of mild TBI were 2.8 times more likely to memory of the photograph. Interestingly, these images develop a psychiatric disorder than patients with no TBI changed with time. For example, when he became con- history.77 In a large military survey, whereas 16% of cerned that his children may be harmed when he was dri- troops who sustained a bodily injury indicated PTSD, ving, his intrusive images changed to include his children 44% of those with MTBI screened positive for PTSD.59 lying dead in the car. Bryant and Harvey62 compared the Further, a large civilian study that employed rigorous intrusive imagery of motor vehicle survivors who either clinical interviews found that sustaining a MTBI signif- (i) had PTSD and no TBI; (ii) had PTSD following severe icantly increased the risk for PTSD.78 This development TBI and reported intrusive memories that were inconsis- is in stark contrast to previously held views that TBI was tent with objective reports of the accident; or (iii) had no protective of PTSD development. PTSD. All participants were asked to listen to an audio This observation may have several possible explanations. tape of a car crash sound effect, and were then inter- The prevailing neurobiological model posits that PTSD viewed about their cognitive and emotional responses. involves exaggerated amygdala response associated with When these responses were independently rated on a impaired regulation by the medial prefrontal cortex.79 range of constructs, it was found that those PTSD partic- The amygdala appears to be pivotal to development and ipants with and without TBI reported comparable levels expression of conditioned fear reactions in human and of vivid imagery, emotional response, involuntariness, and animal studies, and that learning to inhibit these fear sense of reality. The only difference was that those with a reactions (extinction learning) involves inhibition by the TBI tended to report stationary images rather than mov- ventral medial prefrontal cortex.80 Consistent with this ing sequential imagery. This finding highlights that the model, numerous studies have reported that patients reconstructed memories that develop in TBI patients can with PTSD have diminished medial prefrontal cortex be subjectively compelling and share may of the attrib- during processing of fear.81 It is possible that MTBI utes of imagery experienced by people who have contin- enhances risk for PTSD because neural damage sus- uous recall of their trauma. tained in the injury compromises the critical neural cir- cuitry required to regulate fear following the traumatic Postamnesia resolution experience.82 Alternately, the management of post-traumatic stress, as A third possible mechanism is that many people who well as problems caused by ongoing stressors in one’s sustain a TBI, and frequently those with MTBI, suffer environment, requires adequate working memory and traumatic experiences following resolution of their post- cognitive resources83; it is possible that TBI depletes traumatic amnesia. One may be knocked unconscious in these resources to some extent, and this may contribute a motor vehicle accident victim but be fully aware of the to increased PTSD risk. There is much evidence that experience of being cut out of the car by paramedics, PTSD is influenced by the compounding effects of stres- experiencing severe pain, being treated in an emergency sors that occur following the precipitating trauma.84,85 room, and fearing for their safety. These experiences Pain, medical procedures, loss of employment, legal function similarly to any traumatic scenario observed by issues, and interpersonal conflict are commonplace fol- people who develop PTSD in the absence of any TBI. lowing MTBI, and it is possible that the marginal deficits Many MTBI patients will report distressing memories of that may be attributed to MTBI could limit optimal their experience, despite islands of amnesia in which management of these stressors. they cannot recall the point of impact in which they sus- Although MTBI does appear to increase the risk of tained their MTBI. PTSD, it needs to be remembered that the association between TBI and PTSD is complex, and much is not The impact of TBI on PTSD understood. There is evidence of an inverse relationship between extent of one’s memory of the traumatic expe- One of the intriguing findings in recent years is that rience and the occurrence of re-experiencing memories. MTBI appears to increase the risk for PTSD. For exam- One study of 228 motor vehicle accident survivors ple, Fann and colleagues reported from a large-scale indexed the extent to which patients with MTBI recalled

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details of the traumatic accident,87 and found that the it is possible that one explanation of delayed-onset PTSD, less patients recalled of their traumatic event, the less especially in the military, is the pattern of subsequently likely they were to develop PTSD. Another study reconstructing the traumatic events in the wake of assessed 1167 traumatic injury patients in hospital (459 impaired consciousness. The possibility that trauma mem- with mild TBI and 708 with no TBI) for post-traumatic ory reconstruction in the post-deployment period con- amnesia and PTSD in hospital immediately, and subse- tributes to PTSD needs to be studied in military popula- quently reassessed them for PTSD 3 months later.87 tions, and points to the potential importance of ensuring Although this study found an inverse relationship that adaptive, rather than maladaptive, reconstructions between the length of post-traumatic amnesia and intru- of events occur in the months after injury. sive memories in the initial phase after trauma, MTBI patients were more likely to develop PTSD than no-TBI Impairment following MTBI patients, after controlling for injury severity (adjusted odds ratio: 1.86, 95% confidence interval, 1.78-2.94). This There is enormous concern in the wake of the finding suggests that although duration of amnesia Iraq/Afghanistan wars over the impairment caused by appears protective of development of intrusive trau- MTBI. Many millions of dollars are being devoted to matic memories, MTBI nonetheless confers risk for rehabilitation procedures to minimize the potential developing PTSD. It is for this reason that whereas mild adverse effects of MTBI on soldiers affected by it. TBI appears to increase risk for PTSD, presence of Recent studies are indicating, however, that MTBI itself PTSD after more severe TBI (in which there is limited is responsible for minimal impairment. One large-scale encoding of trauma memories) is less common. survey of US troops reported that health impairment was markedly higher in deployed personnel who sus- Delayed-onset PTSD tained a MTBI, including reported poor general health, days off work, and medical visits. Importantly, the influ- Post-traumatic stress symptoms typically occur in the ini- ence of MTBI on these measures of impairment was not tial days and weeks after trauma exposure, and then significant after controlling for the effects of PTSD and gradually abate in most people; a minority of trauma depression.59 This conclusion was supported in a second survivors can suffer persistent PTSD.88 Delayed-onset large-scale military study.92 Similarly, a large-scale study PTSD refers to cases of PTSD in which the condition of civilians found that impaired functioning was not develops at least 6 months after the trauma. Most stud- increased by the presence of MTBI; however, there were ies indicate that delayed-onset PTSD is rare. Although very significant functioning deficits if a patient sustained uncommon following civilian trauma, it has been a psychological disorder in conjunction with the MTBI.78 reported to occur more frequently in troops returning This convergent evidence points to physical, social, and home from deployment.89,90 A review of delayed-onset occupational impairment being strongly related to psy- PTSD studies found that it was rare for PTSD to chological factors occurring after trauma exposure, such develop outside military samples, with up to one third of as PTSD and depression, rather than the presence of military cases presenting as delayed-onset91; specifically, MTBI. it is reported in 38% of military cases compared with 15% in civilian cases. Postconcussive syndrome and PTSD To date, there has not been any systematic study of delayed-onset PTSD following MTBI. It is possible that The issue of postconcussive syndrome is a vexed one, sustaining an mild TBI may contribute to delayed-onset both in terms of its definition and its purported causes. PTSD in the military, and this may be one factor in the It is also an issue that intersects with symptoms of PTSD. increased rates of delayed-onset PTSD in the military. It PCS is generally defined as a syndrome that involves is possible that following MTBI sustained in combat, one headache, dizziness, fatigue, sensitivity to light or sound, feels the need to fill the gap of knowledge of the events sleep disturbance, and concentration difficulties.93 The that affected them. Consistent with reports of TBI definitions of PCS vary, and generally overlap somewhat patients confabulating events in order to make sense of with symptoms of PTSD. For example, the International what occurred to them during the loss of consciousness,61 Classification of Diseases (ICD-10)26 stipulates that PCS

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is defined by headaches, dizziness, general malaise, symptoms and general health problems are largely fatigue, noise intolerance, irritability, emotional lability, related to psychological factors, there are likely risks in depression, or anxiety, concentration or memory diffi- suggesting to troops that the problems experienced fol- culty, sleep disturbance, reduced tolerance to alcohol, lowing MTBI should be attributed to neurological dam- and a preoccupation with these symptoms and fear of age. Communicating to personnel who sustained a permanent brain damage. The Appendix of the DSM-IV4 MTBI that a range of nonspecific symptoms are caused describes PCS as fatigue, sleep disturbance, headaches, by brain damage communicates a cause with a poor dizziness, irritability, anxiety or depression, changes in prognosis. This expectation that common sensations are personality, and apathy. These descriptions clearly over- signs of permanent dysfunction can result in hypervigi- lap with common symptoms of post-traumatic stress, and lance to every sensation, followed by catastrophic attri- represent differential diagnosis problems insofar as how butions about the adverse consequences of the sensa- one attributes these symptoms to PCS or PTSD. tions. This pattern has been well-documented across a Recent evidence is highlighting that symptoms described range of disorders, including panic disorder, health anx- as PCS are common in many populations, and actually iety, and hypochondriasis.105-107 In these disorders, peo- reflect a diffuse collection of frequently experienced sen- ple tend to be hypervigilant to somatic cues because sations. In healthy individuals, headaches, sleep difficulty, they believe they represent a threat to their physical irritability, and memory failures are relatively common in well-being. For example, the patient with panic disorder daily life.97-98 One study found that 72% to 79% of healthy may believe that an alteration in his or her respiration adults reported at least three or more PCS symptoms; fur- is a sign of imminent choking or that a slight pain in the ther, a significant minority of subjects met DSM-IV chest is indicative of an approaching cardiac arrest. (14.6%) or ICD-10 (12.5%) criteria for PCS.99 Similarly, someone with health anxiety may constantly Interestingly, these observed rates of PCS in non-MTBI search their body for any alterations in appearance of are comparable to the rates noted in TBI populations, function to determine if there are signs of malignancy. highlighting the fact that PCS are not unique to TBI. Once the sensation or sign is detected, the person can There has been much debate over the extent to which catastrophize the sign in an extremely negative manner, persistent PCS develops as a result of neurological dam- such that the slightest somatic cue is perceived as age,100 psychological distress,101 or a combination of indicative of dire outcomes. This is a common pattern in both.102 One recent study that assessed PCS in both people with PTSD. Fear network models of PTSD pro- MTBI and non-MTBI injured patients found that com- pose that these individuals preferentially allocate atten- parable proportions of patients reported PCS (MTBI: tion to stimuli of concern because of their fear of 40%; no-TBI: 50%).103 A subsequent follow-up at 3 threat.108 Consistent with this proposal, people with months post-injury found that a similar pattern (mild PTSD are hypervigilent to threat on a range of para- TBI: 46.8%; control: 48.3%).104 Interestingly, across these digms.109-111 Further, people with PTSD not only cata- studies, PCS was predicted by pain levels and PTSD strophize about external threats,112 they also catastro- symptoms. These data indicate that PCS is not unique to phize about somatic and physical sensations.113 MTBI, and that these symptoms that are commonly Therefore, people who are suffering the effects of PTSD attributed to MTBI are more parsimoniously explained will be attentive to any information that is perceived as by the effects of high arousal associated with the stress threatening, and will likely attribute a range of physical, of surviving a traumatic injury. cognitive, and emotional responses to brain injury if this is provided as a salient explanation. This response may The problem of confusing MTBI and PTSD exacerbate the PTSD reaction, as well as promote con- tinued hypervigilence to sensations and subsequent Military agencies have implemented programs for maladaptive appraisals that these reactions are indica- troops in Iraq and Afghanistan targeted towards treat- tive of permanent brain injury. ing the effects of MTBI. Much attention has been given This pattern was reflected in the aftermath of the 1991 to the “problem” of mild TBI, communicating to troops Gulf War, when there were widespread concern of that MTBI is a syndrome that causes marked problems. chemical weapons, which apparently contributed to Given the evidence that so-called postconcussion-like medically unexplained symptoms that were linked to

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concerns about somatic sensations purportedly linked to encoded119; specifically, experiences are often fragmented chemical agents.106,114,115 It seems that a cohort of soldiers because they are encoded under conditions of extreme after the 1991 Gulf War misattributed somatic experi- arousal, and this purportedly disturbs the ability to form ences to chemical agents, which led to persistent con- the required coherent narrative. Fragmented memories cerns about their health. There are potential similarities of the traumatic experience can also occur in the context between Gulf War Syndrome and the manner in which of TBI because of the impaired consciousness secondary MTBI is currently being understood; both comprise gen- to the injury. As noted above, TBI patients can recon- eral sensations that are commonly reported in stress struct aspects of the traumatic experience that were not responses, and both mistakenly attributed to common adequately encoded during the period of impaired con- stress reactions. This can be problematic because it can sciousness. This scenario raises the possibility that treat- reduce people’s optimism or expectancy for recovery. ing PTSD after TBI will require adaptive reconstruction of this narrative in a way that facilitates adaptation Implications for treatment rather than retraumatization. For example, a patient who reconstructs their memory of a car accident in which This review has several implications for how symptoms they were excessively responsible for someone’s death following TBI are addressed in treatment. In terms of will have marked depressive responses relative to a treating the symptoms of PCS, current evidence suggests patient who reconstructs the memory in a way that that simple neuropsychological education is modestly accepts a more reasonable level of responsibility. useful in reducing symptoms of PCS.116 The emerging Alternately, a patient can be encouraged to tolerate a evidence that PCS is predominantly influenced by post- level of uncertainty insofar as there is permanent amne- traumatic stress reactions suggests that addressing these sia of some aspect of the event; inability to tolerate problems may be crucial in alleviating PCS. That is, by uncertainty is linked to enhanced anxiety and worry.120 reducing the arousal-inducing symptoms of PTSD, it is One of the challenges for treating PTSD after TBI is the possible that many of the symptoms associated with PCS patient’s ability to either reconstruct events in a coher- will be alleviated. Similarly, by minimizing catastrophic ent and adaptive way or to accept the uncertainty of how appraisals that exaggerate the severity or adversity of events transpired when they suffered their TBI. PCS sensations it is probable that anxiety about these The extent to which a person with TBI needs to recon- reactions would be eased. For example, patients who are struct the trauma narrative to recover from PTSD has overly concerned about the adverse outcomes of dizzi- yet to be empirically determined. As noted above, sev- ness or sensitivity to light can be taught to normalize eral large-scale studies have reported that MTBI is asso- these reactions in ways that minimize distress about ciated with increased risk for PTSD.59,92,78 One possibility these sensations. Cognitively reframing the perception for this observation may be that people who sustain a of these reactions is akin to established treatments for MTBI do not have a coherent narrative of their trau- panic disorder or health anxiety, in which patients are matic experience because of the impaired consciousness taught to tolerate somatic experiences in ways that dis- secondary to the brain injury, and this may impede their courage inferences involving an adverse outcome. capacity to contextualize the experience in their autobi- Although this approach has been proven to be very ographical memory base. effective in treating panic disorder117 and health anxi- A second implication for PTSD treatment after TBI is ety,118 it has yet to be tested with PCS. that the treatment of choice for PTSD involves trauma- In terms of treating symptoms of PTSD, prevailing cog- focused exposure therapy.121 This treatment is based on nitive models posit that recovery from a traumatic expe- extinction learning, which occurs when a conditioned rience involves integrating the trauma memory into stimulus is repeatedly presented in the absence of an one’s autobiographical memory base in a way that aversive outcome, thereby facilitating new learning that allows a coherent narrative of the experience in which the stimulus is no longer signaling threat. In the context the person can contextualize the experience and conse- of therapy, presenting memories or reminders of the quently currently feel safe.112 This perspective proposes trauma to the patient in the safety of therapy typically that a major reason trauma memories are difficult to leads to symptom reduction. Exposure can either be integrate into memory is the manner in which they are imaginal, which involves focusing on one’s memories of

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the traumatic event, or in vivo, in which approaches and Conclusions remains with reminders that usually trigger anxiety about the event. On the premise that fear conditioning The coexistence of TBI and PTSD is frequent, and the and extinction still occurs in the context of TBI, it would extent to which the symptoms of TBI and PTSD are seem that that exposure-based therapy is the indicated confused may be as frequent. Increasing evidence indi- intervention for PTSD following TBI. Supporting this cates that many previously termed PCS responses are conclusion is evidence in one controlled trial of patients a function of psychological responses, and it hampers a with acute stress disorder following MTBI that CBT patient’s recovery if they mistakenly perceive these effectively treated PTSD symptoms to a similar extent reactions as indicators of a brain injury that may be as when applied to non-TBI samples.122 permanent. In this sense, the field is recognizing the Imaginal exposure with people following TBI will usu- distinction between TBI as an event rather than a syn- ally be dependent on the amount of memory that the drome, whereas PTSD or PCS are symptoms that arise patient is reporting. It may not be as useful to patients secondary to the event. The likelihood that the pre- with more severe TBI because they are largely amnesic sumed sequelae of MTBI are actually attributed to psy- of their trauma. As noted above, some severe TBI chological responses to the traumatic experience is patients can have nightmares or intrusive memories on becoming more apparent. Accurate identification of the basis of reconstructions of their trauma; in these the true nature and cause of the symptoms experienced cases, imaginable exposure to those mental representa- after TBI is important because if stress-related distur- tions that are causing anxiety. In most cases of moder- bances are mistakenly attributed to neurological fac- ate/severe TBI, however, it is more useful to employ in tors, patients may be deprived of effective treatments vivo exposure because reminders of the trauma can elicit that can, in most cases, alleviate the symptoms. As we stronger anxiety in the absence of actual memories or learn more about the interaction of TBI and PTSD, it images. A survivor of a motor vehicle accident who sus- seems that we will be discovering much about how the tained a severe TBI may experience marked fear when brain responds to traumatic experiences, both in cases watching film footage of traffic; in such a case, the when there has and has not been a TBI. Understanding patient could complete exposure by repeatedly watch- this interaction between neurological insult and psy- ing traffic footage. Through these techniques it would be chological response has the potential to shed light on hoped that extinction learning can be achieved, even the key mechanisms underpinning trauma response though the patient may never retrieve direct memories generally, and how it is impacted by different levels of of the traumatic event. brain injury. ❏

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Trastorno por estrés postraumático versus L’état de stress post-traumatique versus daño cerebral traumático lésion cérébrale traumatique

Con frecuencia el trastorno por estrés postraumá- L’état de stress post-traumatique (ESPT) et la lésion tico (TEPT) y el daño cerebral traumático (DCT) coe- cérébrale traumatique (LCT) coexistent souvent car xisten, ya que las lesiones cerebrales a menudo son la survenue de lésions cérébrales est souvent retar- parte de las experiencias traumáticas. Esta revisión dée lors des événements traumatiques. Cet article esquematiza la sobreposición significativa entre souligne le chevauchement significatif entre l’ESPT TEPT y DCT comenzando con un resumen crítico de et les LCT en débutant par une description indis- los síntomas que se sobreponen y de los problemas pensable des symptômes communs et des problè- en el diagnóstico diferencial. A continuación se des- mes liés au diagnostic différentiel. L’influence de la cribe el impacto del DCT en el TEPT y se señala que LCT sur l’ESPT est ensuite décrite, de plus en plus hay una evidencia creciente que sugiere que el DCT d’arguments suggérant qu’une légère LCT aug- leve puede aumentar el riesgo de TEPT. Se ofrecen menterait le risque d’ESPT, ce qui s’explique de dif- algunas explicaciones para este incremento del férents façons : d’après des résultats récents, le défi- riesgo. Hay evidencia reciente que propone que el cit secondaire à une légère LCT est largement deterioro secundario al DCT leve se puede atribuir attribuable aux réactions de stress après la LCT, ce en forma importante a las reacciones de estrés des- qui contredit une croyance ancienne selon laquelle pués del DCT, lo que desafía la antigua creencia de les symptômes post-commotionnels sont fonction que los síntomas post contusionales se producen a d’une lésion neurologique. Ceci ouvre de nouvelles raíz del daño neurológico. Esta evidencia reciente voies de traitement des symptômes post-commo- está apuntando hacia nuevas orientaciones para el tionnels, traiter les facteurs de stress après une LCT tratamiento de los síntomas post contusionales, s’avérant peut-être le meilleur moyen de prendre reconociendo así que el manejo de los factores de en charge les effets des LCT. estrés después de un DCT puede ser la forma óptima de abordar los efectos de muchos DCTs.

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