Evidence Supporting PTSD After TBI
Alongside the studies indicating that subjects who sustain TBI develop PTSD less frequently are several studies suggesting that TBI in trauma survivors is not associated with a lower risk for PTSD. A study that followed victims of motor vehicle accidents during the acute phase of recovery found that symptoms such as fear and intrusive recollections of the accident were present both in those with and in those without head injury, although more commonly in the latter (27). Of those who sustained mild brain injury, 24% met criteria for PTSD in the initial month. Subsequent studies reported that 14% of subjects with mild TBI developed ASD, and an additional 4% to 5% were diagnosed with subsyndromal ASD (35). A 6-month follow-up of the same cohort revealed that 24% had proceeded to develop PTSD, suggesting that risk factors other than ASD were involved (36). A prospective study of 97 people admitted to hospital with mild TBI following motor vehicle accidents found that, after 2 years, 80% of those initially diagnosed with ASD still suffered from PTSD (37). In 2 additional studies, it was reported that 33% of the patients with brain injury met criteria for PTSD (22,38). Another study selected a random sample of 100 subjects from 400 patients with mild-to-severe TBI, and using the Structured Clinical Interview for DSM-IV, diagnosed PTSD in 17% of this sample (39). In a prospective study of 107 road-accident survivors who sought medical attention within 2 days, 36% were diagnosed with PTSD, including 9 out of 16 who had lost consciousness (40). Indeed, there are several case studies of patients with severe head injury who met criteria for PTSD despite extended periods of amnesia and a self-reported inability to recall any aspect of the trauma (41,42).
A few studies examined whether PTSD symptoms with TBI are similar or dissimilar to PTSD symptoms without TBI. For example, ASD and PTSD symptoms in accident survivors with and without TBI were compared after 1 and 6 months. At 1 month, traumatic memories of the accident were less common in the mild TBI group, but by 6 months, this difference was no longer apparent (43). Similarly, patients without brain injury have reported less intrusive memories with time, while those with TBI have displayed increased intrusive memories, suggesting a unique course of posttraumatic adjustment after TBI (27,44).
In a retrospective study of 312 patients with severe TBI referred for neuropsychological assessment (45), 10 had symptoms of PTSD, suggesting that at least 3% of survivors may experience the disorder. In a representative sample of 66 survivors of severe TBI, 18.2% had clinically significant PTSD symptomatology; of these, 6.1% had severe symptoms (46). These rates are lower than rates reported in subjects with mild brain injuries, yet comparisons with other studies are problematic, given varying definitions and methodological differences.
Taken together, these studies support the notion that TBI does not reduce the prevalence of PTSD following exposure to traumatic events. Further, they call into question whether TBI protects trauma survivors from subsequently developing PTSD. However, it is noteworthy that none of these studies carefully addressed memory for the traumatic event as an important variable that differentiates people with TBI. As we discuss in the following section, this factor seems to be of major importance.
TBI-Induced Amnesia and the Risk for PTSD
The assumption underlying many of the studies examining the relation between TBI and PTSD is that impaired consciousness precludes memory of the trauma (47). However, as mentioned before, most studies did not adequately address the degree to which victims of head injury actually remember the traumatic event.
In an effort to fill this gap, we designed and recently completed 2 studies that employed a memory questionnaire requiring participants to assess the degree to which they remember the following 9 domains of the traumatic event: the nature of the event, where it took place, who was involved, when it took place, sounds, sights, odours, things said by the participant during the event, and things said by others. In the first study, we used a prospective design to examine the relation between participants’ appraisal of their memory for details of the traumatic event and the later development of PTSD (48). The participants (n = 120) were admitted to the surgical ward following a trauma involving mild head injury, and we evaluated them at 4 different time points over 6 months (within 24 hours and after 1 week, 1 month, and 6 months). We used the Structured Clinical Interview for Axis I Disorders-Nonpatient Edition (SCID-NP) (49) to diagnose psychiatric disorders and the Clinician-Administered PTSD Scale (CAPS) (50) to assess current PTSD symptoms. Most participants (91%) were motor-vehicle accident survivors with mild physical injury. Responses on the memory questionnaire showed a bimodal distribution in most respondents, with reports of memory for all the domains or for none. Overall, 14% of the participants met full criteria for PTSD 6 months after the trauma. However, PTSD was nearly 5 times more prevalent among participants with memory of the trauma than among those without memory of the trauma. Appraised memory for the traumatic event as early as 24 hours after its occurrence was shown to strongly predict the presence of PTSD at 6 months. It is noteworthy that the positive relation between memory and PTSD was owing primarily to the difference in the reexperiencing cluster. When we accounted for other PTSD risk factors, memory of the traumatic event was associated with more than twice the risk of developing PTSD following a traumatic event involving TBI.
These findings were corroborated in a second study using a retrospective design. We recruited 120 patients with head injury (on average, 3 years posttrauma) from an outpatient neurocognitive clinic and evaluated them in a single, 3-hour interview (51). Overall, 22% of the participants in this study met full criteria for PTSD. The prevalence of PTSD among subjects with memory of the trauma was more than 5 times higher than among participants who did not remember the traumatic event. Moreover, when we accounted for anxiety and depressive symptoms, sex, and age, memory for the details of the traumatic event was associated with a threefold increase in the risk for a PTSD diagnosis. As in the previously mentioned study, the positive relation between memory and PTSD was primarily attributable to a difference in the reexperiencing cluster.
While these 2 studies clearly show the positive correlation between memory for the traumatic event and PTSD, they also show that, in a subset of patients, lack of memory does not fully protect against the development of PTSD. There are several mechanisms by which PTSD could develop in subjects lackng memory of the traumatic event, but a detailed discussion of this complex issue is beyond the scope of this review. Suffice it to say here that emotionally charged traumatic memories may be initially processed via brain circuits that bypass cortical structures and are mediated primarily through the amygdala, resulting in the formation of implicit (unconscious) memories (52). At the same time, stress-induced secretion of glucocorticosteroids, which have been shown to impair hippocampal functioning (53), may disrupt the formation of explicit (conscious) memory.
Conclusions and Implications
This review addresses the relation of traumatic memory to PTSD in the context of TBI, a naturally occurring model for studying the role of memory in trauma response. The literature review is not conclusive, but taken together with the results from our own studies, there seems to be support for the notion that PTSD is more prevalent in TBI victims with memory of the traumatic event and less prevalent when memory of the traumatic event is impaired. This clearly indicates that, at least in this patient population, amnesia regarding the event may protect against the development of PTSD.
While speculative, it is tempting to generalize from this to other traumatic conditions that do not involve head trauma but in which traumatic exposure is nevertheless associated with impaired memory of the event. Taking this even further, one might suggest that deliberately disrupting the memory of the traumatic event might prove therapeutically beneficial. This possibility has been addressed in a recent double-blind study that compared the severity of acute PTSD symptoms in 18 subjects who were given 40 mg of propranolol 6 hours after the trauma with symptoms in 23 participants who received placebo (54). In this study, subjects in the experimental group tended to have lower levels of PTSD symptoms 10 days posttrauma. If further corroborated, these findings may support the notion that not only does lack of memory protect against the development of PTSD but also that pharmacologically induced disruption of traumatic memories can therapeutically benefit trauma survivors.
The above-mentioned study assumed that it is crucial to intervene in the initial process of memory consolidation, which is believed to take place within the first 12 hours after traumatic exposure. However, this may not be the case. Findings from recent studies indicate that memory is a dynamic process: in it, the interplay between retrieval of consolidated memory and its reconsolidation after further processing in the working memory constantly reshapes old memories (52). This ongoing process strengthens the memory, but at the same time it renders retrieved memories amenable to disruption (52). This could indeed be one of the mechanisms by which recurrent intrusive memories in PTSD operate as enhancers, constantly strengthening the memory of the traumatic event and preventing its decay. From a neurobiological perspective, this process reinforces neural networks and involves protein synthesis (52,55). It has been further shown in animal studies that, during this process, retrieved memories are sensitive to pharmacologic disruption (for example, by the use of protein synthesis inhibitors), which may inhibit reconsolidation and result in the extinction of old memories (55,56). Thus, memory disruption can occur in already-consolidated memories, once they are retrieved and processed in the working memory. Taken together with the previously mentioned findings in patients with TBI, this may suggest that old traumatic memories in patients suffering from PTSD could be disrupted by pharmacologic means. If proven empirically, such a possibility might have far-reaching theoretical and practical implications, given that most psychotherapeutic treatments for PTSD emphasize the importance of exposure to and confrontation of the traumatic memories. Currently available treatments for PTSD are frustrating and unsatisfactory; thus, a search for new and different treatment approaches is timely and of great importance.
Funding and Support
Support for this review was provided by the Chutick Fund for the Study of the Injured Brain.
Acknowledgement
The authors thank Dorit Ben-Shachar, David Rabinowitz, and Shimon Marom, for their thoughtful comments.
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Author(s)
Manuscript received and accepted November 2002.
1. Associate Professor, Rappaport Faculty of Medicine, Technion Israel Institute of Technology, Haifa, Israel; Chairman, Department of Psychiatry, Rambam Medical Center, Haifa, Israel.
2. Clinical Psychologist, Department of Psychiatry, Rambam Medical Center, Haifa, Israel; Adjunct Lecturer, Rappaport Faculty of Medicine, Technion Israel Institute of Technology, Haifa, Israel.
3. Adjunct lecturer, Faculty of Social Welfare and Health Studies, Department of Nursing, University of Haifa, Israel; Licensed Clinical Social Worker, Department of Psychiatry, Rabam Medical Center, Haifa, Israel.
Address for correspondence: Dr E Klein, Department of Psychiatry, Rambam Medical Center, PO Box 9602, Haifa 31096, Israel
e-mail: e_klein@rambam.health.gov.il
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