PTSD: Treatment Efficacy and Future Directions

Posttraumatic stress disorder (PTSD) is a severe and often chronic anxiety disorder that can develop following exposure to an event involving actual or perceived threat to the life or physical integrity of oneself or another person. Epidemiological studies such as the National Comorbidity Survey¹ estimate that more than half the population of the United States has experienced one or more traumatic events and that 8% of the population has met criteria for lifetime PTSD. Thus, trauma and PTSD are significant mental health problems.

In this article, we provide a summary of research on the efficacy of treatments for PTSD and suggest directions for future work. Although numerous psychological therapies have been suggested and used in patients with PTSD, most efficacy research using gold standard randomized controlled treatment methodology² has focused on various cognitive-behavioral therapy (CBT) programs. Accordingly, our review will also focus on CBT.

Description of CBT procedures
CBT is a broad term covering a number of interventions designed to challenge and modify erroneous cognitions, reduce the intensity and frequency of distressing negative emotional reactions via exposure to safe but feared situations and objects, and promote effective coping. Two erroneous cognitions commonly found in patients with PTSD are that the world is entirely dangerous and that the person with PTSD is incompetent.³ CBT is a short-term approach, usually involving 9 to 12 individual sessions lasting 60 to 90 minutes, and administered once or twice weekly. Patients are usually assigned homework to practice the specific interventions between sessions.

The most frequently used interventions for PTSD are exposure therapy, stress inoculation training (SIT), and cognitive restructuring. These interventions may be administered as stand-alone treatments or combined into a more comprehensive treatment package. A fourth treatment for PTSD, eye movement desensitization and reprocessing (EMDR),⁴ incorporates elements of exposure and cognitive restructuring with therapist-directed rapid eye movements or other laterally alternating activities.

Exposure therapy
Exposure therapy is a set of treatment procedures designed to help individuals confront feared but safe thoughts, situations, objects, people, places, or activities that elicit anxiety or are otherwise avoided because they are perceived as dangerous by patients with PTSD. Exposure to feared but safe situations is a major component of treatment for other anxiety disorders such as phobias, social anxiety disorder, obsessive-compulsive disorder, and panic disorder/ agoraphobia.⁵

For PTSD, exposure therapy typically involves imaginal exposure to the trauma memory in which patients are instructed to close their eyes and recall the traumatic event by imagining that it is happening right now while simultaneously describing out loud what is being remembered. Patients are encouraged to provide a detailed description of the memory, including all important sights, sounds, smells, tastes, and physical sensations, along with thoughts and emotional reactions that occurred during the trauma. These trauma narratives are repeated several times in the therapy session over the course of 20 to 45 minutes and recorded for the patient to listen to as daily homework.

In addition to imaginal exposure, patients practice in vivo exposure to real life stimuli that trigger trauma-related memories and distress.⁶ This is accomplished through identifying the people, places, situations, and activities that trigger anxiety and avoidance because of the trauma; evaluating each one for safety and for relevance to the patient's normal functioning; then repeatedly confronting selected situations for prolonged periods until there is a significant reduction in the patient's anxiety. To facilitate in vivo exposure, a hierarchy is constructed that begins with targets of moderate difficulty and then moves gradually to more challenging targets as the patient succeeds with the lower items.

The goal of imaginal and in vivo exposure is to help patients process the traumatic memories and correct erroneous cognitions about the world and the self.

Stress inoculation training
SIT is a collection of several techniques designed to manage stressful situations and problematic emotional reactions.⁷ Applied to PTSD,^8-10 SIT consists of training in controlled breathing, progressive muscle relaxation, guided positive imagery, thought stopping, and cognitive restructuring (discussed below). The rationale for SIT assumes that individuals will differ in how they experience and express anxiety, and one goal of treatment is to match interventions with specific symptoms. For example, controlled breathing and progressive muscle relaxation may be used to target the symptoms of physiological arousal, whereas thought stopping is designed to disrupt intrusive recollections about the trauma or other anxiety-provoking thoughts and images (eg, worry, rumination about current life stressors).

Cognitive restructuring
Cognitive therapy, developed initially as a treatment for depression¹¹ and later extended to the treatment of anxiety,¹² is based on the idea that it is not actual events that cause problematic emotional reactions but a person's interpretation of those events. Accordingly, cognitive therapy techniques, of which cognitive restructuring is one of the most basic, are designed to help patients identify and challenge their inaccurate or unhelpful cognitions and replace them with more realistic or helpful ones. Cognitive restructuring is designed to accomplish this through systematic review of evidence for and against a target belief or evaluation of the pros and cons of maintaining the belief. It incorporates careful consideration of the likelihood or actual cost of anticipated consequences, investigating possible alternative explanations for difficult or challenging situations, or attempting to view the situation from the perspective of another.

Eye movement desensitization and reprocessing
EMDR has 2 major components: repeated brief (approximately 30 seconds each) imaginal exposure to trauma- related thoughts, images, and memories (desensitization); and a form of cognitive restructuring called reprocessing. The unique feature of EMDR is that the therapist induces a series of rapid left-to-right eye movements by instructing the patient to follow the therapist's hand as it is moved back-and-forth across the patient's visual field during desensitization and reprocessing. In some cases, therapists may replace eye movements with one of several other possible forms of lateral alternation, such as the patient alternately tapping the left and right hands or the therapist presenting tones alternately to the left and right of the patient. Shapiro,⁴ the originator of EMDR, has hypothesized that trauma can disrupt the normal functioning of the information processing system, which prevents recovery from PTSD symptoms. She has further speculated that "the information-processing mechanism may be activated when attention is elicited by or focused on the external cues [eg, tracking the therapist's fingers] . . . [and that] the simultaneous focus on the traumatic memory may cause the activated system to process the dysfunctionally stored material."

Although much of the initial research on EMDR suffered from significant methodological limitations,^13-17 more recent research has established the basic efficacy of EMDR for PTSD.^18,19 However, dismantling studies have repeatedly failed to find superior outcome for EMDR treatment that includes the use of rapid eye movements compared with a range of control conditions, including conducting EMDR while having patients close their eyes or focus on a set point.²⁰ Accordingly, it would seem likely that the benefit of EMDR is best attributed to the elements it has in common with other forms of CBT (ie, brief imaginal exposure and cognitive restructuring conducted within a supportive relationship).

Efficacy of CBT
The efficacy of CBT in the treatment of PTSD has been studied in a number of randomized controlled studies. A recent meta-analysis of treatments for PTSD identified 26 studies that yielded 44 active treatment conditions, 37 (84%) of which involved CBT, 8 active control conditions (eg, supportive counseling, relaxation), and 15 waitlist control conditions.²¹BT) that produced a mean between-group effect size of 1.11 (CI, 0.76 to 1.47).

Focusing on the CBT conditions, the effect sizes ranged between a mean of 1.43 for EMDR and 1.66 for exposure therapy plus cognitive restructuring, with no significant differences emerging across different CBT categories. Several studies also reported the percentage of patients that no longer met diagnostic criteria for PTSD after completing treatment. Among 29 active treatment conditions, 26 of which were some form of CBT, 67% of patients did not meet criteria for PTSD following treatment, with average rates ranging between 65% for EMDR and 70% for exposure therapy plus cognitive restructuring. Again, there were no significant differences among types of CBT. By comparison, 39% of patients completing an active control treatment and 16% of patients completing waitlist lost the PTSD diagnosis.

In their meta-analysis, Bradley and colleagues²¹ found that the various studies comprised a broad range of trauma populations, including female victims of sexual and physical assault both in adulthood and in childhood, male combat veterans, male and female victims of motor vehicle accidents, male and female refugees, and mixed sex/mixed trauma samples made up mostly of victims of violent crime and motor vehicle accidents. Although their meta-analysis focused exclusively on measures of PTSD, the effects of CBT in the studies analyzed were not limited to PTSD. Concomitant improvements were also found on measures such as depression,^9,10 anxiety,^9,10 anger,²² and guilt.²³ Moreover, follow-up assessments at 3 to 12 months showed that the treatment gains were well maintained.^9,10

Future directions
Although most people in treatment studies benefit from CBT, many patients receive only partial benefit and some patients do not benefit at all. In addition, access to the treatments described above is currently quite limited: nationwide, few therapists are trained to use CBT for PTSD.²⁴ Research on improving treatment outcome and disseminating CBT has begun but is less advanced than research demonstrating the basic efficacy of this approach.

Combining CBT interventions
One method that may improve outcome is to combine separately efficacious treatments. Five studies have investigated whether combining CBT interventions results in greater improvement. Foa and colleagues¹⁰ investigated whether the combination of exposure therapy plus SIT resulted in better outcome than either treatment alone. Marks and coauthors²⁵ investigated whether the combination of exposure therapy plus cognitive restructuring resulted in better outcome than either treatment alone. Unfortunately, neither study found evidence for the superiority of combined treatment over the constituent treatments. Consistent with the study by Marks and coauthors,²⁵ Paunovic and Ost²⁶ and Foa and coinvestigators²⁷ found comparable outcomes between exposure therapy alone and exposure therapy combined with cognitive restructuring.

In contrast, Bryant and colleagues²⁸ found that adding cognitive restructuring enhanced the efficacy of exposure therapy. However, the exposure therapy program in their study included only imaginal exposure, whereas the studies that did not find augmentation of exposure therapy with the addition of either SIT¹⁰ or cognitive restructuring^25-27 used both imaginal and in vivo exposure. Thus, it may be that imaginal exposure alone can be enhanced by the addition of either in vivo exposure or cognitive restructuring, but the combination of imaginal plus in vivo exposure is not further enhanced by the addition of cognitive restructuring or SIT.

Medication and CBT intervention
At present, 2 medications have received FDA approval for PTSD, sertraline^29,30 and paroxetine.^31,32 In a variation of the strategy of combining treatments, Rothbaum and colleagues³³ investigated whether adding exposure therapy to medication for PTSD resulted in enhanced outcome. Patients received 10 weeks of open-label treatment with sertraline and were then randomly assigned to continue receiving sertraline alone for an additional 5 weeks or to continue taking sertraline and receive 10 sessions of exposure therapy administered twice weekly.

Overall, there was a significant reduction in PTSD severity during the course of the initial 10 weeks of treatment with sertraline, followed by a modest effect during the period of augmenting sertraline with CBT. However, an exploratory analysis in which patients were separated based on their response to sertraline at week 10 as either excellent responders or partial responders revealed a substantial augmentation effect for medication partial responders. Among medication partial responders who received only sertraline, there was a 35% reduction in PTSD severity from pretreatment to week 10, and at week 15 the overall reduction was 30%, indicating a small and statistically nonsignificant increase in PTSD severity from week 10 to week 15. Partial responders to medication who received CBT augmentation showed a reduction of 37% from pretreatment to week 10 and overall reduction of 62% from pretreatment to week 15, indicating a clinically and statistically significant (P < .001) improvement from week 10 to week 15. The between-group effect size at week 15 for augmenting sertraline with CBT among medication partial responders was 0.90.

Another strategy for improving outcomes is to provide the same treatment for a longer duration, a strategy that is commonly used in clinical practice: where there is improvement in symptoms but not complete response, continuation with the same treatment is recommended. Efficacy studies, however, typically implement the treatments of interest for a set period without regard to the patient's symptom status. In an exception to the rule, Foa and associates²⁷ used flexible dosing: patients with PTSD symptoms that decreased by at least 70% at session 8 terminated treatment at session 9. The remaining patients were offered additional sessions, to a maximum of 12. Fifty-eight percent of patients who completed at least 8 sessions received extension sessions. Results for this group indicated that further improvement was achieved during the extension period.

On average, these patients showed a 31% reduction in PTSD severity at session 8. After the extension sessions, the average reduction in PTSD severity compared to pretreatment was 60%. Thus, research is beginning to address the need to develop and evaluate strategies for enhancing treatment outcome for those who show partial response to existing treatment programs; however, further research is needed.

Disseminating the use of CBT for PTSD
A second area in which research is just beginning is the development and evaluation of methods to disseminate the use of CBT for PTSD.^34,35 Foa and coauthors²⁷h sites for the duration of the study.

Results indicated that, before treatment, patients were comparable across sites on PTSD severity and depression. More important, the effects of treatment were comparable across sites. This study demonstrated that CBT could be transported from academic-based clinics to community-based clinics under conditions of close collaboration with an academic center. Additional research is needed to determine whether community-based institutions can sustain their use of CBT when the level of contact with the academic center is substantially reduced, along with research to identify the most efficient methods to disseminate CBT to large numbers of therapists.

References:

References:1. Kessler RC, Sonnega A, Bromet E, et al. Posttraumatic stress disorder in the national comorbidity survey. Arch Gen Psychiatry. 1995;52:1048-1060.
2. Foa EB, Meadows EA. Psychosocial treatments for posttraumatic stress disorder: a critical review. Ann Rev Psychol. 1997;48:449-480.
3. Foa EB, Ehlers A, Clark D, Tolin DF. Posttraumatic cognitions inventory (PTCI): development and comparison with other measures. Psychol Assess. 1999;11:303-314.
4. Shapiro F. Eye Movement Desensitization and Reprocessing: Basic Principles, Protocols, and Procedures. New York: Guilford; 2001.
5. Barlow DH. Anxiety and Its Disorders: The Nature and Treatment of Anxiety and Panic. 2nd ed. New York: Guilford; 2002.
6. Foa EB, Rothbaum BO. Treating the Trauma of Rape: Cognitive-Behavior Therapy for PTSD. New York: Guilford; 1998.
7. Meichenbaum DH. Stress Inoculation Training. New York: Pergamon Press; 1985.
8. Veronen LJ, Kilpatrick DG. Stress management for rape victims. In: Meichenbaum D, Jaremko ME, eds. Stress Reduction and Prevention. New York: Plenum Press; 1983:341-374.
9. Foa EB, Rothbaum RO, Riggs DS, Murdock TB. Treatment of posttraumatic stress disorder in rape victims: a comparison between cognitive-behavioral procedures and counseling. J Consult Clin Psychol. 1991;59:715-723.
10. Foa EB, Dancu CV, Hembree EA, et al. A comparison of exposure therapy, stress inoculation training, and their combination for reducing posttraumatic stress disorder in female assault victims. J Consult Clin Psychol. 1999; 67:194-200.
11. Beck AT. Cognitive Therapy and the Emotional Disorders. New York: International Universities Press; 1976.
12. Beck AT, Emery G, Greenberg RL. Anxiety Disorders and Phobias: A Cognitive Perspective. New York: Basic Books; 1985.
13. Acierno R, Hersen M, Van Hasselt VB, et al. Review of the validation and dissemination of eye-movement desensitization and reprocessing: a scientific and ethical dilemma. Clin Psychol Rev. 1994;14:287-299.
14. Herbert JD, Mueser KT. Eye movement desensitization: a critique of the evidence. J Behav Ther Exp Psychiatry. 1992;23:169-174.
15. Lohr JM, Kleinknecht RA, Conley AT, et al. A methodological critique of the current status of eye movement desensitization (EMD). J Behav Ther Exp Psychiatry. 1992;23:159-167.
16. Lohr JM, Kleinknecht RA, Tolin DF, et al. The empirical status of the clinical application of eye movement desensitization and reprocessing. J Behav Ther Exp Psychiatry. 1995;26:285-302.
17. Lohr JM, Tolin DF, Lilienfeld SO. Efficacy of eye movement desensitization and reprocessing: implications for behavior therapy. Behav Ther. 1998;29:123-156.
18. Rothbaum BO. A controlled study of eye movement desensitization and reprocessing in the treatment of posttraumatic stress disordered sexual assault victims. Bull Menninger Clin. 1997;61:317-334.
19. Rothbaum BO, Astin MC, Marsteller F. Prolonged exposure versus eye movement desensitization and reprocessing (EMDR) for PTSD rape victims. J Traumatic Stress. 2005;18:607-616.
20. Cahill SP, Carrigan MH, Frueh BC. Does EMDR work? And if so, why? A critical review of controlled outcome and dismantling research. J Anxiety Disord. 1999;13:5-33.
21. Bradley R, Greene J, Russ E, et al. A multidimensional meta-analysis of psychotherapy for PTSD. Am J Psychiatry. 2005;162:214-227.
22. Cahill SP, Rauch SA, Hembree EA, Foa EB. Effect of cognitive behavioral treatment for PTSD on anger. J Cognitive Psychother. 2003;17:113-131.
23. Kubany ES, Hill EE, Owens JA. Cognitive trauma therapy for battered women with PTSD: preliminary findings. J Traumatic Stress. 2003;16:81-91.
24. Becker, Becker CB, Zayfert C, Anderson E. A survey of psychologists' attitudes towards and utilization of exposure therapy for PTSD. Behav Res Ther. 2004;42:277-292.
25. Marks I, Lovell K, Noshirvani H, et al. Treatment of posttraumatic stress disorder by exposure and/or cognitive restructuring. Arch Gen Psychiatry. 1998;55:317-325.
26. Paunovic N, Ost LG. Cognitive-behavior therapy vs exposure therapy in the treatment of PTSD in refugees. Behav Res Ther. 2001;39:1183-1197.
27. Foa EB, Hembree EA, Cahill SP, et al. Randomized trial of prolonged exposure for PTSD with and without cognitive restructuring: outcome at academic and community clinics. J Consult Clin Psychol. 2005;73:953-964. 28. Bryant RA, Moulds ML, Guthrie RM, et al. Imaginal exposure alone and imaginal exposure with cognitive restructuring in treatment of posttraumatic stress disorder. J Consult Clin Psychol. 2003;71:706-712.
29. Brady K, Pearlstein T, Asnis GM, et al. Efficacy and safety of sertraline treatment of posttraumatic stress disorder. JAMA. 2000;283:1837-1844.
30. Davidson JRT, Rothbaum BO, van der Kolk BA, et al. Multicenter, double-blind comparison of sertraline and placebo in the treatment of posttraumatic stress disorder. Arch Gen Psychiatry. 2001;58:485-492.
31. Marshall RD, Beebe KL, Oldham M, Zaninelli R. Efficacy and safety of paroxetine treatment of chronic PTSD: a fixed-dose, placebo-controlled study. Am J Psychiatry. 2001;158:1982-1988.
32. Tucker P, Zaninelli R, Yehuda R, et al. Paroxetine in the treatment of chronic posttraumatic stress disorder: results of a placebo-controlled, flexible-dosage trial. J Clin Psychiatry. 2001;62:860-868.
33. Rothbaum BO, Cahill SP, Foa EB, et al. Augmentation of sertraline with prolonged exposure in the treatment of PTSD. J Traumatic Stress. 2006;19:625-638.
34. Cahill SP, Hembree EA, Foa EB. Dissemination of prolonged exposure therapy for posttraumatic stress disorder: successes and challenges. In: Neria Y, Gross R, Marshall R, Susser E, eds. 9/11:Mental Health in the Wake of Terrorist Attacks. Cambridge, United Kingdom: Cambridge University Press; 2006:475-495.
35. Cahill SP, Foa EB, Hembree EA, et al. Dissemination of exposure therapy in the treatment of PTSD. J Traumatic Stress. 2006;19:597-610.