REVIEW OF POST-TRAUMATIC STRESS DISORDER
There is a growing body of research revealing relationships between injury, pain, and psychological trauma with important implications for the prevention and management of chronic pain and post-traumatic reactions. This chapter will review findings from recent research in consideration of relevant theoretical models between post-traumatic stress disorder (PTSD) and pain in general and more specifically in the case of pain resulting from whiplash injury. A review of emerging interventions and prevention options for PTSD in individuals with whiplash will also be discussed to provide a basis for treatment of individuals and future research.
Diagnosis, Prevalence, Course, Impact
PTSD arises when a person experiences a traumatic event and goes on to develop symptoms of reexperiencing the event, avoidance of trauma stimuli and persistent symptoms of increased arousal.1 PTSD is specified as acute when the symptoms persist from 1-month to 3-months after the traumatic event and Chronic PTSD is specified when symptoms persist for 3-months or more.
In Australia, about 65% of men and 50% of women are exposed to a potentially traumatic event in their lifetime.2,3 Data from the 2007 National Survey of Mental Health and Wellbeing4 indicated that 12.2% met criteria for a lifetime diagnosis of PTSD and 6.4% met criteria for PTSD in the 12 months before the interview.
Development of PTSD most likely depends on a complex interaction between preexisting, pretraumatic and postevent variables that determine risk and resilience to the disorder.5,6 What distinguishes the symptoms as pathological are their intensity, frequency and duration (greater than 1 month for PTSD), as well as the degree of impairment the symptoms cause, indicating a failure of stress adaption.7,8 Epidemiological studies clearly indicate that PTSD is becoming a major health concern worldwide as it is generally poorly diagnosed and treated and provokes significant occupational, psychiatric, medical and psychosocial disability and costs to survivors, their families and society.9,10
Association With Arousal
Early research into predictors of PTSD found that the degree of physiological arousal, particularly cardiovascular reactivity, initially experienced by an individual soon after a traumatic event strongly predicted the development of chronic PTSD.11,12 PTSD has also been associated with increased sympathetic activity (elevated heart rate, galvanic skin response and blood pressure and low frequency components of heart rate variability) at baseline compared to individuals with panic disorder and normal controls.13 It has been argued that it is the “timeless” quality of such physiological reactivity14 that creates the perception of current threat.15
Association With Pain
In the past decade, research has begun to focus on the potential shared neurobiological pathways between PTSD and pain.16,17 Some studies report that individuals with PTSD have a low pain threshold, lower b-endorphin levels, and decreased production and release of methionine enkephalin and stress-induced analgesia.18,19 Other studies demonstrated hypoalgesia (i.e., decreased sensitivity) to noxious stimuli20 and a hyperalgesic effect (i.e., increased pain sensitivity) to stimuli above the pain threshold.20,21 The ventral basal ganglia dopamine neurotransmitter system has been implicated in stress response, negative emotion, and pain regulation,22 suggesting that pain and the negative affect and stress associated with the response to trauma may share similar neurobiological mechanisms.
PTSD and Whiplash
In recent years research and clinical practice has begun to identify the comorbidity of PTSD and pain because of whiplash injury. Whiplash injury differs from most other musculoskeletal pain syndromes in that it is generally precipitated by a traumatic event, usually a motor vehicle crash (MVC). As discussed above, PTSD is also a common psychological sequelae of severe injuries after a MVC23 Yet, it is only recently that evidence has emerged to show that it may also play a role in less severe road accident injuries including whiplash.
Clinically significant PTSD-like symptoms have been found in more than 50% of patients receiving treatment for chronic pain after MVC24 with 14.6% of MVC survivors with chronic pain meeting full DSM-III criteria for current PTSD and a further 9.1% exhibiting PTSD in partial remission.23 With regard to individuals with persistent whiplash symptoms, at least 15% to 25% of patients meet diagnostic criteria for PTSD.25,26 Chronic pain has also been found to be common in patients with PTSD with 25% to 30% of outpatient samples with PTSD.27,28 Given these findings of high rates of comorbidity between PTSD and whiplash research has increasingly focused on identifying the mechanisms through which these disorders may increase risk and or maintain each other.
There has been an increasing recognition of a shared pattern of aetiology between whiplash and PTSD29 as similar abnormalities of the hypothalamic–pituitary–adrenal axis of enhanced negative feedback have been identified in these disorders.30,31 Also documented are stress-induced changes in neurogenesis and brain functioning,32,33 which play an important role in the onset of chronic widespread musculoskeletal pain.34 It has been hypothesized that PTSD symptoms impact on recovery from and maintenance of whiplash.
Evidence that PTSD symptoms may influence the course of whiplash symptoms was provided by Sterling et al35 in a study which revealed that early reexperiencing and avoidance post-traumatic stress symptoms where associated with relatively persistent whiplash complaints at 6-months follow-up.
A prospective study investigating changes during the acute phase of whiplash associate disorder (WAD) was conducted by Sterling et al.36 This study found that initial post-traumatic reactions were linked to greater pain symptoms over time. Importantly, trauma symptoms were able to differentiate patients with mild or abated whiplash symptoms at 6 months, who reported low, stable trauma scores, from patients who developed moderate to severe whiplash symptoms (reporting moderate elevations in initial trauma symptoms). This study highlights association between trauma experiences and chronic whiplash pain and emphasizes the fact that it is not so much exposure to a traumatic event that predicts chronic pain, but rather the individual's perception and response to such an experience.
A study by Buitenhuis et al37 aimed to further explore the relationship between PTSD symptoms and whiplash complaints over a 12 month follow-up and also included the hyperarousal symptom cluster which was not included in earlier research. In line with previous research, the study found that the presence of PTSD symptoms was associated with more severe whiplash complaints in individuals involved in a motor vehicle accident (MVC). Interestingly, this relationship was especially pronounced for the PTSD hyperarousal symptoms with the mean number of hyperarousal symptoms three to five times higher among participants with WAD at 6 and 12 months follow-up.
Buitenhuis et al37 suggested that the presence of symptoms of PTSD may be involved in the development of WAD in several ways. One way in which PTSD symptoms may influence the course of whiplash complaints is via the anxiety features of PTSD that may alter acute pain experiences and perception and physical complaints38 and thus lead to avoidance behaviors that facilitate a chronic course.39–41 Furthermore, anxiety-induced heightened vigilance may inflate the perception of pain.42 PTSD symptoms may also fuel a vulnerability to catastrophization of the physical sensations that accompany hyperarousal and are associated with pain. These sensations may subsequently be attributed to WAD or aggravate its symptoms.29,43–45 Finally, it is suggested that as PTSD shares several symptoms with acute whiplash syndrome, including insomnia, irritability, and cognitive problems, these symptoms may further intensify the perception of symptoms or lead to misattribution.37
Models of PTSD: Arousal and Pain
A number of theoretical models have drawn on and in some cases combined findings and models from both chronic pain and PTSD research to explore the biological, psychological, and social mechanisms for the development and maintenance of this comorbid pain and PTSD.
More recently, the exploration of the direct impact of PTSD on the experience of pain has become a focus of research and physiological arousal has been identified as a possible mechanism for this relationship. McLean et al17 propose that abnormal stress system function during and after a stressor may disrupt the neurobiological processes involved in adaptive stress responses and thus increase the risk of an individual's development of both PTSD and pain after a MVC. Extending and unifying cognitive-behavioral and biological theories McLean et al's model proposes that the acute physical (tissue damage) and emotional (responses to threat of accident and injury) effects of a MVC interact with an acute stress response. These in turn impact on central pain processing pathways that are highly sensitive to cognitive and emotional modulatory input. In cases where the stress system is dysregulated (due to genetic factors and prior traumatic experience), amplified pain signaling may occur and interact with post-MVC behaviors to produce further amplification and reverberating activity that becomes self-sustaining (see the McLean et al model for further details).17
McLean et al's model incorporates many of the factors identified in prior biopsychosocial theories of chronic pain development after injury and enhances the understanding of stress systems and CNS pain-modulating pathways. This model provides numerous specific, testable hypotheses regarding the complex interactions between central neurobiological processes and psychosocial factors during the transition from acute injury to chronic disorder. Further empirical research is required to assess the prediction that that various factors which predict vulnerability to PTSD in prospective studies may also predict vulnerability to WAD and longitudinal studies will be needed to examine the influence of central factors in the development of chronic WAD and PTSD and allow for evaluation of mediating factors to explore and validate the model. This research is likely to lead to more effective acute, post-trauma interventions to prevent development of both PTSD and chronic pain.
Data from a recent longitudinal study by Jenewein et al46 explored the directional relationships between PTSD and chronic pain in 323 survivors of accidents. Results of the study indicated a mutual maintenance of pain intensity and post-traumatic stress symptoms at 5-days postinjury but by 6-months postinjury (chronic stage), results indicated a significant unidirectional impact of PTSD symptoms on pain but not vice versa. Although this study did not specifically focus on whiplash injury, it provides indication that addressing PTSD symptoms in the chronic stage of WAD may allow for a beneficial effect on levels of pain and disability.
Intervention for PTSD in Whiplash
Patients with both PTSD and pain generally present more complicated clinical profiles than those with either disorder alone.43 In the past treatment implications and associations between pain and psychiatric disorders have focused on pharmacologic interventions.47 Findings from a recent clinical trial investigating the effectiveness of physical therapy for chronic whiplash found that individuals with moderate or greater PTSD symptoms showed no significant change in pain and disability levels.48 The authors of the study suggest that the physical and psychological interactions occurring in these patients are too complex to be addressed by physical treatment alone and highlight the need for the exploration of the relationships between physical and psychological factors that could assist in determining the nature and timing of various intervention forms. More recently, research has begun to assess the effectiveness of psychological treatments aimed at PTSD for individuals with comorbid pain, given the demonstrated effectiveness of these interventions in MVC related PTSD.49,50
There is general support for effectiveness of CBT in reducing PTSD symptoms in individuals with chronic pain.51,52 Mixed results have been found regarding the impact of trauma-focused CBT on pain variables with some studies reporting slight short-term reductions in pain at post-treatment and 4-month follow-up51 whereas other studies reported no unique advantage of CBT on physical functioning or pain severity.52
There has been limited research examining the impact of PTSD treatment in individuals with comorbid pain because of whiplash. In the only published study, Jaspers25 examined a case study of exposure based CBT for PTSD in a patient with chronic whiplash. Jaspers25 concluded that through alleviating the PTSD symptoms, the patient was able to cope more effectively with the chronic WAD complaints and argued that that psychotherapeutic treatment for patients with comorbid PTSD and whiplash should be aimed primarily at trauma not pain.
In a recent unpublished randomized control trial, Dunne et al53 allocated individuals with comorbid chronic pain due to Whiplash and PTSD to either CBT (n = 13) or a waitlist control (n = 13). Treatment effects were evaluated at 10 to 12 weeks and 6-month follow-up, using a structured clinical interview, self-report questionnaires and measures of physiological arousal and sensory pain thresholds. Results indicated clinically significant reductions in PTSD symptoms in the CBT group compared to the waitlist group at the postassessment. Further gains in the PTSD group were also noted at the follow-up. The treatment of PTSD was also associated with improvements in self-reported disability, physical, emotional and social functioning and reduced physiological reactivity to trauma cues, and a nonsignificant trend for change in sensory pain thresholds were observed between groups or over time. This study provides support for the effectiveness of trauma-focused CBT to target PTSD symptoms within chronic WAD. The finding that treatment of PTSD resulted in improvements in self-reported disability and quality of life with minimal changes in sensory pain thresholds highlights the complex and interrelating mechanisms that underlie both WAD and PTSD. As this research has been conducted on chronic whiplash, there is an urgent need to replicate these promising results in an acute whiplash sample.
PREVENTION AND EARLY INTERVENTION
Disclosure and Information
The most widely used approaches to prevention of traumatic stress involve disclosure of the circumstances of the trauma including thoughts and feelings. This approach sometimes called debriefing has been demonstrated as being at best ineffective, and at worst detrimental to recovery.54 It is unclear why this is the case however these approaches should generally be avoided. Simple information based approaches may hold more promise.55,56 Information-based prevention can be delivered in a variety of media and during face-to-face consultations by nonpsychologists during standard clinical exchanges. These approaches also have negligible costs attached to them.
A number of drugs have been identified as having possible prophylactic properties for traumatic stress. These include the beta-blocker propranolol,57 and opioids.58 The mechanisms of action are still unclear as if their efficacy. However it is likely that the mechanisms will involve influence of pain and/or arousal. Routine application in the acute post-trauma period is unlikely at this stage, however in certain situations such as burn injury there is a higher probability of use of opioids.58
An alternative to a prevention approach is to address the symptoms of traumatic stress as early as practicable. The work of Bryant59 has demonstrated the feasibility of this approach through a number of randomized controlled trials of early intervention for acute stress disorder, which is a partial precursor condition for PTSD. It might be possible that more “pared-down” interventions could be delivered concurrent with the treatment of acute whiplash in those at risk.
Post-traumatic stress plays an important role in a significant proportion of whiplash sufferers as its presence seems to deleteriously impact recovery. Thus the presence of post-traumatic stress should be assessed as part of the routine clinical assessment of whiplash. There is emerging evidence that treatment of post-traumatic stress in the context of whiplash has clinically significant impact on whiplash. On the basis of the evidence to date recommended clinical practice for chronic whiplash would be to treat, where present, post-traumatic stress before the whiplash. However, there is an urgent need to replicate and extend this work to acute whiplash.
- Post-traumatic stress occurs relatively frequently in the context of a whiplash injury.
- The most likely mechanisms for this co-occurrence relate to elevated arousal and pain-related distress.
- There is emerging evidence on effective intervention for post-traumatic stress in the context of whiplash, as well as some possible directions for preventative approaches.
1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th ed. (Text Revised edition) Washington, DC: American Psychiatric Association; 2000.
2. Creamer M, Burgess P, McFarlane AC. Post-traumatic stress disorder
: findings from the Australian National Survey of Mental Health and Well-being. Psychol Med. 2001;31:1237–47.
3. Kessler RC, Sonnega A, Bromet E, et al. Posttraumatic stress disorder in the National Comorbidity Survey. Arch Gen Psychiatry 1995;52:1048–60.
4. Australian Bureau of Statistics. National Survey of Mental Health and Wellbeing Summary of Results (ABS cat no. 43260)
. Canberra: ABS; 2008.
5. Brewin CR, Andrews B, Valentine JD. Meta-analysis of risk factors for posttraumatic stress disorder in trauma-exposed adults. J Consult Clin Psychol 2000;68:748–66.
6. Ozer EJ, Best SR, Lipsey TL, et al. Predictors of posttraumatic stress disorder and symptoms in adults: a meta-analysis. Psychol Bull 2003;129:52–73.
7. Blanchard EB, Hickling EJ, Barton KA, et al. One-year prospective follow-up of motor vehicle accident victims. Behav Res Ther 1996;34:775–86.
8. McFarlane AC. Traumatic stress in the 21st century. Aust N Z J Psychiatry 2000;34:896–902.
9. Brunello N, Davidson JRT, Deahl M, et al. Posttraumatic stress disorder: diagnosis and epidemiology, comorbidity and social consequences, biology and treatment. Neuropsychobiology 2001;43:150–62.
10. Chan AOM, Air TM, McFarlane AC. Posttraumatic stress disorder and its impact on the economic and health costs of motor vehicle accidents in South Australia. J Clin Psychiatry 2003;64:175–81.
11. Shalev AY, Rogel-Fuchs Y. Psychophysiology of the posttraumatic stress disorder: from sulfur fumes to behavioral genetics. Psychosom Med 1993;55:413–23.
12. Shalev AY, Freedman S, Peri T, et al. Prospective study of posttraumatic stress disorder and depression following trauma. Am J Psychiatry 1998;155:630–7.
13. Cohen H, Benjamin J, Geva AB, et al. Autonomic dysregulation in panic disorder and in post-traumatic stress disorder
: application of power spectrum analysis of heart rate variability at rest and in response to recollection of trauma or panic attacks. Psychiatry Res 2000;96:1–13.
14. Pitman RK, Orr SP, Shalev AY. Once bitten, twice shy: beyond the conditioning model of PTSD. Biol Psychiatry 1993;33:145–6.
15. Ehlers A, Clark DM. A cognitive model of posttraumatic stress disorder. Behav Res Ther 2000;38:319–45.
16. Asmundson GJG, Coons MJ, Taylor S, et al. PTSD and the experience of pain
: research and clinical implications of shared vulnerability and mutual maintenance models. Can J Psychiatry 2002;47:930–7.
17. McLean SA, Clauw DJ, Abelson JL, et al. The development of persistent pain
and psychological morbidity after motor vehicle collision: integrating the potential role of stress response systems into a biopsychosocial model. Psychosom Med 2005;67:783–90.
18. Friedman MJ. What might the psychobiology of posttraumatic stress disorder teach us about future approaches to pharmacotherapy? J Clin Psychiatry 2000;61 (Suppl 7):44–51.
19. Schwartz AC, Bradley R, Penza KM, et al. Pain
medication use among patients with posttraumatic stress disorder. Psychosomatics 2006;47:136–42.
20. Geuze E, Westenberg HGM, Jochims A, et al. Altered pain
processing in veterans with posttraumatic stress disorder. Arch Gen Psychiatry 2007;64:76–85.
21. Defrin R, Ginzburg K, Solomon Z, et al. Quantitative testing of pain
perception in subjects with PTSD—implications for the mechanism of the coexistence between PTSD and chronic pain
22. Scott DJ, Heitzeg MM, Koeppe RA, et al. Variations in the human pain
stress experience mediated by ventral and dorsal basal ganglia dopamine activity. J Neurosci 2006;26:10789–95.
23. Kuch K, Cox BJ, Evans R, et al. Phobias, panic, and pain
in 55 survivors of road vehicle accidents. J Anxiety Disord 1994;8:181–7.
24. Hickling EJ, Blanchard EB. Post-traumatic stress disorder
and motor vehicle accidents. J Anxiety Disord 1992;6:285–91.
25. Jaspers JPC. Whiplash
and post-traumatic stress disorder
. Disabil Rehabil 1998;20:397–404.
26. Mayou R, Bryant B. Psychiatry of whiplash
neck injury. Br J Psychiatry 2002;180:441–8.
27. Amir M, Kaplan Z, Neumann L, et al. Posttraumatic stress disorder, tenderness and fibromyalgia. J Psychosom Res 1997;42:607–13.
28. Beckham JC, Crawford AL, Feldman ME, et al. Chronic posttraumatic stress disorder and chronic pain
in Vietnam combat veterans. J Psychosom Res 1997;43:379–89.
29. McFarlane AC, Atchison M, Rafalowicz E, et al. Physical symptoms in post-traumatic stress disorder
. J Psychosom Res 1994;38:715–26.
30. Heim C, Ehlert U, Hellhammer DH. The potential role of hypocortisolism in the pathophysiology of stress-related bodily disorders. Psychoneuroendocrinology 2000;25:1–35.
31. Pillemer SR, Bradley LA, Crofford LJ, et al. The neuroscience and endocrinology of fibromyalgia. Arthritis Rheum 1997;40:1928–39.
32. Korte SM, Koolhaas JM, Wingfield JC, et al. The Darwinian concept of stress: benefits of allostasis and costs of allostatic load and the trade-offs in health and disease. Neurosci Biobehav Rev 2005;29:3–38.
33. McEwen BS. The neurobiology of stress: from serendipity to clinical relevance. Brain Res 2000;886:172–89.
34. McBeth J, Silman AJ, Gupta A, et al. Moderation of psychosocial risk factors through dysfunction of the hypothalamic–pituitary–adrenal stress axis in the onset of chronic widespread musculoskeletal pain
: findings of a population-based prospective cohort study. Arthritis Rheum 2007;56:360–71.
35. Sterling M, Kenardy J, Jull G, et al. The development of psychological changes following whiplash
36. Sterling M, Jull G, Vicenzino B, et al. Physical and psychological factors predict outcome following whiplash
37. Buitenhuis J, de Jong PJ, Jaspers JPC, et al. Relationship between posttraumatic stress disorder symptoms and the course of whiplash
complaints. J Psychosom Res 2006;61:681–9.
38. Chibnall JT, Duckro PN. Post-traumatic stress disorder
in chronic post-traumatic headache patients. Headache 1994;34:357–61.
39. Arntz A, De Jong P. Anxiety, attention and pain
. J Psychosom Res 1993;37:423–31.
40. Arntz A, Dreessen L, De Jong P. The influence of anxiety on pain
: attentional and attributional mediators. Pain
41. Vlaeyen JWS, Linton SJ. Fear-avoidance and its consequences in chronic musculoskeletal pain
: a state of the art. Pain
42. Roelofs J, Peters ML, Vlaeyen JWS. Selective attention for pain
-related information in healthy individuals: the role of pain
and fear. Eur J Pain
43. Barsky AJ, Borus JF. Functional somatic syndromes. Ann Intern Med 1999;130:910–21.
44. Hickling EJ, Blanchard EB. The International Handbook of Road Traffic Accidents & Psychological Trauma: Current Understanding, Treatment and Law. Vol. 412. New York: Elsevier Science; 1999.
45. Sharp TJ, Harvey AG. Chronic pain
and posttraumatic stress disorder: mutual maintenance? Clin Psychol Rev 2001;21:857–7.
46. Jenewein J, Wittmann L, Moergeli H, et al. Mutual influence of posttraumatic stress disorder symptoms and chronic pain
among injured accident survivors: a longitudinal study. J Trauma Stress 2009;22:540–8.
47. Stewart JW, McGrath PJ, Quitkin FM, et al. Treatment of atypical depression. In: Hippius H, Stefanis CN, Miller-Spahn F, eds. Research in Mood Disorders: An Update. Psychiatry in Progress Series. Vol. 1. Ashland: Hogrefe & Huber Publishers; 1994:125–31.
48. Jull G, Sterling M, Kenardy J, et al. Does the presence of sensory hypersensitivity influence outcomes of physical rehabilitation for chronic whiplash
?—A preliminary RCT. Pain
49. Blanchard EB, Hickling EJ, Malta LS, et al. Prediction of response to psychological treatment among motor vehicle accident survivors with PTSD. Behav Ther 2003;34:351–63.
50. Ehlers A, Clark DM, Hackmann A, et al. A randomized controlled trial of cognitive therapy, a self-help booklet, and repeated assessments as early interventions for posttraumatic stress disorder. Arch Gen Psychiatry 2003;60:1024–32.
51. Beck JG, Coffey SF, Foy DW, et al. Group cognitive behavior therapy for chronic posttraumatic stress disorder: an initial randomized pilot study. Behav Ther 2009;40:82–92.
52. Wald J, Taylor S, Chiri LR, et al. Posttraumatic stress disorder and chronic pain
arising from motor vehicle accidents: efficacy of interoceptive exposure plus trauma-related exposure therapy. Cogn Behav Ther 2010;39:104–13.
53. Dunne RL, Kenardy J, Sterling M. A Randomised Control Trial of Cognitive Behavioural Therapy for the Treatment of PTSD in the Context of Chronic Whiplash
. Brisbane: University of Queensland; 2011.
54. Kenardy J. The current status of psychological debriefing. Br Med J 2000;321:1032–3.
55. Kenardy J, Piercy JA. Effect of information provision on trauma symptoms following therapeutic writing. Aust Psychol 2006;41:205–12.
56. Kenardy J, Thompson K, Le Brocque R, et al. Information–provision intervention for children and their parents following pediatric accidental injury. Eur Child Adolesc Psychiatry 2008;17:316–25.
57. Pitman RK, Sanders KM, Zusman RM, et al. Pilot study of secondary prevention of posttraumatic stress disorder with propranolol. Biol Psychiatry 2002;51:189–92.
58. Saxe G, Stoddard F, Courtney D, et al. Relationship between acute morphine and the course of PTSD in children with burns. J Am Acad Child Adolesc Psychiatry 2001;40:915–21.
59. Bryant RA, Harvey AG. Acute Stress Disorder: A Handbook of Theory, Assessment and Treatment. Washington, DC: American Psychological Association; 2000.