More threads by David Baxter PhD

David Baxter PhD

Late Founder
Fibromyalgia Syndrome: A Role for Sexual Abuse and Other Traumatic Events?
by Karen G. Raphael, Ph.D.
Primary Psychiatry. 2006;13(9):61-65

Although numerous studies and some reviews contend that fibromyalgia syndrome (FMS) may be caused by sexual and physical abuse and other forms of psychologically traumatic stress, this article does not support such a conclusion. Many studies have methodologic problems that preclude conclusions about the relationship between traumatic stress and FMS onset. Further, existing data suggest that a better explanation of the association between FMS and traumatic stress is that individuals with FMS have a dysregulated physiologic stress response system that may predate the onset of symptoms. Thus, individuals characterized by biologic ?stress vulnerability,? are at increased risk not only for FMS, but for posttraumatic stress disorder and possibly other psychiatric disorders associated with life stress as well.

Traumatic events and associated psychological factors are often invoked for conditions in which pathogenesis is unknown. At least one article on emotional trauma and abuse1, including physical and sexual victimization, suggests that these factors are of etiologic importance in the development of fibromyalgia syndrome (FMS) and that, therefore, FMS may be viewed as a stress disorder. This article critically reviews the evidence linking traumatic life events and psychosocial stressors, including sexual abuse, to the onset of FMS. Focus is placed on events that are presumed to exert their primary impact through psychological trauma and the cascade of physiologic alterations in response to psychological stressors, rather than through physical trauma directly affecting peripheral nociceptive input. (For further coverage, see Staud in this issue.2

Sexual and Physical Abuse
To a limited extent, a first glance at studies on the topic seems to support a role for psychologically traumatic events in the pathogenesis of FMS. The most commonly investigated traumatic events are sexual or physical abuse in childhood or adulthood. Several studies, using either self-report questionnaires3 or interviews4,5 to assess abuse history suggest that patients with FMS report elevated rates of lifetime physical abuse and sexual abuse,3 overall victimization,4 and childhood adversities,5 compared to patients with medically explained pain5 or other rheumatic disease.3,4 Nevertheless, another questionnaire-based study6 reached different conclusions. Contrasting a small sample of FMS patients with a convenience sample drawn from multiple sources, the groups did not significantly differ in self-reported history of lifetime sexual abuse. A more recent and larger study7 using a similar questionnaire found that frequency of reported abuse in childhood and adulthood was higher in FMS patients than those with soft tissue rheumatic disease or healthy volunteers, but not higher than among patients with rheumatoid arthritis. Finally, another study8 compared questionnaire-assessed history of childhood trauma among patients with FMS and three other pain disorders, concluding that rates of childhood abuse did not differ among the groups. However, if FMS patients were contrasted with a combined sample of other pain disorders, reanalysis of their data indicates that FMS patients were significantly more likely than non-FMS pain patients to report childhood abuse histories.

In a study contrasting a combined sample of patients with either FMS or chronic fatigue syndrome (CFS), among whom 43% met American College of Rheumatology (ACR) criteria for FMS, findings were also mixed.9 Assessing history of physical or sexual abuse through a brief self-report questionnaire, FMS/CFS patients did not report higher rates of sexual abuse or harassment than a medical control sample with either multiple sclerosis or rheumatoid arthritis or than a healthy control group. Physical abuse reports also did not differ between the FMS/CFS group and the medical control sample, but were higher in the FMS/CFS group than among controls. Using broader definitions of emotional neglect or abuse, group differences in the predicted direction were found.

Thus, case-control studies comparing patients with FMS to other pain patients or healthy controls sometimes, but not always, conclude that FMS patients have elevated reports of sexual and physical abuse either in childhood, adulthood, or both. The fact that there are negative findings in some studies indicates that these associations are not particularly large or robust. This conclusion is consistent with conclusions regarding the probable small relationship, if any, between childhood victimization and pain in adulthood in general.10

A somewhat different research approach was used by Finestone and colleagues,11 who compared women attending a therapy group for victims of childhood sexual abuse to a combined control sample of psychiatric patients who did not report abuse histories to nurses. The former group was more likely than the control group to report that they had received a diagnosis of FMS. Those reporting childhood sexual abuse also indicated much greater medical resource utilization than controls.

Methodologic Problems in the Research on Traumatic Abuse and Fibromyalgia Syndrome
In light of the findings of Finestone and colleagues,11 an important problem is illustrated. Specifically, receiving a diagnosis of FMS is highly selective and is likely dependent on the extent of health care that a symptomatic individual pursues. Although it has been shown that receiving the diagnostic label of FMS does not have a major negative effect on long-term clinical outcome,12 only a very small proportion of those in the community who meet ACR criteria for FMS report ever receiving the diagnosis (ie, 28% and 12% in studies by White and colleagues12 and Raphael and colleagues,13 respectively). Moreover, diagnosis of FMS is much more likely to be made by a tertiary care rather than primary care physician.14 Thus, elevated rates of receiving FMS diagnoses among those reporting a history of childhood abuse may have been secondary to the increased healthcare utilization of that group, rather than representing a group increase in rates of those who more often met syndromal status for FMS per se.

Similar concerns about the problem of biased sampling have been reached in a study by Alexander and colleagues,15 which compared abuse histories of FMS patients to FMS ?nonpatients,? who were defined as individuals who met ACR criteria for FMS but who had not sought care for their symptoms. Finding that abuse histories were not significantly higher in FMS nonpatients than controls, they concluded that sexual and physical abuse histories in FMS are associated with healthcare seeking rather than the syndrome of FMS itself. Given research showing that those reporting a history of victimization have greater healthcare utilization for other pain conditions as well,16-18 clinicians assessing their patients for a history of abuse and even studies recruiting care-seeking patients may suffer from a so-called ?clinician?s illusion?19 in which some clinicians invariably treat and researchers usually study an unrepresentative group of individuals with a given syndrome (ie, individuals who have symptoms of longer duration and whose pattern of healthcare seeking has led them to receive a specialized diagnostic label).

Use of a community sample of individuals with FMS mitigates the sampling bias problem. A recent article by Ciccone and colleagues20 examined lifetime sexual and physical abuse histories in a community sample of women who met ACR criteria for FMS. Compared to community women without FMS, self-reported sexual and physical abuse histories were not elevated among women with FMS. Although women with FMS were more than 3 times as likely as control women to report having been raped, no other specific traumatic event differed between groups. Since this study did not record the date of the rape event, the finding of elevations in rape histories among women with FMS is subject to multiple interpretations, including the possibility that rape events caused temporary or even prolonged increases in nociceptive input, rather than being associated with psychological trauma per se. Similar associations between adult rape and FMS, and adult physical assault in general and FMS, have been reported in a tertiary care sample.4

Combining Ciccone and colleagues?20 overall negative findings with the findings of Alexander and colleagues15 in their study of nonpatients with FMS, it seems likely that prior studies reporting elevated rates of abuse histories in FMS patients overestimated the relationship by focusing on biased, care-seeking samples of individuals with FMS.

The second major weakness of all the studies reviewed to date is their reliance on self-report of physical or sexual abuse. Reliance on retrospective reports of abuse has been criticized, as retrospective report of childhood trauma is marked by poor recall21,22 and unreliability.23 Traumatic events of all types tend to be unreliably reported,24 especially when using typical questionnaire methods.25 Although simple unreliability in recalling earlier traumatic events would lead to an underestimate of the relationship between FMS and abuse, more insidious is the problem of recall bias. Recall bias,26 in which individuals with an unexplained illness such as FMS exert more effort to recall prior life events than healthier individuals, or in which ill and inevitably distressed individuals recall prior experiences in a mood-congruent way,27 can inflate the true relationship between FMS and abuse. As Widom and colleagues28 conclude, ?recall bias in retrospective studies can wreak havoc with measures of association and conclusions about possible relationships between child maltreatment and health in adulthood.?

Fortunately, the problem of recall bias is not an issue for two prospective studies29,30 that have tested the relationship between court-documented abuse in childhood and pain in adulthood. Although neither was designed to focus specifically on FMS or widespread pain consistent with FMS, an analog of this examination was performed in the former study,29 which failed to find any relationship between the number of medically unexplained painful body sites and documented abuse. Interestingly, and consistent with some of the earlier case-control studies, both found a relationship between self-reported childhood abuse histories and pain in adulthood. In any case, the discrepant conclusions arising when focusing on court-documented versus self-reported abuse fails to inspire confidence in the relationship between childhood abuse and pain in adulthood. Notably, such discrepancies are not found for some other health outcomes.31-34 For example, self-report and court-documented abuse records both confirm a relationship between childhood abuse and posttraumatic stress disorder (PTSD).34 Thus, the relationship between true childhood victimization and adult health is clearly less dramatic, less robust, or nonexistent for pain syndromes and symptoms compared to a variety of other adult health outcomes.

Posttraumatic Stress Disorder
The comorbidity between FMS and PTSD has been documented in studies assessing PTSD through both standardized structured questionnaires35,36 and psychiatric examination.37 This association does not appear to be an artifact of selection bias, as a more recent study confirmed the comorbidity for FMS and psychiatric interviewer-assessed PTSD in a community sample.13

Finding high rates of PTSD in FMS but no convincing increase in rates of exposure to psychologically traumatic events in FMS may seem, at first, hard to reconcile. Another apparent contradiction lies in findings from a community study that did not find new onsets of FMS to be increased following exposure to the World Trade Center terrorist attacks of 2001,38 even though that study and other studies39 found high community rates of PTSD symptoms following the attacks. A second study also failed to find changes in pain symptoms following the terrorist attacks of 2001, in a clinic sample of FMS patients.40 Admittedly, such findings contradict a general conclusion41 that medically unexplained physical symptoms increase following community-level disasters, but prevalence rates of specific unexplained symptoms may vary greatly in response to disaster.

In a report of separate analyses, which found that women with FMS symptoms were at increased risk for new PTSD following the September 11th terrorist attacks,42 despite the fact that onsets of FMS symptoms were unrelated to such traumatic exposures,38 Raphael and colleagues42 suggested:

Women with [FMS] are at risk for PTSD because they have a biological or constitutional propensity for PTSD, not because they are exposed to more traumatic events than other women. Thus, when confronted with a fixed number or fixed magnitude of traumatic events, women with [FMS] are more vulnerable to PTSD than are other women...This hypothesis is consistent with the view of [FMS] as part of [a]...spectrum which there is shared constitutional risk to several syndromes, including major depression, PTSD, and [FMS].​

This view is consistent with views of Yehuda,43 one of the leading researchers in PTSD, who remarks that PTSD is best conceived as an extreme response to common stressful events rather than a common response to inherently traumatic events. Major stressful events are much more common in the community than are diagnoses of PTSD. Thus, syndromes such as PTSD and FMS would be better characterized as indicative of disorders of ?stress vulnerability? rather than ?stress disorders.?

Stress Vulnerability and FMS
Given that very few individuals exposed to traumatic stress develop FMS or even disorders like PTSD, which is linked nominally to stress, the principal causal variable may lie in individual predispositions rather than exposure to environmental stressors.

Dysfunctions in aspects of physiologic stress response systems have been well-documented in FMS.44-46 Similar dysfunctions have been documented in PTSD.47,48 Much of this research is ambiguous with regard to cause and effect, because studies almost always accrue chronic patients. However, two recent studies may provide stronger evidence for the view that abnormalities in the stress response system are an antecedent of FMS. In the first prospective study,49 perturbations involving the hypothalamic-pituitary-adrenal (HPA) axis and the autonomic nervous system predicted which individuals developed symptoms involving pain and other medically unexplained symptoms after brief exercise cessation. The authors specifically suggest that a variety of stressors, including psychological traumas, may trigger a change in lifestyle (eg, sleep disruption and exercise cessation) that may in turn contribute to symptom development in those with antecedent abnormalities of the stress response system. In the second study,50 individuals who were free of chronic widespread pain but who were judged to be at high risk of developing it based on earlier research51 showed disturbances in HPA function. While these data suggest that HPA axis dysfunction may precede the development of FMS, studies involving follow-up with at-risk individuals are needed to confirm the causal implications of these intriguing findings.

It should be acknowledged that living with pain is itself likely to be a powerful and ongoing stressor for those with chronic FMS. Indeed, momentary variation in pain severity relates to salivary cortisol levels in FMS.52 Thus, the stress of living with chronic pain may further exacerbate HPA axis dysfunction in already vulnerable individuals.

The literature reporting HPA axis dysregulation as a function of childhood trauma53 should be acknowledged, as such findings are consistent with an alternative view that HPA axis perturbations, which appear to antedate FMS symptom onset, are themselves a consequence of earlier childhood victimization. While this alternate view of the causes and consequences of HPA axis alterations in FMS is theoretically possible, the weak evidence for an overall relationship between early childhood victimization and pain in adulthood renders it an improbable explanation.

Furthermore, the probability that that HPA axis dysfunction predates the onset of FMS symptoms but is independent of early abuse experiences is supported by genetic research on FMS. A familial disorder, studies have suggested that FMS is associated with a variety of genetic polymorphisms in genes encoding for serotoninergic and catecholaminergic systems relevant to physiologic stress-response systems.54 Some of the same gene regions identified in studies of FMS55,56 have been identified in studies of depression, another syndrome that may involve stress vulnerability,57 and suggest a genetic explanation for familial aggregation of depression in FMS.58,59 Clearly, genetic risks predate even the earliest exposures to environmental stressors. Thus, the ?trait? of stress vulnerability may combine with the stressful ?state? of the individual living with painful FMS, to influence HPA axis dysfunction.

While this article suggests that stress vulnerability is likely to be important in the pathogenesis of FMS rather than early stressful exposures per se, a final caution must be added. The search for cause of a complex syndrome, whose very case definition rests on a single validation study designed to operationalize diagnostic views of expert clinicians,60 is unlikely to be resolved with a single answer. As Merskey61 notes, ?monism of experience cannot and does not translate into singularity of causes.? Stress vulnerability alone may ultimately explain the onset of FMS for only a subset of sufferers, but this conceptualization may be valuable if it advances treatment of this poorly understood disorder for even a few individuals.

David Baxter PhD

Late Founder
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2. Staud R. Fibromyalgia syndrome: mechanisms of abnormal pain processing. Primary Psychiatry. 2006;13(9):66-71.

3. Boisset-Pioro MH, Esdaile JM, Fitzcharles MA. Sexual and physical abuse in women with fibromyalgia syndrome. Arthritis Rheum. 1995;38(2):235-241.

4. Walker EA, Keegan D, Gardner G, Sullivan M, Bernstein D, Katon WJ. Psychosocial factors in fibromyalgia compared with rheumatoid arthritis: II. Sexual, physical, and emotional abuse and neglect. Psychosom Med. 1997;59(6):572-577.

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6. Taylor ML, Trotter DR, Csuka ME. The prevalence of sexual abuse in women with fibromyalgia. Arthritis Rheum. 1995;38(2):229-234.

7. Castro I, Barrantes F, Tuna M, et al. Prevalence of abuse in fibromyalgia and other rheumatic disorders at a specialized clinic in rheumatic diseases in Guatemala City. J Clin Rheumatol. 2005;11(3):140-145.

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9. Van Houdenhove B, Neerinckx E, Lysens R, et al. Victimization in chronic fatigue syndrome and fibromyalgia in tertiary care: a controlled study on prevalence and characteristics. Psychosomatics. 2001;42(1):21-28.

10. Raphael KG, Chandler HK, Ciccone DS. Is childhood abuse a risk factor for chronic pain in adulthood? Curr Pain Headache Rep. 2004;8(2):99-110.

11. Finestone HM, Stenn P, Davies F, Stalker C, Fry R, Koumanis J. Chronic pain and health care utilization in women with a history of childhood sexual abuse. Child Abuse Negl. 2000;24(4):547-556.

12. White KP, Nielson WR, Harth M, Ostbye T, Speechley M. Does the label “fibromyalgia” alter health status, function, and health service utilization? A prospective, within-group comparison in a community cohort of adults with chronic widespread pain. Arthritis Rheum. 2002;47(3):260-265.

13. Raphael KG, Janal MN, Nayak S, Schwartz JE, Gallagher RM. Psychiatric comorbidities in a community sample of women with fibromyalgia. Pain. In press.

14. Gamez-Nava JI, Gonzalez-Lopez L, Davis P, Suarez-Almazor ME. Referral and diagnosis of common rheumatic diseases by primary care physicians. Brit J Rheumatol. 1998;37(11):1215-1219.

15. Alexander RW, Bradley LA, Alarcon GS, et al. Sexual and physical abuse in women with fibromyalgia: association with outpatient health care utilization and pain medication usage. Arthritis Care Res. 1998;11(2):102-115.

16. Biggs AM, Aziz Q, Tomenson B, Creed F. Do childhood adversity and recent social stress predict health care use in patients presenting with upper abdominal or chest pain? Psychosom Med. 2003;65(6):1020-1028.

17. Drossman DA, Leserman J, Nachman G, et al. Sexual and physical abuse in women with functional or organic gastrointestinal disorders. Ann Intern Med. 1990;113(11):828-833.

18. Leserman J, Li Z, Drossman DA, Hu YJ. Selected symptoms associated with sexual and physical abuse history among female patients with gastrointestinal disorders: the impact on subsequent health care visits. Psychol Med. 1998;28(2):417-425.

19. Cohen P, Cohen J. The clinician’s illusion. Arch Gen Psychiatry. 1984;41(12):1178-1182.

20. Ciccone DS, Elliott DK, Chandler HK, Nayak S, Raphael KG. Sexual and physical abuse in women with fibromyalgia syndrome: a test of the trauma hypothesis. Clin J Pain. 2005;21(5):378-386.

21. Williams LM. Recall of childhood trauma: a prospective study of women’s memories of child sexual abuse. J Consult Clin Psychol. 1994;62(6):1167-1176. Erratum in: J Consult Clin Psychol. 1995;63(3):343.

22. Widom CS, Morris S. Accuracy of adult recollections of childhood victimization, Part 2: Childhood sexual abuse. Psychol Assess. 1997;9(1):34-46.

23. Fergusson DM, Horwood LJ, Woodward LJ. The stability of child abuse reports: a longitudinal study of the reporting behaviour of young adults. Psychol Med. 2000;30(3):529-544.

24. Hepp U, Gamma A, Milos G, et al. Inconsistency in reporting potentially traumatic events. Br J Psychiatry. 2006;188:278-283.

25. Raphael KG, Cloitre M, Dohrenwend BP. Problems of recall and misclassification with checklist methods of measuring stressful life events. Health Psychol. 1991;10(1):62-74.

26. Raphael K. Recall bias: a proposal for assessment and control. Int J Epidemiol. 1987;16(2):167-170.

27. Raphael KG, Cloitre M. Does mood-congruence or causal search govern recall bias? A test of life event recall. J Clin Epidemiol. 1994;47(5):555-564.

28. Widom CS, Raphael KG, DuMont KA. The case for prospective longitudinal studies in child maltreatment research: commentary on Dube, Williamson, Thompson, Felitti, and Anda (2004). Child Abuse Negl. 2004;28(7):715-722.

29. Raphael KG, Widom CS, Lange G. Childhood victimization and pain in adulthood: a prospective investigation. Pain. 2001;92(1-2):283-293.

30. Brown J, Berenson K, Cohen P. Documented and self-reported child abuse and adult pain in a community sample. Clin J Pain. 2005;21(5):374-377.

31. Luntz BK, Widom CS. Antisocial personality disorder in abused and neglected children grown up. Am J Psychiatry. 1994;151(5):670-674.

32. Perez CM, Widom CS. Childhood victimization and long-term intellectual and academic outcomes. Child Abuse Negl. 1994;18(8):617-633.

33. Widom CS, Ireland T, Glynn PJ. Alcohol abuse in abused and neglected children followed-up: are they at increased risk? J Stud Alcohol. 1995;56(2):207-217.

34. Widom CS. Posttraumatic stress disorder in abused and neglected children grown up. Am J Psychiatry. 1999;156(8):1223-1229.

35. Sherman JJ, Turk DC, Okifuji A. Prevalence and impact of posttraumatic stress disorder-like symptoms on patients with fibromyalgia syndrome. Clin J Pain. 2000;16(2):127-134.

36. Cohen H, Neumann L, Haiman Y, Matar MA, Press J, Buskila D. Prevalence of post-traumatic stress disorder in fibromyalgia patients: overlapping syndromes or post-traumatic fibromyalgia syndrome? Semin Arthritis Rheum. 2002;32(1):38-50.

37. Roy-Byrne P, Smith WR, Goldberg J, Afari N, Buchwald D. Post-traumatic stress disorder among patients with chronic pain and chronic fatigue. Psychol Med. 2004;34(2):363-368.

38. Raphael KG, Natelson BH, Janal MN, Nayak S. A community-based survey of fibromyalgia-like pain complaints following the World Trade Center terrorist attacks. Pain. 2002;100(1-2):131-139.

39. Galea S, Ahern J, Resnick H, et al. Psychological sequelae of the September 11 terrorist attacks in New York City. N Engl J Med. 2002;346(13):982-987.

40. Williams DA, Brown SC, Clauw DJ, Gendreau RM. Self-reported symptoms before and after September 11 in patients with fibromyalgia. JAMA. 2003;289(13):1637-1638.

41. van den Berg B, Grievink L, Yzermans J, Lebret E. Medically unexplained physical symptoms in the aftermath of disasters. Epidemiol Rev. 2005;27:92-106.

42. Raphael KG, Janal MN, Nayak S. Comorbidity of fibromyalgia and posttraumatic stress disorder symptoms in a community sample of women. Pain Med. 2004;5(1):33-41.

43. Yehuda R, McFarlane AC. Conflict between current knowledge about posttraumatic stress disorder and its original conceptual basis. Am J Psychiatry. 1995;152(12):1705-1713.

44. Crofford LJ. The hypothalamic-pituitary-adrenal stress axis in fibromyalgia and chronic fatigue syndrome. Z Rheumatol. 1998;57(suppl 2):67-71.

45. Crofford LJ, Demitrack MA. Evidence that abnormalities of central neurohormonal systems are key to understanding fibromyalgia and chronic fatigue syndrome. Rheum Dis Clin North America. 1996;22(2):267-284.

46. Spaeth M. Fibromyalgia syndrome: the role of neurochemicals. Primary Psychiatry. 2006;13(9):72-75.

47. Yehuda R. Biology of posttraumatic stress disorder. J Clin Psychiatry. 2001;62(suppl 17):41-46.

48. Ehlert U, Gaab J, Heinrichs M. Psychoneuroendocrinological contributions to the etiology of depression, posttraumatic stress disorder, and stress-related bodily disorders: the role of the hypothalamus-pituitary-adrenal axis. Biol Psychol. 2001;57(1-3):141-152.

49. Glass JM, Lyden AK, Petzke F, et al. The effect of brief exercise cessation on pain, fatigue, and mood symptom development in healthy, fit individuals. J Psychosom Res. 2004;57(4):391-398.

50. McBeth J, Chiu YH, Silman AJ, et al. Hypothalamic-pituitary-adrenal stress axis function and the relationship with chronic widespread pain and its antecedents. Arthritis Res Ther. 2005;7(5):R992-R1000.

51. McBeth J, Macfarlane GJ, Benjamin S, Silman AJ. Features of somatization predict the onset of chronic widespread pain: results of a large population-based study. Arthritis Rheum. 2001;44(4):940-946.

52. McLean SA, Williams DA, Harris RE, et al. Momentary relationship between cortisol secretion and symptoms in patients with fibromyalgia. Arthritis Rheum. 2005;52(11):3660-3669.

53. Bevans K, Cerbone AB, Overstreet S. Advances and future directions in the study of children’s neurobiological responses to trauma and violence exposure. J Interpers Violence. 2005;20(4):418-425.

54. Buskila D, Neumann L. Genetics of fibromyalgia. Curr Pain Headache Rep. 2005;9(5):313-315.

55. Ebstein RP, Buskila D, Cohen H, Neumann L. An association between FMS and the serotonin transporter promoter region (5-HTTLPR) polymorphism and relationship to anxiety-related personality traits. Am J Med Genet. 2001;105(7):627.

56. Offenbaecher M, Bondy B, de Jonge S, et al. Possible association of fibromyalgia with a polymorphism in the serotonin transporter gene regulatory region. Arthritis Rheum. 1999;42(11):2482-2488.

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58. Arnold LM, Hudson JI, Hess EV, et al. Family study of fibromyalgia. Arthritis Rheum. 2004;50(3):944-952.

59. Raphael KG, Janal MN, Nayak S, Gallagher RM, Schwartz JE. Familial aggregation of depression in fibromyalgia: a community-based test of alternate hypotheses. Pain. 2004;110(1-2):449-460.

60. Wolfe F, Smythe HA, Yunus MB, et al. The American College of Rheumatology 1990 Criteria for the Classification of Fibromyalgia. Report of the Multicenter Criteria Committee. Arthritis Rheum. 1990;33(2):160-172.

61. Merskey H. Distortion of the biopsychosocial approach. Pain. 2005;113(2):240-242.

Dr. Raphael is associate professor in the Departments of Psychiatry and Diagnostic Sciences at the University of Medicine and Dentistry of New Jersey in Newark.

Please direct all correspondence to: Karen G. Raphael, PhD, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, 183 S. Orange Ave, BHSB F1512, P.O. Box 1709, Newark, NJ 07101-1709; Tel: 973-972-5462; Fax: 973-972-8305; E-mail:


have to say that while the title of this article did interest me.. i quickly lost interest because i found it more professional typeperson orientated and way toolong.. as well as my usual not understanding some of the terms.

sorry to be critical of this.. but to me it's def not a laymans article.



... existing data suggest that a better explanation of the association between FMS and traumatic stress is that individuals with FMS have a dysregulated physiologic stress response system that may predate the onset of symptoms. Thus, individuals characterized by biologic ?stress vulnerability,? are at increased risk not only for FMS, but for posttraumatic stress disorder and possibly other psychiatric disorders

I would guess, from my unprofessional standpoint and just based on personal opinion, that stress vulnerability/sensitivity does predate the "triggering" of these disorders. Like, they wouldn't manifest without a vulnerability in place first before they are able to manifest/happen, and something has to come along to add to the vulnerability to create a manifestation of fibro or ptsd or or or ...

On the other hand, I also think that vulnerability can be created through physical and/or pysiological (correct word?) changes to the brain due to extreme trauma or injury and effect its function and vulnerability.

Just my opinions here, and in the end, I guess a lot more studies and "proof/evidence" is needed in these areas ;)

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