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Judicial Evaluation of Traumatically Induced Fibromyalgia

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Notes

  1. See Vargas v. Lee, 317 F.3d 498 (5th Cir. 2003).

  2. See Jones v. Conrad, 2001 WL 1001083 (Ohio App. Sept 4, 2001).

  3. See Black v. Food Lion, 171 F.3d 308 (5th Cir. 1999).

  4. See Alder v. Bayer, 61 P.3d 1068 (Utah 2002).

  5. See Gross v. King David Bistro, Inc., 83 F. Supp. 2d 597 (D. Md. 2000).

  6. See Minner v. American Mortgage & Guaranty Co., 791 A.2d 826 (Del. Cty. Ct. 2000).

  7. Id. at 469.

  8. Id. at 468.

  9. Most texts and treatises note the possible link between trauma (of various forms) and fibromyalgia but still conclude that the causes of fibromyalgia remain uncertain. The court’s comment in Reichert v. Phipps, 84 P.3d 353, 363 (Wyo. 2004) is illustrative: “Although scientists acknowledge the potential for a link, they consistently indicate that such a cause-effect connection has not been scientifically established.”

  10. See Robert W. Teasdell & Harold Merskey, The Quebec Task Force on Whiplash-Associated Disorders and the British Columbia Whiplash Initiative: A Study of Insurance Industry Initiatives, 4 Pain Research & Management 141 (1999).

  11. See Muhammad B. Yunus et al., Fibromyalgia Consensus Report: Additional Comments, 3 J. Clinical Rheumatology 324 (1997). The “biologic plausibility” of a link between trauma and fibromyalgia is discussed more fully in Michael Finch, Law and the Problem of Pain, 74 U. Cin. L. Rev. 285, 325–26 (2006) (discussing the emerging biological model of chronic pain as the product of abnormalities in the central nervous system which can be activated by disease and trauma).

  12. See Anil Kumar Jain et al., Fibromyalgia Syndrome: Canadian Clinical Working Case Definition, Diagnostic and Treatment Protocols B A Consensus Document, 11 J. Musculoskeletal Pain 3, 44–45 (2003) (“There is strong consistency in documentation that physical trauma such as a fall or motor vehicle accident… can trigger fibromyalgia in some patients”).

  13. For criticism of the influence of “insurance interests” in developing the first Consensus Report, see Teasdell & Merskey, supra note 10.

  14. Almost 22% of persons suffering a neck injury developed fibromyalgia, which compares to a much smaller rate of fibromyalgia in the general population. Compare id. with Jain et al., supra note 12, at 5 (studies estimate the population prevalence of fibromyalgia as resting between 2% and 10%).

  15. A more recent cohort study of widespread bodily pain, not fibromyalgia specifically, also reported a significant association between low-impact trauma and pain. See Elaine F. Harkness et al., Mechanical Injury and Psychosocial Factors in the Work Place Predict the Onset of Widespread Chronic Pain, 50 Arthritis & Rheumatism 1655 (2004).

  16. Moshe Tishler et al., Neck Injury and Fibromyalgia—Are They Really Associated? 33 J. Rheumatology 1183 (2006).

  17. See, e.g., David Egilman et al., Proving Causation: The Use and Abuse of Medical and Scientific Evidence Inside the Courtroom: An Epidemiologist’s Critique of the Judicial Interpretation of the Daubert Ruling, 58 Food & Drug L.J. 223, 225, 246 (2003); Erica Beecher-Monas, The Heuristics of Intellectual Due Process: A Primer for Triers of Science, 75 N.Y.U.L. Rev. 1563, 1605 (2000).

  18. See, e.g., Lawrence A. Bradley & Graciela S. Alarcon, Fibromyalgia, in 2 Arthritis & Allied Conditions 1816, 1823 (William J. Koopman ed., 14th ed. 2000) (between 14% and 23% of patients with fibromyalgia report that their symptoms began following a physical injury or trauma such as surgery); Katrina Berne, Chronic Fatigue Syndrome, Fibromyalgia and Other Invisible Illnesses 35 (2002) (based on 2000 patient records of one rheumatologist, 65% of patients reported onset of fibromyalgia after trauma); Daniel J. Wallace & Janice Brock Wallace, All About Fibromyalgia 18 (2002)(reporting 30% nationwide incidence of post-traumatic fibromyalgia); Stuart Greenfield, Mary-Ann Fitzcharles, & John M. Esdaile, Reactive Fibromyalgia Syndrome, 35 Arthritis & Rheumatism 678 (1992) (23% of fibromyalgia patients reported that trauma or illness preceded onset); Frederick Wolfe, The Clinical Syndrome of Fibrositis, 81 Am. J. Medicine 7 (1986) (24% of patients implicated trauma as causative factor for fibromyalgia); George W. Waylonis, Patrick Ronan, & Chrisanne Gordon, A Profile of Fibromyalgia in Occupational Environments, 73 Am. J. Physical Medicine & Rehabilitation 112 (1994) (38% of fibromyalgia patients describe onset of symptoms after a traumatic event); D.L. Goldenberg, M.G. Nadeau, & K. Kaplan, Clinical Characteristics of 500 Patients with Fibromyalgia, Proceedings of the American College of Rheumatology, Atlanta, Ga. (October 1992) (50% of patients reported onset of fibromyalgia after infectious disorder or trauma); George W. Waylonis & Robert H. Perkins, Post-traumatic Fibromyalgia: A Long-Term Follow-up, 73 am. J. Physical Medicine & Rehabilitation 403 (1994) (over 10-year period, 773 patients diagnosed with post-traumatic fibromyalgia); David A. Fishbain & Hubert L. Rosomoff, Posttraumatic Fibromyalgia at Pain Facilities Versus Rheumatologists’ Offices, 77 Am. J. Physical Medicine & Rehabilitation 562 (1994) (70% of patients at pain center attributed onset of chronic pain to some form of trauma); D.J. Wallace, M. Linker-Israeli, D. Hallequa, S. Silverman, D. Silver, & M.H. Weisman, Cytokines Play an Aetiopathogenetic Role in Fibromyalgia: A Hypothesis and Pilot Study, 40 Rheumatology 743, 744 (2001) (32% of patients related onset of fibromyalgia to trauma); Leon Chaitow, Fibromyalgia Syndrome, A Practitioner’s Guide to Treatment 103 (2000) (23% of fibromyalgia patients nationally reported physical trauma as trigger).

  19. See Jain et al., supra note 12, at 44 (“There is a strong consistency in documentation that physical trauma...can trigger fibromyalgia in some patients”).

  20. See Kevin P. White et al., Perspectives on Posttraumatic Fibromyalgia: A Random Survey of Canadian General Practitioners, Orthopedists, Physiatrists, and Rheumatologists, 27 J. Rheumatology 790, 791–92 (2000).

  21. See Don L. Goldenberg & H. S. Sandhu, Fibromyalgia and Post-Traumatic Stress Disorder: Another Piece in the Biopsychosocial Puzzle, 32 Seminars in Arthritis & Rheumatism 1 (2002).

  22. Food Lion, supra note 3.

  23. See id. at 309.

  24. See id. at 310.

  25. See id. at 313 n.5.

  26. See id. at 312.

  27. See id. at 313.

  28. See id.

  29. See id. at 314.

  30. See, e.g., Gross, supra note 5, at 600, 601 n.4 (D. Md. 2000) (finding that the “pathogenesis of fibromyalgia remains in doubt“); Wynacht v. Beckman Instruments, Inc., 113 F.2d 1205, 1209, 1210 (E.D. Tenn. 2000) (noting that expert could not explain “how these various chemicals caused toxic...fibromyalgia” and “how they led to [plaintiff’s] myriad diseases and conditions”); Riccio v. S&T Contractors, 2001 WL 1334202 at *6 n.18, 10,11 (Pa. Comm. Pl. 2001) (noting the lack of a scientific consensus concerning the “etiology or pathogenesis” of fibromyalgia and noting the possibility that future research might reveal the “precise mechanism by which fibromyalgia is caused”); Jones, supra note 2, at *2, 3 (expert “could not identify the biological process that causes fibromyalgia to develop after a trauma”); Vargas, supra note 1, at 501 (reaffirming Food Lion’s pathogenesis requirement).

  31. Although a biological model of some chronic pain may be emerging, the specific mechanisms linking trauma to fibromyalgia are still uncertain. See generally Michael Finch, Law and the Problem of Pain, 74 U. Cin. L. Rev. 285, 325–26 (2006).

  32. See, e.g., Minner, supra note 6, at 855 (“there appears to be a consensus that there is no known cause of FM”); Riccio, supra note 30, at *6 (noting defendants’ principal support of their Daubert motion was the 1994 Consensus Report); Jones, supra note 2, at *3 (impeaching plaintiff’s expert by exposing his lack of familiarity with the Consensus Report); Vargas, supra note 1, at 501 (noting expert opinion in the Consensus Report has not been altered by later studies); Reichert, supra note 9, at 363 (noting that the defendant’s expert was unaware of the “seminal Consensus Report on FM”).

  33. See, e.g., Riccio, supra note 30, at *9 (“a catalog of patient self-reports does not constitute an epidemiological study and is insufficient to demonstrate anything more than temporal coincidence”); Vargas, supra note 1, at 502 (evidence that a high percentage of doctor’s patients reported the onset of fibromyalgia symptoms following trauma does not establish reliability of causation theory).

  34. See generally Vargas, supra note 1; Reichert, supra note 9; Warren v. Topolski, 2008 WL 836022 (Del. Super. 2008).

  35. See, e.g., Maras v. Avis Rent A Car Systems Inc., 393 F. Supp. 2d 801 (D. Minn. 2005); Grant v. Boccia, 132 Wash. App. 1016 (2006).

  36. “General acceptance” is also a criterion used under the Daubert standard.

  37. Courts tend to use the phrase “differential diagnosis” even though they might more precisely refer to a clinician’s determination of causation as one of “differential etiology.”

  38. See 211 F.3d 1008 (2000).

  39. See id. at 1019, 1020.

  40. Id. at 1019.

  41. Id. at 1020.

  42. 61 P.3d 1068 (2002).

  43. Id. at 1089.

  44. Id. at 1090.

  45. Reichert, supra note 9.

  46. Id. at 364.

  47. 715 N.W. 2d 501 (Neb. 2006)

  48. Id. at 651.

  49. Id.

  50. 977 So. 2d 543 (Fla. 2007).

  51. Id. at 549. The Court alternatively held that because the expert physicians’ opinions were “pure opinion” based on their clinical experience and training, their opinions were not subject to scrutiny under the Frye standard. Id. at 548.

  52. See, e.g., Wendy Michelle Ertmer, Just What the Doctor Ordered: The Admissibility of Differential Diagnosis in Pharmaceutical Product Litigation, 56 Vand. L. Rev. 1227, 1240 (2003); Jean Macchiaroli Eggen, Clinical Medical Evidence of Causation in Toxic Tort Cases: Into the Crucible of Daubert, 38 Houston L. Rev. 369 (2001).

  53. See Eggen, supra note 52, at 412.

  54. Kumho Tire Co. v. Carmichael, 526 U.S. 137, 152 (1999).

  55. See Eggen, supra note 52, at 413.

  56. See Joseph Sanders & Julie Machal-Fulks, The Admissibility of Differential Diagnosis Testimony to Prove Causation in Toxic Tort Cases: The Interplay of Adjective and Substantive Law, 64 Law & Contemp. Probs. 107, 108 (2001).

  57. The division in circuit court authority is discussed in Eggen, supra note 52, at 394–409.

  58. See Sanders, supra note 56 at 122–24. Experts employing differential diagnosis do not usually insist on supporting evidence of general causation. See Ertmer, supra note 52 at 1254.

  59. See Kevin Patterson, What Doctors Don’t Know (Almost Everything), N.Y. Times Magazine, May 5, 2002.

  60. See id.

  61. Id.

  62. See id.

  63. See Marcia Angell, Science on Trial 23, 103, 105 (1997) (discussing anecdotal reports that led to silicone breast implant litigation, and how “magnet” doctors draw patients based on their reputation for believing in a causal theory); Bert Black & David E. Lilienfeld, Epidemiological Proof in Toxic Tort Litigation, 52 Fordham L. Rev. 732, 743 (1984) (noting courts’ uncritical deference to experts testifying that trauma causes cancer); Michael D. Green, Expert Witnesses and Sufficiency of Evidence in Toxic Substances Litigation: The Legacy of Agent Orange and Bendectin Litigation, 86 NW. U. L. Rev. 643, 659 (1992) (noting expert’s reliance on differential diagnosis to show causation in Agent Orange litigation).

  64. Jack B. Weinstein, Improving Expert Testimony, 20 U. Rich. L. Rev. 473, 482 (1986).

  65. See, e.g., Reichert, supra note 9, at 358–59 (experts were unfamiliar with the Consensus Report); Jones, supra note 2, at *3 (expert could not name studies supporting opinion on traumatically induced fibromyalgia and was unfamiliar with the Consensus Report); Food Lion, supra note 3, at 309 (expert casually attributed plaintiff’s fibromyalgia to “hormonal” changes precipitated by an accident). Even to date, there is little indication that plaintiff’s experts have attempted to explain to courts the biological evidence concerning central sensitization and the possible mechanisms of chronic pain.

  66. Although “biopsychosocial” theories of chronic pain are well attested and provide useful context for understanding pain, opponents of pain-based diagnoses in litigation often contend that the “psychosocial” components of pain are indistinguishable from malingering or outright fraud. See generally George Mendelson, “Compensation Neurosis” Revisited: Outcome Studies of the Effects of Litigation, 39 J. Psychosomatic Res. 655–96 (1995). Even when the pain diagnosis is not being discredited, some experts exceed their expertise in identifying the alleged causes of pain. Apparently no court has found inconsistency in the willingness of defense experts to argue psychogenic explanations of pain while defense counsel argues at the same time that all causal evidence is unreliable! A conspicuous example of this is the testimony of Dr. Frederick Wolfe, co-author of the tender point test and editor of the Consensus Report. Although testifying that science has been unable to “unravel causal issues in fibromyalgia,” Dr. Wolfe has nonetheless attributed a plaintiff’s pain to “pre-existing psychological and behavioral factors that can be seen to be developing in the decade before the accident.” See Riccio, supra note 30, at *5.

  67. Hollander v. Sandoz Pharmaceuticals Corp., 289 F.3d 1193, 1210 (10th Cir. 2002).

  68. The “chain” or web, of causation is considered the “pathogenesis” or “pathophysiology” of a disease. See Mary Sue Henifin et al., Reference Guide on Medical Testimony, in Reference Manual on Scientific Evidence 451 (2d ed. 2000).

  69. See 171 F.3d at 314.

  70. Numerous courts have required that plaintiffs or claimants show their causation theory is biologically plausible. See, e.g., Falksen v. Secretary of the Dept. of Health & Human Serv., 2004 WL 785056 *12 (Ct. Fed. Claims March 30, 2004); In re Phenylpropanolamine (PPA) Products Liability Litigation, 289 F. Supp. 2d 1230, 1239, 1246–48 (W.D. Wash. 2003). Biological plausibility has also been used as a criterion for assessing the association between herbicide exposure and veterans’ diseases under federal compensation programs. See, e.g., Lefevre v. Sec. Dept Veterans Affairs, 66 F.3d 1191, 1193094 (Fed. Cir. 1995). Apparently, the pathogenesis requirement was not even urged in briefing to the Fifth Circuit. See Black v. Food Lion, Appellant’s Brief, WL 34081729 (1999).

  71. See Steve Baughman Jensen, Keep Good Science in Toxic Tort Cases, 39 Trial 18, 21 (2003) (discussing criticisms of Daubert methodology in the proposed Restatement (Third) of Torts).

  72. See Carl F. Cranor et al., Judicial Boundary Drawing and the Need for Context-Sensitive Science in Toxic Torts After Daubert v. Merrell Dow Pharmaceuticals, Inc., 16 Va. Environmental L.J. 1, 76 (1996).

  73. See, e.g., Jerome P. Kassirer & Joe S. Cecil, Inconsistency in Evidentiary Standards for Medical Testimony: Disorder in the Courts, 288 JAMA 1382 (2002) (“The courts appear to be asserting standards that they attribute to the medical profession, but that are inconsistent and sometimes more demanding than actual medical practice….Courts are misled if they think they are representing medical practice”); Development in the Law, Confronting the New Challenges of Scientific Evidence, 108 Harv. L. Rev. 1509, 1516 (1995) (“A final evasive technique judges employ is to craft their own criteria haphazardly”).

  74. See, e.g., Troyen Brennan, Causal Chains and Statistical Links: The Role of Scientific Uncertainty in Hazardous-Substance Litigation, 73 Cornell L. Rev. 469, 486 (1988) (“But for causation theory assumes the existence of causal chain analysis, depends on a mechanistic understanding of causation, and coincides with everyday, common sense notions of causation.”); Susan R. Poulter, Science and Toxic Torts: Is There a Rational Solution to the Problem of Causation?, 7 High Technology L.J. 189, 209 (1993) (noting “courts’ preference for mechanistic causal explanations”).

  75. See Michael D. Green, Expert Witnesses and Sufficiency of Evidence in Toxic Substances Litigation: The Legacy of Agent Orange and Bendectin Litigation, 86 Northwestern L. Rev. 643, 644–45 (1992); see also Margaret A. Berger, Upsetting the Balance Between Adverse Interests: The Impact of the Supreme Court’s Trilogy on Expert Testimony in Toxic Tort Litigation, 64 L. & Contemp. Probs. 289, 298 (2001) (noting that causing in toxic tort cases does not turn on explaining the causal process, since “we do not yet fully comprehend the mechanisms that produce birth defects and illnesses, such as cancers and auto-immune diseases”).

  76. See, e.g., Egilman et al., supra note 17, at 245 (“Scientists do not understand exactly how tobacco smoke causes cancer, yet tobacco smoke is a long-recognized cause of cancer”); Joelle Anne Moreno, Beyond the Polemic Against Junk Science: Navigating the Oceans That Divide Science and Law With Justice Breyer at the Helm, 81 B.U.L. Rev. 1033, 1080 (2001) (noting that the link between smoking and lung cancer was based on the strength of associations “even though we do not yet know how it does so”).

  77. See The Health Consequences of Smoking: A Report of the Surgeon General 22 (2004) (“[I]n 1964 the Surgeon General’s committee found a causal association of smoking with lung cancer to be biologically plausible. Nearly 40 years later, this association remains biologically plausible”).

  78. See Bert Black, A Unified Theory of Scientific Evidence, 56 Fordham L. Rev. 595, 624 (1988) (noting that there is presently “no overarching concept of carcinogenesis“); Mark Geistfield, Scientific Uncertainty and Causation in Tort Law, 54 Vand. L. Rev. 1011, 1012 (2001) (“we do not...adequately understand the etiology of cancer”); Susan R. Poulter, Science and Toxic Torts: Is There a Rational Solution to the Problem of Causation?, 7 High Technology & L.J. 189, 209–10 (1992) (“Scientists know very little about how, in a mechanistic sense, toxic substances cause diseases such as cancer or injuries such as birth defects”). Arthur C. Houts, Discovery, Invention, and the Expansion of the Modern Diagnostic and Statistical Manual of Mental Disorder, in Rethinking the DSM 40–41 (Larry E. Beutler & Mary L. Malik eds. 2002) (observing that most psychiatric disorders are at a “primitive stage of development” where pathophysiology of disorders is not yet known). A pathogenesis requirement would be particularly fatal to the study of rheumatic illnesses, which include common illnesses like arthritis and fibromyalgia, whose pathogenesis is “extraordinarily” complex. See Primer on the Rheumatic Diseases 99 (John H. Klippel, ed. 2001).

  79. See David L. Eaton, Scientific Judgment and Toxic Torts—A Primer on Toxicology for Judges and Lawyers, 12 J.L. & Policy 5, 39–40 (2003); Douglas L. Weed & Stephen D. Hursting, Biologic Plausibility in Causal Inference: Current Method and Practice, 147 Am. J. Epidemiology 415, 416 (1998); Douglas L. Weed, Causation: An Epidemiologic Perspective, 12 J.L. & Policy 43, 46 (2003). Hill’s criteria have been called the “gold standard” of epidemiological proof. See Kenneth R. Foster & Peter W. Huber, Judging Science: Scientific Knowledge and the Federal Courts 28 (1999).

  80. Biological plausibility is also a criterion used by toxicologists.

  81. Sir Austin Bradford Hill, The Environment and Disease: Association or Causation? 58 Proceedings of the Royal Society of Medicine 295, 298 (1965). Hill cautioned, however, that causal interpretations “should not seriously conflict with the generally known facts of the...biology of the disease.” Id.

  82. See Weed & Hursting, supra note 79.

  83. Id. at 416.

  84. See id. at 416, 417.

  85. See id. at 419.

  86. Id. at 421. See also Egilman et al., supra note 17, at 245 (“The contemplation of biologic plausibility is the most onerous of Hill’s considerations to satisfy in that it demands a level of detail of a disease=s etiology that is sometimes impractical or unobtainable.”) This view is also echoed in latest recent Surgeon General’s report on smoking. Regarding the cumulative significance of the epidemiological criteria of biologic plausibility, coherence, and analogy, the report observes that Ain practice they have been treated essentially as one idea: that a proposed causal relationship not violate known scientific principles, and that it be consistent with experimentally demonstrated biologic mechanisms and other relevant data”). See Report of the Surgeon General, supra note 77, at 22.

  87. The epidemiological standard of “biological plausibility” is a different matter. As mentioned earlier, the opinion that trauma plays a role in the onset of fibromyalgia is biologically plausible and, emerging evidence suggests, probable. Although these suspected mechanisms underlying traumatically induced fibromyalgia cannot yet be validated by the kind of physiological evidence required by Food Lion and its progeny, they have the biological plausibility that epidemiologists seek in causal theories.

  88. Bert Black, Learn the Science in Your Cases, 39 Trial 18, 19 (2003). See also Egilman et al., supra note 17, at 249 (courts have “moved beyond their role as gatekeepers of evidence and, without the appropriate training or background...have rendered determinations regarding the reliability of scientific evidence”).

  89. “Hard science” has been defined as “scientific methodologies characterized by careful quantification and rigorous testability. In the context of medical causation, the reference is primarily to population studies and laboratory experimentation, the methodologies associated with epidemiology and toxicology, respectively.” Note, Navigating Uncertainty: Gatekeeping in the Absence of Hard Science, 113 Harv. L. Rev. 1467, 1484 n.6 (2000).

  90. See, e.g., Michael D. Green, Expert Witnesses and Sufficiency of Evidence in Toxic Substances Litigation: The Legacy of Agent Orange and Bendectin Litigation, 86 N.W.L. Rev. 643, 659–62 (1992); Peter H. Schuck, Multi-Culturalism Redux: Science, Law, and Politics, 11 Yale L. & Policy Rev. 1, 7–11 (1993); Donald A. Lawson, Hopkins v. Dow Corning Corporation: Silicone and Science, 37 Jurimetrics 53, 56–68 (1996).

  91. According to one system of epidemiological ranking, case reports constitute Aclass III@ evidence, with class II evidence limited to well-designed clinical studies and class I evidence limited to random, controlled experiments. See D.S. Goodin et al., The Relationship of MS to Physical Trauma and Psychological Stress, 52 Neurology 1, 2 (1999).

  92. See Egilman et al., supra note 17, at 225, 246.

  93. Bert Black, Francisco J. Ayala, & Carol Safran-Brinks, Science and the Law in the Wake of Daubert: A New Search for Scientific Knowledge, 72 Tex. L. Rev. 715, 765 (1994).

  94. Frye’s “general acceptance” standard remains one of the formal criteria considered under Daubert.

  95. The Florida Supreme Court’s approach in Marsh, supra note 50, is consistent with this approach. In Marsh, the court seems to have refined Frye to require that the methodology on which an expert relies be “generally accepted,” even though the expert’s causal opinion (regarding general causation) is not.

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Finch, M. Judicial Evaluation of Traumatically Induced Fibromyalgia. Psychol. Inj. and Law 2, 24–33 (2009). https://doi.org/10.1007/s12207-009-9031-x

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