Why Are PTSD and Fibromyalgia So Common Together in Veterans?

Veterans who live with PTSD are far more likely than the general population to also live with fibromyalgia. That overlap is real, it is measurable, and it is not a coincidence. But the reason the two travel together is more interesting — and more medically defensible — than the shorthand you usually hear.

This article explains what is actually happening in the nervous system, why sleep sits at the center of it, what the evidence does and does not establish, and how the VA's rules treat fibromyalgia depending on where and when a veteran served.

How often do PTSD and fibromyalgia occur together?

In a study of 395 consecutive fibromyalgia patients across eight German treatment centers, 45.3% met criteria for PTSD, compared with 3.0% of age- and sex-matched people from the general population.²¹ That is roughly a fifteen-fold difference.

A meta-analysis of 71 controlled studies found that people reporting trauma exposure were about 2.7 times more likely to have a functional somatic syndrome — a category that includes fibromyalgia, chronic widespread pain, irritable bowel syndrome, and chronic fatigue syndrome. The association was stronger still in people who met full PTSD criteria.²²

Among veterans specifically, the pattern shows up in deployment data. In the Iowa Persian Gulf Study, fibromyalgia symptoms were reported by 19.2% of Gulf War veterans versus 9.6% of nondeployed controls.²⁵ A later VA cohort study that examined veterans in person ten years after the war found physician-confirmed fibromyalgia in 2.0% of deployed veterans versus 1.2% of nondeployed veterans (odds ratio 2.32).²⁴ The two figures differ because one measured self-reported symptoms and the other required examination — a gap worth remembering whenever anyone quotes a single prevalence number.

What is fibromyalgia, in plain terms?

Fibromyalgia is a disorder of pain processing. The problem is not primarily in the muscles or joints where the pain is felt; it is in how the nervous system amplifies, sustains, and fails to dampen pain signals.¹

A useful analogy: the body has something like a volume control for pain. In fibromyalgia, that control sits too high, and the mechanism that normally turns it back down does not work well.

Current diagnosis uses the 2016 revision of the American College of Rheumatology criteria, which require all of the following:²

• Generalized pain in at least four of five body regions
• Symptoms present at a similar level for at least three months
• A Widespread Pain Index of 7 or more with a Symptom Severity Scale of 5 or more, or a Widespread Pain Index of 4–6 with a Symptom Severity Scale of 9 or more

One feature of the 2016 criteria matters a great deal in disability work: a fibromyalgia diagnosis is valid regardless of other diagnoses. Having degenerative disc disease, or PTSD, or an autoimmune condition does not rule fibromyalgia out.²

Note that the 2016 criteria dropped the tender-point examination that the 1990 criteria relied on. The VA's rating code still refers to tender points. That mismatch is discussed further below.

What is actually happening in the nervous system?

Five mechanisms are described repeatedly in the peer-reviewed literature. They are not competing theories; they overlap, and most researchers regard them as different views of one dysregulated stress-and-pain system.

The rest of this section is more technical. If you want the practical material, skip ahead to the sleep section.

Central sensitization

Central sensitization is an increase in the responsiveness of pain-signaling neurons in the spinal cord and brain. After sustained input, those neurons fire more readily, respond to weaker stimuli, and keep firing after the stimulus ends.⁴ Clinically this produces hyperalgesia (ordinary painful things hurt more) and allodynia (things that should not hurt at all, like a waistband or a light touch, do).

Fibromyalgia is the most studied example of a centrally sensitized pain state.¹³ The relevance to PTSD is that the same brain regions involved in threat appraisal and emotional regulation — the amygdala, anterior cingulate, and insula — also participate in the affective dimension of pain. A nervous system already tuned toward threat detection is operating on the same circuitry that governs how loudly pain registers.

Impaired descending pain inhibition

The brainstem sends signals down the spinal cord that suppress incoming pain traffic. This descending inhibitory system is why a soldier can sustain an injury in contact and not feel it until afterward.

In fibromyalgia, that system underperforms. In a controlled study using a spatial summation procedure, healthy volunteers and patients with chronic low back pain recruited endogenous inhibition normally, while fibromyalgia patients did not.⁵ This is one of the more direct pieces of evidence that fibromyalgia involves a failure of pain suppression, not just an excess of pain input.

The finding is not unanimous. Studies using conditioned pain modulation have produced mixed results, with some showing impaired modulation in fibromyalgia and others showing hypersensitivity without a clear modulation deficit.²⁷ The honest summary is that the descending inhibition finding is well replicated but method-dependent.

Descending inhibition depends heavily on serotonin and norepinephrine — which is why serotonin–norepinephrine reuptake inhibitors are among the better-supported drug treatments for fibromyalgia, and why the same class is used in PTSD.

Autonomic hyperarousal

PTSD involves persistent sympathetic activation: elevated resting heart rate, exaggerated startle, reduced heart rate variability. Fibromyalgia shows a strikingly similar autonomic profile — relentless sympathetic activity with blunted responsiveness to actual stressors, sometimes described as a system that is always on but no longer able to mount a proportionate response.⁷

This matters practically. A veteran whose autonomic system never stands down does not get restorative sleep, does not recover normally after exertion, and experiences flares after emotional stress. The VA's own rating criteria acknowledge this pattern: the 20% level under Diagnostic Code 5025 explicitly contemplates exacerbations precipitated by emotional stress.

HPA-axis dysregulation

The hypothalamic–pituitary–adrenal axis is the body's slower stress-hormone system. Chronic traumatic stress alters it, and both PTSD and fibromyalgia are associated with atypical cortisol dynamics — flattened diurnal curves, altered awakening responses, and abnormal feedback sensitivity rather than simple over- or under-production.⁷²⁸

Two cautions belong here. First, the cortisol findings in both conditions are heterogeneous across studies; there is no single "PTSD cortisol pattern" or "fibromyalgia cortisol pattern." Second, HPA measures are not diagnostic. They describe a shared physiology; they do not identify individuals.

Neuroinflammation

This is the newest strand and the one moving fastest. Positron emission tomography studies using translocator protein tracers have shown elevated glial activation in the brains of fibromyalgia patients compared with controls, across multiple sites and multiple tracers.⁹¹⁰ Cerebrospinal fluid studies have found inflammatory mediator profiles consistent with both systemic inflammation and neuroinflammation.¹¹

Separately, a 2021 study transferred immunoglobulin G from fibromyalgia patients into mice and reproduced pain hypersensitivity in the animals — evidence that at least some of the pain sensitivity is carried by circulating antibodies.¹² And skin biopsy work has documented reduced small-fiber density in a substantial subgroup of fibromyalgia patients.¹³

PTSD, for its part, is associated with elevated peripheral inflammatory markers.⁸ The plausible link is that sustained traumatic stress contributes to an inflammatory state that primes glial cells and lowers the threshold for persistent pain.

These findings are recent and still being replicated. They should be described as an emerging mechanism, not settled biology.

Why does nonrestorative sleep deserve its own section?

Because in the PTSD–fibromyalgia relationship, sleep is not a symptom sitting alongside the others. It is one of the main mechanisms connecting them, and it has better causal evidence behind it than almost anything else in this article.

Sleep disruption can produce fibromyalgia symptoms in healthy people

In 1975, researchers deprived healthy volunteers of slow-wave sleep by introducing auditory tones whenever delta activity appeared. The volunteers developed musculoskeletal aching and tenderness — the core features of what was then called fibrositis.¹⁴ The experiment has been repeated in modern form: selectively disrupting slow-wave sleep in healthy middle-aged women produced musculoskeletal pain and fatigue.¹⁵

This is experimental evidence, in humans, that disrupted deep sleep causes pain sensitivity rather than merely accompanying it. Very little else in the fibromyalgia literature has that design.

Poor sleep prospectively predicts fibromyalgia

A Norwegian population study followed 12,350 women who had no fibromyalgia, no musculoskeletal pain, and no physical impairment at baseline. Ten years later, women reporting frequent sleep problems at baseline had a substantially elevated risk of incident fibromyalgia, with a dose–response gradient — the worse the reported sleep, the higher the risk.¹⁷

The study drew a published methodological critique, primarily regarding reliance on self-reported physician diagnosis and the possibility that sleep problems reflected undetected early disease.¹⁸ That objection is fair and should be acknowledged whenever this study is cited. It does not eliminate the finding, and it is reinforced rather than contradicted by the experimental sleep-deprivation work above.

The physiology connects cleanly

Polysomnography in fibromyalgia shows reduced slow-wave sleep and intrusion of alpha rhythms into non-REM sleep — the electrical signature of wakefulness bleeding into deep sleep.¹⁶ Sleep loss impairs descending pain inhibition and promotes pain facilitation, which is precisely the mechanism described earlier.¹⁶¹⁹

PTSD attacks sleep directly

Sleep disturbance is not incidental to PTSD; it is close to definitional. Insomnia and nightmares are among the most persistent PTSD symptoms and among the most treatment-resistant, and disturbed REM sleep is a candidate mechanism in PTSD's maintenance.²⁰ Hypervigilance at bedtime, trauma-related nightmares, and fragmented sleep architecture all reduce exactly the slow-wave sleep that the experiments above show is protective against pain sensitivity.

Why this matters for a claim

If a veteran's records show PTSD-related sleep disruption beginning years before the onset of widespread pain, that is a documented mechanistic sequence, not a coincidence of timing. Sleep is often the best-documented link in the chain, because sleep complaints tend to appear in treatment records early and repeatedly — in primary care notes, mental health notes, sleep studies, and medication histories — long before anyone writes down the word "fibromyalgia."

Does this mean PTSD causes fibromyalgia?

Not automatically, and any medical opinion that says so without qualification is a weaker opinion for it.

Most of the human evidence linking trauma, PTSD, and fibromyalgia is cross-sectional and retrospective. People who already have chronic pain are asked about past trauma. That design carries a known problem: recall of adverse events is influenced by current symptom state and mood. The meta-analytic association is robust, but the underlying studies mostly cannot establish sequence.²²

Several alternative explanations deserve honest treatment:

• Shared antecedent. Trauma exposure may independently raise the risk of both conditions, making them comorbid without either causing the other.²¹
• Shared vulnerability. Genetic and early-life factors influence both stress reactivity and pain sensitivity.
• Reverse causation. Chronic pain is itself distressing and can worsen or unmask psychiatric symptoms.
• Detection bias. Veterans in active PTSD treatment see clinicians more often and are more likely to have widespread pain recognized and labeled.

What does strengthen a causal inference in an individual case is the ordinary set of considerations clinicians use everywhere: a plausible biological mechanism, documented temporal sequence, dose–response (worse PTSD tracking with worse pain), and coherence with what is independently known about the physiology. Several of those elements are present in the general literature, and several can be established or excluded in a specific veteran's records.

A precise clinical opinion says that trauma and PTSD are well-supported contributing factors in the development and maintenance of fibromyalgia in some patients, and then argues from that veteran's actual chronology, not from the population data alone.

How does the relationship run in both directions?

The Häuser study did something unusual: it asked when. Among fibromyalgia patients with PTSD, the most burdensome traumatic experience and PTSD symptoms preceded the onset of chronic widespread pain in 66.5% of cases, followed the pain onset in 29.5%, and occurred in the same year in 4.0%.²¹

That distribution is the clearest available statement of bidirectionality. In most patients the trauma came first. In nearly a third, it did not.

PTSD worsening fibromyalgia. Sympathetic hyperarousal, HPA dysregulation, fragmented sleep, and impaired descending inhibition all push pain sensitivity upward. Fibromyalgia patients with comorbid PTSD report more somatic and psychological symptoms, more disability, and more work impairment than fibromyalgia patients without PTSD.²¹

Fibromyalgia worsening PTSD. This direction is underappreciated and often decisive in a claim:

• Sleep. Pain fragments sleep, and fragmented sleep intensifies nightmares, irritability, and concentration problems.
• Depression and anxiety. Loss of physical capacity, occupational function, and independence are established drivers of depressive and anxious symptoms.
• Avoidance and withdrawal. Pain and fatigue narrow a person's world. That narrowing looks like — and reinforces — PTSD avoidance.
• Loss of coping tools. Exercise is one of the best-supported interventions for both PTSD and fibromyalgia. Pain and post-exertional worsening take it away.
• Hypervigilance turned inward. A nervous system trained to scan for external threat begins scanning bodily sensation, which amplifies symptom perception.

For VA purposes this matters because the framework does not require a single direction. Causation and aggravation are separate legal theories, and aggravation runs in whichever direction the evidence supports.

What does a psychiatric assessment actually contribute?

A rheumatologist establishes the fibromyalgia diagnosis. A psychiatric evaluation addresses a different set of questions — and in a case built on the PTSD relationship, they are the questions that decide it.

Chronology. Building an accurate timeline of trauma exposure, first psychiatric symptoms, first sleep complaints, first pain complaints, and first diagnosis. This is painstaking record work, and it frequently reveals that symptoms were documented years before anyone attached a diagnostic label. Given the Häuser data on temporal ordering, chronology is not a formality — it is the evidence that distinguishes one theory of the case from another.

Trauma exposure. Characterizing the nature, duration, and severity of the stressor, including chronic operational stress and military sexual trauma, which are systematically underrepresented in service treatment records.

Sleep. Reconstructing the sleep history in detail: onset, architecture, nightmares, medication effects, comorbid sleep-disordered breathing. Given how much causal weight sleep carries, a superficial sleep history weakens an otherwise good opinion.

Symptom interaction. Distinguishing what is attributable to fibromyalgia, what is attributable to the psychiatric condition, and what is genuinely inseparable. This cuts both ways — it can support attribution, and it can identify where attribution is not supportable.

Medication effects. Psychiatric medications alter sleep architecture, pain thresholds, weight, and fatigue. Some antidepressants used for PTSD are also used for fibromyalgia pain, which complicates any argument about treatment response. A physician who prescribes these drugs can address this; a reviewer working from records alone often cannot.

Functional impairment. Describing, concretely, what the veteran can no longer do — occupationally, socially, and in daily activity — and which condition accounts for which limitation. Rating criteria turn on function, not diagnosis.

Differential diagnosis. Ruling in and out the conditions that mimic this picture: sleep apnea, thyroid disease, inflammatory arthritis, medication side effects, substance use. An opinion that never considered alternatives is easy to discount.

How can the VA connect fibromyalgia to service?

There are four distinct routes. They rest on different legal authorities and require different evidence. Conflating them is the most common error in this area.

1. Gulf War presumptive service connection

Fibromyalgia is named by statute as an example of a medically unexplained chronic multisymptom illness for Persian Gulf veterans, alongside chronic fatigue syndrome and irritable bowel syndrome. 38 U.S.C. § 1117; 38 C.F.R. § 3.317(a)(2)(i)(B).

For a qualifying veteran, this route does not require proof of an individualized causal nexus. The connection to service is supplied by law. What still must be shown is qualifying service, a qualifying chronic disability (generally symptoms present six months or more), and objective indications of that disability. 38 C.F.R. § 3.317(a)(3)–(4).

There is an important wrinkle that is widely misreported. The regulation, 38 C.F.R. § 3.317, still states that the disability must have become manifest during qualifying service or to a degree of 10 percent or more "not later than December 31, 2026," and still defines the Southwest Asia theater without the countries Congress later added. That text has not been amended since September 2021.

The statute it implements was amended by section 405 of the PACT Act on August 10, 2022. 38 U.S.C. § 1117(a)(1) now reads that compensation may be paid for a qualifying chronic disability "that became manifest to any degree at any time." The same amendment expanded the definition of a Persian Gulf veteran to include service in Afghanistan, Israel, Egypt, Turkey, Syria, and Jordan. 38 U.S.C. § 1117(f).

The VA acknowledged the discrepancy and proposed removing the outdated regulatory language in a proposed rule published October 1, 2024, but the regulation has not yet been amended. Where a statute and an implementing regulation conflict, the statute controls.

Veterans and advocates should treat the December 31, 2026 date with care. It is not a claim-filing deadline, and under the current statute it is not a manifestation deadline either. That said, the regulation still prints it, and until the rulemaking is finished, it remains a point that may need to be argued rather than assumed.

2. Direct service connection

Under 38 C.F.R. § 3.303, fibromyalgia can be directly connected where the evidence shows in-service onset, or continuity of symptoms from service, or a competent medical link between an in-service event and the current condition. This route is available to any veteran regardless of where they served, and it is often the right theory where widespread pain is documented in service treatment records but was never named.

3. Secondary service connection — causation

Under 38 C.F.R. § 3.310(a), a condition proximately due to a service-connected disability may be service connected. This is the route where the PTSD-to-fibromyalgia mechanism does the work, and it requires an individualized medical opinion addressing whether it is at least as likely as not (50% or greater probability) that the service-connected psychiatric condition caused the fibromyalgia.

4. Secondary service connection — aggravation

Under 38 C.F.R. § 3.310(b) and Allen v. Brown, 7 Vet. App. 439 (1995), a non-service-connected condition that is chronically worsened by a service-connected disability may be compensated for the degree of worsening. Aggravation is a separate and independent theory from causation. A veteran whose fibromyalgia predated service, or arose from another cause, may still have a viable claim if a service-connected condition made it measurably worse.

In practice, causation and aggravation should be analyzed and stated separately rather than blended together, because they can succeed or fail independently.

Where a veteran qualifies under more than one theory, the theories are not mutually exclusive. A Gulf War veteran with PTSD may have both a presumptive route and a secondary route available.

How does the VA rate fibromyalgia?

The VA rates fibromyalgia under 38 C.F.R. § 4.71a, Diagnostic Code 5025. Each level requires widespread musculoskeletal pain and tender points, with or without associated fatigue, sleep disturbance, stiffness, paresthesias, headache, irritable bowel symptoms, depression, anxiety, or Raynaud's-like symptoms.

Rating	Criteria
40%	Symptoms that are constant, or nearly so, and refractory to therapy
20%	Symptoms that are episodic, with exacerbations often precipitated by environmental or emotional stress or by overexertion, but that are present more than one-third of the time
10%	Symptoms that require continuous medication for control

A note to the code defines widespread pain as pain on both the left and right sides of the body, above and below the waist, affecting both the axial skeleton (cervical spine, anterior chest, thoracic spine, or low back) and the extremities.

Two observations about this rating code.

It is out of step with current diagnostic practice. DC 5025 was added in 1996 and requires "tender points" — a feature of the 1990 ACR classification criteria that the 2016 revision no longer uses.² A rheumatologist following current standards may never perform a tender-point count. This creates a documentation gap that is worth anticipating rather than discovering later.

Associated symptoms are already contemplated. The code lists depression, anxiety, headache, and irritable bowel symptoms among fibromyalgia's associated features. Whether a separately diagnosed condition can also be separately evaluated turns on the rule against pyramiding at 38 C.F.R. § 4.14, which prohibits evaluating the same disabling manifestation under multiple codes. Separate diagnoses with separate manifestations may be separately evaluated; overlapping symptoms may not.

For advocates, VSOs, and family members

A few points that come up repeatedly and are worth knowing regardless of your role:

The Gulf War route and the secondary route are different claims. They require different evidence and different development. Filing a secondary claim for a veteran who qualifies for the presumptive route can add unnecessary work — and vice versa, since presumptive eligibility depends on service location and dates that not every veteran meets.

Do not let the December 2026 date drive a panic. It appears in the regulation but not in the controlling statute. If someone tells a veteran their claim is dead after that date, they are reading a regulation the VA itself has proposed to amend.

Sleep records are often the most valuable documents nobody thinks to gather. Primary care notes mentioning insomnia, sleep study reports, medication trials for sleep, and a spouse's observations frequently establish the timeline better than the pain records do.

Lay statements carry real weight on chronology and function. A family member is competent to describe what they observed and when: the year the veteran stopped sleeping through the night, the year they stopped doing yard work, the point at which they stopped attending family events. That is factual observation, not medical opinion, and it can fill gaps that treatment records leave open.

Symptoms predate diagnoses, usually by years. Fibromyalgia is often diagnosed long after widespread pain begins, particularly in veterans who normalized pain during service. When reconstructing a timeline, look for the first documented symptom, not the first documented diagnosis.

Function is what gets rated. "I have a lot of pain" is less useful than "I can no longer stand for more than ten minutes, I miss two days of work a month, and I stopped driving my grandchildren to school." Specific functional loss maps onto the rating criteria; general distress does not.

If you are supporting someone with both conditions, the pain and the psychiatric symptoms are not separate problems. They feed each other through mechanisms described above. Treatment that addresses only one often stalls. That is a clinical observation, not a claims strategy — but it is also why the two so often need to be evaluated together.

Where to go from here

If you are researching how the PTSD–fibromyalgia relationship is documented in a medical opinion, our fibromyalgia nexus letter page explains what that evaluation involves and what it addresses. Veterans whose psychiatric picture includes a separately diagnosed mood disorder may also find the depression nexus letter page relevant.

For anyone simply trying to understand their own situation better, the mechanisms above are worth discussing with your own treating providers. A rheumatologist, a sleep specialist, and a mental health clinician are each looking at a different part of the same system.

Legal and regulatory authorities: 38 U.S.C. § 1117; Sergeant First Class Heath Robinson Honoring our PACT Act of 2022, Pub. L. No. 117-168, § 405; 38 C.F.R. § 3.317; 38 C.F.R. § 3.303; 38 C.F.R. § 3.310(a), (b); 38 C.F.R. § 4.14; 38 C.F.R. § 4.71a, Diagnostic Code 5025; Allen v. Brown, 7 Vet. App. 439 (1995).

Bibliography

1. Clauw DJ. Fibromyalgia: a clinical review. JAMA. 2014;311(15):1547–1555. ↩
2. Wolfe F, Clauw DJ, Fitzcharles MA, et al. 2016 revisions to the 2010/2011 fibromyalgia diagnostic criteria. Semin Arthritis Rheum. 2016;46(3):319–329. ↩
3. Sluka KA, Clauw DJ. Neurobiology of fibromyalgia and chronic widespread pain. Neuroscience. 2016;338:114–129. ↩
4. Woolf CJ. Central sensitization: implications for the diagnosis and treatment of pain. Pain. 2011;152(3 Suppl):S2–S15. ↩
5. Julien N, Goffaux P, Arsenault P, Marchand S. Widespread pain in fibromyalgia is related to a deficit of endogenous pain inhibition. Pain. 2005;114(1–2):295–302. ↩
6. Martínez-Lavín M. Biology and therapy of fibromyalgia: stress, the stress response system, and fibromyalgia. Arthritis Res Ther. 2007;9(4):216. ↩
7. Michopoulos V, Powers A, Gillespie CF, Ressler KJ, Jovanovic T. Inflammation in fear- and anxiety-based disorders: PTSD, GAD, and beyond. Neuropsychopharmacology. 2017;42(1):254–270. ↩
8. Albrecht DS, Forsberg A, Sandström A, et al. Brain glial activation in fibromyalgia — a multi-site positron emission tomography investigation. Brain Behav Immun. 2019;75:72–83. ↩
9. Mueller C, Fang YD, Jones C, et al. Evidence of neuroinflammation in fibromyalgia syndrome: a [18F]DPA-714 positron emission tomography study. Pain. 2023;164:2285–2295. ↩
10. Bäckryd E, Tanum L, Lind AL, Larsson A, Gordh T. Evidence of both systemic inflammation and neuroinflammation in fibromyalgia patients. J Pain Res. 2017;10:515–525. ↩
11. Goebel A, Krock E, Gentry C, et al. Passive transfer of fibromyalgia symptoms from patients to mice. J Clin Invest. 2021;131(13):e144201. ↩
12. Üçeyler N, Zeller D, Kahn AK, et al. Small fibre pathology in patients with fibromyalgia syndrome. Brain. 2013;136(Pt 6):1857–1867. ↩
13. Moldofsky H, Scarisbrick P, England R, Smythe H. Musculoskeletal symptoms and non-REM sleep disturbance in patients with "fibrositis syndrome" and healthy subjects. Psychosom Med. 1975;37(4):341–351. ↩
14. Lentz MJ, Landis CA, Rothermel J, Shaver JL. Effects of selective slow wave sleep disruption on musculoskeletal pain and fatigue in middle aged women. J Rheumatol. 1999;26:1586–1592. ↩
15. Choy EH. The role of sleep in pain and fibromyalgia. Nat Rev Rheumatol. 2015;11(9):513–520. ↩
16. Mork PJ, Nilsen TI. Sleep problems and risk of fibromyalgia: longitudinal data on an adult female population in Norway. Arthritis Rheum. 2012;64(1):281–284. ↩
17. Wolfe F. Sleep problems and risk of fibromyalgia — untenable conclusions: comment on the article by Mork et al. Arthritis Rheum. 2012;64(5):1692–1693. ↩
18. Finan PH, Goodin BR, Smith MT. The association of sleep and pain: an update and a path forward. J Pain. 2013;14(12):1539–1552. ↩
19. Germain A. Sleep disturbances as the hallmark of PTSD: where are we now? Am J Psychiatry. 2013;170(4):372–382. ↩
20. Häuser W, Galek A, Erbslöh-Möller B, et al. Posttraumatic stress disorder in fibromyalgia syndrome: prevalence, temporal relationship between posttraumatic stress and fibromyalgia symptoms, and impact on clinical outcome. Pain. 2013;154(8):1216–1223. ↩
21. Afari N, Ahumada SM, Wright LJ, et al. Psychological trauma and functional somatic syndromes: a systematic review and meta-analysis. Psychosom Med. 2014;76(1):2–11. ↩
22. Yavne Y, Amital D, Watad A, Tiosano S, Amital H. A systematic review of precipitating physical and psychological traumatic events in the development of fibromyalgia. Semin Arthritis Rheum. 2018;48(1):121–133. ↩
23. Eisen SA, Kang HK, Murphy FM, et al. Gulf War veterans' health: medical evaluation of a U.S. cohort. Ann Intern Med. 2005;142(11):881–890. ↩
24. Iowa Persian Gulf Study Group. Self-reported illness and health status among Gulf War veterans: a population-based study. JAMA. 1997;277(3):238–245. ↩
25. Institute of Medicine. Chronic Multisymptom Illness in Gulf War Veterans: Case Definitions Reexamined. Washington, DC: National Academies Press; 2014. ↩
26. Gerhardt A, Eich W, Treede RD, Tesarz J. Conditioned pain modulation in patients with nonspecific chronic back pain with chronic local pain, chronic widespread pain, and fibromyalgia. Pain. 2017;158(3):430–439. ↩
27. Yehuda R, Hoge CW, McFarlane AC, et al. Post-traumatic stress disorder. Nat Rev Dis Primers. 2015;1:15057. ↩