Table of Contents
Introduction: The Unseen Storm
For Elara, it began as a whisper, a persistent, dull ache that settled deep into her muscles and soft tissues, a “body toothache that stays with me all the time”.1
It was a pain without borders, present on both sides of her body, above and below the waist, a constant companion that defied explanation.2
This was accompanied by a profound, bone-deep fatigue that no amount of sleep could erase; she would wake up feeling as if she hadn’t slept at all.2
Her thoughts became clouded by a cognitive haze she privately dubbed “fibro fog,” a frustrating phenomenon that made focusing on even simple mental tasks feel like wading through M.D.2
Her symptoms were an invisible storm raging within her.
Yet, to the outside world, and to the medical instruments meant to find disease, she appeared healthy.
X-rays and routine blood tests consistently came back normal, offering no clues.4
This led to a bewildering and frustrating cycle of medical appointments, each one ending with a variation of the same dismissive conclusion: “There is nothing wrong”.4
This chasm between Elara’s debilitating lived experience and the lack of objective proof created a profound internal conflict.
It forced her to confront the question that millions of others with similar symptoms have been forced to ask: “Is this real, or is it all in my head?”.6
Her journey became not just a search for a diagnosis, but a desperate quest for validation—for acknowledgment that her suffering was rooted in a real, physical condition that has been historically and tragically misunderstood.8
The answer, as modern science is now demonstrating with resounding clarity, lies not in the muscles or joints where the pain is felt, but deep within the central nervous system, in the very way the brain and spinal cord process the world.2
Chapter 1: A History of Doubt – The Labyrinth of Misdiagnosis
Elara’s journey through the modern medical system was a lonely echo of a long and troubled history.
She encountered physicians who were hesitant, some who were openly dismissive, and one who suggested her condition was little more than a “fashion tag”.13
Her chart filled with tentative diagnoses—rheumatoid arthritis, lupus, or simply “stress” and “depression”—each one leading to treatments that failed to touch her core symptoms.6
This experience was not a unique personal failure but a reflection of the medical community’s own centuries-long struggle to understand a condition that defied its conventions.
Historical Context
The condition now known as fibromyalgia has long suffered from an identity crisis.
Early descriptions of similar symptom clusters appeared as far back as the 1600s under the term “muscular rheumatism”.9
In the 19th century, figures like Dr. William Balfour began to provide more detailed clinical descriptions, even noting the presence of tender points.10
A pivotal moment came in 1904 when Sir William Gowers coined the term “fibrositis”.8
This name gave the condition a medical identity but also sent medical science down a dead-end path for decades.
The suffix “-itis” implies inflammation, and so researchers began a fruitless search for inflammation in the fibrous and muscle tissues of patients—a search that consistently came up empty.9
This failure to find a clear physical cause created an explanatory vacuum.
In the absence of objective evidence, the condition was relegated to the realm of psychology.
In 1947, the term “psychogenic rheumatism” was introduced, defining the condition as a “musculoskeletal expression of functional disorders, stress states, or psychoneurosis”.9
This damaging detour solidified the belief that the pain was not “real” in a biological sense, a stigma that directly fueled the disbelief Elara and countless others would face generations later.
The name was officially changed to “fibromyalgia” in 1976, a critical step that correctly removed the implication of inflammation.8
However, the legacy of doubt was deeply entrenched.
The Diagnostic Quagmire
The historical confusion continues to manifest in modern clinical practice.
Research reveals that fibromyalgia is frequently misdiagnosed, as its symptoms overlap significantly with other conditions like hypothyroidism, sleep apnea, rheumatoid arthritis, and lupus.6
The diagnostic process is fraught with uncertainty.
Studies show a startling discordance between clinical practice and established criteria: only about one-third of patients who receive a physician’s diagnosis of fibromyalgia actually meet the formal diagnostic criteria.
Conversely, two-thirds of patients who
do meet the criteria remain clinically undiagnosed.15
This has led to the characterization of fibromyalgia diagnosis in the community as a “subjective and negotiated” process, one that is often biased, with women being more than three times as likely as men to receive a clinical diagnosis compared to their prevalence by formal criteria.15
The 1990 American College of Rheumatology (ACR) criteria attempted to standardize the diagnosis by focusing on a history of widespread pain and the presence of pain in at least 11 of 18 specific “tender points” on the body.3
While this provided a valuable tool for research, it was later criticized for its variable reliability and for oversimplifying a complex, multi-symptom illness.17
Investigators soon realized that the tenderness in fibromyalgia was diffuse and widespread, not confined to these arbitrary points.18
This historical journey, from a mysterious “rheumatism” to a misunderstood “psychogenic” ailment, and finally to a controversially defined syndrome, directly shaped the confusing and invalidating experience of patients today.
Table 1: The Evolution of Understanding Fibromyalgia
| Era/Year | Dominant Term/Concept | Underlying Theory | Key Discoveries/Criteria | Impact on Patients |
| 1600s | Muscular Rheumatism | Fluid imbalance (“Rheuma”) | Vague descriptions of widespread pain and fatigue | Symptoms acknowledged but poorly defined 9 |
| 1904 | Fibrositis | Inflammation of fibrous tissue | “Tender points” described by Gowers; term coined | Condition named, but based on an incorrect premise 8 |
| 1947 | Psychogenic Rheumatism | Psychological distress | No physical cause found, attributed to “stress states” | Dismissal, stigma, and belief that pain was “not real” 9 |
| 1976 | Fibromyalgia | Unknown; shift away from inflammation | Name changed to remove “-itis”; sleep disturbances identified | Inflammation theory debunked, but still no clear cause 8 |
| 1990 | Fibromyalgia Syndrome (ACR Criteria) | Pain disorder | 1990 ACR criteria established based on widespread pain and 11/18 tender points | Validation through standardized criteria; focus on pain 8 |
| 1990s-Present | Central Sensitization Syndrome | Neurological Dysfunction / Pain Processing Disorder | Neurotransmitter imbalances (Substance P, Serotonin) found; fMRI shows brain changes; tender points de-emphasized in updated criteria | Scientific validation of a neurological basis; shift toward a multi-symptom understanding 8 |
The long, winding path to understanding fibromyalgia is not merely a historical curiosity; it is the direct source of the diagnostic challenges and patient stigma that persist.
The initial “fibrositis” label sent medicine on a decades-long hunt for inflammation that did not exist.8
The failure of this search created an explanatory void that was tragically filled by the “psychogenic” theory, which incorrectly located the problem in the patient’s mind rather than their body.9
This history of doubt, combined with the lack of a simple blood test or scan, fostered an environment where diagnosis could become a subjective, “negotiated” process.15
It is this very history that patients today are fighting against when they are told their symptoms are “all in your head”.7
Recognizing this flawed history is the first step for both patients and clinicians to dismantle the biases that still impede accurate diagnosis and compassionate care.
Chapter 2: The Turning Point – Unveiling a Disorder of the Nervous System
After years adrift in a sea of uncertainty, Elara finally met a neurologist who offered not just a diagnosis, but an explanation that resonated with every fiber of her being.19
The diagnosis was fibromyalgia, but the revelation was the framework behind it: this was not a problem with her muscles, nor a figment of her imagination.
It was a neurological disorder, a condition of the central nervous system itself.
For Elara, this was the epiphany.
The scattered, confusing pieces of her suffering—the pain, the fog, the fatigue—suddenly clicked into a coherent, scientifically validated picture.
2.1 The Brain’s “Volume Knob”: Demystifying Central Sensitization
The clinician began by explaining the core mechanism of fibromyalgia: a phenomenon called “central sensitization”.11
He described it as the central nervous system—the brain and spinal cord—becoming perpetually stuck in a state of high alert, or “hypersensitivity”.22
To make this abstract concept tangible, he used a series of powerful analogies.
“Imagine your nervous system has a ‘volume knob’ for pain,” he explained.
“In most people, it’s set at a reasonable level.
In fibromyalgia, that knob is involuntarily turned up to the maximum”.24
He offered another image: “Think of it like an electric guitar.
To make the music louder, you can either strum the strings harder or turn up the amplifier.
In fibromyalgia, the amplifier—your brain and spinal cord—is set way too loud.
So even the softest strum of the strings, a minor sensation, comes through as a deafening blast of pain”.26
This state of sensitization, also known as nociplastic pain, means the central nervous system fundamentally misinterprets sensory information.
It treats normal, safe signals as dangerous threats, triggering intense pain even in the absence of any new injury or tissue damage.23
This explains the two hallmark features of fibromyalgia pain:
allodynia, where a normally non-painful stimulus like the brush of clothing or a gentle hug becomes painful, and hyperalgesia, an exaggerated and amplified pain response to a stimulus that would normally be only mildly painful.21
2.2 A Symphony of Imbalance: The Role of Neurotransmitters
This faulty “volume knob,” the clinician continued, is regulated by a delicate balance of chemicals in the brain and spinal cord known as neurotransmitters.
In fibromyalgia, this chemical symphony is profoundly out of tune.11
The system is flooded with excitatory, or “accelerator,” neurotransmitters that facilitate and amplify pain signals.
Key among these are Substance P, a chemical messenger involved in pain perception, which has been found in concentrations two to three times higher than normal in the cerebrospinal fluid of fibromyalgia patients, and glutamate, the main excitatory neurotransmitter in the brain.1
At the same time, there is a critical shortage of inhibitory, or “brake,” neurotransmitters that are supposed to dampen pain signals.
Levels of serotonin and norepinephrine, which are crucial for the brain’s descending pain modulatory pathways, are significantly decreased.1
These descending pathways act as the brain’s natural pain-relief system, sending signals down the spinal cord to turn down the volume on incoming pain messages.
In fibromyalgia, this system is impaired, leaving the “volume knob” stuck on high.17
2.3 A Brain Rewired: Objective Evidence from Neuroimaging
The most validating part of the explanation for Elara was the objective proof.
This was not a theory; it was something scientists could now see.
Modern neuroimaging has provided a window into the fibromyalgia brain, refuting the “it’s all in your head” myth with concrete, visual evidence.
Functional magnetic resonance imaging (fMRI) studies, which measure brain activity, have shown that when a person with fibromyalgia is subjected to a mildly painful stimulus, their brain doesn’t just react—it overreacts.
The pain-processing regions of their brain “light up” far more intensely and across a wider area compared to a healthy person receiving the exact same stimulus.21
This is the visual signature of “central amplification”.24
The changes are not just functional; they are structural.
MRI studies have identified physical differences in the brains of people with fibromyalgia, including a measurable reduction in gray matter volume in key pain-processing and emotion-regulating areas like the prefrontal cortex.11
Some research even suggests a pattern of premature brain aging, with an accelerated loss of gray matter over time.11
Furthermore, research into the brain’s electrical activity has revealed that the neural networks in fibromyalgia are primed for a state of hyperreactivity called “explosive synchronization (ES).” In this state, a minor stimulus can trigger a dramatic, widespread, and synchronized network response, much like a power grid cascading into failure.
The degree of this electrical instability has been shown to correlate directly with the intensity of pain the patient reports.32
2.4 Beyond the Brain: The System-Wide Neurological Impact
The problem, Elara learned, is not confined to the brain.
It is a system-wide dysregulation of the entire nervous system.
The autonomic nervous system (ANS), which controls involuntary functions like heart rate, digestion, and the sleep-wake cycle, is also profoundly affected.
Research monitoring heart rate variability over a 24-hour period found that people with fibromyalgia exhibit a “relentless hyperactivity of the sympathetic nervous system”—the body’s “fight or flight” response.33
This system remains overactive even during sleep, which helps explain why sleep is so consistently unrefreshing.
In contrast, the body’s response to actual stress is blunted (a state of sympathetic hypo-reactivity), which could explain the overwhelming fatigue and other symptoms associated with low blood pressure.33
The story also extends to the peripheral nervous system.
While fibromyalgia was long considered a purely central disorder, mounting evidence points to problems in the nerves throughout the body.
A significant subset of patients are found to have small fiber neuropathy (SFN), a condition involving damage or reduction in the small nerve fibers in the skin.
This neuropathy can independently cause pain and also contribute to the dysfunction of the autonomic nervous system.33
In a different line of research, scientists discovered an “enormous increase” in sensory nerve fibers wrapped around tiny blood vessels in the skin of the palms.
This abnormal nerve growth could disrupt normal blood flow and is a potential explanation for the common complaints of pain and tenderness in the hands and feet.33
Table 2: Key Neurological Mechanisms in Fibromyalgia
| Neurological Domain | Key Mechanism | Primary Evidence/Finding | Key Citations |
| Central Pain Processing | Central Sensitization | Presence of allodynia (pain from non-painful touch) and hyperalgesia (amplified pain response). | 21 |
| Brain Structure & Function | Amplified Pain Response & Network Instability | fMRI shows exaggerated brain activation to pain stimuli; Brain networks exhibit “explosive synchronization.” | 31 |
| Structural Changes | Reduced gray matter volume in prefrontal cortex; signs of premature brain aging. | 11 | |
| Neurochemical Balance | Excitatory Neurotransmitter Excess | Increased levels of Substance P and glutamate in cerebrospinal fluid and brain. | 1 |
| Inhibitory Neurotransmitter Deficit | Decreased levels of serotonin and norepinephrine, impairing the brain’s descending pain-inhibition pathways. | 21 | |
| Autonomic Nervous System | Sympathetic Hyperactivity | 24-hour heart rate monitoring shows a relentless “fight or flight” state with no proper rest cycle, even during sleep. | 11 |
| Peripheral Nervous System | Small Fiber Neuropathy (SFN) | Skin biopsies reveal a reduced density of small nerve fibers in a subset of patients. | 33 |
| Abnormal Nerve Growth | Excessive sensory nerve fibers found around blood vessels in the skin of the hands. | 33 |
The neurological basis of fibromyalgia is not a single, isolated defect but a multi-system failure that cascades across the central, peripheral, and autonomic nervous systems.
The various scientific findings—from central sensitization and neurotransmitter imbalances to small fiber neuropathy—are not competing theories but interconnected facets of the same core pathology.
Central sensitization explains the amplification of signals within the CNS.21
The neurochemical imbalances provide the
mechanism for that faulty amplification and failed inhibition.24
Autonomic dysfunction demonstrates that the nervous system’s fundamental regulatory controls for stress and rest are also broken.33
And the discovery of peripheral issues like SFN suggests that the problem may not always originate in the brain but can involve the entire nervous system, with peripheral nerve abnormalities generating the initial “static” that the sensitized CNS then amplifies into a roar of pain.33
This comprehensive view is crucial, as it explains the vast and seemingly unrelated constellation of symptoms that define the fibromyalgia experience.
Chapter 3: The Echoes of Pain – The Lived Experience of a Neurological Disorder
Armed with this new neurological framework, Elara began a process of re-interpretation.
Her life’s narrative, once defined by confusion and self-doubt, was now viewed through a lens of scientific clarity.
The “why” of the science provided a profound validation for the “what” of her daily suffering, connecting the abstract mechanisms of the nervous system to her most intimate and frustrating symptoms.
3.1 More Than Pain: Deconstructing Fibro Fog, Fatigue, and the Emotional Toll
The neurological explanation illuminated the full spectrum of her condition.
The so-called “comorbidities” were not separate, secondary problems but integral manifestations of the primary neurological dysregulation.
Her “fibro fog”—the debilitating cognitive dysfunction marked by poor concentration, memory lapses, and mental slowing—was no longer a sign of personal failure.2
She understood it as a direct consequence of the chaos in her nervous system.
The same neurotransmitter systems that regulate pain—involving serotonin, norepinephrine, and dopamine—also govern focus and executive function.11
Furthermore, the brain’s resources were being constantly exhausted by the task of processing a relentless barrage of amplified pain signals, leaving little energy for higher-level cognitive tasks.11
Her profound fatigue and non-restorative sleep were explained by the objective finding of a sympathetic nervous system stuck in overdrive.33
Her body was in a constant “fight or flight” mode, never able to access the deep, restorative stages of sleep necessary for physical and neurological repair.
Abnormal brain waveforms detected during sleep studies in fibromyalgia patients further confirmed that the very architecture of their sleep is disrupted.1
This creates a vicious cycle where pain disrupts sleep, and poor sleep, in turn, lowers the pain threshold and worsens fatigue.2
The high prevalence of anxiety and depression was also reframed.1
It was not simply that depression was causing her to feel pain.
Rather, both fibromyalgia and mood disorders can arise from shared genetic vulnerabilities and dysfunction in the very same monoaminergic neurotransmitter systems.21
The constant, invisible, and often invalidated experience of chronic pain is also an immense psychological stressor in its own right, capable of triggering mood disorders independently.2
3.2 The Weight of Invisibility: Stigma, Self-Concept, and the Power of Validation
This new understanding allowed Elara to confront the deep psychological wounds inflicted not just by the illness, but by years of medical dismissal.
The experience of being disbelieved, of having her reality questioned, had eroded her sense of self.
Research confirms this is a common experience, leading to a “precarious or negative self-image,” low self-esteem, and a damaged sense of self-efficacy.35
She learned about alexithymia, a trait characterized by difficulty identifying and describing one’s own emotions, which is found in nearly half of all people with fibromyalgia.36
This is not a personality flaw but can be understood as a consequence of a nervous system so overwhelmed with sensory static that the more subtle signals of emotion become lost in the noise, or as a protective mechanism to cope with chronic physiological hyperactivation.36
For Elara, the turning point was the power of the neurological diagnosis.
It was a shield against stigma and a definitive rebuttal to the myth that the pain was “all in your head”.7
The objective evidence from fMRI scans, neurotransmitter studies, and autonomic testing provided the external validation she had been denied for so long.11
This validation was not just comforting; it was a therapeutic intervention.
It allowed her to stop blaming herself for her symptoms and to shift her focus from a desperate search for legitimacy to a proactive effort toward management.13
Chapter 4: Reclaiming Control – A Neurologically-Informed Path Forward
The final chapter of Elara’s diagnostic journey was one of empowerment.
Understanding the neurological “rules” of her condition transformed her from a passive sufferer into an active manager.
The goal was no longer a futile search for a cure for an invisible injury, but a practical, science-based mission to improve her function and reclaim her quality of life through a multimodal approach.17
4.1 A Multimodal Approach: Retraining the Nervous System
The new therapeutic goal was clear: to “turn down the volume” on her sensitized nervous system.25
This complex task requires a combination of strategies, as no single treatment is a panacea.16
The first and most crucial step was patient education.
Understanding the concept of central sensitization is key to patient engagement, as it provides a logical framework for why certain treatments are recommended and helps patients shift from a passive to an active role in their recovery.16
Exercise, which at first seemed counterintuitive, became a cornerstone of her management.
While initial activity could increase pain, starting slowly with gentle aerobic exercises like walking, swimming, or water aerobics and gradually increasing the duration and intensity has been shown to be one of the most effective non-pharmacological treatments.37
The mechanism is neurological: exercise helps modulate the body’s own pain-inhibiting systems and can positively influence neurotransmitter levels.18
Cognitive Behavioral Therapy (CBT) was presented not as a treatment for a psychological illness, but as a practical tool for retraining the brain.
CBT helps patients identify and change the negative thought patterns and behaviors (like pain catastrophizing) that can inadvertently amplify the pain experience and worsen disability.16
Finally, stress management and sleep hygiene became non-negotiable parts of her routine.
Techniques like mindfulness, deep-breathing exercises, and maintaining a strict sleep schedule directly target the underlying neurological dysregulation.
They help to calm the hyperactive sympathetic nervous system and support the restorative processes that are essential for CNS regulation.11
4.2 Pharmacological Tools: Modulating the Signals
Elara learned that the most effective medications for fibromyalgia are not traditional painkillers.
Because there is no peripheral inflammation or acute injury to target, drugs like NSAIDs (e.g., ibuprofen) and most opioids are largely ineffective and can carry significant risks, including opioid-induced hyperalgesia, a condition where opioids can paradoxically worsen pain sensitivity.4
Instead, the focus is on neuromodulators—drugs that work centrally to rebalance the nervous system.
The three medications currently FDA-approved for fibromyalgia in the United States are:
- Pregabalin (Lyrica): A gabapentinoid that works by calming over-excited nerve cells. It is thought to reduce the release of excitatory neurotransmitters like glutamate, thereby dampening the “accelerator” signals.16
- Duloxetine (Cymbalta) and Milnacipran (Savella): These are serotonin-norepinephrine reuptake inhibitors (SNRIs). They work by increasing the availability of the brain’s key “brake” chemicals—serotonin and norepinephrine. By boosting these inhibitory neurotransmitters, SNRIs help to strengthen the brain’s own descending pain-control pathways, effectively helping the brain turn its own volume down.16
Table 3: A Multimodal Management Toolkit for Fibromyalgia
| Treatment Category | Specific Intervention | How It Helps (Symptom Impact) | Neurological Rationale (How It Targets the CNS) | Key Citations |
| Pharmacological | SNRIs (Duloxetine, Milnacipran) | Reduces pain, fatigue, and depression. | Boosts inhibitory neurotransmitters (serotonin/norepinephrine) to strengthen descending pain-control pathways. | 16 |
| Gabapentinoids (Pregabalin) | Reduces pain and can improve sleep. | Calms over-excited neurons by reducing the release of excitatory neurotransmitters (e.g., glutamate). | 16 | |
| Exercise | Graded Aerobic Exercise (Walking, Swimming) | Improves pain, physical function, sleep, and quality of life. | Modulates endogenous pain inhibition systems; alters neurotransmitter levels. | 18 |
| Psychological Therapies | Cognitive Behavioral Therapy (CBT) | Improves pain coping, reduces disability and catastrophizing. | Retrains the brain’s cognitive and emotional responses to pain signals, altering pain-related neural pathways. | 16 |
| Lifestyle / Self-Care | Strict Sleep Hygiene | Improves sleep quality and reduces fatigue. | Supports restorative sleep processes essential for CNS regulation and preventing pain amplification. | 37 |
| Stress Management (Mindfulness, Relaxation) | Reduces anxiety and stress-related symptom flares. | Calms the hyperactive sympathetic nervous system and helps regulate the HPA axis. | 33 |
Effective fibromyalgia management is fundamentally a process of neuromodulation.
The most successful strategies, whether they are pills, therapies, or lifestyle changes, all converge on a single goal: to recalibrate the sensitized central nervous system.
This understanding shifts the patient’s role from that of a passive recipient of painkillers to an active participant in the complex but achievable task of retraining their own nervous system.
Conclusion: A New Narrative of Empowerment
The question of whether fibromyalgia is a neurological disorder can now be answered with a definitive, evidence-based affirmation.
It is unequivocally a disorder of the central nervous system, characterized by aberrant pain processing, neurochemical imbalances, and functional and structural changes in the brain.
This conclusion is not based on a single study but is supported by decades of converging research from neurochemistry, autonomic testing, advanced neuroimaging, and clinical observation.
We return to Elara one last time.
The pain has not vanished entirely, but her relationship with it—and with herself—has been fundamentally transformed.
The diagnosis is no longer a source of shame or a label of mystery, but a map.
It is a scientific framework that gives her symptoms context, her suffering validation, and her management plan a clear rationale.
She has moved from being the victim of an unknown assailant to being an informed manager of a well-defined, albeit complex, neurological condition.
The journey from “it’s all in your head” to “it’s all in your nervous system” represents a monumental paradigm shift.
It is a shift that dismantles generations of stigma, provides profound psychological relief to those who have been disbelieved, and illuminates a clear, multimodal path forward.
While a cure remains elusive, this new narrative—grounded in the hard-won truths of neuroscience—is one of hope, understanding, and, most importantly, empowerment.
Works cited
- Fibromyalgia – Overview and Clinical Manifestations – Johns Hopkins Arthritis Center, accessed on August 12, 2025, https://www.hopkinsarthritis.org/arthritis-info/fibromyalgia/
- Fibromyalgia – Symptoms & causes – Mayo Clinic, accessed on August 12, 2025, https://www.mayoclinic.org/diseases-conditions/fibromyalgia/symptoms-causes/syc-20354780
- Fibromyalgia | Arthritis Foundation, accessed on August 12, 2025, https://www.arthritis.org/diseases/fibromyalgia
- Fibromyalgia case study – Faculty of Pain Medicine, accessed on August 12, 2025, https://fpm.ac.uk/sites/fpm/files/documents/2020-06/FMS%20case%20study%20for%20EPM.pdf
- Fibromyalgia Case Study – Physiopedia, accessed on August 12, 2025, https://www.physio-pedia.com/Fibromyalgia_Case_Study
- Common Misdiagnoses of Fibromyalgia – WebMD, accessed on August 12, 2025, https://www.webmd.com/fibromyalgia/common-misdiagnoses-of-fibromyalgia
- Blog | Fibromyalgia: Facts vs. myths – Reid Health, accessed on August 12, 2025, https://www.reidhealth.org/blog/fibromyalgia-facts-vs-myths
- History of fibromyalgia: past to present – PubMed, accessed on August 12, 2025, https://pubmed.ncbi.nlm.nih.gov/15361321/
- What Is Fibromyalgia?: A History of the Condition – Swing Care, accessed on August 12, 2025, https://www.swing.care/blog/what-is-fibromyalgia/
- History of Fibromyalgia | Fibromyalgia Association Canada (FAC), accessed on August 12, 2025, https://fibrocanada.ca/en/history-of-fibromyalgia/
- Fibromyalgia – StatPearls – NCBI Bookshelf, accessed on August 12, 2025, https://www.ncbi.nlm.nih.gov/books/NBK540974/
- Fibromyalgia: Background, Pathophysiology, Etiology – Medscape Reference, accessed on August 12, 2025, https://emedicine.medscape.com/article/329838-overview
- The fibromyalgia diagnosis – hardly helpful for the patients? A …, accessed on August 12, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC3379768/
- Was Your Fibromyalgia Diagnosis Actually Something Else? – AOTC Jax, accessed on August 12, 2025, https://arthritisjax.com/blog/was-your-fibromyalgia-diagnosis-actually-something-else/
- The Problematic Nature of Fibromyalgia Diagnosis in the …, accessed on August 12, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC6857982/
- Fibromyalgia: Diagnosis and Management | AAFP, accessed on August 12, 2025, https://www.aafp.org/pubs/afp/issues/2023/0200/fibromyalgia.html
- Fibromyalgia: evolving concepts over the past 2 decades – PMC, accessed on August 12, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC3778468/
- Neurobiology of fibromyalgia and chronic widespread pain – PMC – PubMed Central, accessed on August 12, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC5083139/
- Fibromyalgia | Memorial Hermann, accessed on August 12, 2025, https://memorialhermann.org/services/conditions/fibromyalgia
- Can a Neurologist Diagnose Fibromyalgia? – Jeff Steinberg MD, accessed on August 12, 2025, https://drjeffsteinberg.com/can-a-neurologist-diagnose-fibromyalgia/
- Fibromyalgia: Pathogenesis, Mechanisms, Diagnosis and Treatment …, accessed on August 12, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC8068842/
- Central Sensitivity Syndromes: Symptoms and Chronic Pain – Verywell Health, accessed on August 12, 2025, https://www.verywellhealth.com/central-sensitivity-syndromes-716160
- What is Central Sensitization? | MoreGoodDays® Pain-management …, accessed on August 12, 2025, https://www.moregooddays.com/post/what-is-central-sensitization
- The Science of Fibromyalgia – PMC – PubMed Central, accessed on August 12, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC3258006/
- Understanding Centralized Pain – Arthritis Foundation, accessed on August 12, 2025, https://www.arthritis.org/health-wellness/healthy-living/managing-pain/understanding-pain/understanding-centralized-pain
- What Is Fibromyalgia? | MoreGoodDays Pain-management Program, accessed on August 12, 2025, https://www.moregooddays.com/post/what-is-fibromyalgia
- Central Sensitization: When It Is Not “All in Your Head” | AAFP, accessed on August 12, 2025, https://www.aafp.org/pubs/afp/issues/2023/0100/curbside-central-sensitization.html
- Central sensitization, chronic pain, and other symptoms: Better …, accessed on August 12, 2025, https://www.ccjm.org/content/90/4/245
- Fibromyalgia: Understanding, Diagnosis and Modern Approaches to Treatment – MDPI, accessed on August 12, 2025, https://www.mdpi.com/2077-0383/14/3/955
- Serotonin in Fibromyalgia and Chronic Fatigue Syndrome – Verywell Health, accessed on August 12, 2025, https://www.verywellhealth.com/serotonin-in-fibromyalgia-chronic-fatigue-syndrome-716052
- Evidence of a persistent altered neural state in people with fibromyalgia syndrome during functional MRI studies and its relationship with pain and anxiety | PLOS One, accessed on August 12, 2025, https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0316672
- New research reports that hyperreactive brain networks could spark fibromyalgia, accessed on August 12, 2025, https://www.summitpainalliance.com/blog/new-research-reports-that-hyperreactive-brain-networks-could-spark-fibromyalgia
- Research Fibromyalgia – FND Hope International, accessed on August 12, 2025, https://fndhope.org/fnd-research/fibromyalgia-research-articles/
- Fibromyalgia – Wikipedia, accessed on August 12, 2025, https://en.wikipedia.org/wiki/Fibromyalgia
- Psychological impact of fibromyalgia: current perspectives – PMC, accessed on August 12, 2025, https://pmc.ncbi.nlm.nih.gov/articles/PMC6386210/
- Alexithymia and Psychological Distress in Patients With Fibromyalgia and Rheumatic Disease – Frontiers, accessed on August 12, 2025, https://www.frontiersin.org/journals/psychology/articles/10.3389/fpsyg.2019.01735/full
- Fibromyalgia – Diagnosis & treatment – Mayo Clinic, accessed on August 12, 2025, https://www.mayoclinic.org/diseases-conditions/fibromyalgia/diagnosis-treatment/drc-20354785
- What Are the Symptoms of Central Sensitization in Fibromyalgia? – Upper Cervical Chiropractor in Seneca, accessed on August 12, 2025, https://www.uppercervicalseneca.com/central-sensitization-fibromyalgia/
- New Treatments for Fibromyalgia (2025) – DVC Stem, accessed on August 12, 2025, https://www.dvcstem.com/post/new-treatments-for-fibromyalgia
