Fibromyalgia (FM) is a chronic pain disorder characterized by widespread musculoskeletal pain that persists over a long period. This pain is often accompanied by profound fatigue, poor sleep quality, and cognitive difficulties, sometimes referred to as “fibro fog.” Neuropathy involves damage or dysfunction of the peripheral nerves—those outside the brain and spinal cord—leading to weakness, numbness, and pain, often described as tingling or burning. Given the shared element of chronic pain, patients frequently wonder if the pervasive pain of fibromyalgia is actually a form of nerve damage. This question of a direct causal relationship between the two conditions is a major focus in current pain research.
The Direct Answer: Identifying the Neuropathic Link
Yes, research suggests a strong association, and often a potential causal link, between fibromyalgia and a specific type of nerve damage. The prevalence of neuropathy is notably higher in FM patients than in the general population. While FM was historically viewed as a centralized pain syndrome originating solely from the brain and spinal cord, evidence now points to a peripheral component in a substantial subset of patients. The specific form of nerve damage most frequently co-occurring with FM symptoms is Small Fiber Neuropathy (SFN).
SFN is a condition where the thinnest nerve fibers—those responsible for transmitting pain, temperature, and autonomic functions—are damaged. The presence of SFN does not replace an FM diagnosis, but it offers a measurable physical pathology for the pain experience in many individuals. Studies estimate that between 40% and 60% of fibromyalgia patients show objective signs of SFN. This tissue-level pathology provides new avenues for diagnosis and treatment that move beyond therapies aimed only at the central nervous system.
Small Fiber Neuropathy The Primary Connection
Small Fiber Neuropathy (SFN) affects the small, unmyelinated C-fibers and thinly myelinated A-delta fibers of the peripheral nervous system. These fibers transmit sensory information related to pain and temperature, unlike the large, myelinated fibers that handle motor function, vibration, and light touch. Damage to these small sensory fibers often results in a characteristic burning pain, tingling, and numbness. These small fibers also control certain autonomic functions, such as heart rate, blood pressure, and sweating.
Diagnosing SFN involves specialized testing for objective signs of nerve damage. The gold standard diagnostic tool is a 3-millimeter skin punch biopsy, typically taken from the calf or thigh, to measure the Intraepidermal Nerve Fiber Density (IENFD). A reduced IENFD—meaning fewer nerve fibers are present in the skin—confirms the anatomical presence of SFN.
Another diagnostic measure is the Quantitative Sudomotor Axon Reflex Test (QSART), which assesses the function of the small autonomic nerve fibers that innervate the sweat glands. An abnormal QSART result indicates a dysfunction in the small nerves controlling sweating. The unmyelinated C-fibers are directly implicated in central sensitization, the heightened pain state seen in FM, suggesting that peripheral damage can contribute to the central pain mechanism.
Distinguishing Symptoms of FM and SFN
Fibromyalgia and Small Fiber Neuropathy share a significant overlap in symptoms, including generalized pain and fatigue, making distinction difficult without objective testing. However, SFN introduces specific neuropathic signs that help differentiate the cause of the pain. These symptoms often include a prominent burning, prickling, or electric-shock-like sensation, known as paresthesia or dysesthesia.
The presence of allodynia—pain caused by a stimulus that normally does not provoke pain, such as light touch—is a strong indicator of SFN-related hypersensitivity. SFN frequently causes autonomic dysfunction symptoms, which are less common in FM alone. These can manifest as dry eyes or mouth, blood pressure instability, and Postural Orthostatic Tachycardia Syndrome (POTS), characterized by an abnormal increase in heart rate upon standing.
Understanding this distinction guides the treatment approach. Fibromyalgia treatments focus on modulating the central nervous system with medications like certain antidepressants and anticonvulsants, exercise, and cognitive therapies. If SFN is confirmed, treatment can be targeted specifically at the neuropathic component, possibly involving medications that stabilize nerve membranes or immunotherapies if an underlying immune cause is suspected. The presence of SFN provides an objective, measurable target for therapeutic intervention.
Scientific Theories Connecting Fibromyalgia and Neuropathy
The exact mechanism connecting fibromyalgia and small fiber neuropathy is still under investigation, but current scientific theories converge on several distinct hypotheses. One prominent theory involves neuroinflammation, where chronic low-grade inflammation in the peripheral nerves or the dorsal root ganglia (DRG) causes nerve damage. The DRG, which house the cell bodies of the sensory nerves, may act as a site where peripheral injury triggers central nervous system sensitization.
Another area of focus is on channelopathies, which are dysfunctions of the ion channels, particularly voltage-gated sodium channels, in the small nerve fibers. These channels are responsible for initiating and propagating nerve signals. Their malfunction can cause the nerve to become hyperexcitable, spontaneously firing pain signals even without an external stimulus. Researchers are investigating specific sodium channel subtypes, such as NaV 1.8, as potential targets for new analgesic medications.
Immune system dysregulation is also being explored, suggesting that an autoimmune process may target and damage the small nerve fibers. This hypothesis is supported by the fact that a small subset of patients with SFN and FM features have shown improvement with immunotherapies like intravenous immunoglobulin (IVIg). The growing evidence for a physical, measurable neuropathy in a significant portion of FM patients supports the view of fibromyalgia as a neurological entity with both central and peripheral components.