Fibromyalgia (FM) is a chronic disorder defined by widespread musculoskeletal pain, profound fatigue, and cognitive difficulties often referred to as “fibro fog.” The pain is diffuse and persistent, leading many to question if this constant ache represents true “nerve pain.” Understanding the mechanism behind this pervasive discomfort is fundamental to diagnosing and effectively treating the condition. The answer lies in distinguishing between pain types, as FM is often a complex, multi-layered disorder of the nervous system.
Understanding Fibromyalgia Pain vs. Neuropathic Pain
Chronic pain is generally categorized by its underlying source, most commonly split into nociceptive and neuropathic types. Nociceptive pain arises from actual or potential tissue damage, such as from a sprain or inflammation, and typically presents as a throbbing, aching, or sharp sensation. Neuropathic pain, by contrast, is a malfunction within the somatosensory nervous system itself, signaling pain without an ongoing injury. This true nerve pain is often described as burning, shooting, stabbing, or tingling sensations, like an electric shock. While fibromyalgia pain can feel burning or electric-like, the primary cause has historically been attributed to a separate central process, not peripheral nerve damage.
Central Sensitization: The Core Mechanism of Fibromyalgia
The dominant theory explaining the widespread pain in most fibromyalgia cases is a phenomenon known as central sensitization (CS). CS is a form of neuroplasticity where the nervous system becomes persistently hyper-responsive to sensory input. This process involves an amplification of pain signals within the spinal cord and brain, essentially turning the nervous system’s “volume control” up too high.
This central amplification leads to two hallmark symptoms: allodynia and hyperalgesia. Allodynia is the experience of pain from a stimulus that should not be painful, such as the gentle touch of clothing. Hyperalgesia involves an exaggerated pain response to a mildly painful stimulus, making even a small bump feel excruciatingly painful.
The mechanism is supported by neurochemical changes, including elevated levels of excitatory neurotransmitters like Substance P and glutamate in the cerebrospinal fluid. These chemicals lower the threshold required for neurons to fire, keeping the central nervous system in a state of high alert.
Small Fiber Neuropathy: The Direct Nerve Connection
Although central sensitization explains the widespread hypersensitivity, research suggests a subset of fibromyalgia patients experiences true peripheral nerve damage. Studies indicate that approximately 40% to 60% of people diagnosed with fibromyalgia also meet the criteria for Small Fiber Neuropathy (SFN). SFN is a condition involving the damage or loss of the small, unmyelinated nerve fibers found primarily in the skin.
These fibers transmit pain and temperature sensations, meaning damage constitutes a measurable, physical peripheral neuropathy. Diagnosis of SFN is confirmed objectively through a skin punch biopsy, which measures the intraepidermal nerve fiber density (IENFD). A reduced IENFD count provides direct evidence of peripheral nerve damage, distinct from central amplification. SFN is true neuropathic pain, and its presence in many patients indicates that “nerve pain” is a real component of the condition.
Managing Fibromyalgia Pain Based on Mechanism
Understanding the mechanism driving an individual’s pain—whether central sensitization, peripheral SFN, or both—is guiding treatment strategies. Therapies for central sensitization aim to modulate the hyperactive central nervous system.
Medications like pregabalin work by binding to voltage-gated calcium channels, which reduces the release of excitatory neurotransmitters that amplify pain signals. Other pharmaceutical options, such as the serotonin-norepinephrine reuptake inhibitor (SNRI) duloxetine, increase levels of these neurotransmitters, boosting the body’s natural descending pain inhibitory pathways.
Non-pharmacological approaches are also geared toward retraining the sensitized nervous system. Exercise therapy and cognitive behavioral therapy (CBT) help patients manage their response to pain and gradually increase physical activity.
For patients whose symptoms are strongly linked to SFN, treatment may focus on identifying and addressing the underlying cause of the nerve damage, if one is found. This mechanism-based approach ensures that treatment is personalized, targeting the brain’s pain processing center, the physical peripheral nerve damage, or a combination of both.