Fibromyalgia (FM) is a chronic condition defined by persistent, widespread pain accompanied by symptoms like fatigue, sleep disturbance, and cognitive difficulties. The pain is real, yet its source is often confusing because it does not follow the traditional pattern of pain caused by localized injury or inflammation. This complexity leads to the question of whether FM pain is a form of nerve damage or something fundamentally different. Clarifying the origin of this discomfort is essential for effective diagnosis and management. This article explains the unique neurological mechanism behind FM pain and contrasts it with traditional nerve pain.
The Nature of Fibromyalgia Pain
The fundamental mechanism driving the pain experience in fibromyalgia is central sensitization. This process involves an amplification of pain signals within the central nervous system (the brain and spinal cord). Essentially, the nervous system’s pain “volume knob” is stuck on a high setting, causing a heightened response to normal sensations.
Central sensitization transforms how the body processes incoming sensory information, leading to two types of pain hypersensitivity. The first is allodynia, where a non-painful stimulus is perceived as painful. The second is hyperalgesia, meaning an already painful stimulus is felt much more intensely than it should be.
This amplification occurs because specific neurons in the spinal cord and brain become hyperexcitable, maintained by alterations in neurotransmitter levels. Studies suggest increased levels of excitatory neurotransmitters like Substance P contribute to this hyperexcitable state.
Functional brain imaging studies support this model by showing increased activation in pain-processing regions of the brain in people with FM. The pain is therefore an over-processing of signals by a hypersensitive nervous system. This mechanism explains why common treatments aimed at reducing peripheral inflammation, such as nonsteroidal anti-inflammatory drugs (NSAIDs), are often ineffective.
Distinguishing Fibromyalgia from Neuropathy
The unique nature of FM pain distinguishes it from classic neuropathy, which is pain caused by damage or disease affecting the peripheral nerves. Traditional nerve pain, such as diabetic neuropathy or sciatica, results from direct physical injury or compression of nerve fibers. Neuropathic pain is often described as shooting, burning, electrical, or tingling sensations, and is usually localized to the area supplied by the damaged nerve.
In contrast, the defining symptom of fibromyalgia is widespread pain across the entire body, driven by the central nervous system’s heightened sensitivity. The peripheral nerves themselves are generally intact in people with FM. The problem lies in how the spinal cord and brain process the signals sent by those nerves, confirming the pain source is centralized.
A subset of individuals diagnosed with FM may also exhibit small fiber neuropathy (SFN). SFN involves damage to small sensory and autonomic nerve fibers in the skin, causing symptoms like burning and numbness, especially in the hands and feet. While SFN may contribute to some peripheral symptoms, the widespread nature of FM is fundamentally rooted in the central sensitization mechanism.
Establishing a Fibromyalgia Diagnosis
Because fibromyalgia is a disorder of pain processing rather than tissue or nerve damage, no definitive lab test or imaging study exists to confirm the diagnosis. Doctors rely on meeting specific clinical criteria and systematically ruling out other conditions that mimic FM symptoms. This ensures the widespread pain is not mistakenly attributed to an underlying inflammatory, autoimmune, or thyroid disorder.
The current diagnostic criteria from the American College of Rheumatology (ACR) focus on two main components: the Widespread Pain Index (WPI) and the Symptom Severity (SSS) score. The WPI quantifies the number of body areas where the patient has experienced pain over the past week. The SSS assesses the severity of general symptoms like fatigue, unrefreshed sleep, and cognitive problems.
For a diagnosis of FM, a patient must meet specific thresholds on both the WPI and SSS, and the symptoms must have persisted for at least three months. This standardized approach has replaced the older reliance on counting “tender points” during a physical exam.
Treatment Approaches Targeting Centralized Pain
Treatment strategies for fibromyalgia are designed to address central sensitization by modulating the central nervous system. Since the pain originates from faulty signal processing, treatments focus on “turning down the volume” of the nervous system rather than blocking peripheral pain. This explains why common pain relievers and anti-inflammatory drugs often provide minimal relief.
Pharmacological options include FDA-approved medications that target brain chemicals and nerve activity. These often belong to the classes of certain anticonvulsants, which calm overactive nerve cells, and serotonin-norepinephrine reuptake inhibitors (SNRIs). These drugs modulate neurotransmitters involved in pain pathways and mood regulation, normalizing the dysfunctional signaling that causes hypersensitivity.
Non-pharmacological approaches are also important, focusing on retraining the brain’s pain response. Cognitive behavioral therapy (CBT) helps patients understand their pain and develop coping strategies to influence central pain processing. Graded aerobic and strengthening exercise is recommended to help reset the nervous system’s response to physical activity and improve related symptoms like sleep quality and fatigue.