Pain is a complex sensory and emotional experience. Modern pain science recognizes that the experience of pain can extend beyond simple injury or nerve damage. In 2017, the International Association for the Study of Pain (IASP) formally recognized a third category of pain, moving beyond the historical two-part classification. This newest descriptor is called nociplastic pain, which arises from altered nociception without clear evidence of actual or threatened tissue damage or a lesion of the somatosensory system. The recognition of this distinct mechanism is a significant step toward better understanding chronic pain conditions.
Distinguishing Nociplastic Pain from Other Pain Types
Pain has historically been classified into two main types based on the source of the discomfort. Nociceptive pain results from actual or threatened damage to non-neural tissue, such as a sprained ankle or inflammation associated with arthritis. This type of pain is typically localized, serves a protective function, and resolves as the tissue heals.
The second established category is neuropathic pain, which is caused by a lesion or disease directly affecting the somatosensory nervous system itself. Conditions like diabetic neuropathy or sciatica, where a nerve is compressed or damaged, fall into this group. Neuropathic pain is often described with distinct qualities, such as burning, shooting, or electric-shock sensations, and is typically limited to the distribution of the affected nerve.
Nociplastic pain stands apart because it is neither caused by clear tissue damage nor by a demonstrable disease or lesion of the nerve structures. The source of the pain is a dysfunction of how the central nervous system processes sensory information. This means pain signals are generated or amplified within the spinal cord and brain, even when the initial cause has long since healed or was never present. It is characterized by pain that is often more widespread or intense than expected based on physical findings.
Understanding Central Sensitization
The primary mechanism underlying nociplastic pain is a phenomenon known as central sensitization. This process involves the central nervous system—the brain and spinal cord—becoming hyper-responsive to incoming sensory signals. The chronic signaling of pain, even from a minor initial injury, can lead to structural and chemical changes in the central nervous system that effectively “turn up the volume” on pain perception.
One clear manifestation of central sensitization is hyperalgesia, which is an increased pain response to a stimulus that is already recognized as painful. Another common feature is allodynia, where a stimulus that should not cause pain at all, such as a light touch or the pressure of clothing, is perceived as painful. These altered responses indicate that the central pathways are now interpreting normal, non-threatening sensations as danger signals.
At a cellular level, this hypersensitivity involves changes like the enhanced excitability of neurons in the spinal cord and reduced effectiveness of the body’s natural pain-inhibitory pathways. These changes mean the brain’s filtering and modulation systems are compromised, leading to an amplified and persistent experience of pain that is disproportionate to any ongoing peripheral cause.
Common Conditions Associated with Nociplastic Pain
Nociplastic processes are often the dominant or contributing factor in several chronic pain syndromes that lack clear structural pathology. Fibromyalgia is the archetypal condition associated with this mechanism, characterized by widespread pain, fatigue, and hypersensitivity to touch across multiple body regions. The symptoms of these conditions frequently include co-occurring non-pain symptoms, such as sleep disturbances, cognitive difficulties, and mood problems, reflecting the centralized nature of the dysfunction.
Other common disorders where nociplastic pain plays a significant role include Irritable Bowel Syndrome (IBS) and chronic widespread low back pain that has persisted beyond the expected healing time. Temporomandibular Disorder (TMD) is also frequently associated with this mechanism, presenting as chronic facial and jaw pain without clear joint damage.
Comprehensive Management and Treatment Approaches
The management of nociplastic pain is fundamentally different from treating pain caused by a simple injury, requiring a shift in therapeutic focus. The goal is not to fix a damaged body part, but to “retrain” the nervous system to decrease its hypersensitivity. A coordinated, multimodal approach that integrates both non-pharmacological and pharmacological strategies is considered the most effective way to address this centralized mechanism.
Non-Pharmacological Strategies
A cornerstone of non-pharmacological treatment is patient education, often referred to as Pain Neuroscience Education. This involves explaining to the patient that their pain is real and biological, but is caused by a sensitive nervous system, not by ongoing tissue damage. This understanding is a powerful therapeutic tool, helping to reduce the fear and anxiety that can otherwise contribute to pain amplification.
Psychological interventions, such as Cognitive Behavioral Therapy (CBT) and mindfulness, help patients manage the cognitive and emotional dimensions of their chronic pain. These therapies focus on modifying maladaptive thoughts and behaviors to reduce stress and its impact on the nervous system. Graded exercise and physical therapy are also employed, but they focus on gradually increasing movement and function without provoking fear, thereby signaling safety to the sensitized nervous system.
Pharmacological Strategies
Traditional pain relievers like opioids and non-steroidal anti-inflammatory drugs (NSAIDs) are generally ineffective for nociplastic pain and are often strongly discouraged due to potential risks. Instead, medications that modulate nerve function and neurotransmitter levels in the central nervous system are used. These include certain classes of antidepressants, specifically Serotonin–Norepinephrine Reuptake Inhibitors (SNRIs) like duloxetine, and anticonvulsants, such as gabapentinoids, which work by calming the hyper-excitable central pathways.