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Updated 09/3/2026
Central sensitization can contribute to increased pain sensitivity in some people with chronic pain. But chronic pain and central sensitization are not the same thing. As acute pain becomes persistent, changes in the nervous system may increase sensitivity to pain and other sensory input. These changes are part of the nervous system's ability to adapt—a process known as neuroplasticity. Central sensitization is one possible mechanism involved in some chronic pain conditions. It can contribute to the amplification and persistence of pain, but it is not present in everyone with chronic pain, and chronic pain cannot be explained by central sensitization alone. What is central sensitization? The International Association for the Study of Pain (IASP) defines central sensitization as: "Increased responsiveness of nociceptive neurons in the central nervous system to their normal or subthreshold afferent input.” In simpler terms, the nervous system can become more responsive to sensory signals, so stimuli that might normally produce little pain—or no pain—can sometimes produce a stronger pain response. Central sensitization is a neurophysiological process, not simply another name for chronic pain. In clinical practice, it can only be inferred indirectly from findings such as increased sensitivity to normally painful stimuli (hyperalgesia) or to non-painful stimuli (allodynia). What might it feel like? In some people, increased sensitivity may mean that relatively light touch, pressure, or movement feels unusually painful. Pain may also become more widespread rather than remaining limited to the original area of injury. People may describe their pain in different ways, including:
These experiences are real. However, experiencing widespread pain or sensitivity does not by itself prove that central sensitization is present. Central sensitization is a physiological mechanism that cannot be diagnosed simply by the presence of these symptoms. How is central sensitization related to chronic pain? Features and mechanisms associated with central sensitization have been identified across a range of chronic pain conditions, including fibromyalgia, some forms of headache, osteoarthritis, chronic low back pain, temporomandibular disorders, whiplash-associated disorders, and some visceral pain conditions. However, the extent to which central sensitization contributes varies among individuals and conditions. This is important because not everyone with the same diagnosis has the same pain mechanisms. For example, two people may both have chronic low back pain, but their pain may be influenced by different combinations of biological, psychological, and social factors. Central sensitization may be one contributor for some people, not the explanation for everyone's pain. Central sensitization is not the same as nociplastic pain These terms are sometimes used interchangeably, but they are not identical. Central sensitization refers to a specific neurophysiological process involving increased responsiveness of nociceptive neurons in the central nervous system. Nociplastic pain, on the other hand, is a clinical pain mechanism defined by the IASP as pain arising from altered nociception despite no clear evidence of ongoing tissue damage activating nociceptors or a lesion or disease of the somatosensory nervous system. Central sensitization may contribute to nociplastic pain, but the two terms describe different concepts. Understanding this distinction helps prevent an overly simple explanation such as "your nervous system is misfiring, so that's why you hurt." Pain is more complicated than that. Changing the pain experience The good news: the nervous system can change. Neuroplasticity means that the nervous system is capable of changing its function in response to experience. That includes changes that may contribute to persistent pain—but neuroplasticity also means that the nervous system can adapt in helpful ways. This is one reason rehabilitation focuses on more than simply trying to eliminate pain. Rather than trying to "turn off" central sensitization, the goal is often to improve function, reduce fear and sensitivity, build physical capacity, and help the nervous system respond more appropriately to movement and everyday activities. Research supports multimodal approaches that may include pain education, appropriately progressed exercise, psychological strategies, sleep and stress management, and individualized medical treatment. A biopsychosocial approach There is no single treatment that works for everyone with chronic pain or increased pain sensitivity. A biopsychosocial approach recognizes that pain can be influenced by interacting biological, psychological, and social factors. Depending on the individual, treatment and self-management may include:
The goal isn't necessarily to eliminate every pain signal. The goal is to help you reduce the impact of pain, improve function, build confidence, and regain control over your life. I experienced this multidisciplinary approach firsthand through the Mayo Clinic Pain Rehabilitation Center, where I received a heavy dose of education, physical rehabilitation, psychological strategies, and self-management skills. The bottom line Central sensitization is a real neurophysiological phenomenon that can contribute to increased pain sensitivity in some people. But central sensitization is not synonymous with chronic pain. Chronic pain is complex, and different people can have different combinations of mechanisms contributing to their pain. Understanding how the nervous system can become more sensitive can be helpful—but it is equally important not to replace one overly simple explanation with another. Your pain is real. Your nervous system can change. And there are evidence-informed ways to improve how you live with pain, even when pain persists. Learn more
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