Can Chronic Pain Changes be Reversed?

plasticityNeuroplasticity refers to the nervous system’s ability to change its structure and function. The brain’s ability to reorganize itself has been demonstrated many times including when it is recovering from a stroke or from a traumatic injury.  What are neuroplasticity’s implications for pain?

Recent neuroplasticity studies have shown that chronic pain can lead to many changes in the nervous system on a chemical, functional, and anatomical level.1 A striking example of this phenomenon can be seen following major trauma, such as spinal cord injury or limb amputation, where regions of the brain that typically respond to stimuli from the missing or damaged part of the body can be activated by input from adjacent body regions.2 Although the exact mechanisms behind this reorganization are still poorly understood, such changes seem to be strongly associated with pain.

Other examples of chemical and structural reorganization of the nervous system as a result of pain or injury involve receptor and neurotransmitter changes leading to dysfunctional pain modulation and central sensitization.3,4 This can increase the intensity of pain in conditions such as fibromyalgia, by amplifying peripheral pain signals.  Although neuroplasticity is a normal repair mechanisms of the central nervous system, it may be a maladaptive process when it comes to pain.

However, there is hope. Although nervous system changes occur in chronic pain patients, they are not necessarily irreversible. For example, a large number of people suffering from hip osteoarthritis demonstrated rapid reversal of neuroplastic changes after total hip replacement, regardless of the severity or duration of the pain prior to surgery.5

These findings have contributed to better understanding of central pain processing mechanisms and may lead to better treatment options for chronic pain in the near future.

Meriem Mokhtech, BS
Senior Laboratory Technician
UF Center for Musculoskeletal Pain Research



  1. Seifert F, Maihofner C. Functional and structural imaging of pain-induced neuroplasticity. Curr Opin Anaesthesiol 2011; 24: 515-523
  2. Wrigley PJ, Press SR, Gustin SM, et al. Neuropathic pain and primary somatosensory cortex reorganization following spinal cord injury. Pain 2009;141: 52-59.
  3. Price DD, Verne GN, Schwartz JM. Plasticity in brain processing and modulation of pain. Prog Brain Res 2006; 157: 333-352.
  4. Latremoliere A, Woolf CJ. Central sensitization: a generator of pain hypersensitivity by central neural plasticity. J Pain 2009; 10: 895-926.
  5. Gwilym SE, Filippini N, Douaud G, et al. Thalamic atrophy associated with painful osteoarthritis of the hip is reversible after arthroplasty: a longitudinal voxel-based morphometric study. Arthritis Rheum 2010; 62: 2930-2940.