Neuroplastic Pain

Neuroplastic Pain: refers to pain cause because of changes within the nervous system. These structural and functional changes can occur at every level of the nervous system.

Neuroplasticity: refers to the ability of the nervous system to alter its structure and function.

Neuroplastic Changes Related to Pain Occur at Multiple Levels of the Human Somatosensory System.

The mechanisms of chronic pain differ from those of acute pain.

Traditionally, pain has been regarded as being either nociceptive (arising in response to tissue injury) or neuropathic (arising in response to nerve injury). Although this distinction has had some therapeutic utility, it has served to maintain the Cartesian concept of a fixed immutable pain system that faithfully transmits information from a site of injury to pain centres within the brain. Although this is largely true after acute injury, it is clear from epidemiological studies that in the presence of persistent disease a range of additional factors, often unrelated to the musculoskeletal system, serve to modify activity within pain (nociceptive) pathways. Implicit in recent classification schemes is the notion that acute and chronic pain states are different and that functional changes within the nociceptive system are important in determining the signs and symptoms experienced by individuals with somatic disease [2]. Currently, four different pain states are recognized (Figure 1). The first of these, nociceptive pain, refers to those transient symptoms and signs that arise in response to acute injury and reflects the activation of specialized pain receptors (nociceptors) and corresponding activity in more central pathways. Under these conditions, symptoms broadly reflect the initiating stimulus or injury; treatment at a peripheral level is likely to be successful.

In contrast, neuroplastic pain (also called inflammatory pain) occurs in response to more persistent tissue injury and is the most common pain state associated with musculoskeletal disease [3]. It arises as a result of mediators released from damaged tissues acting to increase the excitability of the nociceptive pathway and has the effect of making everyday activities such as standing or walking painful. Effective therapy requires that attention be directed to both the originating injury and those additional factors (see below) that influence nociceptive activity. Third, neuropathic pain occurs in the presence of nerve injury, as might occur in association with carpal tunnel syndrome or after lumbar disc prolapse. Ectopic expression of ion channels, receptors and related phenomena occur in both injured and neighbouring non-injured neurons, with resultant regional pain hypersensitivity and sensory disturbance. There is currently debate as to the origins of a fourth pain category, idiopathic pain, which covers such medically unexplained disorders as fibromyalgia syndrome, irritable bowel syndrome and tension headache. In all of these disorders, evidence for peripheral pathology is minimal and symptoms are considered to reflect disordered pain processing at more central levels.