Chronic Pain - Pathophysiology

Pathophysiology

Under persistent activation nociceptive transmission to the dorsal horn may induce a wind up phenomenon. This induces pathological changes that lower the threshold for pain signals to be transmitted. In addition it may generate nonnociceptive nerve fibers to respond to pain signals. Nonnociceptive nerve fibers may also be able to generate and transmit pain signals. In chronic pain this process is difficult to reverse or eradicate once established.

Chronic pain of different etiologies has been characterized as a disease affecting brain structure and function. Magnetic resonance imaging studies have shown abnormal anatomical and functional connectivity, even during rest involving areas related to the processing of pain. Also, persistent pain has been shown to cause grey matter loss, reversible once the pain has resolved.

These structural changes can be explained by the phenomenon known as neuroplasticity. In the case of chronic pain, the somatototic representation of the body is inappropriately reorganized following peripheral and central sensitization. This maladaptative change results in the experience of allodynia and/or hyperalgesia. Brain activity in individuals suffering from chronic pain, measured via electroencephalogram (EEG), has been demonstrated to be altered, suggesting pain-induced neuroplastic changes. More specifically, the relative beta activity (compared to the rest of the brain) is increased, the relative alpha activity is decreased, and the theta activity both absolutely and relatively is diminished.