Pathophysiology Under persistent activation, the transmission of pain signals to the dorsal horn may produce a pain wind-up phenomenon. This triggers changes that lower the threshold for pain signals to be transmitted. In addition, it may cause nonnociceptive nerve fibers to respond to, generate, and transmit pain signals. The type of nerve fibers that are believed to generate the pain signals are the C-fibers, since they have a slow conductivity and give rise to a painful sensation that persists over a long time. In chronic pain, this process is difficult to reverse or stop once established. In some cases, chronic pain can be caused by genetic factors which interfere with neuronal differentiation, leading to a permanently lowered threshold for pain. Chronic pain of different causes has been characterized as a disease that affects brain structure and function. MRI 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, which is reversible once the pain has resolved. These structural changes can be explained by neuroplasticity. In the case of chronic pain, the somatotopic representation of the body is inappropriately reorganized following peripheral and central sensitization. This can cause allodynia or hyperalgesia. In individuals with chronic pain, EEGs showed altered brain activity, suggesting pain-induced neuroplastic changes. More specifically, the relative beta activity (compared to the rest of the brain) was increased, the relative alpha activity was decreased, and the theta activity was diminished. Dysfunctional dopamine management in the brain could potentially act as a shared mechanism between chronic pain, insomnia and major depressive disorder. Astrocytes, microglia, and Satellite glial cells have also been found to be dysfunctional in chronic pain. Increased activity of microglia, alterations of microglial networks, and increased production of chemokines and cytokines by microglia might aggravate chronic pain. Astrocytes have been observed to lose their ability to regulate the excitability of neurons, increasing spontaneous neural activity in pain circuits.
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