2022 Volume 62 Issue 1 Pages 50-56
Insight regarding the mechanism of chronic pain without a diagnosed underlying disease is expanding, particularly where neuroinflammation is concerned. Neuroinflammation occurs in the central nervous system. Recent understanding of neuroinflammation has developed dramatically for some diseases. New therapies, such as anti-C5 antibody therapy for neuromyelitis optica spectrum disorders, have been introduced into clinical practice to target neuroinflammation. The association between glial activation and inflammatory mediators in chronic pain has long been studied. Inflammatory mediators produced by activated glial cells in the central nervous system enhance neural activity, resulting in hypersensitivity.
The 18kDa-translocator protein is an emerging ligand used in PET studies to show glial activation. Stronger PET signals have been detected in certain brain areas of study participants with chronic pain. Such studies are expected to deepen our understanding of the pathophysiology of chronic pain.
Synaptic pruning is a phenomenon through which synapses are eliminated by glial cells. It is believed to be associated with the development of schizophrenia and autism spectrum disorders, and studies show it is related to learning and memory. Synaptic pruning may also play a role in some types of chronic pain. Big data studies of genes related to chronic pain indicate common risk factors, including depression, post-traumatic stress disorder, and autoimmune diseases. Understanding of the chronic pain mechanisms is deepening, and the development of new biomarkers and treatments that are useful in the clinical setting can be expected in the near future.
