Emerging relationships between exercise, sensory nerves, and neuropathic pain
Twenty-five million Americans are encumbered by acute pain and over 50 million suffer from varying chronic pain syndromes, leading to a medical cost of over $635 billion a year. This enormous health plight highlights the need to find novel interventions to reduce the burden of chronic pain. Generally speaking, chronic pain undergoes a progressive movement from peripheral tissues, such as the hands and feet, to the central nervous system which often leads to even more debilitating and chronic effects as the disease progresses. The perception of pain is a very broad and complex mechanism to study, having multiple origins including nerve damage, metabolic disease, and numerous others. Each form of pain may be unique not only in its development but also in the treatments necessary to provide relief. Unfortunately, current therapies available for the treatment of these pain states are still associated with pain abatement and do not address underlying mechanisms driving the development of varying forms and levels of sensory discomfort.
Physical activity offers a wide array of benefits and is well documented to help in a myriad of diseases, however the mechanisms by which exercise exerts its benefits are poorly understood. The complexities of understanding how global cross organ communication and changes induce molecular changes to provide benefits in disease makes exercise research often hard to perform on a basic level. However, the clear benefits of exercise provide a strong rational to continue to study this complex intervention.
Nociceptive and neuropathic pain syndromes both receive physiological and behavioral benefits from exercise intervention, even though they are thought to have separate physiological characteristics. Nociceptive pain results from an expected noxious stimulus, while neuropathic pain occurs in the absence of a stimulus, or with a normally innocuous stimulus. The neuronal pathway of nociceptive pain starts with a noxious stimulus detected by a peripheral sensory peripheral terminal, of an Aδ- or C-fiber. The electrical signal is then propagated up through spinal and thalamic pathways to terminate in an appropriate somatotopic region of the cortex. In the case of neuropathic pain, adaptations occur in Schwann cells, satellite cells, the peripheral immune system, spinal microglia, and astrocytes that lead to the development of a painful syndrome when one would not normally exist. Important areas to examine in these pain pathways are interneuronal interactions and the molecular and cellular changes that are initiated within them. This is an important aspect of any therapeutic target for pain due to the activity-dependent neuronal plasticity that occurs in the nervous system.
In response to new information about neuronal activity-dependent plasticity, a new and rapidly growing area within both pain research and neural physiology has begun to examine the effects of exercise on peripheral and central nervous system components. However, the scarcity of well-controlled basic research in this area hampers the utilization of exercise as a therapy for neuropathic and other chronic pain syndromes. While exercise intervention is growing quickly as a clinical therapeutic tool for many diseases, its use to reduce pain states is still relatively new and the research available leaves an incomplete picture of the molecular pathways affected. Continued research therefore is vital to gain a better understanding of how exercise benefits the management of various pain syndromes and for the implementation of this therapeutic technique on a broader scale by physicians.
Read the full article on Frontiers in Neuroscience Diabetes.
Posted: Aug. 23, 2016