"For one in five Americans, chronic pain is inescapable, calmed only by a laundry list of medications and being forced to scale back on the demands of everyday life. Of the 51 million adults suffering from chronic pain, recent surveys show three in four endure some degree of disability, leaving many unable to work or function. The causes of chronic pain, from shoulders and backs to knees and feet, have long been debated, with no clear answer coming out on top."
"In a new study, researchers aimed to understand how acute, or temporary, pain becomes chronic. To do so, they honed in on a pathway in the brain between the caudal granular insular cortex (CGIC), a sugar cube-sized cluster of cells deep within a bodily sensation processing part of the brain called the insula, and the primary somatosensory cortex, which perceives pain and touch."
"Injuries to the sciatic nerve have been shown to cause allodynia, which makes touch feel painful. Using gene editing to turn off certain neurons, the researchers found that while the CGIC played a limited role in processing acute pain, it sent signals to parts of the brain that process pain to tell the spinal cord to keep chronic pain from dissipating."
A neural pathway linking the caudal granular insular cortex (CGIC) and the primary somatosensory cortex promotes the persistence of chronic pain. Mouse models of sciatic-nerve injury that produce allodynia demonstrated that CGIC signals reach pain-processing brain regions and instruct the spinal cord to sustain chronic pain. Gene-editing inhibition of neurons in the CGIC pathway reduced pain behaviors and reversed allodynia, despite the CGIC having a limited role in acute pain processing. Targeting the CGIC pathway could enable development of medications or treatments to prevent or reverse chronic pain.
Read at Mail Online
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