What causes chronic pain? A new study identifies a key culprit | CU Boulder Today
A newly identified neural circuit deep within the brain may hold the key to understanding—and potentially stopping—the transition from temporary pain to chronic pain, according to research from the University of Colorado Boulder. The study, published in the Journal of Neuroscience, details how silencing this specific pathway can prevent or even reverse long-lasting pain conditions.
Unraveling the Mystery of Chronic Pain
Chronic pain affects a significant portion of the population. Approximately one in four adults experience chronic pain, and for nearly one in ten, this pain interferes with daily life and work, according to the Centers for Disease Control. While acute pain is a normal response to injury, serving as a warning signal, chronic pain persists long after the initial injury has healed.
Researchers have long sought to understand why pain becomes chronic. Linda Watkins, distinguished professor of behavioral neuroscience, explains, “Why, and how, pain fails to resolve, leaving you in chronic pain, is a major question that is still in search of answers.” This new research focuses on a region of the brain called the caudal granular insular cortex (CGIC), a “sugar-cube-sized cluster of cells” within the insula.
The Role of the CGIC
The study utilized advanced techniques, including fluorescent proteins and “chemogenetic” tools, to observe and manipulate neuron activity in rats with sciatic nerve injuries. Researchers discovered that the CGIC has a minimal role in processing acute pain, but is crucial in the development of persistent pain. The CGIC signals the brain’s pain processing center, the somatosensory cortex, which then instructs the spinal cord to continue registering pain.
According to Jayson Ball, the study’s first author, “We found that activating this pathway excites the part of the spinal cord that relays touch and pain to the brain, causing touch to now be perceived as pain, as well.” Silencing the CGIC pathway, however, had a dramatic effect. When the pathway was disabled immediately after injury, the rats experienced only short-lived pain. In animals already suffering from chronic pain, disabling the pathway brought relief.
What’s Next for Pain Research?
The current research was conducted on rats, and further investigation is needed to determine if these findings translate to humans. It remains unclear what initially triggers the CGIC to begin sending chronic pain signals. However, the findings open the door to potential new therapies.
Ball envisions a future where pain is treated with targeted infusions or brain-machine interfaces that modulate specific brain cells, avoiding the systemic side effects and risk of dependency associated with opioids. He notes that a “gold rush of neuroscience” is underway, with numerous startups developing brain-machine interfaces for various health applications. He believes that the increasing sophistication of tools for manipulating brain cells is accelerating the pace of discovery.
Frequently Asked Questions
What is the difference between acute and chronic pain?
Acute pain is a temporary warning sign triggered by injury, while chronic pain is a persistent signal that continues long after the initial injury has healed, functioning more like a false alarm.
Where is the caudal granular insular cortex (CGIC) located?
The CGIC is a small cluster of cells located deep within the folds of the insula, a portion of the human brain.
What happened when researchers silenced the CGIC pathway in rats?
Silencing the CGIC pathway immediately after injury resulted in short-lived pain, and in rats already experiencing chronic pain, disabling the pathway caused the pain to cease.
As neuroscience continues to advance, could a future free from the burden of chronic pain be within reach?