Why Pain Memory May Drive Chronic Back Pain
For years scientists have considered inflammation as a primary mechanism for pain. This is certainly true for acute pain, but new research suggests that it is not the case for chronic pain lasting beyond the injury healing period, typically three months. This explains why analgesics such as NSAIDs (ibuprofen, aspirin, naproxen) that work well to reduce pain for acute injuries don’t work well for chronic back pain. According to researchers, chronic pain is caused by central sensitization, a state of hypersensitivity in the central nervous system (spinal cord and brain), resulting from neuroplasticity: the ability of brain cells (neurons) to change the way they fire based on changes in the environment (McCarberg & Peppin, 2019; Mansour, Farmer et al., 2014).
Neuroplasticity is a form of learning. It takes place throughout the lifespan and is an evolutionary survival mechanism. For our Paleolithic ancestors, successful defense against predatory animals was key to survival. Remembering these strategies enabled parents to teach their children self-defense. Today, this form of neuroplasticity serves the same purpose. As children, we learn not to touch a surface that’s too hot or too cold and create a memory to avoid these pain triggers in the future. However, when pain becomes chronic, this system of neuroplasticity and memory formation becomes dysfunctional. The body is no longer protecting itself against a pain trigger, rather, the brain has created a pain memory that perpetuates pain past the healing stage of the initial injury.
Learning and memory take place in two adjacent regions: the amygdala and hippocampus, located in the medial temporal lobes on both sides of the brain. These structures are part of the limbic system, the part of the brain that controls emotions and behaviors related to survival. Emotional memory formation takes place in the amygdala, while semantic and spatial memory formation (related to language acquisition and the ability to navigate) take place in the hippocampus. Given that these two structures are adjacent, it is no surprise that they interact. Emotions such as anxiety, stress and depression that often accompany chronic pain can intensify a person’s perception of pain intensity, and conversely, pain intensifies the aforementioned emotions.
Studying the biological mechanisms behind pain memory may be the key to more effective therapeutic treatment. Reconsolidation is a mechanism by which a pain memory can be updated, either with drugs or behavioral therapy. Researchers are investigating ways of opening the “reconsolidation window,” enabling neuroplasticity to erase the pain memory, and hence the patient’s perception of pain (Price & Inyang, 2015). While this research remains exploratory, it offers hope for millions of individuals living with chronic pain, for whom traditional treatment strategies have been ineffective.