Medical Director Shanti Auto Injury and Accident Scottsdale, Arizona, United States
Objectives: The concept of pain memory, recalled pain, and memory cells is not a new once. It likely dates to the era of Ronald Melzack and colleagues, from decades ago. We remind ourselves here of the mechanisms that cause changes in gene expression in peripheral nociceptors and that permanently alter the phenotype and function of crucial neurons for pain plasticity. In addition, we elucidate the changes in circuitry and synaptic strength in the dorsal horn controlled by mechanisms that affect sustaining a chronic pain syndrome.
For those of us who are clinically practicing, it is a common clinical happening that many of our patients ask us questions to interpret a "similar pain experience", or "brings back memory of previous pain I had". We unfortunately come short in interpreting their statements. We have to familiarize ourselves with these terms, including "memory cells", "recalled pain", and similar pain memory experiences.
Design: Thorough review of published data on PubMed, Ovid, Cochrane Library, NIH, US National Library of Medicine
Results: In neurobiology, altered responses to the same stimulus means “learning”, whereas the retention of these changes is “memory”. These terms encompass a variety of neuronal and behavioral processes, including chronic pain.
When chronic pain persists after an injury has healed, it results in significant functional and structural changes in the nervous system similar to memory processes. As a result, chronic pain has been defined as “a persistence of the memory of pain and/or the inability to extinguish the memory of pain evoked by an initial inciting injury” (Apkarian et al.,2009).
How and where is the nociceptive memory stored is a very complex question and entails multiple levels of the pain pathway, from the initial peripheral nociceptors all the way to the cerebral cortex. The latter no doubt modulates and perceives pain. The term “pain matrix,” was discovered as a group of brain regions consistently activated by acute pain.
Conclusions: We need to familiarize ourselves with the cellular mechanisms, particularly neurons and immune cells, that can "remember" an injury or a pain.
Evidence points that chronic pain is a type of nociceptive memory. It is stored through epigenetic modifications, changes in gene expression, and cellular communication, affecting future pain experiences. Alterations in immune cells, like macrophages, leads to a lasting "memory" that worsens pain and plasticity.
At a cellular/molecular level, pain memory involves alterations in gene expression, how cells transcribe/translate proteins, and the physical structure of DNA.
Chronic pain changes structures of neurons, such as the dendritic spines, affecting connections between cells and the ability to recall pain memory.
Pain memories are stored in neurons, including those in prefrontal cortex, involved in emotion and learning. Immune cells, like macrophages, can also carry a long-lasting memory of pain.
More research is needed to study pathways at cortical, subcortical, spinal, peripheral levels.
