In 2011, the Institute of Medicine (1) reported that 100 million Americans, or almost one-third of the population, are affected by chronic pain. Half that number, or 50 million people, experience severe or daily pain, with increased debility and costs to the health care system (2). Chronic pain is persistent pain, continuing after an injury heals, or emerging in the absence of an apparent injury (3). And so, a significant minority of our patients experience chronic pain, as well as the impairment in daily functioning, sleep and psychological and social well-being that accompanies it.
The disparaging comment that patients (rightly) dread is, “It’s all in your head,” is no less inaccurate than the more acceptable idea that pain is a strictly body-based phenomenon. Chronic pain is a body-mind phenomenon, and current research on the theory of Central Sensitization elucidates the mechanisms by which chronic pain emerges (4). Data supporting Central Sensitization suggests that chronic pain results from three types of changes in the central nervous system: Sensitization of pain circuits, generalization of pain to non-pain circuits, and failure of inhibitory pathways to dampen pain. Central Sensitization can occur after a single injury, repeated injury, or even no apparent injury to the body. Sensitization of central nervous system pain circuits mean that mild or even benign stimuli (e.g., a gust of wind across the cheek of a Trigeminal neuralgia patient) produce pain. Further, non-pain-related central nervous system circuits (e.g., those that carry temperature signals between brain and body) get “hijacked” into the pain system, generalizing, and thus enhancing, the pain experience. Finally, central nervous system pathways from brain to body that inhibit pain fail to work effectively, creating another avenue by which pain is intensified. Interestingly, Central Sensitization is being explored as the common underpinning for seemingly diverse conditions such as chronic pain, irritable bowel syndrome, and PTSD.