Pain that lasts beyond the expected time after an injury or pain that seems to develop for no apparent reason continues to baffle scientists and pain specialists around the world. This type of pain labeled chronic has been the focus of neuroimaging studies for the last two decades. Neuroimaging has opened our eyes to the changes in the brain that accompany chronic pain. Changes that affect the anatomy, biochemistry, and neurochemistry of the nervous system.
What kinds of studies make up this category of neuroimaging? And what have they shown us? Positron Emission Tomography known as PET scans and Functional Magnetic Resonance Imaging (fMRI) head the list. But other methods include magnetoencephalography (MEG) and the more traditional electroencephalgraphy (EEG). These techniques have made it possible to study the brains of patients with chronic pain compared to individuals without pain. Measuring density of brain tissue, connections between brain structures, brain biochemistry, and location and type of neurotransmitters and their receptors has helped explain more about central pain processing. Central pain processing refers to how pain is processed in the central nervous system (brain and spinal cord).
The question this information brings then is this: is chronic pain a disease? Answering that question is important — both for the millions of people who suffer from chronic pain and because billions of dollars are spent on trying to solve the problem by eliminating (or at least reducing) pain for these folks. Right now, truly effective treatment methods just aren’t available. It seems like a process of trial and error to find what will work with each person — even though the brain scans show similar changes in the structure and function of the nervous system.
Some experts suggest that with visible and measurable changes in the brain, chronic pain fits the medical definition of disease. And that definition is disease is a disorder of structure or function in a human, animal, or plant; especially one that produces specific symptoms. But others call this decision to consider chronic pain a disease into question because it’s not always clear which came first: the pain or the brain changes?
In the case of an injury to the soft tissue or nerves, acute pain is expected. What isn’t clear is why this pain can become persistent (chronic) but only in some people. And what about people who develop chronic pain problems like fibromyalgia, irritable bowel syndrome, and interstitial cystitis (chronic bladder infection) without a traumatic event first? Can stress be considered the triggering trauma? The problem of explaining, describing, and/or categorizing chronic pain as a disease falls into the catch-22 phrase of which came first: the chicken or the egg? In other words, do the painful symptoms develop because of brain changes or do the brain changes occur because of the change in body structure and function?
Right now, we still have more questions than answers. But the current evidence from neuroimaging studies points to chronic pain as a disease state with functional, structural, and chemical brain changes. Chronic pain isn’t just a collection of symptoms that place it in the category of syndrome. With observable changes in the brain, it makes sense to think that the disordered brain function could be considered a disease.
So, where does that leave chronic pain sufferers? Does this change in how we view chronic pain (as a disease state) change anything? Not yet, but maybe it will change the way we treat chronic pain patients and hopefully so in the very near future. Armed with this new information, scientists are changing their focus of study. Now, they are looking at groups of patients with the same problem (e.g., fibromyalgia, irritable bowel syndrome, depression, arthritis) and examining what’s going on in the brain associated with these conditions.
They are finding that common disturbances are present in the brains of people who have the same disorder. For example, patients with knee osteoarthritis have increased brain activity in three areas: the amygdala (survival center), thalamus (relays sensation and motor signals to the main part of the brain), and cingulate cortex (emotion processing and formation). It may be possible to find ways to shift brain activity or change the pain experience through direct brain stimulation. If there are people with a particular pattern of biochemistry more likely to anticipate pain or amplify pain, there may be ways to alter the body chemistry to change their response to pain.
The bottom line is that chronic pain is linked with structural changes and altered neurochemistry in the brain. This information alone gives a focus and direction for research that may ultimately result in changes not only in the way we view chronic pain (disease rather than syndrome), but also in finding more effective ways to treat it centrally (at the brain level). The results of these neuroimaging studies also open the door for changes in treatment for other chronic nervous system-related problems that are currently considered irreversible such as Parkinson disease, post-stroke, and drug addiction (narcotics).