Most people, including doctors, do not appreciate that the organ that produces pain is the brain. A broken bone, damaged tissue or a bleeding wound is often the focus, but the experience of pain is the sum total of more than just the physical injury – it is the result of information sent from our nerves being filtered through an individual’s unique psychological makeup, genetics, gender, beliefs, expectations, motivations and emotional context. Pain is therefore an individual experience, and often confounds and frightens us, as well as those we love and who love us.
Acute pain is a life-preserving sensory and emotional experience, like hunger or thirst, and is produced by the brain to alert us to an actual or potential threat to our survival from damage to our bodies. It is a complex biological alarm system and, like all systems, may malfunction. When it becomes dysfunctional, the individual experiences pain without identifiable damage. The disease state that results is called chronic pain. At the moment, it cannot be cured – in other words, there is no bone that can be mended or wound that can be stitched that will cause the alarm to be switched off.
For people who report chronic pain with nothing to show for it when examined or scanned, a biomarker, or scientific measurement that could objectively show the abnormality in their system has long been a goal of researchers. In a recent study by the University of California, San Francisco, Prasad Shirvalkar and colleagues studied four individuals who suffer from chronic pain.
The team implanted electrodes into areas of the brain responsible for planning, expectation and emotion, which are important in the genesis of the experience of pain. They then correlated the brain activity in these areas using machine learning, with daily self-reported pain intensity scores from the four individuals over six months. The research enabled them to objectively demonstrate that the information-processing areas of the brain in chronic pain are distinct from that of acute pain.
Rather than just relying on the individual’s report of pain as the evidence for their experience, abnormal neural activity correlated with their report provides objective evidence of the presence of chronic pain. In a sense, it allows researchers to visualise the condition, like one could a broken bone on an X-ray.
Because chronic pain is not associated with ongoing tissue damage, often individuals who report pain where there is no evidence of injury are not believed. Consider, for example, someone who reports persistent pain following a whiplash injury but does not have any orthopaedic damage. This person may be accused of feigning the experience of pain for the sake of a compensation claim.
The conditions that can lead to chronic pain are varied. The study looked at one person with chronic pain after amputation, which results in a condition called phantom limb pain. The brain struggles to cope with the loss of sensory input to the brain from the missing limb, and tries and fails to reorganise that part of the brain responsible for sensation in the missing limb, resulting in pain. Pain can also be caused in this condition due to nerves that have been cut as a result of the loss. Three other individuals studied had pain after brain damage from a stroke. The damaged nerves in the brain short-circuit, and pain is experienced in the body parts that the damaged nerves are responsible for controlling.
Although chronic pain can arise from different causes, understanding the similar brain areas responsible for chronic pain may in the future yield treatments aimed at specifically addressing these dysfunctional regions. This could be by modulating the nervous system, through the application of electricity, to cause the release of chemicals that can inhibit the abnormal nervous system activity that causes the experience of persistent pain. Stimulation of the spinal cord with an electrical current is routinely used to treat nerve pain from diabetes and pain from injured spinal nerves caused by a prolapsed disc (sciatica). A similar approach could work in the brain.
We are in our infancy in terms of understanding how and why our nervous system changes to produce chronic pain that is ubiquitous and disabling. But we do know chronic pain often has pejorative connotations. People who have cancer are generally regarded as heroic for their perseverance through suffering. Raising awareness for cancer treatment and prevention is often much easier than promoting the plight of individuals who suffer with chronic pain.
Individuals who report pain in the absence of visible damage are often not believed or the condition is dismissed. The universality of the acute-pain experience and the widespread understanding that pain must always be due to tissue damage also hampers research and support for people who suffer with chronic pain.
Chronic pain often joins us on our journey in life, particularly as we age. Although Shirvalkar’s research is promising as a gateway to future pain therapies, and is yet another step towards recognising chronic pain as a disease in its own right, we do not as yet have reliable and effective treatments for managing it. So, ultimately, prevention is better than long-term opioid use or risky interventions. Attention to exercise, nutrition, sleep and psychological wellbeing are strategies available now to improve health overall and delay the onset of chronic pain from strokes.