While we all can understand why pain has to exist in our bodies, it can be pretty terrible at times. Occasional pain is one thing; it tells us to stop grabbing that sharp object or to stop walking on hot rocks, but chronic pain with what can appear to be little hope of relief can be crushing. Research into chronic pain has been vast over many years, with some success in identifying, treating and preventing some types of pain. More recently, insights in neuroscience have expanded how we understand and think about chronic pain conditions.
Chronic pain is in the brain. Studies have demonstrated that conditions creating chronic pain change the brain structurally and chemically (May, 2011; Seminowicz et al., 2009; Balaki et al., 2011). This has been called the “centralization of pain”- which is exactly what it sounds like. This centralization of pain takes pain and makes it the absolutely most important thing around, altering sensory, emotional and modulatory circuits by decreasing gray matter in these areas and thus decreasing their communication (Borsook, 2012). These circuits are normally responsible for inhibiting pain, but in their altered state they are less effective at doing so. Moreover, these altered circuits may lead to altered cognition and emotional responses, creating a kind of negative feedback loop in which the brain is unable to regulate the pain as it normally would, making the pain even less bearable (May, 2011).
Some researchers think that chronic pain can be a manifestation of a breakdown of the brains reward system, and treatments that can alter the brain’s reward circuitry can be an effective way to treat chronic pain (Blum et al., 2012). In fact, this is already heavily practiced- the most commonly used painkillers for chronic pain are opioids. Opioids both block pain sensors while targeting the brain’s reward system, causing a release of dopamine, the neurotransmitter that regulates emotion, cognition, pleasure and other actions in the brain (Rosenblum et al., 2009). Part of the reason that opioids are so good at regulating pain might be their ability to both block pain sensors and help boost the reward system (Argoff, 2010). The main issue with them, however, is the ever-present threat of misuse, abuse and addiction that comes from drugs acting in the brain’s reward circuits.
With our new insight into how pain might manifest itself in the brain, however, new treatment and prevention options are emerging. Researches have recently identified a host of genetic factors that contribute to pain syndromes. Among a multitude of genetic contributions to pain, researchers found epigenetic contributions to chronic pain, which hopefully might lead to ways to counteract these effects. Epigenetics describes the ability of the environment to active or deactivate sections of the genetic code. Recently, multiple epigenetic contributions have been found that may lead to the development and maintenance of chronic pain, such as the increased cortical representation of pain in patients with chronic pain (Denk & McMahon, 2014). Understanding these epigenetic contributions is the first step in preventing them, and while this field is still very young, it offers hope for new treatments of chronic pain.
For some types of pain, our new insight has led to bizarre but effective treatments. For amputee patients experiencing phantom limb pain, immersive virtual reality via a complex virtual reality system allows a person with an amputation to “see” their limb as it previously was, completely intact. During this therapy, they act as if they had a normal limb, and the majority of patients reported pain alleviation to some degree. It is thought that seeing a virtual limb makes the primary motor cortex fool itself into thinking that the limb is still there, in addition to making mirror neurons fire as the phantom limb ‘moves’ (Murray et al., 2006). For some reason not yet well understood (more research is currently underway), this suppresses the pain response in the brain.
Another treatment involves transcranial magnetic stimulation (TMS), stimulating the motor cortex. Why motor activity or stimulating the motor cortex helps alleviate chronic pain is yet unknown, but TMS has powerful pain-relieving results. Researchers believe that it may disrupt the malfunctioning connection between the motor circuits and sensory processing circuits that are malfunctioning in those with chronic pain (Flor & Diers, 2009). This is a major breakthrough in the treatment of chronic pain in the brain, and offers hope for more treatment options in the future.
Chronic pain has long plagued people all around the world, and understanding more about how chronic pain manifests in the brain will help us treat and alleviate it. Our broadened understanding about neuronal plasticity and epigenetic contributions to pain will allow us to expand our treatment options and understand how chronic pain affects millions of people’s lives.
A more in depth look at curing chronic pain can be found here-
A Future Without Chronic Pain: Neuroscience and Clinical Research by David Borsook
Argoff CE (2010). Clinical implications of opioid pharmacogenetics. Clinical Journal of Pain. 26, S16–20.
Baliki MN, Schnitzer TJ, Bauer WR, Apkarian AV (2011) . Brain morphological signatures for chronic pain. PLoS One. 6(10):e26010
Blum, K., Gardner, E., Oscar-Berman, M., & Gold, M. (2012). “Liking” and “Wanting” Linked to Reward Deficiency Syndrome (RDS): Hypothesizing Differential Responsivity in Brain Reward Circuitry. Current Pharmaceutical Design, 18(1), 113–118.
Borsook, D. (2012). A Future Without Chronic Pain: Neuroscience and Clinical Research. Cerebrum: The Dana Forum on Brain Science, 2012, 7.
C.D. Murray, E. Patchick, S. Pettifer, T. Howard, F. Caillette (2006). Investigating the efficacy of a virtual mirror box in treating phantom limb pain in a sample of chronic sufferers Int J Disabil Hum Dev, 8 , pp. 167–174
Denk F, McMahon SB (2012). Chronic pain: Emerging evidence for the involvement of epigenetics. Neuron.73(3):435–444
Flor H, Diers M. Sensorimotor training and cortical reorganization. NeuroRehabilitation. 2009;25(1):19–27
May A (2011). Structural brain imaging: A window into chronic pain . The Neuroscientist;17(2):209–220
Ramachandran VS (2005). Plasticity and functional recovery in neurology.Clinical Medicine. (4):368–373.
Rosenblum, A., Marsch, L. A., Joseph, H., & Portenoy, R. K. (2008). Opioids and the Treatment of Chronic Pain: Controversies, Current Status, and Future Directions. Experimental and Clinical Psychopharmacology, 16(5), 405–416. http://doi.org/10.1037/a0013628
Simons, L., Elman, I., & Borsook, D. (2014). Psychological Processing in Chronic Pain: A Neural Systems Approach. Neuroscience and Biobehavioral Reviews, 0, 61–78. http://doi.org/10.1016/j.neubiorev.2013.12.006
Seminowicz DA, Laferriere AL, Millecamps M, Yu JS, Coderre TJ, Bushnell MC (2009). MRI structural brain changes associated with sensory and emotional function in a rat model of long-term neuropathic pain. NeuroImage.47(3):1007–1014
Tegeder I, Costigan M, Griffin RS, Abele A, Belfer I, Schmidt H, Woolf CJ (2006). GTP cyclohydrolase and tetrahydrobiopterin regulate pain sensitivity and persistence. Nature Medicine.12(11):1269–1277
de Vries B, Frants RR, Ferrari MD, van den Maagdenberg AM (2009). Molecular genetics of migraine. Human Genetics. 126, 115–132