Pain is a complex condition that is not easily explained. We may think that it is very straightforward – an injury occurs and neurons fire, indicating a feeling of Pain. What causes pain and how the body processes and remembers it is not so simple. New research is looking more deeply into how pain originates and what that means for diagnosis and treatment.
What causes pain?
In September 2015, neuroscientists at Aalto University collaborated with researchers at Helsinki University Hospital and Harvard Medical School to begin to answer this question. Focusing on complex regional pain syndrome (CRPS), researchers studied the brains of patients suffering from this condition and made a novel connection. The size of the choroid plexus in the brains of CRPS patients was almost 20% larger than that of those with no such condition.
The choroid plexus is a crucial part of the transmission of pain. It manufactures cerebrospinal fluid, a protective cushion that not only surrounds the brain but is also responsible for the passage of fluid from the blood into the cerebrospinal fluid, brain, and spinal cord. As pain move through the spinal cord and into the brain, this key piece of research may explain not only CRPS but also other chronic pain syndromes.
This larger choroid plexus may also help define what causes pain in terms of inflammation. It also connects inflammation that occurs on the edges of the body and its interaction with the brain.
This particular research has made the first connection to what causes pain, but there is another potential cause on a cellular level as well. Researchers looking to identify a pain “on/off” switch have found that a series of events in the S1 cortex that may contribute to pain.
A pain “on and off switch”?
The S1 cortex is an area of the brain that is not affected by injury to the spinal cord. Researchers at the National Institute for Physiological Sciences (NIPS) looked at how manipulating the S1 cortex affected allodynia, a type of pain in which the sufferer is hypersensitive to the slightest touch. They found that stimulating the S1 cortex deep in the brain resulted in relief from neuropathic pain.
Study first author Sun Kwang Kim believes that this relief might be a result of manipulating a specific type of cell in this area, noting:
“Direct manipulation of the S1 cortex has been shown to relieve neuropathic pain in humans and animals. This suggests the S1 cortex might act as a sort of central processing unit within the brain networks that mediate and/or sustain chronic neuropathic pain. We hypothesized that S1 astrocytes, a type of glial cell, may show functional changes following peripheral nerve injury, resulting in mechanical allodynia.”
What causes pain to become chronic?
What causes pain to begin is the first part of the question researchers are looking to answer. What causes pain to become chronic is the second.
King’s College London looked at cell memory and the “footprint” of pain that makes it become chronic. They found that pain left epigenetic marks on genes in some immune cells that eventually influenced which genes were expressed and which were not. In some cases, epigenetic marks don’t have any actual consequences. They just indicate more potential for a condition. In other cases, epigenetic marks can affect the function of the cell.
Looking at chronic pain in mice, the study found that the epigenetic marks didn’t change the function but increased the potential for pain to be remembered in such a way that it became chronic.
Dr. Giovanna Lalli, Neuroscience & Mental Health Senior Portfolio Developer at the Wellcome Trust, which partially funded the study, said:
“People develop chronic pain for a huge variety of reasons. We therefore need an equally diverse range of treatments to tackle the different root causes. The clues from this study, suggesting epigenetic changes may be involved in pain persisting, will hopefully lead us to better understand the mechanisms underlying chronic pain.”
Professor Stephen McMahon from the IoPPN at King’s College London believes that these marks may ultimately raise more questions than they answer, leading to a deeper understanding of chronic pain, noting:
“This research raises many interesting questions: do neurons also acquire epigenetic footprints as a result of nerve injury? Do these molecular footprints affect the function of proteins? And are they ultimately the reason that chronic pain persists in patients over such long periods of time?”
Ultimately, researchers are looking at the whole of what causes pain, from stimulating areas of the brain to cell memory to even empathetic pain. It seems that the common denominator in many studies is how the brain experiences, processes, and ultimately expresses what we know of as “pain.”
Studying empathetic pain
Take the case of empathetic pain. Empathetic pain is pain that is felt when a person hears about or sees pain happen to someone else. Even in the cases of empathetic pain, the anterior insula region and the cingulate cortex of the viewer (as opposed to the one experiencing the pain) changes to process the pain not only as if they were experiencing the physical sensation but also the emotional one. This process results in the viewer having a learning experience about avoiding the painful stimuli but also produces an empathetic response in the brain.
Anita Tusche, a neuroscientist at the Max Planck Institute in Leipzig and one of the authors of the study, points out that this learning process is an important function for humans to be able to build social relationships, noting:
“The fact that our brain processes pain and other unpleasant events simultaneously for the most part, no matter if they are experienced by us or someone else, is very important for social interactions because it helps to us understand what others are experiencing.”
Continuing to look into what causes pain – physically, mentally, and emotionally – may lead to breakthroughs in treatments for all aspects of pain. What aspects of this recent research into what causes pain is most interesting to you?
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