It was June 12, 2011. I was out on an evening walk when a very fast car decided to join my friend and I on the sidewalk. I will spare both you and myself the details of the accident and instead, focus on my nervous system and it’s interpretation of pain over the years…yes, years.
At the time of the accident there was significant tissue damage. Significant enough to warrant a large amount of pain however, I felt nothing. My brain had decided that the threat of my injuries did not outweigh the threat of the car that was still present and trying to reverse to flee the scene. So I quickly got up and ran out of harm’s way kind of like a super human.
Once out of harm’s way, my super human powers disappeared and I started to experience pain. Bummer. Simplified for teaching purposes, there are three nerves that pass a message from the injured tissue to the brain for interpretation. Peripheral nerves go from the body to spinal cord, in the spinal cord there is a small interneuron that acts as a gateway to the third nerve which is ironically called a second order neuron because medical terminology likes to be confusing. This second order neuron travels up the spinal cord to the brain where multiple areas go into the processing of the signal to determine what meaning the message has.
Upon impact, my injured tissues started sending signals through peripheral nerves to my spinal cord. At first, they were either stopped by the interneuron or my brain decided they weren’t a threat because a bigger threat (the car) was present. Once I was removed from danger, the messages were allowed to pass through and my brain interpreted them as the next most immediate threat so I started to perceived pain. At first, the pain experienced directly correlated to the extent of my injuries but over time, my pain became disproportionate to the tissue damage.
At first, my body’s top priority was to heal and in order to heal, the body must rest. Even as tissues started to repair, my nerves remained extra sensitive and my brain continued to interpret everything as a threat (pain) so I would minimize my movement and allow for further healing. Makes sense right? Now typically this protective pain will go away once the tissues have healed because it is no longer needed but 1 in 4 people will experience persistent pain long after the injury has resolved. I am one of those lucky people. Yay me! At first I thought this was just due to chance but knowing what I now know about pain, I believe this has nothing to do with chance and everything to do with the adaptations of my nervous system.
Let’s start with the peripheral nerves: the ones going from the body to the spinal cord. Nerves have a level of charge that must be met in order to send a message. If the threshold is met, the nerve will fire. Nerves reach their firing charge by allowing ions from the outside to the inside through ion channels. There are many types of ion channels that open or close in response to different stimuli. Some respond to chemicals (stress, immune, inflammatory) while others respond to mechanical stimuli like tension and pressure. Temperature also opens and closes ion channels. The more ion channels that are open, the more likely the nerve is to fire. With my original injury, the mechanical impact and the inflammatory response opened more than enough ion channels for nerve firing. Ion channels are only present where there isn’t myelin (a sheath that improves the speed of signaling). Over time, inflammatory chemicals can demyelinate nerves allowing an increase in ion channels and a perpetually more sensitive nerve long after the inflammation is gone. So fast forward a few months and even a few years, my nerves still have increased ion channels and still reach their firing threshold more easily. I experience pain when I’m sick, when I’m stressed and even when I’m cold all because there are more ion channels.
Moving on to the spinal cord where the peripheral nerves meet interneurons before going to the brain for interpretation. If this interneuron is bombarded by messages, it will die off. This eliminates the gate keeper of messages and allows all of them to get to the brain easier. I’m pretty sure my interneurons were obliterated. My injuries took a really long time to heal on a tissue level which meant a lot of messages were sent for a long time. The brain can also ease the passing of messages from the body through the spinal cord if it believes there is a threat. The brain becomes more interested in the danger signals and will therefore increase nerve sensitivity by keeping ion channels open longer so it can receive more information more often. For good reason, my brain perceived threat for a long time so it likely made it as easy as possible for messages to pass through.
Another thing to note is that the nervous system is messy in its organization and adaptations. These changes occurred at the nerves corresponding to the areas that were injured but there is crossover in representation of an area as the nerves enter the spinal cord and within the brain. As a consequence, the area of my perceived pain spread over time. Not because of further tissue damage but because the adaptations of my nervous system and the interpretation of where the signals were coming from are not precise.
Just like the rest of the nervous system, the brain is also adaptable. When an area of the body is used more or generates a disproportionate amount of signals, the representation of that area in the brain will grow and borders of it will become less defined. This is another reason why pain can go from being isolated to the injured tissues, to being more diffuse.
All of the magic really happens in the brain. Up to this point, all messages are just an electrical signal traveling down a nerve. It’s the brain that gives meaning to this electrical charge. It’s the brain that decides whether the message is pain, a different sensation or not worthy of any feeling at all. Many areas of the brain participate in this decision making process. The areas for sensation, emotions, memory, cognition, movement planning and stress response have all been shown to be activated during the experience of pain. This complex interaction varies for each individual and each pain experience. The specific pattern of activation is called a neurotag. Other experiences and memories also have their own neurotag. The more often a neurotag is used, the more it becomes reinforced and the easier it will be accessed. This is where the phrase “its like riding a bike” comes from. The more we practice something, the easier it is to do automatically and this can occur with a movement, a memory or the experience of pain. Specific movements and activities had become so strongly associated with the experience of pain within my neurotag that even after my body healed, these movements still generated pain.
So with all of these adaptations, am I destined to be in pain for the rest of my life because I am literally wired to experience more pain? For years, the answer was yes but once I started learning about pain neuroscience, the answer became heck no. If the nervous system can adapt in one direction, it is also capable of reverse adaptations and the key to this switch is actually quite simple. It all lies in the perception of threat.
Stay tuned for the final post of this series: How to Decrease Pain by Decreasing the Perception of Threat.
Louw A. Why Do I Hurt? A Neuroscience Approach to Pain. Minneapolis: OPTP; 2013. Textbook.
Moseley, G.L., A pain neuromatrix approach to patients with chronic pain. Man Ther, 2003. 8(3): p. 130-40. Full text.
Melzack, R., Pain and the neuromatrix in the brain Journal of Dental Education, 2001. 65: p. 1378-1382. Full text.
Woolf CJ. Central sensitization: uncovering the relation between pain and plasticity. Anesthesiology. Apr 2007;106(4):864-867. Full text.
Moseley GL. Reconceptualising pain acording to modern pain sciences. Physical Therapy Reviews. 2007;12:169-178. Full text.
Gifford LS. Pain, the tissues and the nervous system. Physiotherapy. 1998;84:27-33. Full text.
Woolf CJ, Salter MW. Neuronal plasticity: increasing End the gain in pain. Science. Jun 9, 2000;288(5472):1765-1769. Full text.