Pain is an experience to which all of us are subjected at some point in our lives, either from a slight strain which subsides after a short time or a persistent condition that lasts. Understanding how pain operates within our body will help us gain control over pain and even reduce its intensity. One theory of pain management is the gate control theory which suggests that our body’s interpretation and processing of pain is more intricate than one might think. This blog post will explore this theory as well its application to spinal cord injury patients and examine the physiological mechanisms and their role in pain management.
The gate control theory of pain states that “the transmission of pain signals can be modulated at the spinal cord level, by non-painful inputs as well as descending signals from the brain”. Put simply, we can attune signals either to or from our central nervous system (CNS) almost like a tap controlling the volume of water coming out. Our body is equipped with small receptors known as nociceptors (Noi-see-sep-tors), these specialized nerve ending receptors are responsible for detecting pain and form first-order neurons (our receptors) in the pain pathway.The axons of these neurons (think of axons like a sheath that covers nerve fibres that help modulate the speed of transmissions in between neurons) form 2 specific small-diameter nerve fibers: fast A-delta fibres, which are responsible for the initial sharp pain perceived at the time of injury, and slow C-fibers which are responsible for a dull, longer-lasting pain.
These signals travel via the dorsal horn of the spinal cord, synapse with 2nd order neurons in the white matter of our spinal cord which sends the signals all the way up to an area of our brain called the thalamus then our 3rd order neurons will send these signals to the specific area in the brain in relation to where the site of the pain initiated from (e.g., knee pain signals will be sent to the primary somatosensory cortex).
To ensure the signal reaches the brain, as pain is an important signal to receive, our nerves inhibit the inhibitory interneurons, thus opening the gate, allowing transmission of pain signals to reach the brain. When pain occurs, we halt our body’s ability from stopping this process in order to alert the brain of areas of concern i.e a pain signal.
However, according to the gate theory of pain, perception of pain is not simply due to stimulation of nociceptors. There is a so-called nerve gates, located in the dorsal horn of the spinal cord that controls the passage of pain signals to the brain. These nerve gates consist essentially of interneurons (nerves between nerves) that inhibit second-order neurons, thereby stopping or reducing signal transmission.
If the same painful area also receives non-painful stimuli (non-painful stimuli are associated with closing the gate) such as touch, pressure, or change in temperature, this activates a different kind of nerve fiber, large-diameter A-beta fibers. These fibers then re-trigger the inhibitory neurons, which interrupt the transmission of pain signals and begin to close the gate by turning down the voltage.
So, when pain occurs and inhibits the inhibitor we can re-activate the inhibitor with non-painful stimuli.
This mechanism underlies the pain-relieving effects of skin rubbing, or temperature based therapies for pain relief. Hence why when we bump our knee, our instinctive reaction may be to rub or squeeze it or why you may reach for a cold pack for the affected area. It is also the basis of pain treatment procedures such as transcutaneous nerve stimulation (TENS), which delivers a small electrical current to activate non-nociceptive receptors in the skin.
So, just as we can send non painful (non-noxious) stimuli up to the brain or spinal cord, we can also send non painful stimuli down to the spinal cord in order to modulate the pain gates by means of endorphins.
Endorphins – morphine-like substances are neurotransmitters released by the brain in response to pleasurable activities as well as painful stimuli, and work to change and alter our brain’s perception of pain.
Endorphins reduce transmission of pain signals between the first and second order neurons by 2 mechanisms: Prevention and Inhibition
Prevention by preventing the release of a key neurotransmitter – substance P (elevated levels of SP are linked to heightened pain sensitivity)
Inhibition by inhibiting action potentials in postsynaptic neurons (halting the neural pain pathway before it reaches the brain).
Endorphin production may be induced by a number of factors including (and not limited to):
Pleasurable activities
Excitement
Meditation
Laughter
Vigorous exercise
The physiological mechanisms by which endorphins work underlies the pain-relieving effects of physical exercise, positive state of mind; and explains, for example, after a sports injury, athletes often continue to play through pain during a high-energy game or match. This is partly because the body releases endorphins in response to the stress of competition, numbing the pain temporarily. It’s only once the excitement of the game has passed that the pain becomes more noticeable.
The gate is particularly important as the inhibitory nerve cells that form the “gate” are easily damaged. This is one of the reasons why people with spinal cord injuries (SCI) experience neuropathic pain. These interneurons or our gates, are commonly damaged when one experiences a spinal cord injury, and just as we’ve mentioned, if our gates are damaged you could begin to imagine where this is going.
Damaged interneurons can present a wide variety of pain related signs and symptoms, most noticeably a significant change in perception of pain.
Pain can be expressed far higher to what is stimulating the pain pathway and vice versa can dwell high levels of incoming pain stimuli. This may also mean neurons can start firing erratically and start sending signals up to the brain with no stimulus, this is known as loss of inhibition. This can also transcend to other types of pain such as musculoskeletal where pain can be expressed stronger due to the reduced ability of these inhibitory cells to turn down the volume of pain in the spinal cord.
For those managing chronic pain, the pain itself can cause the gate to open further or increase the pain intensity. Physical factors that transcend to behavioural factors like sleep deprivation can trigger emotional states, such as anxiety, tension, or stress, which can influence the gate to open greater.
When continuous signals of pain travel through our nervous system, they activate a mechanism that changes painsensitivity similar to a volume control.
This acts as a safety control as our body perceives pain as danger and will bring attention to it if it doesn’t cease. This is known as sensitization, whereby the nervous system is rendered more sensitive or “sensitized” due to prolonged pain. Hence why the active practice of non-nociceptive stimuli can assist as a ploy to reduce the sensitization of our nervous system and subsequently reduce the severity of perceived pain for people with SCI. Countless research has been made and drawn correlations between the practice of mindfulness, mediation and other modalities which result in a quieter and calmer mind and the overall reported reduction in pain. This being said, pain management should always be multidisciplinary and practised in a healthy adherable way which is inline with your goals and your health professional’s advice..
In final analysis, the use of physical/mental non-nociceptive stimulation can be a handy strategy within your toolbox of pain relief management. For example, physical stimulation like rubbing or massaging the painful area, heat or cold, or TENS (Transcutaneous Electrical Nerve Stimulation). As well as managing emotional states with relaxation techniques like deep focused breathing, meditation, breathwork (if there are no respiratory contraindications) or mindfulness to encourage endorphin release. Cognitive approaches such as positive thoughts/affirmations, also reduce painexperience by creating a facilitatory state for your CNS to contribute to prevention and inhibition, actually dampeningthe amplitude, duration and frequency of pain signals.
Astokorki, A. H. Y., & Mauger, A. R. (2017). Transcutaneous electrical nerve stimulation reduces exercise-induced perceived pain and improves endurance exercise performance. European Journal of Applied Physiology, 117(3), 483–492. https://doi.org/10.1007/s00421-016-3532-6
Khelemsky, Y., Malhotra, A., & Gritsenko, K. (Eds.). (2019). Academic Pain Medicine. Springer International Publishing. https://doi.org/10.1007/978-3-030-18005-8
Murray, R., Perry, K. N., McCabe, R., Siddall, P., & Katte, L. (2014). Spinal Cord Injury Pain Book. HammondCare.
Trachsel, L. A., Munakomi, S., & Cascella, M. (2023, April 17). Pain Theory – StatPearls – NCBI Bookshelf. National Center for Biotechnology Information. https://www.ncbi.nlm.nih.gov/books/NBK545194/
Zeidan, F., & Vago, D. R. (2016). Mindfulness meditation-based pain relief: a mechanistic account. Annals of the New York Academy of Sciences, 1373(1), 114–127. https://doi.org/10.1111/nyas.13153
Written by Lenny Kechayas
Exercise Scientist & Allied Health Assistant
At The Next Step Recovery and Wellness Centre in Melbourne, our mission is to provide tailored programs and services for athletes recovering from spinal cord injuries and neurological conditions. Our Athlete Scholarship Program secures generous funding for athletes without financial support.
