When the central nervous system gets involved in the transmission of pain, it can make commands on a whim. If your brain feels like it, it will exaggerate it or even produce it out of thin air. It can change the way things normally feel, making you feel when you shouldn’t. It can make normal sound, touch and light intolerable.
All of this is possible when your central nervous system has been sensitised. Central sensitisation is a phenomenon that has gained notoriety since 1983 when it was first described as more and more people suffer from chronic pain and long-term health issues 1. It is the neurophysiological underpinning of chronic pain and conditions such as fibromyalgia 2, migraine headaches 3 and irritable bowel syndrome 4. The hallmark of central sensitisation is that pain is no longer useful or protective 1.
Why does the central nervous system do this? Ultimately, it is to protect you, but you first need to understand how the nervous system works. The CNS is composed of two main parts: the brain and the spinal cord. The brain and body communicate with each other through nerves that travel from the periphery (body) to the central nervous system giving important sensory information about the environment, both internal and external 5. The main point where information is gated is the spinal cord, specifically in the dorsal horn. This is where information that is going to help protect us will be sorted with priority and ascend to the brain and the brain’s response will be sent to the body.
Non-threatening information is normally desensitised: sight, sound, taste, and touch flit by our central nervous system quickly like putting on clothes. Once they are on, you don’t feel them the whole day, unless there is a change in the way they are sensed. Pain does that. Think about when you get a sunburn. Even the most delicate of clothing can feel irritating and uncomfortable.
With noxious information, the central nervous system can amplify it so you don’t damage yourself. This can also happen if the stimulus is repetitive or if it the brain has decided there should be pain1. The latter is more apparent when pain appears out of nowhere and happens anytime the brain has believed there is a threat. Pain is the way the brain communicates with us. If we don’t listen, it will turn up the volume.
What Influences Pain Perception?
The perception of pain either from acute injury or clinical pain states undergoes significant processing in the central nervous system with the brain being increasingly recognised as a major player in the presentation and modulation of pain 6. Pain has a number of different inputs and outputs depending on context or meaning, psychological state, prior learning of pain, cultural beliefs, gender and your own expectations 7. These various inputs target many different regions in the brain in a way that is unique to you 8. It is these brain regions and the interplay with our senses that make pain persist and why pain has been called an illusion 9. They can also abolish pain. How often have you been deceived by what you see?
Persistent Pain is Maladaptive
This is maladative plasticity: a variety of structural and functional changes in the neural elements and connections that make pain last far beyond the time the tissue has healed. These changes make pain appear out of the blue, come back consistently to the same place, swap sides, become widespread and are definitely not serving any function.
Chronic pain perception becomes damaging not only to the brain but also to the quality of life and ability to thrive, which is the hallmark of many clinical pain syndromes 10. However, pain and suffering do not have to be intertwined. The biopsychosocial model, which takes into account who you are and how you interact with your environment, has led to many interventions and therapies that allow anyone with chronic pain to regain function and experience major improvements in quality of life 11. It starts with the right education about your pain.
- Latremoliere A and Woolf C. Central sensitisation: a generator of pain hypersensitivity. Journal of Pain. 2209: 10(9): 895-926. doi: 10.1016/j.jpain.2009.06.012
- Siracusa R, Di Raola R, Cuzzocrea S. Fibromyalgia: pathogenesis, mechanisms, diagnosis and treatment options update. Int J Mol Sci. 2021; 22(8): 3891. doi: 10.3390/ijms22083891.
- Iyengar S, Johnson KW, Ossipov MH et al. CGRP and the trigeminal sustem in migraine. Headache. 2019; 59(5): 659-681. doi: 10.1111/head.13529.
- Ustianowski K, Ustianowski L, Machaj F et al. The role of the human microbiome in the pathogenesis of pain. Int J Mol Sci, 2022; 23(21): 13627. doi: 10.3390/ijms232113267.
- Azarfar A, Calcini N, Huang C, et al. Neural coding: a single neuron’s perspective. Neurosci Biobehav Rev. 2018; 94:238-247. doi: 10.1016/j.neubiorev.2018.09.007.
- Apkarian A, Bushnell CM, Treede R-D et al. Human brain mechanisms of pain perception and regulation in health and disease. European Journal of Pain. 2005; 9: 463-484. doi: 10.1016/j.ejpain.2004.11.001.
- Baliki MN, Apkarian AV. Nociception, Pain, Negative Moods, and Behavior Selection. Neuron. 2015 Aug 5;87(3):474-91. doi: 10.1016/j.neuron.2015.06.005.
- Tracey I, Mantyh PW. The cerebral signature for pain perception and its modulation. Neuron. 2007 Aug 2;55(3):377-91. doi: 10.1016/j.neuron.2007.07.012.
- Pozeg P, Palluel E, Ronchi R, at al. Virtual reality improves embodiment and neuropathic pain caused by spinal cord injury. Neurology. 2017;89(18):1894-1903. doi: 10.1212/WNL.0000000000004585
- Baliki MN, et al. Beyond feeling: chronic pain hurts the brain, disrupting the default-mode network dynamics. J Neurosci. 2008. PMID: 18256259. doi: 10.1523/JNEUROSCI.4123-07.2008.
- Gatchel R, Peng Y, Peters M et al. The biopsychosocial approach to chronic pain: scientific advances and future directions. Psychol Bull. 2007; Practical Pain Management. 2008; 8(4): 581-684. Doi:10.1037/0033-2909.133.4.581.