The Memory of Pain
Your Pain Is Not in Your Head.
It Is in Your Spinal Cord.
The nervous system does not forget pain. It encodes it — using the same molecule and the same mechanism it uses to encode memory. What you carry after extreme pain is not weakness, not drama, not a disproportionate response. It is biology. And it has a name.
The first time, I did not know what was coming. They operated on bones in my foot. Gave me a spinal block — a needle in the back that switches off sensation below the waist. When it wore off, they asked me to walk. Slowly, on crutches, on the foot that had just been cut open. I made it a few steps. And then the world went black. Not metaphorically. I fainted. From pain. I had not known that pain could reach a threshold where the body decides that consciousness is the wrong response, and simply opts out of it.
That was surgery one. There were three. And there is a fourth I need — and cannot make myself do. I will come back to why. It has to do with a specific molecule in the neurons of my spinal cord, and once you understand what that molecule does, the fact that I cannot walk into that operating theatre a fourth time will make complete neurological sense. It is not a failure of courage. It is a consequence of learning.
I have a small list of experiences in this category. At fourteen, I had a large abscess pressing on the nerves of my spinal cord. When they inserted the needle to drain it, I learned something about pain that I would spend years trying to understand. I know what it is to break bones — although that, to my surprise, was never the worst of it. And I know what severe period pain is. A professor of reproductive health at University College London described his patients' reports of severe menstrual cramps as "almost as bad as having a heart attack." I believe them. The mechanism — uterine prostaglandins triggering ischaemic-type muscle cramping — is not fundamentally different from cardiac ischaemia in terms of what it asks the body to process.
I have not given birth. That experience — consistently the one people reach for when describing the upper limit of survivable pain — belongs in this post even though it does not belong to my own list. Not yet, anyway.
What I want to tell you is that there is a reason your worst pain experiences stay with you. Not just as memory. Not just as fear. At the cellular level. In the neurons of your spinal cord. In a molecule that uses exactly the same mechanism as learning. You are not making it up. You are not catastrophising. You are not weak. You are sensitised. And sensitisation is a neurological diagnosis, not a character assessment.
Wind-Up — Watching the Nervous System Amplify
Send repeated pain signals and watch the dorsal horn neurons respond with increasing intensity — until they fire without any new input at all
Pain is supposed to be self-limiting. A signal arrives, the nervous system responds, the signal stops, the neurons return to baseline. This is acute pain — clean, informative, functional. The problem begins when the signal does not stop, or when it is repeated enough times that the neurons no longer wait for it. This is wind-up: a progressive increase in the response of dorsal horn neurons to repeated C-fibre stimulation, first described in 1965, still one of the most clinically relevant phenomena in pain neuroscience.
Wind-up itself is short-lived. What it leads to is not. When repeated nociceptive stimulation is sustained, the dorsal horn undergoes a more lasting change: central sensitization. The neurons become hypersensitive not just to painful stimuli but to everything — touch, movement, temperature. The threshold drops. The response amplifies. And the change persists long after the original injury has healed. You are no longer reporting the pain in your tissue. You are reporting the pain your nervous system has learned to expect.
Central sensitization shares its mechanism with memory. A landmark review in Trends in Neurosciences established that central sensitization and long-term potentiation — the synaptic mechanism underlying learning and memory in the hippocampus — involve the same receptor, the same calcium influx, and the same structural synaptic changes. The NMDA receptor is the key to both. In the hippocampus, repeated stimulation unblocks the NMDA receptor, floods the synapse with calcium, activates protein kinases, and structurally remodels the synapse — encoding a memory. In the dorsal horn, the same sequence encodes pain. The authors named this a "pain engram" — the spinal cord equivalent of a memory trace. [1,2]
Women show significantly greater experimentally induced central sensitization than men. A 2024 study published in Pain — using standardised experimental pain protocols in healthy volunteers — found that women show significantly more experimentally induced central sensitization than men. The mechanisms are partly hormonal: estrogen modulates NMDA receptor expression and glutamate signalling at the spinal cord level, increasing sensitization susceptibility in ways that fluctuate across the menstrual cycle. This is not evidence that women feel pain more. It is evidence that the spinal cord's pain-learning machinery is more sensitive in female biology — with direct implications for chronic pain prevalence, for post-surgical sensitization, and for why dismissing women's pain as disproportionate is not just wrong but neurologically backwards. [3]
Surgical incision creates latent sensitization that persists for over a year. A 2021 study in Neuropharmacology documented that after a single surgical incision, NMDA receptor signalling in the dorsal horn creates a state of latent sensitization — heightened reactivity that is kept partially suppressed by endogenous kappa opioid receptors, but that can be reactivated by stress, re-injury, or re-exposure to the original context. This sensitization persisted for over a year in the study model. The study also identified sex-dependent differences in the mechanisms maintaining this sensitization. Three surgeries on the same site, each producing a round of post-operative C-fibre activation, means three rounds of NMDA-mediated sensitization — stacked, cumulative, and long-lasting. [4]
The descending pain modulation system can amplify as well as inhibit. The brain is not a passive recipient of pain signals. It sends pathways back down to the spinal cord — the descending modulation system — that can either reduce the pain signal (through endogenous opioids, noradrenaline, serotonin) or amplify it (through threat appraisal, fear, and cortical sensitization). A comprehensive review in Physiological Reviews established that in chronic and post-surgical pain, the descending inhibitory system becomes progressively dysfunctional — opioid tone falls, the noradrenergic pathway loses efficiency — while the threat-responsive amplification system becomes overactive. The brain is now turning up the volume on the signal, not just receiving it. [5]
The mechanism by which your nervous system learned to fear that movement — learned to anticipate that surgery — is identical to the mechanism by which you learned your own name. The spinal cord is not being irrational. It is doing exactly what it was built to do. It is remembering.
The Pain Volume — Ascending and Descending
Toggle between the three states of the pain system — the brain is not just receiving signals, it is sending them back down
The NMDA receptor is one of the most studied molecules in neuroscience. It is the gateway through which the nervous system learns. In the hippocampus, under repeated stimulation, it opens — calcium floods in — and the synapse is physically remodelled to be more responsive to future signals. You call this memory. In the spinal cord, the same receptor, under the same conditions, undergoes the same change. The synapse becomes more responsive. The neuron fires more easily, more intensely, for longer. The pain threshold falls. You call this chronic pain. The neuroscience calls them the same mechanism in different locations.
The NMDA Receptor — How Pain Becomes Memory
Step through the mechanism that makes pain persistent — and understand why "it's all in your head" is, in the most literal sense, wrong
The fourth surgery. This is what is happening, neurologically.
The first surgery sensitised the dorsal horn neurons in and around my foot. Post-operative C-fibre activation — the signal that fires after tissue is cut, hours after the spinal block wears off, while you are being asked to walk on crutches on a freshly operated foot — produced the conditions for NMDA receptor activation and synaptic remodelling. A latent sensitization was encoded. The second surgery re-activated it, amplified it, and extended it. The third layered on top of the second. Three rounds of extreme nociceptive input to the same site, each one building on the structural changes left by the last.
The descending modulation system has been recruited. My brain, having processed three experiences of extreme pain in this specific context — this specific foot, this specific surgical environment — has learned that this context equals extreme threat. The amygdala activates. The descending amplification pathway — the one that turns the pain volume up — fires before a single incision has been made. Before I have even walked into the theatre. The anticipatory experience is itself painful, because the nervous system is doing its job: protecting the organism from a threat it has encoded as catastrophic.
This is not weakness. This is not a disproportionate response. This is a nervous system that has learned something true — that this procedure is extremely painful — and is acting on that information with precision. The fact that the fourth surgery is probably necessary, that avoiding it causes its own harm, that the sensitization itself will make recovery harder the longer it is delayed — none of that changes what the nervous system is doing or why. Understanding the mechanism does not dissolve it. But it changes the frame. It means that when I eventually go back — and I will — the preparation, the perioperative pain management, the specific attention to descending modulation and to the NMDA pathway, will matter more than in most surgical cases. This is not about being brave. It is about being specific.
The Fear-Avoidance Cycle
Click any node to see what is driving it — and what can actually break it
Central sensitization and the fear-avoidance cycle are both real and both reversible — or at least modifiable. Not by willpower. By specific interventions that target the specific mechanisms. This is what the research supports, and what the clinical conversation around chronic pain in women has been slow to incorporate.
Ketamine is an NMDA receptor antagonist — it blocks the receptor and prevents the calcium influx that encodes sensitization. Sub-anaesthetic ketamine given before and during surgery demonstrably reduces post-operative pain, reduces opioid consumption, and reduces the risk of chronic post-surgical pain. For someone with pre-existing surgical sensitization — like three previous operations on the same site — perioperative ketamine is not an optional add-on. It is the specific pharmacological intervention for the specific mechanism causing the problem. Asking for it by name, and explaining why, is a reasonable clinical request.
Avoidance paradoxically increases pain-related fear. A 2021 study found that the perceived opportunity to avoid a painful event increased — not decreased — fear in patients with chronic pain, because avoidance prevents the nervous system from learning that the feared outcome does not always occur. The alternative is graded exposure: systematic, controlled, graduated re-engagement with the feared stimulus. Not jumping in. Not ignoring the fear. Introducing the context in small, manageable doses that allow the nervous system to update its prediction — and reduce the amygdala's threat appraisal over repeated safe encounters. In practice, for surgery: visiting the ward beforehand. Meeting the surgical team. Understanding the post-operative pain management plan in specific terms. Giving the nervous system information, not surprise.
A 2023 paper in PNAS identified that the pain engram encoded in the dorsal horn — the synaptic remodelling that maintains central sensitization — can be destabilised and reversed. When a sensitized sensory pathway is reactivated under specific conditions, the NMDA receptor plays a non-ionotropic role in degrading the excitatory proteins that maintain the sensitization. The pain memory can be reconsolidated — rewritten — rather than simply suppressed. This is the most recent and most hopeful development in chronic pain neuroscience. It means sensitization is not necessarily permanent. The same mechanism that encoded the pain can be engaged to undo it, if the conditions are right.
The descending opioid system — the brain's own inhibitory pathway — is activated by movement, specifically by aerobic exercise. Exercise-induced hypoalgesia is one of the most robustly documented effects in pain neuroscience: regular aerobic exercise reliably reduces pain sensitivity, restores descending inhibitory tone, and reduces the amygdala's reactivity to pain-related threat cues. In women, this effect is cycle-dependent — highest in the follicular and ovulatory phases when estrogen supports both descending opioid tone and exercise recovery. The goal is not to push through pain. The goal is to restore the system that dampens it.
Almost everyone has a version of this story. A procedure that left them changed. A pain experience so extreme that the body filed it somewhere beyond conscious memory — in the tissues, in the spinal cord, in the lowered threshold that means the same stimulus never quite feels the same again. A fear of returning to a context that was once the site of something unbearable. These experiences are universal and they are, almost universally, undertreated in women specifically. Women's pain is documented to be dismissed, undertreated, and more slowly managed than men's in emergency settings. The same experience, in a female body, receives less medication and less clinical urgency. That is not a perception bias. It is a documented pattern in the research, and it has consequences that compound over time — because undertreated acute pain is one of the most reliable predictors of chronic sensitization.
What I want for you is the same thing I eventually found for myself: the frame. The one that says this is biology, not character. That the pain you carry — from surgery, from childbirth, from a lifetime of menstrual pain that was waved away as part of being a woman, from an abscess at fourteen that nobody adequately managed — is real and measurable and encoded at the molecular level. You did not catastrophise it. Your spinal cord catalogued it. And knowing that is the starting point for asking for the interventions that actually address the mechanism rather than just the surface.
You are not alone in this. And you are not making it up. You never were.
Your nervous system was doing its job. Love, Nina ❤References
- Woolf, C. J. (2011). Central sensitization: Implications for the diagnosis and treatment of pain. Pain, 152(3 Suppl), S2–S15. https://doi.org/10.1016/j.pain.2010.09.030
- Ji, R. R., et al. (2003). Central sensitization and LTP: Do pain and memory share similar mechanisms? Trends in Neurosciences, 26(12), 696–705. https://doi.org/10.1016/j.tins.2003.09.017
- Guekos, A., et al. (2024). Healthy women show more experimentally induced central sensitization compared with men. Pain, 165(6), 1413–1424. https://doi.org/10.1097/j.pain.0000000000003144
- Custodio-Patsey, L., et al. (2020). Sex differences in kappa opioid receptor inhibition of latent postoperative pain sensitization in dorsal horn. Neuropharmacology, 163, 107726. https://doi.org/10.1016/j.neuropharm.2019.107726
- Sandkühler, J. (2009). Models and mechanisms of hyperalgesia and allodynia. Physiological Reviews, 89(2), 707–758. https://doi.org/10.1152/physrev.00025.2008