少点错误 04月09日 19:59
Learned pain as a leading cause of chronic pain
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文章探讨了神经可塑性疼痛,这是一种由大脑学习产生的慢性疼痛,而非由持续的组织损伤引起。文章强调了这种疼痛的常见性、诊断方法以及有效的治疗手段,并结合作者自身的经历,深入浅出地解释了这种疼痛的机制和应对方法。文章指出,传统的医疗方法可能无法有效缓解神经可塑性疼痛,而针对性的心理疗法能够带来显著改善。

🧠 神经可塑性疼痛是一种由大脑学习产生的慢性疼痛,与组织损伤无关。这种疼痛源于大脑将疼痛作为一种学习反应,而非对持续组织损伤的直接反应,这与传统的疼痛机制有所不同。

🧐 诊断神经可塑性疼痛需要综合考虑多种因素,包括疼痛起始于压力时期、无明显损伤、多部位症状、症状不一致、症状扩散或改变、情绪触发、与身体无关的触发因素、对称性症状等。具备多个特征可增加诊断的可能性。

💡 神经可塑性疼痛的治疗方法主要集中于“解学习”疼痛模式,这包括躯体追踪等心理学方法。这些方法旨在改变大脑对疼痛的认知和反应,从而减轻疼痛。文章强调,针对性的心理疗法可以带来显著改善。

📚 神经可塑性疼痛的证据基础广泛,世界卫生组织已将其纳入疼痛分类。现代医学教科书和课程中也开始介绍这种疼痛,这表明其在医学界的重要性日益增加。

Published on April 9, 2025 11:57 AM GMT

Epistemic status: Amateur synthesis of medical research that is still recent but now established enough to make it into modern medical textbooks. Some specific claims vary in evidence strength. I’ve spent ~20 hours studying the literature and treatment approaches.

Disclaimer: I'm not a medical professional. This information is educational only, not medical advice. Consult healthcare providers for medical conditions.

Key claims

This post builds on previous discussions about the fear-pain cycle and learned chronic pain. The post adds the following claims:

    Neuroplastic pain - pain learned by the brain (and/or spinal cord) - is a well-evidenced phenomenon and widely accepted in modern medical research (very high confidence).It explains many forms of chronic pain previously attributed to structural causes - not just wrist pain and back pain (high confidence). Other conditions include everything from pain in the knees, pelvis, bowels, neck, and the brain itself (headaches). Some practitioners also treat chronic fatigue (inc. Long-COVID), dizziness and nausea in a similar way but I haven't dug into this.It may be one of the most common or even the single most common cause of chronic pain (moderate confidence).There are increasingly useful resources, well-tested treatments with very large effect size, and trained practitioners.Doctors are often unaware that neuroplastic pain exists because the research is recent and not their specialty. They often attribute it to tissue damage or structural causes like minor findings in medical imaging and biomechanical or blood diagnostics, which often fuels the fear-pain cycle.

My personal experience with with chronic pains and sudden relief

My first chronic pain developed in the tendons behind my knee after running. Initially manageable, it progressed until I couldn't stand or walk for more than a few minutes without triggering days of pain. Medical examinations revealed inflammation and structural changes in the tendons. The prescribed treatments—exercises, rest, stretching, steroid injections—provided no meaningful relief.

Later, I developed unexplained tailbone pain when sitting. This quickly became my dominant daily discomfort. Specialists at leading medical centers identified a bone spur on my tailbone and unanimously concluded it was the cause. Months later, I felt a distinct poking sensation near the bone spur site, accompanied by painful friction when walking. Soon after, my pelvic muscles began hurting, and the pain continued spreading. Steroid injections made it somewhat more tolerable, but despite consulting multiple specialists, the only thing that helped was carrying a specially shaped sitting pillow everywhere.

None of these pains appeared psychosomatic to me or to my doctors. The sensations felt physically specific and emerged in plausible patterns that medical professionals could link to structural abnormalities they observed in imaging.

Yet after 2-3 years of daily pain, all of these symptoms largely disappeared within 2 months. For reasons I'll touch on below, it was obvious that the improvements resulted from targeted psychological approaches focused on 'unlearning' pain patterns.  This post covers these treatments and the research supporting them.

For context, I had already written most of this post before applying most of these techniques to myself. I had successfully used one approach (somatic tracking) for my pelvic pain without realizing it was an established intervention.

What is neuroplastic (learned) pain?

Consider two scenarios:

    You touch a hot stove and immediately feel painYou develop chronic back pain that persists for years despite no clear injury

Both experiences involve the same neural pain circuits, but they serve different functions. The first is a straightforward protective response. The second represents neuroplastic pain - pain generated by the brain as a learned response rather than from ongoing tissue damage.

This might pattern-match to "it's all in your head," but that's a bit of a misunderstanding. All pain, including from obvious injuries, is created by the brain. The distinction is whether the pain represents: a) An accurate response to tissue damage b) A learned neural pattern that persists independently of tissue state.

Strength of evidence

The overall reality of neuroplastic pain as a common source of chronic pain has a broad evidence base. I haven't dug deep enough to sum it all up, but there are some markers of scientific consensus:

Side note: With obvious caveats, LLMs think that there is strong evidence for neuroplastic pain and various claims related to it[1].

Why we learn pain

(This part has the least direct evidence, as it’s hard to test.)

Pain is a predictive process, not just a direct readout of tissue damage. Seeing the brain as a Bayesian prediction machine, it generates pain as a protective output when it predicts potential harm. This means pain can be triggered by a false expectation of physical harm.

From an evolutionary perspective, neuroplastic pain confers significant advantages:

    False Positive Bias: Mistakenly producing pain when no damage exists (false positive) is less costly than failing to produce pain when damage does exist (false negative). Perhaps this is part of the reason why people with anxious brains, which tend to focus more on threats, are more prone to neuroplastic pain.Predictive Efficiency: The brain generates pain preemptively when contextual cues suggest potential danger. This is especially protective when engaging in an activity that has caused (perceived) damage in the past.

As Moseley and Butler explain, pain marks "the perceived need to protect body tissue" rather than actual tissue damage. This explains why fear amplifies pain: fear directly increases the brain's estimate of threat, creating a self-reinforcing loop where:

    The brain detects a plausibly threatening sensation and generates mild painWe become afraid this pain signals tissue damage (often due to prior experience or general anxiety)This fear directly increases the brain's threat assessment and attention to the sensationsThe brain produces more pain as a protective responseIncreased pain confirms our fear, amplifying it and repeating the cycle

This cycle can also be explained in terms of predictive processing.

In chronic pain, the system becomes "stuck" in a high-prior, low-evidence equilibrium that maintains pain despite absence of actual tissue damage. This mechanism also explains why pain-catastrophizing and anxiety so strongly modulate pain intensity.

Note: Fear is broadly defined here, encompassing any negative emotion or thought pattern that makes the patient feel less safe.

Diagnosing neuroplastic pain

The following patterns suggest neuroplastic pain, according to Alan Gordon’s book The Way Out. Each point adds evidence. Patients with neuroplastic pain will often have 2 or more. But some patients have none of them, or they only begin to show during treatment.

Some (but not many) other medical conditions can also produce some of the above. For example, systemic conditions like arthritis will often affect multiple locations (although even arthritis often seems to come with neuroplastic pain on top of physical causes).

Of course, several alternative explanations might better explain your pain in some cases - such as undetected structural damage (especially where specialized imaging is needed), systemic conditions with diffuse presentations, or neuropathic pain from nerve damage. There's still active debate about how much chronic pain is neuroplastic vs biomechanical. The medical field is gradually shifting toward a model where a lot of chronic pain involves some mixture of both physical and neurological factors, though precisely where different conditions fall on this spectrum remains contested.

Case study: my diagnosis

I've had substantial chronic pain in the hamstring tendons, tailbone, and pelvic muscles. Doctors found physical explanations for all of them: mild tendon inflammation and structural changes, a stiff tailbone with a bone spur, and high muscle tension. All pains seemed to be triggered by physical mechanisms like using the tendons or sitting on the tailbone. Traditional pharmacological and physiotherapy treatments brought partial, temporary improvements.

I realized I probably had neuroplastic pain because:

Finally, the most convincing evidence was that pain reprocessing therapy (see below) worked for all of my pains. The improvements were often abrupt and clearly linked to specific therapy sessions and exercises (while holding other treatments constant).

If you diagnose yourself, Gordon’s book recommends making an ‘evidence sheet’ and building a case. This is the first key step to treatment, since believing that your body is okay can stop the fear-pain cycle.

Belief barriers

Believing that pain is neuroplastic, especially on a gut level, is important for breaking the fear-pain cycle. But it is difficult for several reasons:

    Evolutionary programming: Pain evolved specifically to make us believe something is physically wrong. This belief is feature, not a bug - it made us avoid dangerous activities.Medical diagnostics: Some findings seem significant but appear commonly in pain-free individuals. For example, herniated discs (37% of asymptomatic 20-year-olds) or bulged disks, mild tendon inflammation, muscle tension, minor spine irregularities and degradation/arthritis, body asymmetries, poor posture, bone spurs, and meniscus tears. Doctors found physical reasons for all three of my chronic conditions but the conditions all went away without changing the physical findings.Conditioned responses: Pain often follows predictable patterns that seem to confirm structural causes. For example, my own wrist pain increased reliably the longer I typed. This created a compelling illusion of mechanical causation, but is also common for people with neuroplastic pain because the brain fears the most plausible triggers.

Treatment Approaches

Pain neuroscience education

Threat Reprocessing

General emotional regulation and stress reduction

Traditional medical treatments

(Reminder that I’m not a medical professional, and this list misses many specialized approaches one can use.)

Resources

I recommend reading a book and immersing yourself in many resources, to allow your brain to break the belief barrier on a gut level. Doing this is called pain neuroscience education (PNE), a well-tested intervention.

My recommendation: “The Way Out” by Alan Gordon. I found the book compelling and very engaging. The author developed one of the most effective comprehensive therapies available (PRT, see below).

Books

Treatment Programs

Therapists

Online Resources

Appendix: Chronic fatigue, dizziness, nausea etc

'Central Sensitivity Syndromes' can allegedly also produce fatigue, dizziness, nausea and other mental states. I haven't dug into it, but it seems to make sense for the same reasons that neuroplastic pain makes sense. I do know of one case of Long COVID with fatigue, where the person just pretended that their condition is not real and it resolved within days. 

I’d love to hear if others have dug into this. So far I have seen it mentioned in a few resources (1, 2, 3, 4) as well as some academic papers.

It seems to make sense that the same mechanisms as for chronic pain would apply: For example, fatigue can be a useful signal to conserve energy (or reduce contact with others), for instance because one is sick. But when the brain reads existing fatigue as evidence that one is sick, this could plausibly lead to a vicious cycle where perceived sickness means there is a need for more fatigue.

  1. ^

    For example, here is Claude 3.5’s assessment of how much evidence there is in specific areas:

      Strongest Evidence (multiple RCTs, consistent mechanistic understanding):
        Brain imaging shows identical activation patterns between acute pain and neuroplastic pain that is experimentally induced by giving fake electric shocks etc.Pain often persists unchanged despite tissue healingStructural abnormalities correlate poorly with pain levelsWHO's official recognition of "nociplastic pain" (2019)
      Strong Evidence (some RCTs, strong observational data):
        Psychotherapy approaches targeting neural patterns can cure chronic pain (as measured by both self-reports and brain imaging)Stress and emotional states modulate pain intensityPain patterns often violate anatomical expectations
      Moderate Evidence (limited RCTs, good observational data):
        Neuroplastic pain may be the primary cause of most chronic painSpecific treatment protocols' relative effectiveness
      Areas of Uncertainty:
        Optimal treatment protocolsIndividual patient susceptibility factors


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神经可塑性疼痛 慢性疼痛 大脑 心理疗法
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