Sensible advice for aches, pains & injuries

The Basic Types of Pain

Nociceptive, neuropathic, and “other”

by Paul Ingraham, Vancouver, Canadabio
I am a science writer and a former Registered Massage Therapist with a decade of experience treating tough pain cases. I was the Assistant Editor of for several years. I’ve written hundreds of articles and several books, and I’m known for readable but heavily referenced analysis, with a touch of sass. I am a runner and ultimate player. • more about memore about


There are two main classifications of pain: the common sensical sort that arises from damaged tissue (nociceptive pain), and the more exotic kind that comes from damage to the system that reports and interprets damage, the nervous system (neuropathic pain). This is the difference between engine trouble and trouble with that light on your dashboard that claims there’s engine trouble. Oddly, there is still no official “other” category for the pain of conditions like fibromyalgia and irritable bowel syndrome, which involve dysfunction of the nervous system, as opposed to damage; names like nocipathic or algopathic are on the table.

full article 3250 words

There are two well-recognized broad categories of pain: the common sensical sort (the pain of damage), and the somewhat more exotic kind that comes from damage to the system that reports and interprets damage, the nervous system. It’s the difference between engine trouble and trouble with that light on your dashboard that says there’s engine trouble. More specifically:

  1. Nociceptive pain arises from various kinds of trouble in tissues, reported to the brain by the nervous system.1 This is the type of pain everyone is most familiar with, everything from bee stings and burns and toe stubs to repetitive strain injury, nausea, tumours, and inflammatory arthritis. Nociceptive pain typically changes with movement, position, and load.
  2. Neuropathic pain arises from damage to the nervous system itself, central or peripheral, either from disease, injury, or pinching.2 The simplest neuropathies are mechanical insults, like hitting your funny bone or sciatica, but this is a big category: anything that damages neurons, from multiple sclerosis to chemotherapy to alcoholism to phantom limb pain. It’s often stabbing, electrical, or burning, but nearly any quality of pain is possible. Unfortunately, it’s also more likely to lead to chronic pain: nerves don’t heal well.3

Obviously these kinds of pain can overlap. Some medical problems, like injuries, can affect both nerves themselves and other tissues, causing both kinds of pain. However, it’s surprising how little overlap there is: look at any list of the most painful conditions [NHS] and they all fit pretty clearly into one category or the other.

Pain is predictably unpredictable, thanks to brains. Regardless of type, all pain is weird in some typical ways, because it’s all under the total control of our brains,6 and brains have complicated and conflicting priorities for us that we are oblivious to.7 The result is that pain is often weird, a somewhat paranoid guess about how much danger we’re in, and that’s when everything’s working correctly. If the nervous system is damaged (neuropathic pain), then the brain is getting bad information, and pain gets even weirder. But when the nervous system misbehaves, pain can get so wonky that a whole new category of pain might be needed.

Venn diagram showing the intersection of neuropathic pain, nociceptive pain, and “other” pain. In the centre is the word “hell.”

Although the different kinds of pain certainly can overlap, mercifully it’s relatively rare to end up in “hell” at the centre of this Venn diagram. Unfortunately, the “other” category often does arise from a history of other kinds of pain.

File under “other”: pain problems for which we might need a new word

Some common kinds of pain are not a great fit for either of the two official categories. The canonical example is the pain of fibromyalgia. [Mayo] Other major examples:

Fibromyalgia is probably a pain system dysfunction, a poorly understood multi-system failure causing widespread body pain (and more9), but “dysfunction” of the nervous system is specifically excluded from neuropathic pain, by decree, as of 2011.10 Dysfunction means that fibromyalgia isn’t caused by any (known) damage to the nervous system, but by its misbehaviour, and so it’s not welcome at the neuropathy club. It was before 2011! But not anymore.

Maybe there are unknown lesions? Maybe someday we’ll know that fibromyalgia is caused by some kind of subtle damage to the nervous system.11 There are at least two theories of subtle lesions of this type.12 That would make it just another neuropathy after all, ho hum. But for now it’s still more plausible that it’s a dysfunction, arising from widespread problems in a complex system, and no clear point of failure will ever be discovered.1314 But who knows. Science is not finished with fibromyalgia.

Meanwhile, what do we call it? And other miserable pain problems that arise from what seem to be neurological dysfunction?

Possible names for this other kind of pain

“Other” is a bit vague, so experts have proposed some more descriptive names for this category. There are issues with all of them. (The first three here all come from the same source.15)

The “noci” terms seem a little misguided to me, because the pain of a misbehaving nervous system is so much closer kin to neuropathic pain.18 Centralization is an important concept and element, but clearly not the whole story19 (and “maladaptive” might be too blamey20). Algopathic gets my vote: suitably neutral and formal, while saying just enough to be better than “other.”

Do sensitization and centralization belong in the “other” category?

Sensitization is the amplification of danger signalling in any part of the system (which can be driven by both peripheral and central neurology, while centralization is referring only to the latter). It seems like a slam dunk to put these in the “other” category, but not so fast: the nervous system is not being dysfunctional just because it overestimates some danger. Many of us experience normal, healthy centralized sensitization every time we go to the dentist, because our nervous system is not an idiot and is very suspicious of dentists based on past experiences. Our brains think the dentist is a threat, and although they are technically wrong — the dentist is actually there to help — the judgement is not “dysfunctional.”

Sensitization is clearly part of the normal function of the pain system — it’ s not a dumb system where pain is always exactly proportionate to tissue danger. It’s more subtle. Sensitization/centralization is only dysfunctional when it’s chronic and seriously disproportionate. And of course there’s a grey zone a mile wide between normal and dysfuntional. It’s a spectrum.

File under “unknown”: pain problems that can’t be categorized yet

Sometimes we just don’t understand a problem well enough to classify it. The best example of this is the sensitive spots in soft tissue that so many people have — “trigger points,” the things that motivate most massage therapy appointments. There is a popular hypothesis that they are caused by a problem with muscle tissue, which would make it a clear case of nociceptive pain from a fairly subtle lesion… but it’s just an hypothesis, and some experts have suggested that trigger points are caused by a problem with nerves themselves, which would make them neuropathic.21 No one actually knows, and it’s not likely to be settled for a long time.

Article Summary

There are two main classifications of pain: the common sensical sort that arises from damaged tissue (nociceptive pain), and the more exotic kind that comes from damage to the system that reports and interprets damage, the nervous system (neuropathic pain). This is the difference between engine trouble and trouble with that light on your dashboard that claims there’s engine trouble. Oddly, there is still no official “other” category for the pain of conditions like fibromyalgia and irritable bowel syndrome, which involve dysfunction of the nervous system, as opposed to damage; names like nocipathic or algopathic are on the table.

About Paul Ingraham

Headshot of Paul Ingraham, short hair, neat beard, suit jacket.

I am a science writer, former massage therapist, and I was the assistant editor at for several years. I have had my share of injuries and pain challenges as a runner and ultimate player. My wife and I live in downtown Vancouver, Canada. See my full bio and qualifications, or my blog, Writerly. You might run into me on Facebook or Twitter.

Related Reading

Appendix: Neuropathic versus nociceptive pain

If you have unexplained pain, can at least diagnose the type? Can you put it in one of the two major pain categories, neuropathic or nociceptive? Sometimes! And often you can’t. These types of pain overlap and often the only clues are the quality of the pain and the messy stories and ideas we have about it: how it started, what makes it worse or better, and so on. We can’t just say that neuropathic pain is “electrical,” because not everyone’s sciatica nerve feels that way.

But we can usually make an educated guess, at least.

Neuropathic pain is mostly more distinctive and specific than nociceptive pain, so it’s best to think in terms of whether pain is or is not neuropathic.

It is usually burning, electrical, or stabbing. The better these words seem to fit, the more likely it is to be neuropathic pain.

Neuropathic pain is sometimes associated with other sensory disturbances like tingling (parasthesia) and numbness, or weakness.

More exotically, neuropathic pain may cause odd effects like exaggerated pain (hyperalgesia), or even pain from stimuli that shouldn’t hurt at all (allodynia), or pain “echoes.” If any of these other non-pain neurological symptoms are present, it’s nearly a diagnostic slam dunk: the pain is probably neuropathic.

Unfortunately, plenty of neuropathic is not conveniently packaged with other obvious neurological effects. So how else can we judge it?

Neuropathic pain is also more likely to occur in some locations. For instance, a very broad rule of thumb is that neuropathic pain is more common in the limbs, and the further you go out towards the tips the more likely it gets, simply because the limbs of are full of long and relatively exposed nerves.

So, if you have stubborn, widespread, burning pain in your limbs that defies acetaminophen… that’s probably neuropathic pain. And yet it’s still not a sure thing!

What’s new in this article?

Five updates have been logged for this article since publication (Aug 29th, 2016). All updates are logged to show a long term commitment to quality, accuracy, and currency. more Like good footnotes, update logging sets apart from most other health websites and blogs. It’s fine print, but important fine print, in the same spirit of transparency as the editing history available for Wikipedia pages.

I log any change to articles that might be of interest to a keen reader. Complete update logging started in 2016. Prior to that, I only logged major updates for the most popular and controversial articles.

See the What’s New? page for updates to all recent site updates.

JulyNew section — “Appendix: Neuropathic versus nociceptive pain.”

JanuaryAdded an important point to the definition of neuropathy: it tends to be more chronic.

2016Added a nice new Venn diagram depicting the intersection of all three kinds of pain in “hell.” Added section “Do sensitization and centralization belong in the “other” category?”

2016Added sidebar about migraine, and converted section about the influence of the brain to a sidebar. Elaborated on overlapping pain problems.

2016Extensive next day revisions.



  1. [Internet]. International Association for the Study of Pain. IASP Taxonomy; 2012 May 22 [cited 16 Sep 1]. The formal definition: “Pain that arises from actual or threatened damage to non-neural tissue and is due to the activation of nociceptors [nerve endings that detect tissue damage].” The next definition is also based on this reference. BACK TO TEXT
  2. Formally: “Pain caused by a lesion or disease of the somatosensory nervous system.” You get a gold star if you notice that “dysfunction” isn’t included there. More on this below. BACK TO TEXT
  3. Cohen SP, Mao J. Neuropathic pain: mechanisms and their clinical implications. BMJ. 2014;348:f7656. PubMed #24500412. BACK TO TEXT
  4. Chakravarty A, Sen A. Migraine, neuropathic pain and nociceptive pain: towards a unifying concept. Med Hypotheses. 2010 Feb;74(2):225–31. PubMed #19765908. “Migraine, neuropathic pain and nociceptive pain are the three commonest pain syndromes affecting human.” BACK TO TEXT
  5. Biondi DM. Is migraine a neuropathic pain syndrome? Curr Pain Headache Rep. 2006 Jun;10(3):167–78. PubMed #18778570. BACK TO TEXT
  6. Pain is an output of the brain.

    Pain is the end result. Pain is an output of the brain designed to protect you. It’s not something that comes from the tissues of the body.

    Lorimer Moseley, from his surprisingly funny TED talk, Why Things Hurt 14:33

    The formal definition of pain emphasizes its subjective, experiential nature: “An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” (IASP Taxonomy). This experience is based on many “inputs,” not just nerve signals about tissue damage.

  7. Although the brain takes data from tissues seriously, it also regularly minimizes, exaggerates, and misinterprets. The brain thinks minor things are serious, or serious things are minor. It’s poor at locating the sources of internal pain. If the nervous system itself is damaged, the brain can really get thrown off (as with phantom limb pain). The brain’s pain policies are warped by moods, anxieties, fatigue, and much more. For much more about this, see Pain is Weird: Pain science reveals a volatile, misleading sensation that is often more than just a symptom, and sometimes worse than whatever started it. BACK TO TEXT
  8. PS Ingraham. Central Sensitization in Chronic Pain: Pain itself can change how pain works, resulting in more pain with less provocation. 4116 words. Pain itself often modifies the way the central nervous system works, so that a patient actually becomes more sensitive and gets more pain with less provocation. This is called “central sensitization.” (And there’s peripheral sensitization too.) Sensitized patients are not only more sensitive to things that should hurt, but also to ordinary touch and pressure as well. Their pain also “echoes,” fading more slowly than in other people. BACK TO TEXT
  9. Poor quality sleep, fatigue, memory and mood issues — the infamous “fibrofog.” BACK TO TEXT
  10. Jensen TS, Baron R, Haanpää M, et al. A new definition of neuropathic pain. Pain. 2011 Oct;152(10):2204–5. PubMed #21764514.

    IASP has recently [2008] published a new definition of neuropathic pain according to which neuropathic pain is defined as ‘pain caused by a lesion or disease of the somatosensory system.’ This definition replaces the 17-year old definition that appeared in the Classification of Chronic Pain published by IASP in 1994, which defined neuropathic pain as ‘pain initiated or caused by a primary lesion, dysfunction, or transitory perturbation of the peripheral or central nervous system’. Even though the definition has not been changed dramatically, there are two important changes in the new version: (1) the word ‘dysfunction’ has been removed and (2) a lesion or disease affecting the nervous system has been specified to be a lesion or disease of the somatosensory system.

    The whole paper is excellent, but skipping to the cogent conclusion:

    A definition of neuropathic pain is only useful if it distinguishes conditions in a clinically meaningful way. If the definition does not provide additional benefit in terms of understanding and treating the condition(s), then there is no reason to keep it. Hopefully, the new definition of neuropathic pain will act as a stimulant to discuss the definition in more detail and provide input for studies that can be used to test the value of the definition.

  11. Multiple sclerosis attacks nerves in quite a dramatic way, which we could see in autopsies, but the lesions were invisible in living patients until the invention of MRI. It’s plausible that there are still plenty of biological “lesions” that we haven’t yet learned to detect, because they are just too small and transient. Despite all of our modern technological wizardy, most of the action in biology happens at the nanoscale, cells moving molecules and atoms around at dazzling speeds through the chaos of the molecular storm (brownian motion). There are probably nanoscale lesions. BACK TO TEXT
  12. Both small fibre peripheral neuropathy and positional cervical cord compression are candidate neuropathic etiologies: both hard to detect, both capable of explaining at least some of the symptoms of fibromyalgia, both associated with people who have diagnosed with fibromyalgia. See the main fibromyalgia article for more information about these. BACK TO TEXT
  13. Lyon P, Cohen M, Quintner J. An evolutionary stress-response hypothesis for chronic widespread pain (fibromyalgia syndrome). Pain Med. 2011 Aug;12(8):1167–78. PubMed #21692974. “Drawing on diverse findings in neurobiology, immunology, physiology, and comparative biology, we suggest that the form of central sensitization that leads to the profound phenomenological features of chronic widespread pain is part of a whole-organism stress response, which is evolutionarily conserved, following a general pattern found in the simplest living systems.” BACK TO TEXT
  14. [Internet]. Hargrove T. A Systems Perspective on Chronic Pain; 2014 Oct 23 [cited 16 Sep 12].

    This deep but beautifully readable article explains, with many pictures and apt examples, how “chronic pain is often driven by dysregulation of a ‘supersystem’ that coordinates defensive responses to injury. The supersystem results from dynamic interaction between different subsystems, most notably the nervous system, immune system, and endocrine system.” It’s hard to believe, but the article also manages to make this information seem quite practical.

  15. Kosek E, Cohen M, Baron R, et al. Do we need a third mechanistic descriptor for chronic pain states? Pain. 2016 Jul;157(7):1382–6. PubMed #26835783. PainSci #53276. BACK TO TEXT
  16. Clauw DJ. Fibromyalgia: a clinical review. JAMA. 2014 Apr;311(15):1547–55. PubMed #24737367. BACK TO TEXT
  17. Topical Issues in Pain ( BACK TO TEXT
  18. Even if this kind of pain does involve an exaggeration of nociception (which it probably does), it still seems to me that nociception itself is innocent. It’s not nociception’s fault! The focus should be on the mechanism of sensitization — that is what makes the problem what it is. BACK TO TEXT
  19. Quintner, J. “Why “Centralized” Is Unacceptable As A Descriptor For The Pain Of Fibromyalgia.” Aug 23, 2016. “Not only does the word itself not imply a mechanism but also it creates potential for confusion with conditions such as ‘central post-stroke pain’ (which is technically ‘neuropathic’) and quite different from the phenomena that underlie fibromyalgia.” BACK TO TEXT
  20. This term has some strong negative connotations. I think this term could strongly stigmatise the patient’s condition, implying that they have “adapted badly” to things that other patients had no problem with. Even if that is technically true from one perspective, it’s not where the emphasis should be. Most patients with these problems have already had lot of difficulty being heard, understood, and respected — let’s not make it harder with a blame-y label. BACK TO TEXT
  21. Quintner JL, Bove GM, Cohen ML. A critical evaluation of the trigger point phenomenon. Rheumatology (Oxford). 2015 Mar;54(3):392–9. PubMed #25477053. Quintner, Cohen, and Bove argue that the common picture of trigger points as lesions in muscle and soft tissue, spelled out most formally in Gerwin 2004, is “flawed both in reasoning and in science.” But not even these critics of trigger points deny that people have pain that seems to come from their muscles. But if it’s not coming from the muscle, where is it coming from? They briefly discuss the possibility of inflamed nerve fibres, which would be a clear case of neuropathy. Neuritis is undoubtedly worth investigating, but it requires us to believe that nerve axons are routinely inflamed for no apparent reason. And the evidence cited to support it is actually much more limited than the evidence for a lesion in muscle. BACK TO TEXT