A semantic argument is not about facts, but about the meaning of words. Both parties agree on what’s real, but disagree on how to describe the reality. For example, in the 2000s there was a debate about whether Pluto was a “planet.” It wasn’t focused on contested facts about Pluto, but rather the pros and cons of different classification systems for celestial bodies. Ultimately, it was decided that Pluto would be called a “dwarf planet.”
Semantic debates can be useful. Good science requires a system of terms which correspond well to the relevant facts, are self-consistent, and establish conventions about how experts communicate. For pain physiology, we need terms that identify important phenomena, distinguish between them, have some internal logic, and get everyone on the same page when they communicate and write about these topics. For this reason, efforts by the IASP to develop a uniform set of terms is useful.
Unfortunately, the debates about pain terminology that I see on social media are generally not useful. Most are just ways to declare opponents “wrong” based on legalistic analysis of language, rather than substantive discussions of pain physiology. The result is confusion and people talking past each other.
Some of these problems are evident in the recent debate about whether “pain” can occur in the absence of “nociception.” A recent paper by Weisman, Quintner, and Cohen addresses this question by arguing that the common aphorism “nociception is neither necessary nor sufficient for pain” is false, and should be replaced with: “nociception is necessary but not sufficient for pain.”
The paper contains some discussion of relevant facts, but its arguments are primarily semantic, and these are confused and self-contradictory. The authors argue that current IASP terminology implies, as a matter of logic, that nociception is necessary for pain. But they also argue that the definitions of both “pain” and “nociception” should be changed to state this. And they stated specifically in an earlier paper that under current definitions, nociception is not necessary for pain. Thus, the paper is not really an attack on the aphorism, but on IASP terminology.
This is like arguing that Pluto is a planet because it would be a planet if we changed the definition of "planet." Here’s a detailed analysis.
The definition of “pain”
Weisman et al. argue that pain requires nociception by definition. Specifically, that the definition of pain proposed by the IASP logically implies that all pain must involve nociception.1 This argument is wrong. Here’s the IASP definition of pain:
An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage.
There’s nothing in this definition that states that pain requires nociception. The only requirement is an unpleasant conscious experience that feels like tissue is being damaged.
Weisman et al. argue that nociception is logically implied in the definition because it references “tissue damage”, and tissue damage implies nociception.2 However, the definition also refers to “potential tissue damage”, and uses the word “resembling” and the phrase “associated with.” These words make clear that the phrase “tissue damage” is there to describe what pain feels like (e.g pain feels like tissue is damaged), not to state a requirement about what causes the feeling.
The authors seem to recognize the point, arguing in various places that the IASP definition of pain is flawed and would need to be “recast” to support their claim that pain requires nociception.3 As detailed in the section below, the same pattern appears in how they use the term “nociception.” They cite the IASP definition of this term, but have previously admitted that it does not support their argument, and would need to be changed to show that pain requires nociception.
The definition of “nociception”
Weisman et al. analyze a list of pain phenomena, including phantom limb pain and experimental brain stimulation, and conclude that all of them involve “nociception.” Therefore, they argue, it is impossible for there to be pain without nociception.
But how are they defining “nociception” here? Are they using the IASP definition, or some other definition they would prefer? Although the paper refers to the IASP definition, this can’t be the basis for the argument that pain requires nociception. How do we know this? Because Weisman, Quintner, and Cohen wrote a previous paper in 2023 stating that under the IASP definition, nociception is not necessary for pain. Here are some details and background.
The term “nociception” was coined by Sherrington more than 100 years ago, but it wasn't formally defined by the IASP until 2008. In the interim, the word was used to mean different things in different contexts.
Sometimes the word is used to convey a broad meaning, encompassing all neural events involved in processing noxious stimuli. For Sherrington, it even included top-down modulation of those signals. In other contexts, the meaning of nociception is narrower, intended to distinguish sensory signaling that arises from detection of noxious stimuli at nerve endings in the periphery, from sensory signaling that originates from “ectopic firing” in nerve trunks as a result of neuropathy. This is an important distinction: in the first case, sensory signals are “encoding” a noxious “stimulus”, but in neuropathy, sensory signals are firing by mistake and not accurately reflecting any stimulus.4
Neither usage is right or wrong in an absolute sense, only right or wrong within a particular context. So what context was the aphorism using when it said you can have pain without nociception? As Weisman et al. themselves point out, the aphorism was first stated by John Loeser in 1980. And Loeser himself has clarified that the word nociception in the aphorism means peripheral nociception.
In 2008, the IASP tried to standardize terminology by defining nociception as: “the neural process of encoding noxious stimuli.” My reading of this language, along with the IASP’s distinction between “neuropathic” and “nociceptive” pain, suggests that the narrow meaning was intended, i.e nociception means sensory signaling originating in the periphery. But I acknowledge this isn’t clear.
More importantly, Weisman and co-authors have themselves conceded that the narrow interpretation of this definition is correct. In a 2023 paper addressing IASP pain terminology, they explicitly stated that the IASP definition of nociception requires transduction in the peripheral nervous system, thus excluding sensory signaling caused by neuropathy. In fact, they specifically stated that under the current IASP definition, nociception is “neither necessary nor sufficient for pain.” In other words, they have already conceded that under IASP definitions, the aphorism is correct. Here are the relevant quotes:
This codification of nociception occurred in 2008, even though the term had been in use for a long time. However, this definitional focus is solely on the transduction and encoding of a noxious stimulus, that is, on the function of the nociceptor and the newly-defined nociceptive neuron.
…
NACD [nociception as currently defined by the IASP] posits that nociception relates only to the recognition of a noxious stimulus via nociceptors, defined in the singular as “a high-threshold sensory receptor of the peripheral somatosensory nervous system that is capable of transducing and encoding noxious stimuli.
…
the concept of NACD [nociception as currently defined] is too narrow. Indeed, this should come as no surprise, given that [nociception as current defined by the IASP] is neither necessary nor sufficient for pain.
I was surprised to find this. I wasn’t expecting that, in my research to find papers that take the opposite position of Weisman, Quintner and Cohen, I would find one written by …. Weisman, Quintner and Cohen. What exactly is going on here?
Let’s review the timeline:
In 2023, they explicitly state that under current IASP definitions, nociception is not necessary for pain. In 2025, they state that nociception is necessary for pain, citing the IASP definitions as authority.
How do we resolve this conflict? A careful read of both papers shows that the authors want to redefine both “pain” and “nociception.”5 They want “pain” changed so that it specifically requires nociception. And they want “nociception” broadened significantly. This can be seen from their references to “nociception-in-some-form” and a “nociceptive apparatus,” terms that they do not define.6 This is a good example of how debates about pain terminology can create more confusion than they resolve.
So is the aphorism correct?
I’m not sure there’s a right or wrong answer in the absolute sense. It depends on the context and how you define nociception. It’s also worth noting that aphorisms are not intended to be precise statements about specific facts. They are short, memorable ways to describe general principles. As such, they lack specific context and do not express precise meanings. Legalistic analysis of their accuracy is therefore unlikely to be informative.
That doesn’t mean we can’t improve the way we talk about pain. Perhaps a better aphorism would be something like: “tissue damage is neither necessary nor sufficient for pain.” Or scientists could stop using it altogether. What would be the effect of this change?
Contrary to suggestions I’ve seen on social media, the aphorism is not a foundational premise upon which other facts and theories are based. It’s an eight-word summary of decades of research on hundreds of separate topics. Changing or “refuting” the aphorism wouldn’t overturn the research illustrating the disconnect between pain and tissue damage, or the role of psychosocial factors in modulating pain. To do that, you need to engage in analysis of research, not argue over definitions.
To their credit, Weisman and colleagues do discuss a variety of factual topics in their paper. These shed light on pain physiology, including phantom limb pain, the thermal grill illusion, and the anecdote about the nail in the boot. These analyses are part of a larger argument that appears in their work, which is that central factors in pain (especially the role of the brain, thoughts, and emotions) have been overrated, and that more peripheral factors such as inflammation have been underrated.
These are legitimate arguments, and I would not be surprised if Weisman and colleagues are correct about some of them. Perhaps the thermal grill illusion will be shown to result from demand characteristics. Perhaps thoughts, emotions, and expectancies have less effect on pain than we think. Perhaps we’ll learn that fibromyalgia is far more peripheral than central, or that the immune system is more powerful than the nervous system in modulating pain. Or that treatments aimed at changing thoughts and emotions (e.g. CBT, CFT, PRP or PNE) are not as effective as advertised.
These are open empirical questions about the relationship between peripheral and central factors in pain. The answers will come from detailed examination of specific evidence in specific contexts, not from redefining terms (and developing long lists of questionable fallacies7) so that the distinction between central and peripheral is blurred, and the role of the brain can no longer be conceived.
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Footnotes
They make this claim several times: “The assertion that nociception is not necessary for pain is found to contradict the definition of pain itself.” Also: “the definition in essence requires that if pain is present then nociception has occurred.” Also: “The IASP definition of pain and its logical implication, that nociception is necessary for pain, constitute the default position that governs this field of scientific and clinical enquiry.”
From the paper: “Both this definition and its predecessor explicitly enshrine a connection between the (subjective) experience of pain and the (objective) phenomenon of tissue damage.”
Some relevant quotes on changing the definition of pain:
It seems reasonable, therefore, to recast the definitional connection of pain from “tissue damage” to the signalling to the organism that tissue damage has occurred or is threatened.
…
As it is improbable that the recently revised definition of pain will be changed in the foreseeable future, the connection (“associated with”) between pain and tissue damage may need to evolve into the more nuanced connection between pain and harm-signalling, which would be a sine qua non for a pain experience.
For example, see this quote from this paper by Cliff Woolf: “The nociceptor is designed to initiate activity only at its peripheral terminal. Any action potentials that originate from the axon or cell body represent pathological ectopic firing and produce sensory inflow in the absence of sensory stimuli.”
Some quotes from the paper about the need to change both the definitions of pain and of nociception: “That paradox can be resolved by operationally reframing the definition as ‘an unpleasant sensory and emotional experience associated with nociception,’ with the vital caveat that nociception itself needs to be redefined. What follows logically from that reframing is that the presence of pain implies that nociception-in-some-form has occurred.” Also: “In a new conceptualisation of nociception as activation of a nociceptive apparatus, which reflects the interaction of a neuronal substrate with cellular and humoral elements of the immune system.”
The 2023 paper suggests that the term “nociceptive apparatus” is a very broad concept which would include activation of the HPA axis.
Weisman, Cohen and Quintner have argued that it’s a “mereological fallacy” to say the brain analyzes evidence of threat, and a “teleological fallacy” to say pain serves a protective function. They have argued that concepts like fear avoidance, pain catastrophizing and kinesiophobia involve fallacious reasoning. They have argued that pain is a sensation, not a perception. These arguments share two common features: they are radical critiques of well-established concepts, and they make it conceptually more difficult to consider the role of the brain in pain.







Strong article, Todd. Really appreciate your insights and balanced approach. This semantic debate is frustrating and I fear might create confusion for people working to recover from pain. I still feel there’s a hidden agenda here that’s unclear. Perhaps a desire to go back or defend current bottom up interventions. Time will tell. Thanks again for your reflections.
“Or scientists could omit this term altogether. What impact would this change have?”
1. Yes!!!
2. Back to the beginning!!!
Sherrington also did some good things. Sherrington laid the foundation for our understanding of spinal reflex arcs and neural circuits.
The sea slug (Aplysia californica) has a nervous system consisting of only about 20,000 nerve cells. It is both simple and complex enough to exhibit a primitive form of learning and memory.
Before we talk about central sensitization, let's look at what habituation actually is.
The concept of habituation plays a central role in pain perception.
Habituation is a learning process in which the response to a constant, repeated stimulus decreases over time. This is crucial for the survival mechanism. The question of whether the response requirement modulates the input at the detection, synapse, or transmission level will be answered in the future.
Repeated manual mobilization (emphasis on repetition) of skin and joints, as well as targeted movements, can promote movement-induced hypoalgesia and improve proprioception and exteroception through tissue contact.