The Peripheral Mind — general introduction

Aranyosi, The Peripheral Mind (OUP 2013)
Aranyosi, The Peripheral Mind (OUP 2013)

This is the first of a series of three blog posts about my book. It will introduce the main idea behind it, and highlight a few applications. The second post will present one of the chapters in a bit more detail. Finally, the last post will try to identify some future venues of research where the hypothesis of the book might prove useful. I will keep the posts without too much detail, so as to induce some curiosity in the reader to pick and read the book itself. The posts will appear here in the next 15 days, and I will try my best to get involved in the discussions, should there be any.

The basic hypothesis of the book is extremely simple. It is that we could take mental states to be realized by, or identical to (I myself assume identity in the book, but nothing hinges on this choice) CNS + PNS neural subsystems. Is this idea new? I provide several quotations from the classical philosophy of mind literature that show how philosophers assume that mental states, both sensory and non-sensory, are realized by brain states. Even the embodied and the extended approaches to the mind seem to neglect such a philosophical hypothesis when it comes to sensory states, such as pain, and some authors who do stress the bodily aspects of non-sensory states assume a body-in-the-brain type of approach, which still has the brain as the central mover, and the body merely as a contributor to a body image in the brain.

Which CNS+ PNS subsystem realizes which type of mental state is an empirical question.I discuss the state of pain, and stress that it is best to be thought of as a state that involves large areas of the brain, a gate system in the spinal cord, as well as various PNS components, depending on what the source stimulus is. Other types of mental states will have other such subsystems as their realizers, and it is a question of empirical research into such correlations to find out which. What is distinctively philosophical here is the conceptual point that there is no a priori or a posteriori reason, for what we know so far, not to postulate that the peripheral components involved in virtually all mental states are not merely causal contributors to the occurrence of those states, but constitutive of them.

For instance, in the standard case of pain, that is, when pain is caused by injury of some bodily tissue, I say that the activity of C fibers A-delta (which are fast conducting, myelinated bundles, responsible for the first, sharp stage of pain) and of A-delta C fibers (slow conducting, unmyelinated bundles, responsible for the second, longer and dull type of pain feeling) is constitutive part of the realizer of the quale of pain. Most philosophers seem to assume that the quale of pain is realized by some region of the brain, and the PNS components, as well as the non-brain-based CNS components (in this case the gate system in the spinal cord) are merely causes of the state of pain. I don’t have an argument for my view, but they don’t have one either for their assumption. So we are doomed to beg the question against one another. The difference is that I beg it with more philosophical benefit, if what I say in the book is more or less right and credible.

So here are some highlights of where the Peripheral Mind Hypothesis proves to have some philosophical payoff, according to what I claim in the book.

Zombies. This is the part I’ve become least sure about, after the experience of not having convinced any of the philosophers who read the manuscript in draft form. However, I still endorse what I say (I’m the author, after all, and the book is fresh 🙂 ). What I try to show is that the zombie intuition can be weakened once we include the PNS as a constitutive component of the neural basis of conscious states. I reject the need to appeal to phenomenal concepts, as well as any physicalism that is based on denying the conceivability-possibility entailment. The first step is to stop thinking in terms of persons as subjects of experience, and think rather in terms of nervous systems. This shouldn’t bother anyone, except substance dualists. Property dualists should be happy with it since they are substance physicalists. And what else is the physical subject of experience than a nervous system? The next step is to ask: what does it mean for a nervous system to be conscious in the actual world? It means to be activated in some ways. The zombie intuition is that you can conceive of a copy of this conscious nervous system such that the copy lacks consciousness. What happens if the property of being conscious is partly realized by the PNS (the model I use in the book for this view is that of distributional properties, first discussed by Josh Parsons — conscious state types are then realized by ways to distribute electrical activity over parts of the nervous system)? I claim that at the level of an individual nerve fiber we have a specific conscious property, the fibers own constitutive contribution to the global state of consciousness. Finally, we ask the question “what does it mean for the fiber to be conscious?”

The basic point is that if we focus on the consciousness specific to an individual peripheral nervous fiber, the intuition is that what it means, not just actually but simpliciter, for that fiber to be conscious is simply for it to be active. At that level of simplicity, at which we got rid of the temptation to involve anything like a person in the thought experiment, to be conscious is for the fiber to fire. This has the consequence that a zombie fiber (a zombie foot, a zombie retina, etc.) is inconceivable. But since we can replicate this all the way up to the higher levels of the nervous system, a zombie brain is equally inconceivable.

The mad pain problem. Mad pain (i.e. a pain quale caused by, say, moderate exercise on an empty stomach, and causing the desire to solve mathematical problems) is logically impossible, because part of the realizer of the pain quale are the nociceptive peripheral fibers. The fibers involved in moderate exercise don’t deserve the name “nociceptive fibers”, hence the alleged quale above does not deserve the name “pain quale”.

The problem of pseudonormal vision. Pseudonormal vision is an alleged actual version of spectrum inversion. There are two types of partial color blindness: (A) when the green photopigment is contained in both the G and the R cones, and (B) when the red photopigment is contained in both the G and R cones. The genes responsible for case (A) and (B) can in rare cases be present in one and the same person, thus such persons, called ‘pseudo-normal’, although not visually defective in terms of normal color discriminations, have their photopigments swapped between the G and R cones. Hence, according to Martine Nida-Rümelin (“Pseudonormal vision: An actual case of qualia inversion?”, Philosophical Studies 82 (2):145-57, 1996) they are actual cases of spectrum inversion. My response is that the above argument depends on assuming that qualia are realized by brain states; once we include cones and photopigments as constitutive of experience, the possibility of inversion vanishes. It is in virtue of the photopigments that that one’s experience has the color quale that it has, hence, me and my alleged pseudonormal twin will experience the same colors, because the same photopigment is activated when we look at the same surface. A photoreceptive cell deserves the name ‘G-cone’ in virtue of containing the G pigment; the morphology of the cones has no relevance, as proven by the history of neuroscience (see the book for details).

The China-brain problem. I think that why most people got moved by Ned Block’s China-brain thought experiment is because they focused their attention on the wrong side of the China system, namely on the brain. Suppose the government of China is a bit less ambitious and is content with only realizing a brief pain sensation via a system of people and radio transmitters. What happens is that I offer my nociceptive nerves and the corresponding motor nerves to be used by China for the experiment. They will put me to sleep, disconnect my pain-related PNS components from my brain and connect them to the China-pain CNS system. I will wake up, suppose, with all the other cognitive components intact, except for those involved in the sensation of pain. Intuitively, I will be zombified, pain-wise: I won’t feel pain; yet, when my skin is hurt, my relevant muscles will contract and I will avoid the stimulus, I will scream, and so on.

What about the CNS states in the China-pain system? If in Block’s experiment you intuited that the China-brain system is not conscious, you will intuit here that the China-pain system is not in pain. I also intuit that in this case I am not in pain and the China-pain system is not in pain either. Yet, I do not intuit that there is no pain at all instantiated by the composite system of my body (PNS) + China-pain (CNS). The only puzzle about the original China-brain system is a puzzle about who is conscious, not about whether there is any consciousness somewhere in the global system.

There are several other puzzles that the PMH offers novel solutions to: the problem of triviality for machine functionalism, the possibility of a brain in a vat, the problem of wide mental states posing a threat to physicalist supervenience, as well as the problem of how to distinguish between causal and constitutive contributions of nervous processes to experience. I will present the last one of these next week in a new blog post, and leave the other three for the readers to check out in the book.


  1. Hi István.

    My personal view is that the whole concept of a “mental state” is misguided, because the word “state” implies a presumption that there is some underlying substance capable of being in that state. I don’t believe there is any such substance, so I think you’re trying to solve a problem that doesn’t actually exist.

    But ignoring that and taking the theory on its own terms, I’m curious to know how you would handle phantom limb pain. It seems like you are going to be forced to say that it isn’t really pain — but perhaps I didn’t understand what you were saying.

    Best regards, Bill

  2. Very interesting work, I have a basic question. You wrote:
    “The basic point is that if we focus on the consciousness specific to an individual peripheral nervous fiber, the intuition is that what it means, not just actually but simpliciter, for that fiber to be conscious is simply for it to be active. ”

    Do you literally think that individual neurons are conscious, such that if we have a cultured set of neurons, there is consciousness there?

    • István Aranyosi

      What I think, and say in the book, is that individual fibers could, for all we know, make a constitutive (not merely causal) contribution to consciousness. If some kind of reductive view of consciousness is true, then these individual fibers activity would actually partially constitute the phenomenology, hence they would literally contribute their own consciousness, or their own bit of consciousness, to what we as persons experience. I appeal to an analogy with our attribution of fear to dogs and even to sea urchins. When sea urchins get scared, they extend their spikes towards the direction above, from where some object casts a shadow. I believe there is no problem in attributing fear to the sea urchin as long as we are aware that it is probably phenomenally different (simpler, more primitive) than our state of fear. By analogy to what I call “sea-urchin-y fear”, we could attribute fear, pain, pleasure, color sensation, to individual fibers, keeping in mind that we are talking about something less complex than what we instantiate at the personal level.

      • Ken

        “If some kind of reductive view of consciousness is true, then these individual fibers activity would actually partially constitute the phenomenology, hence they would literally contribute their own consciousness, or their own bit of consciousness, to what we as persons experience.”

        I think this line overlooks what seems to be a more plausible line that may have been what was troubling Eric. Suppose you think there is a mechanistic (hence in some sense, reductive) explanation of consciousness a la Bechtel, Craver, Machamer, et al. It could be that neuronal activity is part of the mechanistic basis of a conscious experience without the contributing neurons being conscious. You need not explain a person’s conscioiusness as somehow being made up of neuronal consciousnesses.

        • István Aranyosi

          Sure enough, it would be great to come up with such a model for getting full experience out of neuronal “protoexperience”. I do not have such a model in the book, and it is hard, according to some authors, to even see how experience “arises from” more complex firing patterns in the brain.

          • Ken

            Hi, Istvan,

            I don’t think you are speaking to my point. You seem to be proposing that something like creature consciousness be mechanistically explained by something like neuronal “protoconsciousness”. But, why think the mechanistic explanation of consciousness must appeal to protoconsciousness, rather than something non-conscious?

            I am not asking about the details of any proposal, but simply about the apparent presumption that we must bridge from the conscious to the non-conscious by way of the “proto-conscious.”

            It does not seem to follow simply from the desire for some kind of “reductive” view of consciousness.

            Maybe this is something that you take up in more detail in the book.

          • István Aranyosi

            Hi Ken,

            i understand now, and agree. We don’t need to appeal to an intermediary protoconscious level. In fact, I never mention this term “protoconscious” in the book itself; I’ve only used it in tnis post in order to try to boost the antizombie intuition. As in the book I go for an identity theory, creature-conscious states are thought as identical to CNS+PNS incolving loops. On the model of distributional properties, then, the phenomenally conscious property is thought as a way of distributing electrical activity over the nervous system.

  3. Ken

    ” I don’t have an argument for my view, but they don’t have one either for their assumption.”

    Does the scientific literature really contain nothing like some version of phantom limb pain that would challenge this view?

  4. István Aranyosi

    Bill and Ken, thanks for pointing out the case of phantom pain and phantom limbs in general, which is the most obvious apparent counterexample to what I say; I should have mentioned that in my post. Indeed, I address this issue in the book. Merleau-Ponty, who seems to subscribe at one point in his Phenomenology of Perception to my thesis, defends this thesis by pointing out that complete deafferentation makes the sensation of phantom pain disappear. Phantom pain, just like pain in general, arises from some peripheral stimulation, and sometimes from random internal, but still peripheral signals. So it is not as if the phantom limb by itself shows that the PNS is disposable when it comes to explaining and ontically basing the phenomenology. The closest we can get to a case in which the phantom limb could falsify my hypothesis and reinforce the central theory is discussed in recent neuroscience in connection with phantom limb sensations in patients with congenitally missing limbs. These phantoms are interesting in that the patients have never had any limb in their lives, so it is puzzling how these vivid phantom limb sensations arise. However, even in these cases the explanation neuroscientists have recently come up with is that the phantom is a result of “the monitoring of reafference signals derived from the motor commands sent to the phantom during gesticulation” (Ramachandran & Hirstein 1998: 1606), which means, if I have understood it correctly, that ultimately the phantom sensation requires reafference signals, that is some PNS components. Of course, then, someone could easily claim that the PNS signals are merely causes of pain, but I don’t know whether there is a way to empirically establish such a claim.

    • Ken

      “I don’t know whether there is a way to empirically establish such a claim.”

      But, the logic of the case is straightforward. Get a case where you have pain even when you have eliminated the peripheral nervous system that you say is constitutive of pain. The case does not have to be a phantom limb pain, which is why I said “some version of phantom limb pain.” You can look for something like a peripheral degenerative disorder. There is nothing like this in the literature?

      • István Aranyosi

        Ken, what you quote from me and what you say afterwards are not connected, although what you say after the quote is correct. The quote, in context, says that if there is always PNS trigger and/or support whenever there is phantom pain, then to falsify the peripheral theory requires empirical proof that the PNS component is merely causal. And I claim (like some other people in the fields of both philosophy and neuroscience) that such a claim cannot be empirically proven.

        On the other hand, what you say is right: if we find a case when the PNS is totally shut down and there is phantom pain, then of course the peripheral theory is false. As it happens, I could not identify such a case. Phantom pain is most frequently elicited by amputation (which leaves all the sensory PNS above the section functional). The closest we get to what we want is, indeed, congenital lack of limbs, and even in that case there is PNS involvement. I am not aware of any sensory, exclusively PNS-affecting neurodegenerative condition to progress to a total annihilation of the afferent PNS components. The only way to find out what we want would be to section all the afferent nerves at their junction with the spinal cord, and see whether pain can be elicited in the subject. You might think trascranial magnetic or electrical stimulation would also be able to disprove the thesis, but, I argue in the book, (1) TMS and TES work to the extent that they simulate a PNS, so we might equally take the pain induced by such methods as partly embodied in the extracranial material support, and (2) there are recent studies showing that when, for example, TMS is used to generate phosphene experiences in a subject, for some mysterious reason the retina is activated although it does not receive any light stimulus. If such activation is present in other sense modalities, the it looks like we have some empirical plausibility to the peripheral theory. (Note: the retina is considered part of the CNS, but, as I argue in the book, for our purposes, namely, from a functional rather than anatomical and developmental point of view, I consider it as part of the PNS)

          • István Aranyosi

            This issue arises in a chapter where I discuss the brain in a vat, and, indeed, I put forward a principle informally called “the eye for an eye” principle, which states that a controlled pattern of direct brain stimulation will have to simulate PNS – CNS feedback loops, amd thus recreate some of the PNS processes artificially. It doesn’t really take the theory in another direction, as the main point would still remain that simole nervous structures like the ones the PNS consists of serve as partial support or realizer for experiences.

          • Carl Gillett

            Hi Istvan, I am not seeking to press any objections, but just to try to get clearer what the brad shape of your view is. Following along the interchange with Bill, let me see if I got the ideas and position at all straight.

            You accept that an entity that produces stimulation S of the brain is needed to produce pain. And you accept that stimulation S might be produced by something other than the PNS. Is that right?

            But the underlying issue comes down to whether we take the state of being in pain to be composed simply by individuals contained within the brain that are stimulated by S; or whether we take the state of pain to be composed by both the individuals in the brain stimulated by S and the individuals that produce S (which is your view)? Is that right?

            So you are not an identity theorist about being in pain, it is not identical to brain and PNS, rather you take being in pain to be multiply composed — most pains are in fact composed by the individuals in the brain and the PNS, but some pains could be composed by individuals in brain and non-PNS individuals that also produce S. Is that right?

            Pain looks like a nice case for your type of theory, since it has the bodily damage component in our normal usage. Anyway, am I getting you at all right above? Any help is gratefully received. I look forward to working through the book, best, Carl

          • István Aranyosi

            Thanks, Carl. You put it very well. When the brain is directly stimulated in order to generate, say, a pain state, the source of stimulation has to co form to so e ways in which the biological PNS would normally resonate with the brain states thus created.

        • Ken

          Hi, Istvan,

          ” if there is always PNS trigger and/or support whenever there is phantom pain, then to falsify the peripheral theory requires empirical proof that the PNS component is merely causal. And I claim (like some other people in the fields of both philosophy and neuroscience) that such a claim cannot be empirically proven.
          On the other hand, what you say is right: if we find a case when the PNS is totally shut down and there is phantom pain, then of course the peripheral theory is false. ”

          I’m not getting this view. I don’t want to talk about “proof” and “proving” a theory wrong (that seems to be a red herring), but I do think you *can* have empirical evidence against the view. And, in fact, after the “On the other hand” you seem to agree that we could have evidence against the peripheral nerve hypothesis. Moreover, that this evidence could have the character I described.

          I know folks claim that you can’t empirically test constitution versus causal claims, but is this claim correct?

          • István Aranyosi

            Sure, in principle you could have such evidence against the view, namely, a case when there is no PNS left and yet there is experience. I am not aware of any case study when these two conditions are satisfied. My and other folks’ point about lack of evidence pro or contra constitution is related rather to cases when we do have some PNS contribution, but the experimental results, based on lesion or on disconnection studies, do not decide which view is correct. I mention in the book such a debate in neuroscience about the realizer of visual awareness. The experimental results could equally support the view that visual awareness is realized by the primary visual area V1, whose activity always accompanies visual awareness, and the view that it is realized by higher visual areas. Authors who go for the latter theory argue that lesions to V1 merely interrupt the flow of information to higher areas, so V1 is merely a causal contributor, not a realizer of visual awareness.

            But you are right, if it turns out that no PNS activity is necessary for experience, then we have evidence against the peripheral view.

          • Hi Ken,


            The case I cited refers to ‘double-pain’: Some cutaneous wounds initially generate a highly localized ‘first’ pain that is followed by a poorly localized ‘second’ pain (e.g., stubbing a toe). First pain is described as lancinating, stabbing, or pricking; second pain is more pervasive and includes burning, throbbing, and cramping. Compression nerve block of Aδ nociceptors eliminates first, but not second, pain.

            This is highly relevant to Istvan’s PMH because it shows that pain submodality is partly explained by nociceptor (peripheral) specialization. When conduction of Aδ peripheral nerves is blocked, the characteristic conscious qualia of fast pain are entirely absent. Just as nociceptor specificity best describes why pain has different submodalities, the distinct ‘first’ and ‘second’ pain qualia in double pain is best delineated by the differences in signal transmission in Aδ and C nociceptors, respectively (van Rysewyk, 2013).

            Compression nerve block is a well-established experimental technique, e.g.,

            Laursen, R. J., Graven‐Nielsen, T., Jensen, T. S., & Arendt‐Nielsen, L. (1999). The effect of differential and complete nerve block on experimental muscle pain in humans. Muscle & Nerve, 22(11), 1564-1570.

            Yarnitsky, D., & Ochoa, J. L. (1990). Release of cold-induced burning pain by block of cold-specific afferent input. Brain, 113(4), 893-902.


  5. Hi Istvan,

    Fascinating post, I am sure the book is too. 🙂

    First, an error in your post: you confuse C afferent nociceptors with Aδ afferent nociceptors: C fibers are small diameter, unmyelinated and conduct slow ‘second pain’; Aδ fibers are medium diameter, myelinated and conduct fast ‘first pain’. These primary afferents differ from the larger diameter and rapidly conducting Aβ-fibers that respond to innocuous mechanical stimulation (i.e., light touch).

    You wrote: ‘Most philosophers seem to assume that the quale of pain is realized by some region of the brain, and the PNS components, as well as the non-brain-based CNS components (in this case the gate system in the spinal cord) are merely causes of the state of pain. I don’t have an argument for my view, but they don’t have one either for their assumption.’

    Pain, a submodality of bodily sensation, like touch, proprioception and temperature, itself divides into further submodalities: thermal pain (burning skin on a hot surface), mechanical pain (crushing a thumb in a door), and chemical pain (lemon juice in an open wound). I think pain submodality is best described by nociceptor specialization. Each of the pain qualia (i.e., submodalities) is represented by nociceptors that are submodality specific. When a nociceptor is stimulated naturally (e.g., skin burn) or experimentally (e.g., by electrical stimulation of the neuron), the quale experienced is specific to the information normally processed by the neuron (i.e., burnt skin). Accordingly, a mechanical nociceptor (e.g., Aδ) will not fire to noxious heating of the skin or to a touch stimulus that does not noxiously compress the skin. The nociceptor and its connections in the CNS determine the submodality specificity of the neurons forming a somatosensory tract or pathway (e.g., neospinothalamic and paleospinothalamic tracts). Thus, nociceptor specificity best describes why different sensory qualia are different mechanistic submodalities.



    • István Aranyosi

      Thanks, Simon! Sorry for the error, swapping the C and A-delta fiber characteristics– in the book it is correct 🙂

      As about the second observation, at least in the classic analytical philosophy of mind literature, authors indeed assume that a sensation is a point terminus in a region of the brain. I have quite a few quotes in the book where this idea is implicitly present. Otherwise you are totally right about the different types of pain as a consequence of nociceptor specificity.

      • Hi Istvan,

        Sure, you got it. Understood.

        Concerning ‘a sensation is a point terminus in a region of the brain’. Viewing pain as a sensory-neural modality only dominates thinking outside of the interdisciplinary pain community (e.g., in philosophy). Indeed, the Peripheral Mind Hypothesis (PMH) appears to make the same assumption – ‘And what else is the physical subject of experience than a nervous system?’

        Briefly – 3 considerations below concerning pain that challenge a purely unimodal sensory-neural view of the PMH:

        (1) Tissue trauma (i.e., wounding) occurs against background of overall bodily awareness that encompasses interdependent neural, endocrine and immune states. At the periphery, the nervous system cooperates dynamically with the immune system to create inflammation and associated chemotaxis in the acute phase reaction. Nociceptors contribute to inflammation following wounding by releasing substance P (SP), calcitonin gene-related peptide (CGRP), neurokinin A (NKA), and nitric oxide (NO). Thus, nociceptor activation
        initiates neurogenic inflammatory processes that
        amplify responses to subsequent stimuli (noxious
        or innocuous.) (van Rysewyk, 2013)

        (2) Pain is multimodal and typically includes integrated visual, kinesthetic, and enteric sensory modalities in addition to noxious signaling. Concerning multimodal integration in pain, Hollis et al. (2004) studied how catecholaminergic neurons in the solitary nucleus integrate visceral and somatic sensory information during peripheral inflammation. Intense physiological arousal, pre-existing fatigue, dysphoria, or nausea, and a systemic inflammatory response induced
        by proinflammatory cytokines may all contribute information to the brain’s processing load during the construction of pain (van Rysewyk 2013).

        (3) Clinical problems of acute and chronic pain do not conform to a purely sensory neural model. The persistence of chronic pain as a major medical problem reveals that a purely sensory-neural model has largely failed to guide clinicians toward curative interventions (van Rysewyk, 2013).

        Hollis JH, Lightman SL, Lowry CA. (2004). Integration of systemic and visceral sensory information by medullary catecholaminergic systems during peripheral inflammation.
        Ann N Y Acad Sci 1018: 71-75.
        van Rysewyk S. (2013). Pain is Mechanism. PhD Dissertation, University of Tasmania.


  6. Assaf Weksler

    Hi Istvan, long time…

    A very interesting post!

    In your responses to Eric and Ken, you seem to endorse a specific theory of consciousness, according to which individual fibers, say C-fibers, can be conscious, or proto-conscious, in some minimal sense. Is this view compatible with the (widely held!) global workspace theory (GWT) of consciousness? As I understand GWT, contents (and/or representational states, I will ignore this distinction henceforth) become conscious iff they are globally broadcasted. In order for a content, or a piece of information, to be globally broadcasted, it must “win” a competition (for attention?) among various incoming contents. The contents that lose are not conscious *at all*, not even minimally conscious, and those that win are conscious in an ordinary, not minimal, sense (in virtue of being globally broadcasted). On this picture, it seems, there is no place for proto-consciousness or minimal consciousness. Ordinary consciousness, on this picture, is not an aggregate of numerous minimally conscious contents or neuronal states.

    That being said, I realize that I am not sure about what exactly GWT implies (perhaps what the GWT theorist calls “unconscious” content/state is what you’d call “minimally conscious content/state”; perhaps GWT is about access consciousness, *rather than* about phenomenal consciousness, although many think that P-consciousness implies A-consciousness?), so I’d be glad to be corrected.

    • István Aranyosi

      Yes, if the GWT has the implication that a conscious state is ultimately realized only by brain-confined firing patterns, then my view is in conflict with it. But maybe we could think of a version of GWT in which the winner content is distributed not only horizontally (at the same level of neural hierachy, but different regions of it), but also vertically (at different levels of the hierarchy, even including the PNS). The terms “protoconscious” and “minimally conscious” might suggest that individual neurons or fiber bundles could have these consciousness instantiations even when not interacting with the CNS, that is why i don’t actually use such terms in the book, as I think these fibers can only properly be attributed consciousness when they are contributing to the realization lf the conscious state as such, i.e. the state that we as persons are aware of whenever we are conscious.

      • If GWT has well-defined views, they surely must be the views of Bernard Baars. Bernard has been concerned almost entirely with what Block would call access consciousness. Where he has discussed phenomenal consciousness, he has argued that it is actually the same thing as access consciousness. (e.g., Baars, Bernard J. “Evidence that phenomenal consciousness is the same as access consciousness.” Behavioral and Brain Sciences 18.02 (1995): 249-249.) Of course other proponents of GWT might hold different views.

      • Assaf Weksler

        Thanks, Istvan!

        Just to be clear, when you suggest that perhaps the winner content is distributed vertically, do you mean that “global broadcast” involves, inter alia, broadcast *to* the PNS?
        This appears to imply (given your view) that the PNS, or more specifically c-fibers, are constitutive of conscious pain because (or partly because) they are *consumers* (perhaps of a special sort?) of the information that is globally broadcasted. Is this right?
        We know that attention to pain can make it more intense and unpleasant, and lack of attention can make it less painful. Does your suggestion mean (given the tight connection between attention and consciousness) that this phenomenon should be understood in terms of information about pain being broadcasted from the global workspace in the brain to c-fibers, making their signal stronger, thereby making the pain more intense?
        If this is not what you have in mind, then what would you say is the role of broadcasting pain information from the brain to c-fibers?

        • István Aranyosi

          Thanks, Assaf, very interesting. In the specific case of pain, Gate Control Theory also involves the existence of an efferent (downwards conducting) brain trigger mechanism that modulates afferent (upward conducting) nerve impulse from the PNS, whose influences are also mediated through the gate control system. So yes, I think we shouldn’t assume that whenever some cognitive or emotional penetration of more primitive states such as pain, proprioceptive states, vision, etc. takes place, it must always and exclusively act on the higher levels, such as the cortex.

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