Smudging pain neurotags and cortical body maps: explaining the weirdness of pain
Warning: this post is long Audience: health care providers
I use social media to help organize my thoughts and challenge what I think. I usually ask a lot of questions because that has always been my style. I tend to challenge those who are the most similar to me (even if I agree with them) because it helps me “know what I know”.
I recently posted a series of questions on Facebook about Pain Neurotags (the collection of brain cells that are activated throughout the brain to produce pain) and Cortical Body Maps (the regions of the brain that correspond to the physical body parts or to the movements that the body performs).
Below is a summary of the discussion and some relevant reading.
- Graded Motor Imagery Handbook (noigroup.com)
- Explain Pain by Butler and Moseley
- How to Improve Proprioception (a great piece on Cortical Body Maps by Todd Hargrove at www.bettermovement.org)
I initially asked…
1. How do you see cortical body maps being similar to or different from neurotags? Specifically pain tags. Would you view a sensory body representation as being part of a pain neurotag?
2. With pain neurotag smudging (disinhibition of other neurotags) would part of that be due to smudging of the sensory body map and some due to disinhibition of other neurotags?
Bold and italics are mine. I have cut out some information but by and large here is what everyone contributed with a few recaps and extra notes thrown in.
Sigurd Mikelson gave us...
Puh. Now there's a challenge... I'll have to do some thinking and come back to this, but for starters I think of cortical body maps as a more neuroanatomical construct than neurotags which I understand as functional synaptic networks. The term neurotag is also somewhat ambiguous as its "only" a construct of "some kind of activity" that we potentially want to see. The term (in lack of anything better) still serves as a subjective conceptualization of "something going on in there" that is thought to be associated with pain" and helpful in formulating dynamic, clinical frameworks. On the other hand one should be careful in taking them as "true", not that I'm implying you doing so. These considerations about terminology also goes for what is really a "sensory body representation", but yes, whatever that is, I guess it would also be part of what a pain neurotag is, whatever that is... In regards to your last question too, I think disinhibition of functional networks of "brain activity" is the least wrong explanation so far about what might be going on in ongoing pain states and behavioral "disorders".
Lars Avemarie provided a great definition from the GMI Handbook
"A neurosignature (or we call it a neurotag, like a graffiti tag1) is a pattern of activity in the neuromatrix. It is a physical linking of neurones at a particular time and it canlead to an output such as pain, movement or an emotion. We are not conscious of most of these brain constructions and their outputs, but rest assured that it will be a pain neurosignature, absolutely personalised for you that will be the basis behind you experience of pain (Figure 4.3)."
The Graded Motor Imagery Handbook. G. Lorimer MoseleyDavid S. Butler, Timothy B. Beames, Thomas J. Giles. Noigroup Publications, Adelaide, Australia, 2012
In specific reference to the question “Would you view a sensory body representation as being part of a pain neurotag? " Lars responded:
Yes, a sensory body representation can be part of a neurosignature. To my current knowledge.
Ben Cormack (at cor-kinetic.com) asked the clarifying question…
...could we say we may use selected neurones within our cortical maps when we activate a pain tag/signature?
and Sigurd responded:
from my understanding, these "selected neurons", if you talk about neurons located around/in S1, S1, thalamus, insula, ACC are multi-modal and will therefore respond to any stimuli regardless of whether the stimuli is nociceptive or non-nociceptive. Ianetti and Moreaux have done some important work on this.
Whatever gives meaning to the stimuli would partially determine the threat value and emergence of a potential painful experience (or continuous state when thinking of longstanding pain), which would also involve all of the above. The problem is that we don't have solid evidence to suggest that synapses/neurons give meaning to anything, or at least, not enough to formulate/prove a theory that will hold under any condition.
Nevertheless, the neuromatrix-theory binds together these diffuse bits of "knowledge" into a dynamic framework useful for clinical practice. Or, maybe it should be understood as a dynamic model, rather than a theory, like the bio-psycho-social model (which rather should be practiced as a socio-psycho-biological model). Maybe. There are epistemological challenges with both.
Our first three contestants have put forward the idea that neurotags are activations of different brain cells, from different parts of the brain that can produce pain, movement or emotions. Within a neurotag can be our “cortical body representations” or our body maps. The sentiment is that our body maps are more neuroanatomical constructs and the neurosignature is a functional creation that would include activation of body maps as well as the activation of other brain cells.
We have also introduced the idea that a Pain Neurotag can be activated or modulated by other factors than mere information from the body’s booboos. Siggurd has noted the importance of meaning in the creation of the pain experience. This is important because we should view the brain as evaluating all the information it has in relation to the “danger” signals from the body and from other information it possesses. Ultimately, if the brain feels sufficiently threatened pain will be felt.
A new point: There are multiple areas of the brain involved in producing pain. Butler and Moseley call these Ignition Nodes. These nodes are used for:
Butler and Moseley write “Pain just uses this parts to express itself”
With persistent pain these nodes can become sensitized and more easily activated. This means that multiple factors besides the booboo in your back can cause pain.
I very much like Sigurd's notion of the neuromatrix-theory as a dynamic clinical model. I find that as I consider your post Gregory I'm tempted to frame neurotags as memories and cortical body maps as an overall sense of self. In that construct, I see that those neurotags are subsets that help to define the overall sense of self that the cortical body matrix represents. Memory and sense of self are plastic and each influence the other. Good topic to sit with this AM!
Jason Silvernail stepped in and essentially said he would take this topic to the highest authority...Lorimer Moseley :)
“Good question Greg and great comments Sigurd. I think at this point we don't know enough for sure to be able to say one way or another. Greg your suggestion makes sense as part of a framework.
All frameworks are wrong, but some are useful. I think the bigger question is how can we make these concepts useful - in helping practitioners and patients understand, in formulating hypotheses to test, in developing treatment approaches, etc.
In general I have the same overall sense of the interrelation between cortical maps and neurotags as Phillip does - but that division probably reflects my own conceptual model rather than any underlying truth. Would love to get some neuroscientists in a room and ask them. Hey maybe we can ask Lorimer Moseley in San Diego in February…”
I then produced a screen shot from Pg 76 of Explain Pain that describes the phenomenon of ‘smudging of the neurotag”. The relevant quotation from that page being:
another change which is known to occur in the outer brain, the cortex, is “smudging” - brain areas normally devoted to different body parts or different functions, start to overlap. In fact, the longer pain persists, the more advanced the changes int he brain. We think both types of changes might be strategies by which the brain ‘looks out’ for you - by making the body part difficult to use (smudging of the motor areas in the brain, thus limiting movement) or by making neraby body parts sensitive too (smudging of sensory areas in the brain).
Todd Hargrove jumped in with an answer that I tended to agree with. I agree a lot with Todd thats why I argue so much with him. Todd wrote:
Thanks for including me. Why are you asking?
I only browsed the answers above and saw many great points. Here are my answers, which duplicate a lot of what has already been said.
“How do you see cortical body maps being similar to or different from neurotags?”
The cortical maps are anatomically discrete areas of the brain whose activity represents the movement, position and health of the body parts. Neurotags are the patterns of brain activity that create a particular experience of pain. These patterns are widespread throughout the brain, and include activity in the cortical maps. So the neurotag is far broader than the maps.
“Would you view a sensory body representation as being part of a pain neurotag?”
Yes, for the reasons stated above.
“With pain neurotag smudging (disinhibition of other neurotags) would part of that be due to smudging of the sensory body map and some due to disinhibition of other neurotags.”
Personally I never think of pain neurotags as being smudged, as their purpose is not to represent or map the body, but to create an action signal. I think of the cortical maps as being smudged, because when they are smudged they inaccurately map the body, just as smudged map would fail to clarify the outlines of a geographic area. But I do think of the pain neurotags as being disinhibited, or as being activated by lots of stimuli that we don’t want to create pain, such as thinking about herniated discs, arriving at a workplace, or doing a movement that at one time caused nociception but no longer does. I think the easiest way to understand and describe this problem is not by talking about neurotags or disinhibition, but by reference to Pavlovian learning through association.
For example, if I want to explain to someone why movement can help with their pain, I might say that they learned through experience to associate movement with pain, because of a previous injury. The pain continues even though the injury is gone, just as a dog will salivate when a bell is rung, after it learns to associate the bell with dinner. The dog will eventually stop salivating if you ring the bell without bringing dinner, and you will eventually stop feeling pain if you do that movement you have been avoiding without causing reinjury. I wouldn't say anything about disinhibition or neurotags, not because those ideas are wrong, but because these concepts are unnecessarily complex in my opinion, and as Jason said, they are all in service of good communication and understanding, and should be judged on that basis.
Another quick recap…
Todd highlighted the previous views that the cortical body maps are anatomical representations of the body and that Neurotags are Functional/dynamic “patterns of brain activity” that create some experience. A Neurotag is again viewed as something that can encompass a cortical body map.
Todd and Jason discuss the utility of using Neurotags in explaining pain which I think is a very fair point. Todd gives a great example of how we can discuss pain becoming associated with movement (an example of the pain neurotag become more easily activated with other stimuli) without actually ever discussing pain neurotags with a patient.
Todd also provides us with another great reference from Lorimer Moseley on Neurotags and memory.
and Jo Nijs work on altering pain memories through exercise http://www.ncbi.nlm.nih.gov/pubmed/25090974
Ben further added...I like the concept of memories that we then create predictions from. This seems to make sense.
Somewhere down the line if we alter the memories we alter the prediction. I think this has elements of associated learning in it and why I identified with the paper Todd Hargrove reposted on the thread.
I then added:
Thanks Todd Hargrove that's a great response and how I generally view it (but less eloquently put). I got the neurotag smudging from Moseley. See my above pic. I tend to view neurotags as something that would contain cortical body maps as you described.
I suppose smudging is just another way to describe disinhibition of other neurotags. I'm not sure it's the pain neurotags themselves that become disinhibited though. I think it's other neurotags that become disinhibited. Thus they fire with the initial pain tag. Hence we have spreading and diffuse and moving pain
Lars Avemarie Todd Hargrove Great comments, specially this "Personally I never think of pain neurotags as being smudged, as their purpose is not to represent or map the body, but to create an action signal. I think of the cortical maps as being smudged, because when they are smudged they inaccurately map the body, just as smudged map would fail to clarify the outlines of a geographic area. "
This is the same way I view it currently.
Moseley talkes about this here:
“One aspect of the changes that occur when pain persists is that the proprioceptive representation of the painful body part in primary sensory cortex changes. This may have implications for motor control because these representations are the maps that the brain uses to plan and execute movement. If the map of a body part becomes inaccurate, then motor control may be compromised – it is known that experimental disruption of cortical proprioceptive maps disrupts motor planning”
Moseley, G. Lorimer. Reconceptualising pain according to modern pain science. Physical Therapy Reviews 2007; 12: 169–178.
And Hodges here:
“First, chronic pain is commonly associated with reduced tactile sensitivity on the painful body part [70,71,133] and disorganisation of somatotopic maps in SI [71,134–138]. Further, the magnitude of somatosensory disorganisation is a strong predictor of pain severity [134,135,139]. Conversely, tactile discrimination training, which should promote organisation of somatosensory maps, is an effective treatment for chronic pain, presumably by sharpening somatotopic maps of the body in primary somatosensory cortex [140,141]. Intriguingly, the effectiveness of tactile discrimination training increases when CRPS patients view the body part being trained .”
Spine (Phila Pa 1976). 2011 Oct 1;36(21):1721-7. doi: 10.1097/BRS.0b013e31821c4267.ISSLS prize winner: Smudging the motor brain in young adults with recurrent low back pain. Tsao H1, Danneels LA, Hodges PW
With Todd adding:
I think that pain neurotags can be activated by other neurotags, as you say. For example, the neurotag for thinking about work activates the pain neurotag. But does this happen through disinhibition (a mistake) or through learning (neurons that fire together wire together)?
Hopefully the latter because the remedy for unlearning is more clear to me than the remedy for improving inhibition, which might be systemic or genetic. I understand that many intractable problems like migraine, epilepsy, etc. are characterized by failures in inhibition.
By the way, you might be interested in this post, which has four or five paragraphs summarizing what Moseley had to say at a conference about neurotags, disinhibition and maps, including lots of very concrete examples. Still very confusing, but I think it supports my idea that correctable disinhibition is more in the cortical maps than in unwanted connections between pain and non-pain neurotags.) http://www.bettermovement.org/.../review-of-moseley.../
Lars then quotes a great article:
"Chronic pain is impossible to ignore, and commonly dominates the patient’s mental life. Ironically, however, there is also evidence that chronic pain is associated with ‘neglect-like’ symptoms [151–153] or ‘body perception disturbance’ [154,155], in which the affected limb is misperceived. These symptoms reflect a constellation of symptoms with intriguing similarities to disorders of body representation that follow right parietal lobe damage . Some patients report that their affected limb feels ‘‘like dead weight’’ and that focused attention is required to move the limb, while others report feeling that the painful limb feels ‘‘foreign’’ or ‘‘strange’’, as if it were not part of the patient’s body [152–154].
In one large survey of CRPS patients, 84% of patients re-ported at least one such neglect-like symptom . Such reports are intriguingly similar to previous reports of ‘asomatagnosia’ following parietal lobe damage, in which patients report feeling like the contralateral side of their body is absent . In some cases, these feelings of foreignness result in hostility towards the limb (‘misoplegia’) [154,157] and even desire to have the limb amputated [154,158]. In other cases, there is clear evidence for sensory abnormalities related to the affected body part, including unawareness of limb position [155,157], referral of sensations to adjacent body parts [139,159], and displacement of the perceived body midline towards the affected side .
In addition to the neglect-like symptoms caused by chronic pain, visual hemi-neglect itself also alters pain perception. In particular, Liu and colleagues  observed a mislocalization of painful stimuli to the ipsilesional size of the body, and a misidentification of stimulus modality in neglect patients."
"Our review of the neural mechanisms that integrate pain and body representation has several implications for the search for multisensory therapies. First, this search should not be abandoned as hopeless, since there is clear evidence for neurophysiological mechanisms for multisensory interactions involving the nociceptive system, on which such therapies should rely. Second, there is a need for future research to use multiple sensory modalities, and not only vision, as potential interactors with pain. Third, multisensory interactions involving nociception reveal a strong principle of spatial organization. Since chronic pain is often very specifically localized to a single body part, and since reorganization of spatially-mapped cortical areas appears relevant to chronic pain, future research might usefully investigate how to harness the spatial organization of body-pain interactions in order to modulate chronic pain."
Curr Biol. 2013 Feb 18;23(4):R164-76. Spatial sensory organization and body representation in pain perception.Haggard P1, Iannetti GD, Longo MR.
And that was basically it with the discussion. Back to the original questions:
How do you see cortical body maps being similar to or different from neurotags? Specifically pain tags. Would you view a sensory body representation as being part of a pain neurotag?
The consensus was that cortical body maps represent discrete anatomical or movements in the cortex and that Pain Neurotags are probably something larger that can contain those body maps. From reviewing Moseley’s writings in the GMI handbook he views those bodymaps as neurotags as well. This makes sense since those are still parts of the brain that would become activated when moving or sensing a body part.
Moseley uses this definition:
“A neurotag is a network of interconnected neurones, we will call brain cells, that are distributed throughout the brain. When a neurotag is activated it produces an output. The output defines the neurotag”
And goes on to write:
What is important conceptually is that to activate any particular neurotag, two criteria have to be met:
- The member brain cells have to fire. That is, the neurones that make up the neurotag have to fire.
- Nearby brain cells have to NOT fire. If non-member brain cells fire, the neurotag is changed, is imprecise, is wrong if you like.
An important point is that each member brain cell of the neurotag is open to being influenced by other brain cells which is communicates. This is how other variables like thoughts, memories, movements and emotions can influence a pain neurotag
Moseley goes on to write:
When pain persists, the pain neurotag becomes sensitised and disinhibited. Sensitisation of the pain neurotag refers to an increase in the excitability of the member brain cells such that they are more easily activated. The principle of this increase in excitability is the same as that of individual neurones that become potentiated, or ‘wound-up’. Sensitisation of the pain neurotag is like the whole network of brain cells being ‘wound-up’. Sensitisation of the pain neurotag offers the most sensible explanation as to why, as pain persists, pain is evoked more easily and by a wider array of internal and external stimuli than it is initially.
Moseley describes the smudging of a neurotag:
Remember that for a neurotag to be activated, it requires sufficient activation of the member brain cells and sufficient inhibition of the non-member brain cells? Well, disinhibition refers to a decrease in this inhibition of non-member brain cells. This sounds complex but it just means that they’re not dampened down. Perhaps an easier way to think about it is to say that the neurotags lose precision. This effect probably only involves neurotags that are relevant to the pain neurotag. Disinhibition might manifest as spreading pain, pain that moves, pain that is less precisely defined anatomically or qualitatively. The pattern of spread will not adhere to the distribution of a peripheral nerve, or to that of a nerve root. Instead, pain will spread to a whole limb, a body region or to a whole side of the body. Disinhibition of movement neurotags will manifest as imprecise movements or perhaps in the extreme, dystonia.
...and to the last part of the questions
With pain neurotag smudging (disinhibition of other neurotags) would part of that be due to smudging of the sensory body map and some due to disinhibition of other neurotags?
I’m not sure this was solidly answered. Everyone can agree that cortical body maps become disinhibited/smudged and this can contributes to influencing the pain neurotag. I’ve found less discussion in the literature or in our discussion on whether there is “disinhibition of other neurotags” besides the body maps.
Disinhibition is the most likely explanation for the rangeof body-related neurotags that can become disrupted as pain persists. The most investigated of these involves an area of the brain called the primary sensory cortex, or S1.
Todd suggested that it might be more useful to think less about a pain neurotag becoming disinhibited and more that that neurotag becomes coupled with some other neurotag via associated learning. Todd rightly notes that talking about this association with pain and movement is a great way to unlink pain from movement in patients. And perhaps we don’t even have to talk about smudging at all with patients if we just talk about learning. The key here is that other neurotags can more easily activate the pain neurotag. I don’t know, and I don’t think we resolved, if this coupling is due to disinhibition or some other mechanism like learning. I’m not sure it matters in order to explain the symptoms that patients feel or to help guide treatment.
Thanks to everyone for helping out with this.