Thank you so much for a very well laid out hypothesis of changing how we analyze pain. I'd like to also bring one more aspect to the pain assessment approach we use. As a practitioner that deals with persistent pain, I'd like to shift it away from nociceptive analysis, but address other ways of sensing bodily awareness. What if we were to develop better measurement scales that looked at comfort, ease, fluency in movement... The sad truth is our culture knows many descriptive words for pain, but not for its opposite. I look forward to any comments that you help instigate here.

Dear Stacy,

Thank you so much for your comment and for bringing such a necessary and lucid clinical perspective to this theoretical discussion.

Your point is absolutely central. I completely agree that to move beyond the nociception paradigm, we need to develop "better measurement scales" that focus on body awareness. In fact, your proposal to measure "comfort, ease, and fluidity of movement" fits perfectly with what I call the "Integrated Embodiment" pillar in my Five Pillars model. It is precisely this dimension of experience that my instrument, the SCIS scale, attempts to begin to quantify.

Your reflection on how our culture has a very rich vocabulary for pain but not for "its opposite" is brilliant and on point. This is a cultural and linguistic bias that has undoubtedly limited our development of psychometric tools. Part of my goal with Physicobioneurodynamics is precisely to begin to build a language and metric for "coherence," which would be the opposite of pain understood as systemic disorganization.

I would love to continue exploring these ideas with you. I believe that combining a theoretical framework like mine with the practical experience of professionals like you is the only way to create tools that are truly useful for patients.

Thank you again for your valuable input.

Best regards.

I agree that to see pain experience solely through the lens of peripheral nocciceptive pathways misses the importance of cental processes. However, as a balance, I'd like to add that the two are not either/or binary matters, but a complicated, multi-factorial interaction to allow the body to assess the degree of importance of the pain experienced

In effect, the brain receives a generalised neurogenic 'tone' signals from peripheral receptors , largely via autonomic pathways that do not allow exact site localisation (eg compared to sharp pain).

I work with migraines, where I use Botox injected directly within the fascial capsule containing the Corrugator muscles in the brow. This blocks the signalling from particularly relevant routes from the pain receptors in the enthesis of the Corrugator muscles, and reduces the level of central neuronal excitability, in this case in important parts of the trigeminocervical tract in the brainstem. One can consider migraines as a generalised neuronal hyperexcitability state. The Botox reduces the hyperexcitability in the brainstem and thus reduces ongoing the signalling to many other parts of the brain. In effect migraine is a generalised neuronal hyperexcitability state where reducing the generalised effect by reducing one specific area with Botox.

It is interesting to explain the generalised pain state in terms of the theoretical concepts of system entropy, but one can go further to consider pain as an aberration of a normal control process that uses both negative and positive feedback loops at many levels to manage the homeostatic mechanisms that exist throughought the body - including the autonomic processes that interlink in magnificently complicated interactions....

All power to your thoughts and keep me informed :)

Dear Chris,

Thank you so much for such an incredibly lucid, detailed, and constructive comment. Your example of migraine and Botox is an immensely valuable contribution to my argument.

You have articulated, from a neurophysiological perspective, exactly the point my model attempts to capture theoretically. Your description of migraine as a "state of generalized neuronal hyperexcitability" is a perfect operational definition of what I call a "topological breakdown of coherence" or a state of high network entropy. The fact that Botox, acting locally, can reduce this global state of the system is an extremely powerful empirical validation of my central hypothesis: that pain is not a simple signal, but a state of the system as a whole.

Your suggestion to go further and consider pain as a process that utilizes both negative and positive feedback loops at multiple levels, including autonomic processes, is brilliant. This resonates directly with the dynamics I attempt to model in my Neurotopological Coherence equation, where the "synergy factors" (μij) between pillars can be both positive (reinforcing coherence) and negative (generating conflict and increasing entropy).

Please be assured that I will keep you informed about the progress of this work. Finding an interlocutor who can build such a clear bridge between clinical neurophysiology and abstract theory is extremely rare and valuable.

Thank you again for your intellectual generosity.

Best regards.