Could it be because the brain is attempting to identify potential threats and this is one way to ensure ambiguous experiences are interpreted as threat rather than neutral? I'm also of the opinion that perhaps we expect the brain to positively adapt, when maybe we can have dysfunction in the nociceptive system just as we do in every other body system.

I don't think anyone knows for sure why cortical reorganization and disinhibition exist in chronic pain. It's interesting to note, however, that in the hand, the distance between stimulated areas of the hand in patients with pain decreases in patients with chronic upper extremity pain, but it increases (and even changes sides) in patients with chronic low back pain. I think Bronnie's hypothesis makes sense if you think about the high density of senory receptors in the hand versus the skin of the low back. In persistent pain of the upper extremity, perhaps this is the brain's attempt to more localize the threat in the densely innervated hand while in the low back, the brain takes a more "broad sweep" approach to the relatively sparse receptor system (or at least in the skin). I think it comes down to the self-referential brain's attempts to respond to its salience system's assessment of the perceived threat.

Because 98% of chronic pain patients are Neuropathic Pain Patients (NPP). This is what we observed on 2123 chronic pain patients.

As a neuropathic pain is "Pain arising as a direct consequence of a lesion or disease affecting the somatosensory system " Treede et al., Eur J Pain 2007; Treede et al., Neurology 2008, it seems to be logical. On the other hand somatosensory rehabilitation of pain decreases neuropathic pain: the therapy - even a non-pharmacological treatment - is a diagnosis on the opposite side (Carl Rogers).

Dear Claude, do I understand well that you consider chronic low back pain patients to have neuropathic pain? Then what is their lesion or disease?

And second: you answer the WHY from a neurophysiological perspective. Could there be an answer in a functional way? Does the change in the cortex have a function or purpose?

Dear Jean-Paul, Yes it is. We are assessing in my Somatosensory Rehabilitation Centre chronic low back pain patients who present axonal lesions of:

Medial clunial nerve I, or medial clunial nerve II, or medial clunial nerve III or medial clunial nerve IV - NOT medial clunial nerve V which DOESNOT exists. This low back pain is quiet often associated with sciatic neuralgia.

Some others patients present axonal lesions of:

Superior clunial nerve I (associated or not with the iliohypogastric nerve), superior clunial nerve II (associated or not with the ilioinguinal nerve), superior clunial nerve III (associated or not with femoral neuralgia) or superior clunial nerve IV - NOT superior clunial nerve V which DOESNOT exists.

Does the change in the cortex have a function or purpose? Yes, central sensitization mechanisms induce a symptom of hypersensitivity on the skin, which can be map with an allodynography. This hypersensitivity is a paradoxical painful to touch hypo-aesthesia as a consequence of the axonal lesions of these cutaneous branches: "Although the neurofiber Aβ damage is peripheral the mechanisms for pain sensitization are probably centrally driven with referral back to the peripheries where it is perceived as a paradoxical painful to touch hypoaesthesia (McCabe, 2009)."

Claude,

How are you identifying axonal damage in these cluneal nerve branches? Have you published anything? This looks very interesting.

John,

If the skin is numb, we are looking for a partial tactile hypoaesthesia with aesthesiography (Spicher, 2006; Spicher et al., 2013)

If the skin is hypersensitive, we are looking for a paradoxical painful to touch partial tactile hypo-aesthesia (Static Mechanical Allodynia) with allodynography (Spicher et al., 2008).

This a very good question that is being tossed around also among pain-related research. Could the reorganization happen because of an ongoing/prolonged stimulus from the periphery that then draws in and is combined with fear-avoidance behaviour, catastrophizing and/or other affective factors?

Also, studies have shown some intresting findings since if I remember correctly patients with phantom limb pain show cortical reorganization and amputees without pain do not. It also seems that cortical activation patterns are different among patients with pain and healthy controls. One study by Gustin et al. (2012, in J Neur Sci) hyphothezied that a neurapathic component to the pain needs to present for reorgazation to appear. How this relates to the whole phenomena is still a bit unclear to me and what is the relation of these finding (they studied and compared TMD and trigeminal neuralgia) on back pain or other body sites.

One good article in this area

Very nice article indeed, Shankar. But despite it's quality in explaining what happens, it does not adress the WHY. question. Again, it could very well be that we are dealing with some kind of pathology, where the WHY question has no ground. However, it is my assumption that changes in the cortex may provide a purpose. In that case the changes are not so much pathological as more physiological changes guided by the input provided. If we understand what the brain needs or desires, it might be a therapeutic entrance.

Jan-Paul,

I don't think the cortex can be isolated from the peripheral inputs and recruitment and convergence of innocuous sensory signaling of various pathways to pain pathways, hyperexcitable spinal neurons, etc. (Baron, R., Hans, G. and Dickenson, A. H. (2013), Peripheral input and its importance for central sensitization. Ann Neurol., 74: 630–636.)

The increased cortical receptive field sizes may be associated with a series of other events and personal history. How does it serve an organism to develop this particular neuroplastic adaptation? It's almost like a message, "This is extremely important. Pay attention, and I will turn up the volume to make sure you do." Or as if the allocation of priorities has been scrambled. What is the purpose of prioritizing avoidance/pain over other aspects of life?

On reflection, I have seen it serve positive functions to transform and redirect the lives of a few of my patients, as if the extreme pain gave permission to make necessary changes to get out of a particular rut, that the person could not allow themselves otherwise. Others have had severe losses in QoL. However, I have too small a sample to generalize. Especially compared to your 7000. Are you collecting psychosocial data on your patients and their issues, by any chance?

Dear Rosi,

I agree with your perspective! This approach to how the mind works might provide therapeutic entrances, or explain why some interactions work.

We collect psychosocial data to a small extend. We could though implement specific questions in this area for future patients. (500-700 per year)........