When Aunty Sue called in

My friend’s Aunt had a traumatic accident nearly a year ago leading to an above elbow amputation and now a phantom clenched fist at the end of the stump. She called in today to show us her progress through the graded motor imagery programme.

While the phantom sensation was really bugging her, it was great to hear a story of improvement which involved  acceptance,  multiple active coping strategies,  getting on with life, the influence of family and friends and the search for understanding of how and why the brain insisted on constructing a clenched phantom hand. The story had particular resonance because at the same time I was reading what I thought was very special article in the ‘Pain’ journal.

The article
The article (Edwards RR et al 2008 Association of catastrophising with interleukin-6 responses to acute pain. Pain 140: 135-144 abstract attached) really struck home. In essence, these authors demonstrated a link between catastrophisation and elevated levels of the pro-inflammatory cytokine interleukin-6. Interleukin-6 (IL-6) is one of a number of pro-inflammatory molecules produced by immune organs and cells (eg bone marrow, macrophages, glial cells) and is known to be involved in hypersensitivity, such as the aching you get when you get the flu, but also related to the severity of pain in back pain, fibromyalgia, OA and RA and neuropathic pains. This study basically says that the more you catastrophise, the higher the levels of and influence of IL-6 (and surely other cytokines such as TNF alpha). Cognitions and emotional responses are translated into known chemistry. It harks back to Candice Pert’s “Molecules of Emotion.”

The research adds to the growing literature that proinflammatory cytokines play a role in the development and maintenance of persistent pain syndromes. (Watkins and Maier 2002; Marchand, Perretti et al. 2005; Thacker, Clark et al. 2007)

The author’s suggestion is that a range of ongoing pain states such as Type II diabetes and cardiovascular disease, known to be associated with IL-6 levels, may be influenced by catastrophisation and therapy could be directed to it. Said in another way – catastrophisation can lead to tissue inflammation and damage. It is not too much of an extrapolation to add low back pain, whiplash and neuropathic pains to the list – indeed any persistent pain state. By the way, as the authors remind us, catastrophisation is a complex response to varied stimuli and the influences on immune cells and inflammation and pain may be just one of a number of influential pathways. For example, IL-6 can also blunt the endogenous opioid system.

The link with Aunty Sue
So what is the link with the phantom hand in this case, when there is no hand to get inflamed? If pro-inflammatory cytokines are expressed in the body they will be picked up in the bloodstream and by the vagus and hypoglossal nerves and transported back to the brain where glial (astrocytes and microglia) based long range signalling will allow further distant sprouting, sensitization and processes involved in plastic changes.

For the current status on this read (Barres 2008; Saab and Hains 2009).

Phantoms pains are characterized by plastic changes in the brain (Flor, Devor et al. 2003), at least in somatosensory areas.  It is not hard to suggest that managed catastrophisation – especially early post injury – may limit the problem of phantom pains via the cytokines. Nor is it hard to conclude that the reason my friend’s aunt is doing so well, is that the approach she has taken which has minimized catastrophic thoughts and emotions has had a potent effect on potential proinflammatory cytokine inspired plasticity which may also be related to pain. She doesn’t call it ‘pain’ though it is bugging her. Maybe the coping strategies have combined to stop it being a pain.

Your turn

Send in your story of catastrophisation and body awareness to go in the running for a Graded Motor Imagery pack.

Last month’s notes on Christmas Pain
Thanks to all who wrote in on last month’s topic of pain at Christmas. Well done and thanks a bunch Heather from Canada, an Explain Pain audio is coming your way for your story on annual or anniversary pain.

The rest of the stories are in here… and here is Heather’s.

Although I have run into many examples of annual/anniversary pain, the most extreme example was a woman I treated who had a mysterious knee pain that usually went away on its own. This was the third year I had tried to treat it at exactly the same week of the year.

Conversation led me to realize that her husband had died at that time of year. She spontaneously told me about his severe pain prior to death and how hard it was to watch and how she would rather cut her own leg off than have him go through that. With each phrase, she jumped and held her leg while the pain she had tried to absorb on his behalf stabbed her.

Pointing out the connection and a tree planting ceremony that year seemed to help as she seemed better able to lay him to rest and realize it was over for him. To have another human really hear her emotional pain seemed to be helpful too.

Heather, Canada

References
Barres, B. A. (2008). “The mystery and magic of glia: A perspective on their roles in health and disease.” Neuron 60: 430-440.

Flor, H., M. Devor, et al. (2003). Phantom Limb Pain: Causes and Cures. Progress in Pain Research and Management. J. O. Dostrovsky, D. B. Carr and M. Kolzenburg. Seattle, IASP Press. 24.

Marchand, F., M. Perretti, et al. (2005). “Role of the immune system in chronic pain.” Nat Rev Neurosci 6: 521-532.

Saab, C. Y. and B. C. Hains (2009). “Remote neuroimmune signalling: a long-range mechanism of nociceptive network plasticity” Trends in Neurosciences.

Thacker, M. A., A. K. Clark, et al. (2007). “Pathophysiology of peripheral neuropathic pain: immune cells and molecules.” Anesth Analg 105: 838-847.

Watkins, L. R. and S. F. Maier (2002). “Beyond neurons: evidence that immune and glial cells contribute to pathological pain states.” Physiological Reviews 82: 981-1011.



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