On November 22nd 2013, I attended the APA breakfast titled "The immunotherapst and linguist in all of us", presented by David Butler APAM, B.Phty, M.App.Sc., EdD.

David spoke about five key points regarding the role of the neuroimmune system in pain and emphasised the importance of the language ourselves and patients use to describe pain. These points have been summarised below.

Players in the neuro-immune system.

Some of the players involved in the neuro-immune system that we often forget about are the immune cells. In fact each neural synapse is a tripartite synapse with the pre and post synapse interacting with glial cells, helping their function. This exists throughout the human body. Other cells such as astrocytes and microglia also interact with the synapse. A neuron will not function without an immune cell.

The products of immune cells.

The products of immune cells are both pro-inflammatory (interleukin 1, 6 & 15, and TNF [Tumour necrosis factor]) and anti-inflammation (interleukin 4 & 10, and TGF [transforming growth factor]). A disturbance in the balance and increase in pro-inflammatory cells leads to increased pain and stiffness.

Immune signalling.

How does the brain know we are sick? The sickness response is due to neural immune signaling. The vagus and hypoglossal nerves are immuno-modulatory and as cranial nerves can access the brain directly, i.e. neural immune signalling occurs through the blood-brain barrier.

The immune system defies the peripheral-central divide, there is no separation and the immune system can access everything and not just the areas needed for nociception.

Immune modulating and sculpting of the brain leading to behavioural and neural plasticity, cognition and learning.

"In conditions under which the immune system is strongly activated by infection or injury, as well as by severe or chronic stressful conditions, glia and other brain immune cells change their morphology and functioning and secrete high levels of pro-inflammatory cytokines and prostaglandins. The production of these inflammatory mediators disrupts the delicate balance needed for the neurophysiological actions of immune processes and produces direct detrimental effects on memory, neural plasticity and neurogenesis. These effects are mediated by inflammation- induced neuronal hyper excitability and adrenocortical stimulation, followed by reduced production of neurotrophins and other plasticity-related molecules, facilitating many forms of neuropathology associated with normal ageing as well as neurodegenerative and neuropsychiatric diseases" (Yirmiya & Goshen, 2011, p. 181).

Immune response is temporal.

Glial cells may remain experienced and interested in the injured part for at least 21 years. (Banati article, 2001). The same pain tune plays it again when our immune system is down. The immune system knows you and will react when you are not you.

Some other tips from David regarding coping and education:

Explaining pain reduces pain and disability at 6 months and one year with NNT for 50% reduction at three months.
What is said out aloud is unsaid 1000 times.
You have to change their language and the way they describe their pain...the language we choice is so important.
Metaphors of the product of living experience of the disease.
There are three main categories of metaphors.
Invasive metaphors - psychological e.g. ruptured, slipped, out of place, unstable...
Ontological metaphor - the journey e.g. I am going to pieces, I’m falling apart, I’m on struggle street…
Disembodiment metaphor - rename the body part e.g. I want a new one, the back is killing me, this arm is broken…
As physiotherapists we need to use reframing strategies to change the metaphor and convince our patients that the language they use is unhelpful and can trigger inflammation in the brain and pain memories in the brain.

People use metaphors because they try to link their feelings to objects and emotion such as "my back feels fragile like glass". You need to explain that the brain memory is playing a larger role than the body part being injured. As physiotherapists, we need to get our patients to love their body part again and ask them to express themselves differently.

Panel: David Butler, Sara Brentnall, Malcolm Hogg, and Jacqui Stanford.

"What have you heard me say and what do you understand?"

Asking this question back to your patients allows them to express their understanding of the treatment and discussion from that very day. It also allows the therapist to correct any misunderstanding or misinterpretation that may have occurred.

What not to say, "I know what you're going through." "Build a bridge and get over it."
You need to honour and pay attention to the coping strategies they have constructed. You must acknowledge them before you change them.
Don't say "this won’t or shouldn't hurt", maybe say "this may hurt but I will help you get through it".
Careful with saying "It is not your disc, it is a muscle" because they hear disc.
But.... "I don't want to be offensive but".... The but does not make what you are going say ok. Don't say it.
Tell your patients "Well done".
Address flags then and there.
Use the terms primary and secondary hyperalgesia to explain pain so that language used is consistent.
Communicate with the other health professionals and tell them what we are working on and ask them to reinforce this to the patient.
Don't disempower patients with the use of passive therapy. Use passive therapy to empower people with your touch to continue working towards their goals and empower them with the knowledge to manage independently.

Discussing pain and understanding how others experience pain is a continual challenge for therapists. David reminded me of how important it is to reflect on the words and metaphors we use to describe our individual experiences. What we say and what others hear, and vice versa, may have a different meaning. Always make the time to clarify "What have you heard?" and "My understanding of what you have said is.... is this correct?".

Sian

Key references:

Aguzzi, A., Barres, B. A., & Bennett, M. L. (2013). Microglia: scapegoat, saboteur, or something else? Science, 339(6116), 156-161.

Besedovsky, H. O., & del Rey, A. (2011). Central and peripheral cytokines mediate immune-brain connectivity. Neurochemical research, 36(1), 1-6.

Beggs, S., Liu, X. J., Kwan, C., & Salter, M. W. (2010). Peripheral nerve injury and TRPV1-expressing primary afferent C-fibers cause opening of the blood-brain barrier. Molecular pain, 6(1), 74.

Banati, R. B., Cagnin, A., Brooks, D. J., Gunn, R. N., Myers, R., Jones, T., ... & Anand, P. (2001). Long-term trans-synaptic glial responses in the human thalamus after peripheral nerve injury. Neuroreport, 12(16), 3439-3442.

Yirmiya, R., & Goshen, I. (2011). Immune modulation of learning, memory, neural plasticity and neurogenesis. Brain, behavior, and immunity, 25(2), 181-213.