Understanding and Explaining Pain Level 2 Pain Training Fife Integrated Pain Management Service Welcome and thanks for coming Housekeeping

Aims Cross the gap between lab to clinic Understand the pain related biology of the patient in front of you Be able begin to reassure, explain and give understanding to a patient of what is going on State aims as per slide Task 1 - A3 flip chart ask group what is pain? Ask group ‘What is pain?’ - Is it a feeling, if it is a feeling what is a feeling? Where is the feeling coming from? (could mention pain paradox i.e. the pain is in my back not in my brain) - If it is an emotion what is an emotion? What is sad/happy?

“The fear of pain is worse than pain itself” What are the kind of things that we are talking about today? In this case it is your opinions or your patient’s opinion of their pain. We can change opinion through knowledge and questioning of their current opinions People with chronic pain think they are vulnerable – it is theri opinion that makes them vulnerable

Pain as response to threat As we are talking in the first half, even it is technical, it is always worth remembering that the changes are in a response to a real or percieved threat.

In some situations descending inhibition can block any sensation of pain – the rugby player who carries on running with a broken leg or the soldier who doesn’t notice that he has been shot. In another situation there can be no tissue damage, but severe pain. The picture on the right is of a man who was brought into casualty with a nail through his boot. He couldn’t be made comfortable, even with large doses of morphine. When he was anaesthetised & the boot cut off, it was found that the nail had passed right between the 1st two toes without having broken the skin. It’s worth thinking about how this makes us feel – did we make a value judgement about how much pain there should be? Did we laugh at the man with the nail through his boot?

We have used this slide in previous training to discuss hurt and harm beliefs and biomedical model (see below) Today we want to use it to illustrate the link between body and mind. In the biomedical model the focus has been one or the other however what we aim to illustrate today is that you cannot have one without the other. In the biomedical model we try to find the source of the pain. However in Low back pain 85% NSLBP have normal XR’s Jeffrey et al 2005 – depression is a greater predictor of new episodes of low back pain than bulging discs, annular tears, facet joint degeneration What are the problems with the biomedical model? Waddell 2006 ‘has not solved problem and may have contributed’ Increased suffering, social and economic burden Pain beliefs predict QoL greater than intensity (Lame’ et al 2005) Level of disability is better predictor of GP appt than intensity (Ferreira 2009) Pain intensity isn’t that good a predictor of QoL or use of services - beliefs and disability levels have a greater impact. Anguish – Dergalis – deleted picture

60 – 70% people in their 30’s & 40’s have bulging discs, but don’t necessarily have pain

Imagine that you are at home alone and you hear the bins getting knocked over. Your mind starts racing and you think that you maybe broken into (the power cuts out and the phones go dead!)... What do you think, feel, do

But really it is......

Feedback Burglar & Cat Thoughts Feelings Behaviour Bio psycho social response Bio – increase sensitivity to noise, pay more attention, HR and BP increases, bowel/bladder, loss of appetite, muscles tighten, adrenalin, increase blood flow to muscles Psycho – threat/not knowing Social – call friend Behaviour – go to hospital,GP/other AHP, go off work, avoid activities thought to be dangerous With Pain Education we are aiming to change the thoughts or opinions part of the vicious circle thus allowing changes in behaviour and feelings

Structure of the Nervous System (or threat detection system) Incraese knowledge of the threat detection system (aim of which is to preserve homeostasis) Use A3 flip chart to sketch out nervous system Include the risk factors, including not knowing, hurt and harm, rumination, catastrophisation, poor sleep and depression Play How Nerves Work from CD RoM to give overview 1m 37 Receptor we are talking about is nociceptor 2.07 Brain we come to in a wee bit 2.19 Resting potential levels – important 3.04 Action potential 4.10 spinal cord processing 4.44 Synaptic processes including amplification

Threat detection system starts to light up – rememeber it is only looking out for you. REMINDER – nociception isn’t pain just as light striking the eye isn’t seeing/vision

Pain can be modulated at spinal & higher levels

Melzack & Wall Melzack & Wall discovered the pain gate theory in discussion after three or four glasses of wine Pat Wall said – “we’d better not put a diagram in this or people will have to reproduce it in exams for ever after”

But Melzack won the argument

Of course the nervous system & brain are pretty complicated & lots of things have an influence

Spinal cord feedback Location rational “oh bother” Muscle tightening AFFECTIVE Feelings SENSORY Conscious Brain Thinking Fear, anxiety, sleep, punishment autonomic changes Location rational “oh bother” Limbic System feedback Muscle tightening Recruitment Sensitivity Sometimes – most of the time Spinal cord Wind-up and long term potentiation Central sensitization

Timeline of pain Time of injury 3 months Pain? Tissue Healing Worth mentioning at this time about pain without specific injury or onset – - Prolonged stress Time of injury 3 months

Medication for Chronic Pain Medicines just a small part of managing pain Appropriate use of analgesics can control pain sufficiently to allow increased activity & effective self management which may allow a reduction in analgesic use over time Aim…with a little bit more knowledge Patients can make the most of their medicines

The Pain Ladder WHO Pain Ladder…. Step 3 Step 2 Step 1 Mechanical Pain- Paracetamol & Strong Opioid (e.g. morphine) +/- Inflammatory Pain- Anti-inflammatory (e.g. ibuprofen) Nerve pain- adjuvant (e.g. amitriptyline) Step 3 Mechanical Pain- Paracetamol & Weak Opioid (e.g. codeine) +/- Inflammatory Pain- Anti-inflammatory (e.g. ibuprofen) Nerve pain- adjuvant (e.g. amitriptyline) Step 2 Mechanical pain- Paracetamol +/- Inflammatory Pain- Anti- inflammatory(e.g. ibuprofen) Nerve pain adjuvant (e.g. amitriptyline) Step 1 Re-enforce ladder approach- stepping up and down as pain increases/improves, controlled by patient as they know how they are feeling Helps stop tolerance- explain No medication

In Summary Think about medications: Be aware of the limitations of the WHO pain ladder. Regular medication is generally better than PRN. Cocodamol 8/500 confers no better analgesia than paracetamol. Consider topical preparations such as capsaicin. Fewer systemic side effects. Many chronic pains have a mixed aetiology and may benefit from the use of a low dose tricyclic, SNRI or gabapentinoid. Sleep pattern may be improved with low dose tricyclics. Try a periodic reduction in medications. For advice about prescribing Pain medication see Pain Management Guidance, appendix 4C of the Fife Formulary available on http://www.fifeadtc.scot.nhs.uk/

Sensitisation What is it? Why does it happen? How does it happen? Forms of sensitisation – Primary hyperalgaesia Secondary hyperalgaesia Cold hyperalgaesia – risk factor Allodynia Wind up What is it? Increasing sensitivity of the nervous system including sensory, motor, autonomic (therefore sympathetic) in response to a threat. Sensory changes – increase in sensitivity to touch, pressure, light, noise, vibration, chemicals, movement, dizziness (vestibular system), increasing pain and spread of pain, pins and needles. Motor – muscle tightening, muscle weakness, decreased coordintation, giving way or dropping things Autonomic – Digestion altered – IBB, IBS (bladder and bowel), heartburn, poor sleep, temperature dysregulation, fight/flight state, decreased libido Behavioural would include avoidance and depression Why does it happen? Multi factorial – prolonged afferent barrage (poorly controlled or uncontrolled pain) leading to changes in resting levels, genetic transcription of proteins, probably some genetic factors, plasticity, worry and anxiety, downward excitation (response to a threat, top down. ‘The not knowing’), , disinihibition of inhibitory interneurones leading to spread of pain and other symptoms How does it happen? See why Hyperalgaesia – heightened painful response to a painful stimulus Primary – in acute injury is close to injury site – sensitisation to protect – minutes after injury Secondary – increased sensitivity distal from the injury site – reflects central processes causign wideining of the receptive field of the nociceptors – reflects increased activity in threat detection system. Allodynia – painful response to a non painful stimulus – light brushing is painful – central changes, widening of receptive field and wide dyanmic range neurones become more active. Reflects a threat detection system on high alert. Wind up – delayed pain after activity. Can be later the same day or up to 48 hours after. Like a dripping tap. Most patients recognise this.

Central Sensitisation Highly common in chronic pain syndromes e.g. CLBP, FMS, CRPS How to recognise? Sensitive to light, noise, smell, chemicals, to touch, pressure, vibration Is not an indication of harm or damage Can be alarming for patient Can lead to many investigations, tests, appointments

Mechanisms of Central Sensitisation Plasticity - Strengthening of existing synaptic connections - Formation of new ones Hebbian Plasticity ‘Nerves that fire together wire together’ ‘nerves that fire apart wire apart’ ‘past behaviour predicts future behaviour’ Disinhibition accounts for spread of pain and other symptoms. Biological basis of learning Repeat or practice something often enough nervous system responds by strenghtening those connections and becoming more efficient. In sports/music this is seen by improved coordination, more automatic, less concentration, less effort. Bit like forming a new path. In childhood and teenage years we are at our most plastic – the nervous system is highly responsive to input e.g. learning both mental and physical tasks, but also stress. Part of the evolution of language/communication is due to this prolonged plastic childhood as we have the longest childhood of all animals.

Neuropathic Pain Pain caused by a lesion or disease of the somatosensory nervous system. From peripheral nerve, nerve root (peripheral) From spinal cord or brain (central e.g. thalamic pain) Pain often described as shooting, electric shock-like, burning – commonly associated with tingling or numbness The painful region may not necessarily be the same as the site of injury Pain occurs in the neurological territory of the affected structure (nerve, root, spinal cord, brain) Neuropathic pain probably present to a greater or lesser extent in most chronic pain conditions. DN 4 Question 1:Does the pain have one or more of the following characteristics? Burning Painful cold Electric shocks Question 2: Is the pain associated with one or more of the following symptoms in the same area? Tingling Pins and needles Numbness Itching Question 3: Is the pain located in an area where the physical examination reveals one or more of the following characteristics? Hypoaesthesia to touch (reduced sensation) Hypoaesthesia to pin prick (reduced sensation Question 4: In the painful area, can the pain be caused or increased by: Brushing (with a brush or cotton wool) Score of 4 or more will likely diagnose NeP

Putting it all together! One of the aims of today was to help you understand the biological mechanisms of the patient in front of you. Obviously there is a lot of information but this clinical tool may help clarify your thinking. This is a useful clinical decision tool making sheet. We have concentrated on the CNS adaptation (central changes) but the tool includes distribution, behaviour of symptoms to different stimuli, duration etc. Copyright Body in Mind 2012

A Unifying Theory of Pain and its Symptoms – the Neuromatrix Ronald Melzack 1997 He recognised that phantom limb pain (pain from fresh air!), thalamic pain syndrome, i.e. Pain felt in the absence of input from the body. GIST - Homeostasis and response to threat Cognitive – evaluative = what we think about sensory input (could introduce mature organism model here) Sensory – discrimiantive = sensory input Motivational – affective = how threatened or how safe we feel These all mingle together continuously Response can be sensory system, motor system and autonomic nervous system. Goto Diane Jacobs article on desktop for references and Melzack examples Brief mention of theory of self/mention threat to self (this relates back to narrative theory)

Case Studies We are just going to talk through 2 case studies in your groups Bearing in mind what we have talked about can you apply this to the case studies and apply an understanding of pain biology to their presenting symptoms

History - RTA 3 yrs ago, whiplash injury, not sore at time, developed after 1 day. Reports high levels of pain initially. Also reports that has flashbacks to RTA. Legal case. Started as neck/shoulder pain then started spreading down arms and legs. Also headaches and poor sleeper. Recent breavement and isreapplying for DLA and not sure what to fill in diagnosis. Has been for massage and chiropractors, spent a lot of money with no lasting relief. Blood test for rheumatoid factor - negative Constant all over aching, Bad days and worse days aggs doing anything for too long, cold. Uses better days to try and catch up on housework, likes to get job done even though she knows she it will take a long time to settle Eased with rest and heat Fair RoM Hard neurological examination is clear Allodynia and secondary hyperalgaesia on palpation. ACR >11/18 Pain Mechs – as per CLBP plus neuromatrix Treatment options as per CLBP 32

History. -. ‘Failed back surgery’ History - ‘Failed back surgery’. Discectomy 3 years ago, felt worse post op. Wonders if something happened on operating table. 2ndMRI showed no further target for Sx, but some ‘bulging discs’ -Constant burning 9/10. Aggs weight bearing, walking any distance. Eases lying down, recliner chair Recently paid off from job as receptionist, difficulty with children, running house, parents aren’t well and is closet family therefore puts in care. Puts pressure on self to get things done. Examination – antalgic gait, deconditioned. Increasesd extensor tone Reduced RoM esp flexion, ongoing numbness in foot, reflexes OK, weakness in dorsiflexors. Also c/o leg giving way esp when tired. Pain Mechs see CLBP emphasise central and peripheral sensitisation, Treatment Options – as previous + gabapentin, ?? epidural 33

YELLOW FLAGS Attitudes & Beliefs - towards the current problem. Does the patient feel that with appropriate help and self management they will return to normal activities? The most common worry is that the patient feels they have something serious causing their problem. 'Faulty' beliefs can lead to catastrophisation. Behaviours - adopting disabled role, rest, use & abuse of medication Compensation - Is the patient awaiting payment for an accident/ injury at work/ RTA? Diagnosis - or more importantly Iatrogenesis. Inappropriate or confusing communication can lead to patients not being sure what the problem is, the most common examples being 'your disc has popped out' or 'your spine is crumbling'. Emotions - Patients with other emotional difficulties such as ongoing depression and/or anxiety states are at a high risk of developing chronic pain. Family - There can be two problems with families, either over protective or under supportive. Work – If there are difficulties, people are more likely to develop chronic problems.

So sometimes the first step is getting the patient to accept Pain Comes from the Nervous System. And here I describe the nervous system from nociceptor to brain and back again. So I use this diagram here – this is one form our most recent PMP – which may be is something similar to what many people see/use already. I will talk about the nerve endings in the skin of which there is 1300/square inch and foun myself talking to somebody as if they were mini pressure pads when talking about why there back was sensitive. I talk about the spinal cord as being an amplifier, and of course I bring in the brain at this point as I will begin to talk about descending control from what can make you more sensitive and less sensitive. So that is what the plus’s and minus’s are here. GOTO NEXT SLIDE It is when I am talking about the descending inhibition that I will talk about endorphins and the importance of exercise and will point out that opiates and lack of activity will make the endorphin system sluggish in chronic pain. On this slide I have also talked a little bit about why pain can spread talking about interneurons in the spinal cord and also changes in the sensory homunculus.

So this is a bit like the first diagram but on its side – and the emphasis is on the synapse or the connectors in the nervous system and what the plastic changes are in chronic pain. I use the different shapes to indicate neurotranmitters in the synapse, so I will increase the number of triangles to indicate adaptation of the nervous system and also show the growth or development of new synapses or connectors. Again I would reflect back to the things that can drive this from the more and less/sensitive slide. Again the positive message here is that synapses can be weakened and new synapses formed that are nothing to do with pain.

I title this section ‘repairing the alarm system’ as it is obviously very important to build in positive messages into pain ed. I usually ask the patient to contribute to this section. Usually I will do the section on the left and I will ask them do the section on the right. If I am doing this 1:1 I will use my hands to indicate increasing sensitivity and how to reduce sensitivity.

Explain Pain Examples Steve and Neil demonstrate

Small groups Use A3 paper Aim to draw to together what we have covered and discussed and think about how you could incorporate it into your work. You may want to thing about verbal explanations, pictures or diagrams, during assessment, using online material Discuss the above in your groups, throw around ideas and suggestions and feedback to the wider group at the end. Suggestions for ideas board: ‘too much going in and not enough coming out’ ‘overactive nervous system’ Swapping brains scenario

Thank You!