Chronic Primary Pain
Red Flags — exclude new serious pathology in chronic pain patients
| Red flag | Why important | Action |
|---|---|---|
| Saddle anaesthesia + bilateral leg weakness + bladder/bowel dysfunction | Cauda equina syndrome — surgical emergency. Can develop insidiously in pre-existing lumbar back pain. Missing it leads to permanent neurological injury. Saddle anaesthesia (inner thighs, perineum) is the most specific feature. | 999 / Emergency MRI / immediate neurosurgery referral |
| New or significantly changed pain in known cancer patient | Bone metastases; spinal cord compression; malignant nerve infiltration. Pain change in a cancer patient requires imaging before any pain management adjustment. | Urgent MRI / CT; oncology same day |
| New pain with fever + systemic features + focal neurological deficit | Spinal epidural abscess or discitis — can mimic chronic back pain exacerbation. Associated fever and raised inflammatory markers distinguish it. Urgent MRI and infectious disease involvement. | Urgent MRI spine; FBC/CRP/ESR; blood cultures; emergency admission if sepsis |
| Night pain waking from sleep + unexplained weight loss in a patient >50 | Vertebral metastases; multiple myeloma; primary bone tumour. Night pain that wakes from sleep is not mechanical — it is the most sensitive red flag for vertebral malignancy. | Urgent MRI spine; bloods (ESR, LDH, protein electrophoresis, ALP); 2WW if malignancy suspected |
| Suicidal ideation in chronic pain | Suicide risk is significantly elevated in chronic pain (2–3× general population). Pain catastrophising + hopelessness about recovery is the primary driver. PHQ-9 item 9 must be screened at every chronic pain consultation. | PHQ-9; direct suicidal ideation screen; same-day crisis if active ideation with plan |
Safeguarding Considerations in Chronic Pain
💊 Opioid Risk and Diversion
- Chronic opioid prescribing creates risk of misuse, dependence, and diversion to others in the household (including children)
- Assessment: is the patient taking opioids as prescribed? Any dose escalation? Any requests for early prescriptions?
- Children in the household of a patient on high-dose opioids: potential accidental ingestion risk; medication storage discussion mandatory
- Opioid prescribing should be reviewed at every consultation with documented clinical indication and functional benefit assessment
🏠 Domestic Abuse and Chronic Pain
- Chronic pain (particularly widespread musculoskeletal and pelvic pain) has a strong association with domestic abuse and adverse childhood experiences
- Screen using HARK (Humiliation, Afraid, Rape, Kick) questionnaire in unexplained or unusual chronic pain presentations
- Domestic violence can present as chronic pain through: repeated physical injury; stress-related central sensitisation; medically unexplained symptoms from chronic trauma
- Safety planning: MARAC if high-risk; IDVA; children's social care if children in household
🧒 Children in the Household
- Parental chronic pain significantly impacts children: reduced parental engagement; financial hardship from work absence; modelling of pain behaviour (children of chronic pain patients have higher rates of chronic pain themselves)
- PHQ-9 and parenting capacity assessment when parental chronic pain is severely functionally impairing
- Social prescribing: family support; young carers assessment (if children are fulfilling carer roles for a chronically ill parent)
⚠️ Chronic Pain and Self-Harm Risk
- Chronic pain doubles suicide risk; PHQ-9 at every consultation; direct suicidal ideation screen
- Opioid stockpiling: patients with chronic pain on long-term opioids may accumulate doses; at-risk patients may be stockpiling for overdose
- Safe storage and prescription quantities: monthly prescriptions for opioids in patients with any mood instability or suicidal ideation history
- Hopelessness about pain recovery + depression is the highest-risk combination: same-day crisis assessment if active ideation
😤 Invalidation and the "Normal MRI" Trauma
Being told "your scan is normal — you should be fine" when in severe pain is one of the most invalidating experiences in medicine. It implies the pain is imagined, exaggerated, or manipulated. The accumulated effect of repeated invalidation creates a patient who arrives defensive, angry, and with very low expectations of being understood. Reversing this narrative — "normal MRI means the pain is a nervous system phenomenon, not a structural one — it is equally real, equally serious, and differently treated" — is the most therapeutic act of this consultation.
"I want to acknowledge something: you have been in significant pain for 4 years, and you have been told repeatedly that your scan is normal and you should be better. That experience is frustrating and dismissive — the pain is real, and a normal MRI does not mean it is in your imagination. It means the type of pain you have lives in the nervous system's sensitivity, not in the tissue. That changes how we treat it."🧠 Pain Catastrophising
Pain catastrophising — the tendency to ruminate about pain, magnify its significance, and feel helpless — is the strongest predictor of chronic pain disability. It is not a personality trait or a sign of weakness. It is a learned cognitive response to repeated, unpredictable pain that has not been adequately explained or managed. ACT and pain-focused CBT are specifically designed to interrupt the catastrophising cycle: changing the relationship with pain rather than the pain itself.
"When the pain is at its worst, what goes through your mind? Do you find yourself thinking things like 'this is never going to get better' or 'the pain must be doing damage'? Those thoughts are a very important part of what keeps the pain so disabling — and they are something we can actually work on."🚶 Deconditioning and Fear-Avoidance
Margaret has stopped walking — partly because it hurts, partly because she fears it will make things worse. Fear-avoidance is the cycle: fear of pain → avoidance of activity → deconditioning → lower pain threshold → more pain from less activity → more fear and avoidance. This cycle is one of the most powerful perpetuating mechanisms in chronic pain. Exercise — gradually, graded, supported — breaks the cycle. The key cognitive shift: "movement is medicine, not damage."
"I know movement hurts, and I know you are worried about making things worse. But the evidence is clear: for pain of this type, the most effective thing we can do — better than any medication — is to gradually increase movement. Not because it will stop the pain immediately, but because deconditioning is amplifying every signal your nervous system receives."👤 Identity Loss
Margaret was a teacher — an active, engaged professional. Chronic pain has replaced her professional identity with a pain identity. Much of her daily mental and social life is now organised around her pain: monitoring it, managing it, explaining it, advocating about it. This identity reorganisation maintains the pain and reduces quality of life. ACT specifically addresses the identity shift: reorienting toward values (what matters to me) rather than pain (what prevents me from being who I was).
"What mattered to you before the pain — what did you love doing, what gave you a sense of purpose? I ask because one of the treatments I want to offer is specifically about getting back to the things that matter to you, even if the pain is still present."💊 Opioid Dependence and the Escalation Trap
Margaret has been on tramadol for 2 years with "incomplete relief." This pattern — long-term opioid with escalating dose requirement and no functional benefit — is the clinical signature of opioid-induced hyperalgesia. The opioid is paradoxically worsening the central sensitisation that is maintaining the pain. Explaining this to the patient without making them feel blamed for taking a prescribed medication requires skill and empathy. "Your brain has adapted to the tramadol in a way that is actually maintaining the pain sensitivity."
"I want to talk about the tramadol honestly. You have been on it for 2 years and it is not giving you good relief. The research shows that long-term opioids like tramadol can sometimes make the nervous system more sensitive to pain over time — not less. That means the tramadol may actually be part of what is keeping the pain so difficult. I would like to discuss a gradual plan to reduce it."🔮 Prognosis and Possibility
Chronic primary pain is not curable in the sense of eliminating all pain — but it is very manageable. The evidence for exercise and ACT is that 50–70% of patients achieve significant improvement in function and quality of life. The treatment goal is not pain elimination but pain acceptance alongside meaningful living. Many patients describe their lives as fully meaningful and satisfying with reduced but residual pain after effective treatment. Communicating this accurately — not falsely optimistic and not pessimistic — is a key therapeutic act.
"The goal of treatment is not to make you pain-free — though some people do achieve that. The goal is to get you back to living a life that feels meaningful and full, even if some pain is still present. That is achievable. And the treatments that achieve it are not stronger medications."- Prescribing morphine or escalating opioids — NICE NG193 explicitly recommends against this for chronic primary pain
- Not validating the pain before explaining the treatment approach
- Not addressing the "dismissed by previous GPs" experience
- Not screening PHQ-9 for depression
- Not identifying pain catastrophising and fear-avoidance
Same-Day to 2 Weeks
Structural or systemic cause must be excluded- Cauda equina features999 / Emergency MRI / neurosurgery — saddle anaesthesia, bilateral leg weakness, bladder/bowel dysfunction
- Night pain + weight loss (>50 years) — malignancyUrgent MRI spine; 2WW; FBC/ESR/LDH/protein electrophoresis
- Fever + focal neurology + back pain — spinal infectionUrgent MRI; blood cultures; FBC/CRP; emergency admission if septic
- Active suicidal ideation with planSame-day crisis team; adjust opioid prescribing (monthly supply only) if risk present
Weeks
Complex or refractory- Refractory chronic pain despite exercise + ACT + adequate medicationPain clinic / multidisciplinary pain management programme (MPMP)
- Neuropathic pain — specialist assessment neededNeurology; pain medicine; capsaicin patch (specialist-initiated)
- Opioid tapering requiring specialist supportCommunity addiction services; pain clinic shared care
Primary Care
Biopsychosocial management- Established chronic primary painExercise (graded, supervised); ACT or CBT (NHS Talking Therapies pain pathway); self-management programme; social prescribing; address comorbid depression
- Opioid de-prescribing discussionIf on long-term opioids with no functional benefit: 10% taper every 2–4 weeks; pain psychology alongside
- Not re-screening red flags at a chronic pain consultation
- Escalating opioids without explicitly documenting red flag exclusion and NICE NG193 framework
- Missing a new neurological deficit in a patient with pre-existing chronic pain
- Ordering MRI for established chronic primary pain without new red flags — may reinforce structural illness belief
- Not completing PHQ-9 at a chronic pain consultation
"Think of your pain system like a smoke alarm. Normally, the smoke alarm goes off when there is smoke — that is useful, it keeps you safe. After your disc problem, your pain system had a genuine reason to fire — there was an injury. But sometimes, after prolonged pain, the alarm system becomes oversensitive. It starts firing even when there is nothing actually dangerous — it is now responding to tiny signals as if they are major threats. A normal MRI does not mean there is nothing wrong — it means the problem is in the alarm system's sensitivity, not in the structure it is protecting. The good news is that the alarm system can be recalibrated. But the treatments that recalibrate it are not the same as the treatments for a structural injury — and stronger painkillers do not turn down an oversensitive alarm."
"I just need something stronger — if the pain was properly controlled I could get on with my life."
"I understand why that makes sense. But there is an important piece of research I want to share with you: for pain of this type — where the nervous system is oversensitised rather than where there is ongoing tissue damage — opioids actually make the nervous system more sensitive over time, not less. This is called opioid-induced hyperalgesia. It is one of the reasons the tramadol has been getting less effective over time. Morphine would produce the same effect: short-term relief, then escalating tolerance, then increased pain sensitivity. The research shows that patients who taper off opioids and do the exercise and psychological programme end up with less pain and more function than patients who escalate the opioid dose. I know that is the opposite of what you expected to hear — but that is what the evidence shows."
Neuropathic Pain
Post-herpetic neuralgia; diabetic neuropathy; CIPN; spinal stenosis. Treat with duloxetine, amitriptyline, gabapentinoid (note: NOT for primary pain).
Inflammatory (RA, SpA)
Elevated inflammatory markers; synovitis; rheumatology; DMARDs.
Cancer Pain
WHO analgesic ladder applies; opioids appropriate; specialist oncology pain service.
Cauda Equina
Saddle anaesthesia + bladder/bowel → 999; emergency MRI.
Vertebral Malignancy / Infection
Night pain + systemic features → urgent MRI; cancer/infection screen.
- Not explaining why the MRI being normal does not mean the pain is imagined
- Not explaining OIH when declining opioid escalation
- Referring to passive physiotherapy (massage, manipulation) rather than active exercise-based rehabilitation
- Not mentioning pain-focused psychological therapy (ACT/CBT) as part of the management plan
Validate — the experience of inadequate treatment
4 years of inadequate pain relief, being told her scan is normal, and feeling dismissed by previous consultations. This is a genuine failure of healthcare, not a personality problem. Acknowledging it explicitly — without defensively justifying previous clinicians — creates the foundation for honest treatment discussion.
"I want to acknowledge something: 4 years is a long time to be in significant pain, and not having the right treatment for that long is genuinely a failure on the healthcare system's part — not yours. The type of pain you have has traditionally been undertreated because we did not have the right tools. I want to change that today."Explain — why morphine will not work and exercise will
The explanation must be specific, evidence-based, and non-dismissive. The OIH mechanism and the neuroplasticity evidence for exercise must both be named. The patient is intelligent (retired teacher) and will respond to accurate information — not to platitudes about "relaxation" and "positive thinking."
"The research on chronic pain like yours is clear: opioids become progressively less effective over time and increase pain sensitivity. Exercise — even small amounts, gradually — does the opposite. It directly reduces the nervous system's hypersensitivity through mechanisms that no medication can replicate."Offer — a specific, achievable starting point
Do not send the patient away with a general recommendation to exercise — identify one specific, achievable activity. Hydrotherapy, aquatic exercise, gentle walking programme, tai chi, yoga — all have evidence. The first step must be small enough to succeed. Success rebuilds self-efficacy; self-efficacy reduces catastrophising.
"I am not asking you to run a marathon. The evidence is that even a 10-minute walk, three times a day, started today, produces measurable improvement in chronic pain within 6 weeks. Let us identify something that feels possible and build from there."Exercise directly reduces central sensitisation through multiple mechanisms: endogenous opioid release (endorphins); noradrenergic and serotonergic pathway activation (descending inhibition); neuroplastic changes in spinal cord excitability; reduced neuroinflammation; improved sleep (which further reduces sensitisation); improved mood (antidepressant effect). No analgesic achieves all of these simultaneously.
Cochrane meta-analysis: aerobic exercise reduces pain intensity and improves function in chronic primary pain; effect size comparable to SSRI for depression. NICE NG193: offer supervised group or individual exercise. Any modality (walking, swimming, cycling, yoga, tai chi) is effective — the key is gradual progression and consistency. Supervised exercise (physio) is more effective than self-directed for most patients initially.
ACT does not aim to reduce pain intensity. It aims to reduce the suffering caused by pain by changing the patient's relationship with it. Core processes: acceptance (willingness to experience pain without struggle); defusion (seeing painful thoughts as events, not facts: "I am noticing the thought that I will never get better" rather than "I will never get better"); valued action (committed engagement with what matters, despite pain). Reduces catastrophising and increases psychological flexibility.
Standard CBT for pain: challenges the content of catastrophic thoughts ("is this thought realistic?"). ACT: changes the relationship with the thoughts ("this thought is present; it is not a fact I must act on"). Both are effective; ACT has slightly stronger evidence for acceptance-related outcomes and for patients who have already tried CBT without success.
Pain Neurophysiology Education (PNE): systematic patient education about the science of chronic pain — how central sensitisation works, why normal MRI is compatible with significant pain, why exercise helps and opioids eventually worsen it. Cochrane: PNE + exercise is more effective than exercise alone. PNE directly changes the structural illness model and reduces catastrophising before therapy begins.
The GP consultation is the first opportunity for PNE. Resources: "Explain Pain" (Butler and Moseley — the standard patient education book); NHS Chronic Pain Self-Management resources; Live Well with Pain (livewellwithpain.co.uk). The smoke alarm analogy used in Step 5 is a core PNE metaphor.
Pain disrupts sleep; poor sleep reduces descending inhibitory pain pathways (noradrenergic and serotonergic); reduced inhibition amplifies pain signals; more pain disrupts sleep further. Treating the sleep disorder in chronic pain is a direct pain-modulating intervention, not just comfort management. CBT-I for insomnia in chronic pain has evidence for both sleep and pain improvement.
Sleep hygiene (consistent wake time; stimulus control; no screens in bed). Low-dose amitriptyline 10mg nocte: evidence specifically for improved sleep in chronic pain and fibromyalgia. Not recommended for long-term use in primary care but can be useful short-term bridge while exercise and ACT take effect.
Social isolation is a significant chronic pain amplifier — it increases central sensitisation through stress pathway activation and removes positive meaning from daily life. Peer support groups for chronic pain (Action on Pain; Pain Concern) reduce catastrophising and improve function. Social prescribing (link worker referral to community activities) is a NICE NG193-endorsed component of management.
Link worker referral for community activities. Pain support groups. Livewellwithpain.co.uk (online chronic pain self-management resource). Activities chosen around patient values — not generic "just get out of the house" advice. Return to meaningful activities (teaching, reading groups, volunteering) is an ACT target.
Opioid-induced hyperalgesia (OIH): chronic opioids down-regulate descending inhibitory pathways, up-regulate NMDA receptor excitability, and produce tolerance at mu-opioid receptors — net effect is increased pain sensitivity. Tapering opioids allows neuroplastic recovery of pain-inhibitory pathways. Most patients who complete opioid taper report equivalent or improved pain control at lower opioid dose or no opioid.
10% dose reduction every 2–4 weeks. Slower if anxiety or dependence features. Pain psychology mandatory alongside taper. Buprenorphine patch as transition if significant dependence. Never abrupt cessation. Warn about temporary pain increase during taper (expected; not relapse). Document shared decision-making explicitly — patient agreement is essential.
Duloxetine 30mg OD → 60mg OD; or low-dose Amitriptyline 10mg nocte
- Duloxetine: SNRI; licensed for diabetic neuropathic pain and fibromyalgia; significant evidence for pain + depression comorbidity. Not NICE NG193 recommended as first-line for undifferentiated chronic primary pain but appropriate when depression is comorbid.
- Low-dose amitriptyline 10mg nocte: evidence specifically for fibromyalgia sleep and pain (at 10mg — much lower than antidepressant doses). Not to be routinely prescribed for non-specific chronic pain per NICE NG193.
Gabapentin/Pregabalin ONLY for confirmed neuropathic pain — NOT primary pain
- NICE NG193: do NOT offer gabapentinoids for chronic primary pain — high-yield exam point
- Gabapentinoids ARE appropriate for confirmed neuropathic pain (diabetic neuropathy, post-herpetic neuralgia, CIPN) but must not be confused with chronic primary pain treatment
- Class C controlled drugs since 2019; significant dependence and misuse potential; additive respiratory depression with opioids
- Opioids (tramadol, codeine, morphine, oxycodone) — cause OIH; worsen long-term outcomes; do not start; taper if already prescribed
- Gabapentinoids (gabapentin, pregabalin) — no evidence for chronic primary pain; significant harms; do not start
- Paracetamol — insufficient evidence of benefit in chronic primary pain; de-prescribe if no benefit
- NSAIDs (long-term) — insufficient evidence for chronic primary pain; significant CV, GI, renal risks with long-term use
Select clinical scenario — see drug cards below
"This tablet treats both the low mood and the pain by affecting the pathways that regulate both in the brain and spinal cord. Start at 30mg for 2 weeks to help with tolerability, then increase to 60mg. Take it in the morning with food. It takes 4–6 weeks to see the full effect. Do not stop it suddenly — we reduce it gradually."
Duloxetine: NICE NG193 framework — appropriate for chronic pain when depression or neuropathic pain is comorbid; NOT first-line for undifferentiated chronic primary pain without these features. SNRI mechanism enhances descending inhibitory pain pathways. Discontinuation syndrome: always taper.
"Take this at night — 10mg is a very low dose, much lower than when it is used for depression. At this dose it helps with sleep quality and with the pain. You will notice the dry mouth — drinking water helps. Do not drive if you feel drowsy the next morning."
Low-dose amitriptyline (10mg nocte) has specific evidence for fibromyalgia and neuropathic pain. NICE NG193: not recommended for undifferentiated chronic primary pain routinely. More sedating than at antidepressant doses — night-time use is the clinical application. ECG before higher doses. Anticholinergic effects limit use in elderly.
"This tablet is specifically for the nerve pain component — the burning and shooting sensations. It can cause dizziness and drowsiness at first, especially when you stand up. Start slowly and increase only as the dizziness settles. Do not drive until you know how it affects you."
High-yield exam point: NICE NG193 explicitly prohibits gabapentinoids for chronic primary pain. They are only appropriate for confirmed neuropathic pain. Class C CD since 2019. Respiratory depression with opioids (additive). Renal dose adjustment essential. This is one of the most commonly examined NICE NG193 points in SCA.
"I want to explain why I am recommending reducing the tramadol rather than increasing it. The research shows that long-term opioids can actually increase the nervous system's sensitivity to pain over time — this is called opioid-induced hyperalgesia. The tramadol is part of what is keeping your pain difficult. Most patients who complete a gradual reduction end up with equal or better pain control without the opioid. The reduction will be very slow and I will support you throughout."
NICE NG193: opioids should not be started for chronic primary pain; if already prescribed, discuss tapering. OIH must be explained to justify the taper to the patient. 10% reduction every 2–4 weeks; never abrupt; pain psychology alongside. Documenting shared decision-making is essential — patient must understand and agree to the plan.
"Apply a small amount directly to the painful area 3–4 times a day. Rub it in gently. Wash your hands afterwards. If you are going to be outside in sunshine, cover the area — it can make the skin more sensitive to the sun. It should start helping within a few days of regular use."
NICE NG193 preferentially recommends topical NSAIDs over systemic for localised pain. Much safer profile: negligible cardiovascular, GI, and renal effects compared with oral NSAIDs. Appropriate even in mild CKD where systemic NSAIDs are avoided. OTC availability (Voltarol Gel) makes it accessible.
"When you first use this cream it will feel warm or burning — that is expected and means it is working. The burning reduces over the first few days. Use it 3–4 times a day. Wash your hands immediately afterwards and never touch your eyes. It works by reducing the pain signal from the area over time."
Low-strength capsaicin is OTC and appropriate for localised pain; Qutenza 8% patch is specialist-initiated for peripheral neuropathic pain. The burning-on-application is expected and therapeutic — warn the patient to avoid premature discontinuation. NICE NG193: topical agents preferred over systemic for localised pain.
Identity Loss
Margaret was a teacher — active, engaged, purposeful. Chronic pain has progressively stripped her professional role, her physical activities, her social engagements, and her self-concept. Pain has become her identity. ACT specifically addresses this: the treatment is not about reducing pain but about re-engaging with values and meaningful activity alongside pain.
"What mattered to you before the pain — what gave you a sense of who you are? Because one of the treatments I want to offer specifically helps people return to the things that matter to them, even if the pain is still there."Relationship Impact
Chronic pain profoundly affects relationships — partners often feel helpless (cannot fix it), frustrated (by the limitations it imposes on family life), or guilty (for having moments of resentment). The patient feels guilty about the burden she represents. Both partners are suffering, neither knows how to talk about it. Family psychoeducation about chronic pain is underused and highly effective.
"How is your partner managing through this? It affects them too, often in ways neither of you are talking about. Part of the treatment I am recommending involves understanding that — there are resources for families and partners of people with chronic pain."Financial and Occupational Impact
Margaret is retired (somewhat younger than normal retirement age — suggests the pain contributed to early retirement). For patients still working, chronic pain causes significant occupational disruption. The Equality Act 2010: chronic pain that substantially limits daily activities is a disability — workplace adjustments are a legal entitlement. PIP, ESA, Access to Work are relevant for patients with significant disability.
"I want to make sure you are aware of the financial support you may be entitled to — DWP benefits, PIP. These are not "giving up" — they are practical support that might reduce some of the financial stress that amplifies the pain."Medical Invalidation and Distrust
"You've been told your scan is fine and you should be better" is one of the most harmful things healthcare can say to a chronic pain patient. The accumulated effect of this repeated invalidation is a patient who has lost trust in the healthcare system and arrives at every consultation expecting to be dismissed again. Rebuilding trust requires explicit acknowledgment of the invalidation, not just a new diagnosis.
"I want to be direct about something: the experience of being told your scan is normal and you should be fine — when you are clearly not fine — is a failure of how we have communicated about this condition. Your pain is real. The science of how we understand it has changed, and so should the treatment."Social Isolation
Chronic pain progressively reduces social engagement — activities are cancelled, relationships maintained only by the most committed, and isolation deepens. Social isolation amplifies pain through two mechanisms: increased focus on pain (nothing else to think about) and increased activation of central sensitisation pathways (social exclusion activates the same neural pathways as physical pain). Social prescribing and peer support groups are underused but evidence-based interventions.
"You mentioned you have stopped going out as much. I want to be honest: the isolation is actually amplifying your pain — the brain processes social pain and physical pain through the same pathways. Getting back to social connections, even gradually, is part of the treatment."Prognosis
Chronic primary pain is not reliably curable but is very manageable. Most patients who engage with the evidence-based pathway (exercise + ACT + medication optimisation) achieve significant improvement in function and quality of life, with pain reduced but often not eliminated. The framing of "living well with pain" rather than "waiting for the pain to stop before living" is the therapeutic core of ACT and the most important prognostic message.
"The goal is not a pain-free life — though some people do achieve that. The goal is a life that feels full and meaningful, with the pain present but not defining it. Most people who engage fully with this programme describe that as achieved within 6–12 months."4 Weeks — Exercise Progress + Opioid Taper + PHQ-9
Exercise: has the patient started? What activity? What frequency? Barriers to exercise identified and addressed. Tramadol taper: first 10% reduction tolerated? Withdrawal symptoms? Temporary pain increase expected. Duloxetine started? Tolerability. ACT referral confirmed? PHQ-9 trend. Any new red flag symptoms? Self-management resources accessed?
8–12 Weeks — Response Assessment + ACT Progress
Function (not just pain: has the patient walked further? re-engaged with any activity?). Pain NRS vs baseline (function more important than pain intensity). ACT sessions started? Catastrophising reducing? PHQ-9. Opioid taper: next 10% step. Duloxetine at 60mg? Sleep improving? Any new concerns?
3–6 Months — Major Review
Function significantly improved (return to meaningful activities)? Opioid substantially reduced or stopped? PHQ-9 in remission range? Exercise established as habit? ACT complete? Pain NRS. If inadequate response: pain clinic referral; MPMP consideration; review diagnosis. Red flags re-screened. Medication review: is duloxetine still needed?
Annual Review
Annual chronic pain review: PHQ-9; medication review (is each drug still working? is each drug still indicated?); opioid prescribing justification documented; functional status; any new red flags; falls risk if on amitriptyline, pregabalin, or opioids; cardiovascular and renal monitoring if on NSAIDs.
Chronic pain annual review — NICE NG193 minimum standard
At every chronic pain medication review: function assessment (what can the patient do now vs 3/6/12 months ago?); PHQ-9 (comorbid depression; suicide risk); opioid justification (document that opioid is providing functional benefit — if it is not, begin taper discussion); eGFR (NSAID, gabapentinoid, tramadol dose review); falls risk (opioids; amitriptyline; gabapentinoids in elderly); exercise engagement (is the patient engaged with active management?); weight (opioids cause weight gain; sedentary lifestyle compounds this).
⚠ Safety-netting for chronic pain
Documentation requirements for NICE NG193 compliance
- Prescribing morphine or escalating opioids — NICE NG193 explicit recommendation against this for chronic primary pain
- Not validating the pain as real before explaining the biopsychosocial model
- Not explaining OIH as the reason for declining opioid escalation
- Not offering exercise and ACT as specific, evidence-based alternatives
- Not completing PHQ-9
- Not addressing the cauda equina safety-net
- NICE NG193 framework applied; morphine not prescribed; OIH explained
- Exercise and ACT/CBT offered specifically (not generic lifestyle advice)
- Tramadol taper plan discussed (10% per 2–4 weeks)
- PHQ-9; duloxetine for depression + pain
- Cauda equina safety-net given verbally
- Pain validated as real before explaining biopsychosocial model
- "Dismissed" experience acknowledged
- Biopsychosocial model in plain language (smoke alarm analogy)
- ICE all three; catastrophising identified
- Opioid taper discussed non-judgmentally
- Prognosis realistic and hopeful
Who you are
Margaret Davies, 58, retired secondary school teacher (took early retirement 2 years ago, primarily due to the pain). Lives with husband David (62, retired). Two grown-up children. She was previously active — gardening, long country walks, book club. All stopped. She now spends most of her day at home, sitting with heat pads, watching television. She has lost her social circle because she keeps cancelling. Her husband is supportive but frustrated — "he tries to help but doesn't really understand why I'm not getting better." PHQ-9 = 12 (mild-moderate depression — she has not connected her low mood to the pain explicitly; she attributes it to "not being able to do anything"). She is a capable, intelligent, and articulate woman who has been failed by healthcare and arrives defensive and sceptical.
Hidden clinical concerns
Primary demand: Morphine or equivalent. She has read about it online. She believes stronger pain medication is the logical next step after tramadol has been inadequate. She will initially resist the biopsychosocial explanation — "I don't want to be told it's all in my head." She responds positively if the GP clearly distinguishes "in your head" (imagined) from "in your nervous system" (real, just a different mechanism).
Secondary agenda: She wants to be believed. The most therapeutic thing the GP can say is "your pain is real." She has been in pain every day for 4 years and no one has acknowledged that. Everything else is secondary to this.
Catastrophising pattern: "The pain is never going to get better. There must be something the MRI missed. Every time I move it feels like I am doing more damage." She has not been assessed for catastrophising — it will emerge if the GP asks about what goes through her mind when the pain is bad.
Clinical details if asked
- Pain location: central low back, radiating to left buttock and posterior thigh (non-dermatomal — does not reach below knee); no saddle anaesthesia; no bladder/bowel problems; no bilateral leg symptoms
- Pain character: aching, constant 6/10 at rest; 8–9/10 with activity; worse in morning; slightly better after gentle movement but fear prevents her from testing this
- Current medications: tramadol 100mg BD; duloxetine 60mg OD (started 8 months ago — "helps a bit with mood but not much with pain"); paracetamol PRN (rarely takes — "it doesn't do anything")
- Activities: stopped all walking 18 months ago; stopped gardening 2 years ago; drives short distances only; stopped book club 6 months ago
- PHQ-9 = 12 (question 9: passive death wish "sometimes feel life isn't worth living" — 1 point; no active suicidal ideation)
- Catastrophising: "I think every time I try to do something I am making it worse. I lie awake thinking about the pain."
Reactions to key moments
- When pain is validated: Visible relief — "That is the first time a doctor has actually said that." Then willingness to listen.
- On opioid escalation declining: "So you're saying the tramadol is making it worse? That seems mad." → Receptive to OIH explanation if specific and non-blaming.
- On exercise recommendation: "I can't exercise — the pain stops me." → Receptive to graded exercise explanation if the mechanism is explained and a very small starting point is offered.
- On ACT: "I don't want to be told to just accept the pain and move on." → Receptive if ACT is distinguished from dismissal: "It is not about giving up. It is about getting your life back alongside the pain."
- Challenge line: "But if the exercise and the therapy were going to work, why haven't all the previous treatments worked? I've tried physio before and it made things worse."
Resolution: Margaret will accept the plan if the GP: (1) validates her pain as real and explicitly distinguishes "not on the scan" from "in your head"; (2) explains OIH specifically — why tramadol is part of the problem, not just inadequate; (3) explains that the previous physio likely involved passive treatment (massage, manipulation) whereas this referral is for a specific graded exercise programme for central sensitisation; (4) acknowledges her fear of exercise making things worse, with the mechanism of how graded exercise works differently from traditional physio; (5) starts duloxetine optimisation (she is on 60mg — discuss whether this needs review; or add comment about the depression component); (6) completes PHQ-9 and addresses the low mood explicitly; (7) gives the cauda equina safety-net. She will disengage if morphine is prescribed, if her pain is minimised, or if the biopsychosocial explanation is given without first validating that the pain is real.
- Cauda equina: saddle anaesthesia + bilateral leg weakness → 999
- Night pain + weight loss >50y → urgent MRI; malignancy screen
- Fever + back pain + focal neurology → spinal infection; admission
- Suicidal ideation with plan: same-day crisis
- Refractory after exercise + ACT + pharmacotherapy: pain clinic; MPMP
- Confirmed neuropathic pain: duloxetine + gabapentinoid appropriate
- Opioid tapering requiring specialist support
- Chronic primary pain: exercise (graded) + ACT/CBT + comorbid depression treatment
- Opioid de-prescribing: 10% taper every 2–4 weeks