Pain Management

1. Pain Management Greg Hobbs Consultant in Pain Medicine

2. Context • Prevalence of persistent pain • 13% UK adults • Up to 40 000 patients registered with GPs in City • Effects of pain • Mood, sleep, mobility, social role, vocational role • Impact on family/carers • Challenges in treatment • Few highly successful interventions

3. Session Plan Evidence and Pain Who gets pain? Why? What are the consequences? How should we manage these people?

4. Session Plan 2. Analgesics What is the evidence? Opioids

6. Clinic Casemix?

7. Clinic Casemix?

8. Two-thirds will suffer LBP at some time Sciatica less common (1 in 10) but more likely to consult

9. Most will recover quicklySome people (1 in 10) have persistent pain and disability following an episode of LBPWho are these people?Why?

10. Physical risk factors for persistent problems include • pain radiating to the leg • ongoing exposure to lifting heavy and awkward loads • poor physical fitness • heavy smoking

11. Psychosocial Determinants • Pain catastrophising • Inappropriate illness beliefs & attributions to physical injury • people present with physical manifestations of psychological distress and life-trauma • Fear-avoidance • pain is harmful coupled with a fear of movement • Low self-efficacy (low mood and anxiety) • Iatrogenic factors • Perceived injustice (job dissatisfaction) • Litigation, compensation claims

12. Back Pain and Work • Work absence in workers with back pain = 15% • Return to work 68% at 1 month 86% at 1–6 months 93% at ≥6 months • This suggests most return to work • But 32% not back at work at 1 month • This is a crucial point for intervention to prevent long term work absence

13. Putative Cause of Chronic PainUK survey, > 5000 patients • Degenerative 34.2 % • Surgery 22.5 • No definite cause 20.2 • Trauma 18.7 • Infective 7.2 • Inflammatory 6.7 • Tumour 3.5 • Other 6.2

14. Chronic pain after surgery • 30-50% after some operations • Thoracic • Breast • Hernia • 5-10% of these severe pain • Overall 2 in 100 are life-changing

15. Risk factors/predictors of chronic postsurgical pain • Surgical e.g. invasiveness, nerve injury, duration of surgery • Psychosocial e.g. anxiety, catastrophizing, fear of surgery Katz & Seltzer, Expert Rev Neurother 2009 Jung et. al., Pain 2003. Fillingim et. al., J Pain 2009.

16. Effects on Pain-Signalling Systems Acute Pain  Peripheral nociception  Nerve excitability • Hyperalgesia • Allodynia Prolonged pain Chronic pain Damaged spinal pain-signalling systems

19. fMRI • Neuroimaging has provided evidence of structural and functional brain changes in the majority of chronic pain syndromes. • No one region is responsible for chronic pain. • anterior cingulate cortex, insular cortex, prefrontal cortex, primary and secondary somatosensory cortices (S1 and S2), motor cortex (M1) and supplementary motor area, thalamus, basal ganglia, amygdala, hippocampus and cerebellum • multiple regions of the brain are involved in a range of pain, sensory, motor, cognitive, motivational, memory, emotion and fear processes.

20. fMRI • Resting-state fMRI focuses on network-based changes • default mode, executive control, sensory motor networks • changes within these networks with chronic pain • Good cop v bad cop networks • Healthy? Vulnerable? Injured? • That ‘pain is in a patient’s head’ can now be taken more literally. eg maladaptive cortical remapping can itself produce symptoms, potentiate and sustain pain in LBP

21. fMRI • LBP, FMS, neuropathic pain and TMD the most widely studied • Neuroimaging shows considerable individual variability in networks mirrors the variability in pain experience • Challenge for clinical care, but has predictive value • Who will get pain? • Predict the effect of analgesics

22. fMRI • Multivariate pattern analysis, with machine learning, is gaining momentum as a new method of analysis for MRI studies of chronic pain. • Advances in real-time functional MRI, transcranial magnetic stimulation and other neuroimaging-based therapies continue to promise novel and more effective treatments for chronic pain.

23. Genetics Associations between gene/protein level changes and the type of pain pathology implicates a wide range of genetic variants. Search for genetic variants point to a centralised pain processing system. . . . Driven and modulated by neurotransmitters and their receptors . . . Also modulated by a complex system of inflammatory cytokines and growth factors. Genetic studies of musculoskeletal, neuropathic and visceral pain conditions

24. Genetics Somatic mutations acquired during lifetime are not passed on to offspring – implicated in cancer but not associated with chronic pain conditions. 1. High impact genetic inheritance Rare Potassium channel in familial migraine with aura Sodium channel in primary erythromelalgia These are inherited from parents

25. Genetics 2. Low impact but common (>1% population) single nucleotide polymorphisms that have a minimal effect on phenotype Aggregates of these variants are associated with symptoms e.g. sleep disturbance, fatigue, cognitive probs, hypersensitivity etc, Require environmental pressures to manifest. These modulate susceptibility rather than cause the problem - Can predispose or protect.

26. Genetics • GWAS = genome wide association studies • Migraine - most studied. Also FMS • LBP 50% heritability – mainly disc degeneration, protein degradation, inflammatory mechanisms and proinflammatory signalling. • FMS. 50% heritability. Monoaminergic pathway transmitters , neuronal differentiation, alterations synaptic stabilisation. • Stress induced MSK pain • Pain after trauma, psychological or physical; PTSD • Depression is a pre-trauma factor that predicts pain and is presumably a correlate for genetic susceptibility • Postoperative pain. • Treatments???

27. Session Plan Evidence and Pain Who gets pain? Why? What are the consequences? How should we manage these people?

28. Severe chronic pain is a considerable physical and psychological burden to the patient1-4

30. Persistent Pain A quantity of life issue?

31. Assess and manage the patientusing best evidence where possible 1. Use appropriate treatments

32. RCTs

33. Interventions & Treatments • Self-management; improve understanding, expectations, self-efficacy, resilience, social prescriptions . . . • Physical therapies • Psychological therapies egCBT • Pain management programmes • Medication • Procedures Acupuncture & TENS Injections (interventional) Surgery Neuromodulation

34. Low back pain and sciatica in over 16s: assessment and managementNICE guideline [NG59]Published date: November 2016

35. Changes from CG88: What’s Out? • Acupuncture • No different to sham for pain • Contextual not biological effect • Better evidence for other treatments thus resource use • Manual therapy or psychological treatments without exercise and advice on self management • Paracetamol • Opioids except weak opioids ± paracetamol for acute LBP if NSAID not tolerated or ineffective • Amitriptyline • Spinal Fusion for LBP

36. Changes from CG88: What’s In? (LBP) • Exercise: biomechanical, aerobic or mind-body • Manual therapy alongside exercise • Psychological treatments alongside exercise • Combined physical and psychological programmes where psychosocial obstacles to recovery or previous treatments not effective • Promote and facilitate return to work or normal activities of daily living • Radiofrequency denervation for facet joint pain where previous treatment ineffective

37. Changes from CG88: What’s In? (Sciatica) • Neuropathic medication (CG173) • Epidural steroid + local anaesthetic • Surgical decompression • SCS for selected patients according to 2008 Tech appraisal

38. Treatment algorithmfor non-specific LBP and sciatica Risk stratification tool • Do not routinely image • Refer for an opinion, not imaging • Only image in specialist settings if result likely to change management • Consider alternative diagnoses Advice to support self-mgt NSAID or weak opioid ± paracet Sciatica Exercise (group) ± Manual tx ± Psychological tx ± Educ RF Denervation (for subgroups) Neuropathic Rx Epidural steroid + LA All tx explored? Risks v benefits Surgical decompression Additional tx unlikely to benefit Consider Draft for consultation, March 2016 Key: If appropriate Strong rec

39. Decreased fear and avoidance predicts improved mood, less pain interference with daily activity, less medication and healthcare use • Changes in pain account for relatively little or no variance in outcomes • Pain relief is not necessary for patient satisfaction • PMP: 65% increase in physical activity • 66% return to work. • 68% reduction in annual healthcare costs.

40. Medical Service Utilisation: Physician, Specialist & Physiotherapist

41. Procedures, injections

42. MBB Epidural

46. Target Specificity: Transforaminal Epidural Steroid Injections (TFESI) Transforaminal access provides a high concentration of corticosteroid at the locus of inflammation: Ventral and lateral epidural space

47. Target Specificity: Transforaminal Epidural Steroid Injections (TFESI) Transforaminal access provides a high concentration of corticosteroid at the locus of inflammation: Neural foramen

48. SI Joint

49. Self management • Complex skill • Develops over a long timescale • Frequent adjustment • Ongoing skilled judgement and guidance

50. Assess and manage the patientusing best evidence where possible 2. Use an appropriate clinical model