Chronic_Neuropathic_Pain-Slides_Pierce-Smith.ppt

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Chronic_Neuropathic_Pain-Slides_Pierce-Smith.ppt

  1. 1. Chronic Pain Management Beverly Pearce-Smith, MD Clinical Assistant Professor Department of Anesthesiology UPMC-McKeesport Hospital July 2008
  2. 2. IASP Definition of Pain “Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.”
  3. 3. Acute vs Chronic Pain Characteristic Acute Pain Chronic Pain Cause Generally known Often unknown Duration of pain Short, well-characterized Persists after healing, ≥3 months Treatment approach Resolution of underlying cause, usually self-limited Underlying cause and pain disorder; outcome is often pain control, not cure
  4. 4. What is Acute Pain?  Physiologic response to tissue damage  Warning signals damage/danger  Helps locate problem source  Has biologic value as a symptom  Responds to traditional medical model  Life temporarily disrupted (self limiting)
  5. 5. What is Chronic Pain?  Chronic pain is persistent or recurrent pain, lasting beyond the usual course of acute illness or injury, or more than 3 - 6 months, and adversely affecting the patient’s well-being  Pain that continues when it should not
  6. 6. What is Chronic Pain?  Difficult to diagnose & perplexing to treat  Subjective personal experience  Cannot be measured except by behavior  May originate from a physical source but slowly it “out-shouts” and becomes the disease  It has no biologic value as a symptom  Life permanently disrupted (relentless)
  7. 7. Domains of Chronic Pain Social Consequences  Marital/family relations  Intimacy/sexual activity  Social isolation Socioeconomic Consequences  Healthcare costs  Disability  Lost workdays Quality of Life Physical functioning Ability to perform activities of daily living Work Recreation Psychological Morbidity Depression Anxiety, anger Sleep disturbances Loss of self-esteem
  8. 8. Mixed Type Caused by a combination of both primary injury and secondary effects Nociceptive vs Neuropathic Pain Nociceptive Pain Caused by activity in neural pathways in response to potentially tissue-damaging stimuli Neuropathic Pain Initiated or caused by primary lesion or dysfunction in the nervous system Postoperative pain Mechanical low back pain Sickle cell crisis Arthritis Postherpetic neuralgia Neuropathic low back pain CRPS* Sports/exercise injuries *Complex regional pain syndrome Central post- stroke pain Trigeminal neuralgia Distal polyneuropathy (eg, diabetic, HIV)
  9. 9. Possible Descriptions of Neuropathic Pain  Sensations  numbness  tingling  burning  paresthetic  paroxysmal  lancinating  electriclike  raw skin  shooting  deep, dull, bonelike ache  Signs/Symptoms  allodynia: pain from a stimulus that does not normally evoke pain  thermal  mechanical  hyperalgesia: exaggerated response to a normally painful stimulus
  10. 10. Physiology of Pain Perception  Transduction  Transmission  Modulation  Perception  Interpretation  Behavior Injury Descending Pathway Peripheral Nerve Dorsal Root Ganglion C-Fiber A-beta Fiber A-delta Fiber Ascending Pathways Dorsal Horn Brain Spinal Cord Adapted with permission from WebMD Scientific American® Medicine.
  11. 11. Pathophysiology of Neuropathic Pain  Chemical excitation of nonnociceptors  Recruitment of nerves outside of site of injury  Excitotoxicity  Sodium channels  Ectopic discharge  Deafferentation  Central sensitization  maintained by peripheral input  Sympathetic involvement  Antidromic neurogenic inflammation
  12. 12. Multiple Pathophysiologies May Be Involved in Neuropathic Pain  More than one mechanism of action likely involved  Neuropathic pain may result from abnormal peripheral nerve function and neural processing of impulses due to abnormal neuronal receptor and mediator activity  Combination of medications may be needed to manage pain: topicals, anticonvulsants, tricyclic antidepressants, serotonin-norepinephrine reuptake inhibitors, and opioids  In the future, ability to determine the relationship between the pathophysiology and symptoms/signs may help target therapy
  13. 13. Neuropathic Pain  “Pain initiated or caused by a primary lesion or dysfunction in the nervous system” Merskey & Bogduk 1994  Central & peripheral sites  Acute & chronic pain states  CRPS I: consequent of acute, often minor trauma  CRPS II: consequence of nerve injury  Sympathetically maintained Pain (SMP) or independent of the SNS
  14. 14. Neuropathic Pain  Burning, stabbing, paraesthesia, allodynia, hyperalgesia  Threshold for activation of injured 1o afferents is lowered  Ectopic discharges may arise from the injury site or the DRG  2o to changes in Na+ channel expression  Central Sensitisation in the cord  2o to peripheral inputs  2o to central changes  Reduced inhibition  Functional (neurotransmitter) & anatomical (sprouting) changes in Aβ fibres  tactile allodynia (pain induced by light touch)
  15. 15. Acute Neuropathic Pain  Acute causes  iatrogenic, traumatic, inflammatory, infective  Acute neuropathic pain = 1-3%  Based on cases referred to an acute pain service  Majority still present at 12 months  May be a risk factor for chronic pain  Prompt diagnosis & Rx may prevent chronic pain
  16. 16. Examples of Acute NP  Phantom Limb Pain (PLP)  Complex Regional Pain Syndrome (CRPS)  Spinal Cord Injury Pain  Peripheral nerve injury  Post-surgical (eg thoracotomy, mastectomy)
  17. 17. NEUROPATHIC PAIN LESION IN THE NERVOUS SYSTEM  EXPERIENCED IN PARTS OF BODY THAT APPEAR NORMAL  CHRONIC  SEVERE  RESISTANT TO OVER THE COUNTER ANALGESICS  AGGRAVATED BY ALLODYNIA
  18. 18. Chronic Pain Syndromes  Neuralgias  Causalgia  Complex Regional Pain Syndrome (aka: RSD  Hyperesthesias  Myofascial pain syndromes  Hemiagnosia  Phantom limb pain
  19. 19. COMMON TYPES OF NEUROPATHIC PAIN PERIPHERAL • Polyradioculopathy • Alcoholic polyneuropathy • Entrapment neuropathies (carpal tunnel) • Nerve compression by tumor • Diabetic neuropathy • Phantom limb pain • Postherpetic neuralgia • Trigeminal neuralgia CENTRAL  Compressive myelopathy from spinal stenosis  HIV myelopathy  MS  Parkinson disease  Post ischemic myelopathy  Poststroke pain  Posttraumatic spinalcord injury
  20. 20. CLINICAL EVALUATION OF PTS WITH SUSPECTED NEUROPATHIC PAIN  HISTORY- pain intensity (0 to 10), sensory descriptors, temporal variation, functional impact, attempted treatments, alcohol  PHYSICAL- gross motor, DTRs, skin, sensory- light touch, pin prick, vibration, dynamic /thermal allodynia, hyperalgesia, tinel`s  SPECIAL TESTS- CT, MRI, EMG, nerve conduction, clinical biochemistry
  21. 21. NEUROPATHIC PAIN  SPONTANEOUS- CONTINOUS OR INTERMITTENT -Burning, Shooting, Shock-like  STIMULUS EVOKED- ALLODYNIA AND HYPERALGESIA -Extension of allodynia above and below the originally affected dermatomes is a feature of central sensitization.
  22. 22. Copyright ©2006 Canadian Medical Association or its licensors Gilron, I. et al. CMAJ 2006;175:265-275 Neuropathic pain arises following nerve injury or dysfunction
  23. 23. PATHOPHYSIOLOGY  PERIPHERAL MECHANISMS Peripheral nerve injury 1. Sensitization by spontaneous activity by neuron, lowered threshold for activation, increased response to given stimulus. 2. Formation of ectopic neuronal pacemakers along nerve and increased expression of sodium channels and voltage gated calcium channels. (α 2 delta subunit- where gabapentin acts) 3. Adjacent demyelinated axons can have abnormal electrical connections channels and increased neuronal excitability.
  24. 24. PATHOPHYSIOLOGY CENTRAL MECHANISMS Sustained painful stimuli results in spinal sensitization (neurons within dorsal horn) 1. Increased spontaneous activity of dorsal horn neurons, reduced activation thresholds and enhanced responsiveness to synaptic inputs. 2. Expansion of receptive fields, death of inhibitory interneurons (intrinsic modulatory systems). 3. Central sensitization mediated by NMDA receptors that further release excitatory amino acids and neuropeptides. 4. Sprouting of sympathetic efferents into neuromas and dorsal root and ganglion cells.
  25. 25. Pain Treatment Continuum Least invasive Most invasive Psychological/physical approaches Topical medications *Consider referral if previous treatments were unsuccessful. Systemic medications* Interventional techniques* Continuum not related to efficacy
  26. 26. Nonpharmacologic Options  Biofeedback  Relaxation therapy  Physical and occupational therapy  Cognitive/behavioral strategies  meditation; guided imagery  Acupuncture  Transcutaneous electrical nerve stimulation
  27. 27. Pharmacologic Treatment Options  Classes of agents with efficacy demonstrated in multiple, randomized, controlled trials for neuropathic pain  topical analgesics (capsaicin, lidocaine patch 5%)  anticonvulsants (gabapentin, lamotrigine, pregabalin)  antidepressants (nortriptyline, desipramine)  opioids (oxycodone, tramadol)  Consider safety and tolerability when initiating treatment
  28. 28. FDA-Approved Treatments for Neuropathic Pain  Carbamazepine  trigeminal neuralgia  Duloxetine  peripheral diabetic neuropathy  Gabapentin  postherpetic neuralgia  Lidocaine Patch 5%  postherpetic neuralgia  Pregabalin*  peripheral diabetic neuropathy  postherpetic neuralgia *Availability pending based upon controlled substance scheduling by the DEA.
  29. 29. BRAIN Pharmacologic Agents Affect Pain Differently Descending Modulation Central SensitizationPNS Local Anesthetics Topical Analgesics Anticonvulsants Tricyclic Antidepressants Opioids Anticonvulsants Opioids NMDA-Receptor Antagonists Tricyclic/SNRI Antidepressants Anticonvulsants Opioids Tricyclic/SNRI AntidepressantsCNS Spinal Cord Peripheral Sensitization Dorsal Horn
  30. 30. Anticonvulsant Drugs for Neuropathic Pain Disorders  Postherpetic neuralgia  gabapentin*  pregabalin *  Diabetic neuropathy  carbamazepine  phenytoin  gabapentin  lamotrigine  pregabalin *  HIV-associated neuropathy  lamotrigine  Trigeminal neuralgia  carbamazepine*  lamotrigine  oxcarbazepine  Central poststroke pain  lamotrigine *Approved by FDA for this use. HIV = human immunodeficiency virus.
  31. 31. Gabapentin in Neuropathic Pain Disorders  FDA approved for postherpetic neuralgia  Anticonvulsant: uncertain mechanism  Limited intestinal absorption  Usually well tolerated; serious adverse effects rare  dizziness and sedation can occur  No significant drug interactions  Peak time: 2 to 3 h; elimination half-life: *Not approved by FDA for this use.
  32. 32. Gabapentin  Action: ↓ NT release from hyper-excited neurones  variable oral absorption, no interactions, completely renally excreted  Indication:  Protective analgesia  Neuropathic pain treatment (NNT = 4.7)  SE: sedation, dizziness, ataxia, tremor  NNH minor = 4, NNH major =12-18  COST!  Doses:  Pre-op: 600-1200mg (1-2 hours pre-op)  Post-op “prophylaxis”: 100-300mg TDS (? 2 weeks)  Post-op “treatment”: 100-900mg TDS (usu 300-600mg tds) Dahl JB, Mathiesen O, Moiniche S. ‘Protective premedication’: an option with gabapentin and related drugs? A review of gabapentin and pregabalin in the treatment of post-operative pain. Acta Anaesthesiol Scand 2004; 48: 1130—1136 Hurley RW, Cohen SP, Williams KA, Rowlingson AJ, Wu CL. The Analgesic Effects of Perioperative Gabapentin on Postoperative Pain: A Meta-Analysis. Reg Anesth Pain Med 2006;31:237-247.
  33. 33. Pregabalin  Very similar to gabapentin  More reliable oral absorption  Slightly different side effect profile  Doses: 75-300mg BD
  34. 34. Other Anticonvulsants  Effective (NNT 2-3) but less “user friendly”  Most have uncommon but serious SE (eg. aplastic anaemia, hepatotoxicity, Stevens- Johnson syndrome etc)  NNH minor = 3, NNH major = 16 - 24  Consider  Carbamazepine 100mg BD (↑ to 400mg bd/tds)  Valproate 200mg BD (↑ to 1000-2000mg/d)  Phenytoin 100mg nocte (↑ to 500mg/d) Finnerup NB, Otto M, McQuay HJ, Jensen TS, Sindrup SH. Algorithm for neuropathic pain treatment: An evidence based proposal. Pain 118 (2005) 289–305
  35. 35. Topical vs Transdermal Drug Delivery Systems Systemic activity Applied away from painful site Serum levels necessary Systemic side effects Peripheral tissue activity Applied directly over painful site Insignificant serum levels Systemic side effects unlikely Topical (lidocaine patch 5%) Transdermal (fentanyl patch)
  36. 36. Lidocaine Patch 5%  Lidocaine 5% in pliable patch  Up to 3 patches applied once daily directly over painful site  12 h on, 12 h off (FDA-approved label)  recently published data indicate 4 patches (18–24 h) safe  Efficacy demonstrated in 3 randomized controlled trials on postherpetic neuralgia  Drug interactions and systemic side effects unlikely  most common side effect: application-site sensitivity  Clinically insignificant serum lidocaine levels  Mechanical barrier decreases allodynia
  37. 37. Lidocaine  Action: Na+ channel block  Indication: peripheral NP, ? others  Useful IV or topical (NNT = 4.4)  No reliable oral equivalent (mexiletine NNT = 10)  SE: similar rates to placebo for sedation, N/V, pruritis etc  CNS toxicity at plasma levels > 5 mcg/ml  Dose: IV 1-2 mg/kg/hr (??duration)  Patches available in USA, ?EMLA here Challapalli V, Tremont-Lukats IW, McNicol ED, Lau J, Carr DB. Systemic administration of local anesthetic agents to relieve neuropathic pain. Cochrane Database of Systematic Reviews 2005, Issue 4.
  38. 38. Ketamine  Action: NMDA receptor antagonist  ‘anti-hyperalgesic', 'anti-allodynic' and 'tolerance- protective' agent  Indication: Protective analgesia, NP treatment, opioid- tolerant patients  SE: Dysphoria, nightmares, “psychedelic” effects  Dose: Low doses usually well tolerated  Intra-op: 0.5mg/kg bolus then 0.25-0.5 mg/kg/hr (beware prolonged recovery)  Post-op: 0.1-0.2 mg/kg/hr (?duration) Himmelseher S, Durieux ME. Ketamine for Perioperative Pain Management. Anesthesiology 2005; 102:211–20 Australian and New Zealand College of Anaesthetists and Faculty of Pain Medicine. Acute Pain Management: Scientific Evidence, 2nd Ed. Australian and New Zealand College of Anaesthetists, Melbourne, Australia, 2005; 143-144
  39. 39. Principles of Opioid Therapy for Neuropathic Pain  Opioids should be titrated for therapeutic efficacy versus AEs  Fixed-dose regimens generally preferred over prn regimens  Document treatment plan and outcomes  Consider use of opioid written care agreement  Opioids can be effective in neuropathic pain  Most opioid AEs controlled with appropriate specific management (eg, prophylactic bowel regimen, use of stimulants)  Understand distinction between addiction, tolerance, physical dependence, and pseudoaddiction
  40. 40. Opioids  A select group of pain patients benefits from opioids, with resultant pain reduction and improved physical and psychological functioning  They have minimal side effects & show increased activity levels & less pain  Other patients do poorly with opioids, experiencing tolerance and side effects, especially with escalating doses
  41. 41. Distinguishing Dependence, Tolerance, and Addiction  Physical dependence: withdrawal syndrome arises if drug discontinued, dose substantially reduced, or antagonist administered  Tolerance: greater amount of drug needed to maintain therapeutic effect, or loss of effect over time  Pseudoaddiction: behavior suggestive of addiction; caused by undertreatment of pain  Addiction (psychological dependence): psychiatric disorder characterized by continued compulsive use of substance despite harm
  42. 42. Opioids  Action: ↓ NT release, ↓ cell excitability  Indications: Any NP  Oxycodone, morphine (NNT = 2.5)  Tramadol (NNT = 3.9)  SE: usual, and ?OIH  Doses: usual  ? Stay below 100-200mg/d PO Morphine equivalent (ie. 30-60mg/d IV)  ? methadone & buprenorphine less hyperalgesic Finnerup NB, Otto M, McQuay HJ, Jensen TS, Sindrup SH. Algorithm for neuropathic pain treatment: An evidence based proposal. Pain 118 (2005) 289–305
  43. 43. Antidepressants in Neuropathic Pain Disorders*  Multiple mechanisms of action  Randomized controlled trials and meta-analyses demonstrate benefit of tricyclic antidepressants (especially amitriptyline, nortriptyline, desipramine) for postherpetic neuralgia and diabetic neuropathy  Onset of analgesia variable  analgesic effects independent of antidepressant activity  Improvements in insomnia, anxiety, depression  Desipramine and nortriptyline have fewer adverse effects *Not approved by FDA for this use.
  44. 44. Tricyclic Antidepressants: Adverse Effects  Commonly reported AEs (generally anticholinergic):  blurred vision  cognitive changes  constipation  dry mouth  orthostatic hypotension  sedation  sexual dysfunction  tachycardia  urinary retention  Desipramine  Nortriptyline  Imipramine  Doxepin  Amitriptyline Fewest AEs Most AEs AEs = adverse effects.
  45. 45. Tricyclic Antidepressants  Action: Mixed (↑ 5-HT &/ Norad at synapse)  Indication:  All NP treatment (except SCI, PLP, HIV)  NNT: overall = 3.1, central = 4.0, periph = 2.3  PHN prevention: 50% ↓ if used for 90days  SE: dizzy, sedation, anticholinergic  NNH minor = 5, NNH major = 16  Doses  Amitriptylline 10-25mg nocte, max 100mg  Nortriptylline (?less sedating) same doses Finnerup NB, Otto M, McQuay HJ, Jensen TS, Sindrup SH. Algorithm for neuropathic pain treatment: An evidence based proposal. Pain 118 (2005) 289–305
  46. 46. Venlafaxine  Action: SNRI  Indication:  mastectomy pain prophylaxis,  peripheral NP treatment (NNT=5.5)  SE: sedation/insomnia, ataxia, ↑BP, nausea  NNH major = not significant  Doses  Protective 75mg/d (pre-op then for 2wks)  Treatment: 37.5-375mg/d Reuben SS, Makari-Judson G, Lurie SD. Evaluation of efficacy of the perioperative administration of venlafaxine XR in the prevention of postmastectomy pain syndrome. J Pain Symptom Manage. 2004; 27: 133-39.
  47. 47. Calcitonin  Action: uncertain  Indication: PLP, CRPS, ?other NP  SE: N/V, flushing, dizzy, allergy  Skin prick test advised  Dose: 100 IU in 100ml saline over 1hr  Pre-treat with anti-emetics  Repeat daily for 3 days Visser EJ. A review of calcitonin and its use in the treatment of acute pain. Acute Pain 2005;7 :185-189.
  48. 48. Interventional Treatments for Neuropathic Pain  Neural blockade  sympathetic blocks for CRPS-I and II (reflex sympathetic dystrophy and causalgia)  Neurolytic techniques  alcohol or phenol neurolysis  pulse radio frequency  Stimulatory techniques  spinal cord stimulation  peripheral nerve stimulation  Medication pumps CRPS = complex regional pain syndrome.
  49. 49. Summary of Advances in Treatments for Neuropathic Pain*  Botulinum toxin: low back pain  Lidocaine patch 5%: low back pain, osteoarthritis, diabetic and HIV-related neuropathy, with gabapentin  CR oxycodone: diabetic neuropathy  Gabapentin: HIV-related neuropathy, diabetic peripheral neuropathy, others  Levetiracetam: neuropathic pain and migraine  Oxcarbazepine: neuropathic pain; diabetic neuropathy  Bupropion: neuropathic pain  Transdermal fentanyl: low back pain *Applications not approved by FDA.
  50. 50. CURRENT MANAGEMENT NON PHARMACOLOGIC  EXERCISE  TENS  PENS  GRADED MOTOR IMAGERY  CBT
  51. 51. World Health Organization (WHO) Analgesic Ladder.
  52. 52. INTERVENTIONAL PAIN MANAGEMENT  Epidural or Perineural injections of local anesthetics or cortico steroids.  Implantations of epidural and intrathecal drug delivery systems.  Neural ablative procedures.  Insertion of spinal cord stimulators.  Sympathetic nerve blocks.
  53. 53. Treatment Goals - I  Reduce and manage pain  Decreased subjective pain reports  Decreased objective evidence of disease  Optimize medication use  Increase function & productivity  Restore life activities  Increase psychological wellness  Reduce level of disability
  54. 54. Treatment Goals - II  Stop cure seeking  Reduce unnecessary health care  Prevent iatrogenic complications  Improve self-sufficiency  Achieve medical stabilization  Prevent relapse / recidivism  Minimize costs - maintain quality  Return to gainful employment
  55. 55. Chronic Pain Evaluations  Comprehensive multidisciplinary evaluations offers a means of developing an appropriate treatment plan  This can help identify factors which may prolong complaints of pain and disability despite traditional medical care  Such an evaluation can also identify who would benefit from a more structured and intensive functional restoration program
  56. 56. Measuring Opioid Usefulness  Each individual with chronic pain should be viewed as unique and the ultimate outcome of the use of opioid medication must be viewed in terms of  Pain relief  Objective gains (function or increased activity)  Does taking an opioid allow the person to be happier and do more things without unacceptable side effects or do the medications only create more problems and no observable change in activity level?
  57. 57. Adjunctive Treatment Modalities  Joint, bursal & trigger point injections  Botulinum toxin injections  Nerve root and sympathetic blocks  Peripheral and plexus blocks  Facet and medial branch injections  Lidocaine infusions  Epidurals  Neuroablative techniques  Chemical, Thermal, & Surgical  Neuromodulation  Spinal cord stimulators & Implanted spinal pumps
  58. 58. Physical & Occupational Therapy  Active  Improved body mechanics  Spine stabilization  Stretching & strengthening  Aerobic conditioning  Aquatics therapy  Work hardening  Self-directed fitness program
  59. 59. Psychological Approaches  Non-drug pain management skills  Anxiety & depression reduction  Biofeedback, relaxation training, stress reduction skills, mindfulness meditation, & hypnosis  Cognitive restructuring  Improve coping skills  Learn activity pacing  Habit reversal  Maintenance and relapse prevention
  60. 60. Functional Restoration  Locus of control issues  Timely and accurate diagnosis  Assessment of psychosocial strengths and weaknesses including analysis of support system  Evaluation of physical and functional capacity  Treatment planning and functional goal setting for return to life and work activities  Active physical rehabilitation  Cognitive behavioral treatment  Patient and family education  Frequent assessment of compliance and progress
  61. 61. 61 Facial Nerves and Pain  Trigeminal nerve  Largest of 12 cranial nerves  Three major branches  Ophthalmic nerve  Sensory information (tactile, thermoception, nociception, proprioception) from green areas, nasal mucosa,and frontal sinuses  Maxillary nerve  sensory information from pink areas, nasal mucosa, palate, ethmoid and sphenoid sinuses  Mandibular nerve  Sensory input from yellow areas, floor of the mouth, and anterior 2/3 of tongue  Motor control of muscles involved in biting, chewing, and swallowing
  62. 62. 62 Neural Mechanisms of Pain  Gate Control Theory  Melzack and Wall (1965)  Perception of pain mediated by a “gate” located in the dorsal horn of the spinal cord SG- SG+ T cell L-fibers mediating tactile perception (A-α and A-β) S-fibers mediating pain perception (A- δ and C) PAIN Central Control closes gate opens gate - + + + + +
  63. 63. 63 Experimental Evidence for the Gate  Selective inactivation of L- fibers results in greater pain perception from noxious stimuli (Price, Hi, and Dubner, 1977)  Phantom Limb Pain may result from reduced L-fiber input (Melzack, 1970) SG- SG+ T cell L-fibers mediating tactile perception (A-α and A-β) S-fibers mediating pain perception (A- δ and C) PAIN Central Control closes gate opens gate - + + + + +
  64. 64. 64 Endorphins and Pain  Endorphins: neurotransmitters that act as endogenous (naturally-occurring) morphine-like substances  Endorphins bind to same receptor sites in brain stem as opiates  SPA works best when endorphin sites are stimulated— may release endorphins into the nervous system (Hosubuchi et al., 1977)
  65. 65. 65 Endorphins and Pain  Concentration of endorphins is generally less for people suffering from chronic pain (Akil et al., 1978)  Opiate inhibitors (e.g., naloxone) decrease the analgesic effects of acupuncture, SPA, and placebos  Stress-induced analgesia may result from increased release of endorphins during stress
  66. 66. Nociceptors in Skin Epidermi s Dermis Free Nerve Endings
  67. 67. Pain Pathways  Lots of effort to id neural pathways  Found distinct categories of nerve fibres  A δ : mylinated, carry rapidly sharp pains (20- 30 ms-1 )  C : unmylinated, carry slowly burning pain (0.5- 2 ms-1 )
  68. 68. Associated Area of Brain Fibres pass signals up spinal cord as electrical impulses then onto the thalamus Thalamus relays messages to cortex Proved difficult to id. specific area of the cortex that produce pain
  69. 69. Gate Control Theory (Melzack & Wall, 1965) A gate in the substantia gelatinosa of the dorsal horn can be open or closed, blocking pain information. The gate can be closed by descending signals from the brain, or by the balance of activity in A-beta fibres (large myelinated) and C fibres (small non-myelinated)  A-beta fibres produce touch sensations  C fibres produce dull diffuse pain. Greater activity in A-beta fibres closes the gate, greater activity in C fibres opens it.  Other factors influencing the gate include  Attention  Emotional & Cognitive factors  Physical factors Some forms of analgesia, e.g. TENS & acupuncture, might be accommodated within gate control theory.
  70. 70. Gate Control Theory - Melzack & Hall (1965) Experience Behaviour Tissue damage Gate – amplifies or attenuates signal Pain Perception Emotion
  71. 71. Opening & Closing the Gate Factor Opens Closes Physical injury agitation medication Emotional anxiety stress frustration depression tension relaxation optimism happiness Behavioural (Cognitive) rumination boredom enjoyable activities complex tasks distraction social interaction
  72. 72. Problems for Gate Control Theory  Evidence for propsed moderators, but no physical evidence of gate  Still organic basis for pain (phantom limb?)  Not truly integrative re: psyche & soma  Still improvement on stimulus-response paradigm
  73. 73. Subsequent Pain Theories  Reflect trends in general psychology  Fordyce (1976) - pain as behaviour  Reinforcement contingencies  +ve reinforcement (e.g. attention / affection for pain behaviours)  -ve reinforcement (e.g. avoid unpleasant events such as work, school)  Recently, growth in cognitive behaviour models
  74. 74. Fear-Avoidance Theory  (-ve) appraisals (catastrophising) → fear of pain (illness cognitions) & re-injury  Fear of pain → avoidance of potentially painful events (illness behaviour)  Little opportunity to disconfirm beliefs  Avoidance → disuse syndrome & ↑ p (mood problems)
  75. 75. Treatments  Mirror pain theories  Medical (especially acute pain)  Non-anti-inflammatory non-steroid (paracetamol)  Anti-inflammatory non-steroids (eg ibprofen)  Opioids (eg morphine)  Psychological  Behavioural initially
  76. 76. Treatment of Chronic Pain  Surgical procedures to block the transmission of pain from the peripheral nervous system to the brain.  Synovectomy – Removing membranes that become inflamed in arthritic joints.  Spinal fusion – joins two or more adjacent vertebrae to treat chronic back pain.
  77. 77. Psychological Pain Control Methods  Biofeedback – provides biophysiological feedback to patient about some bodily process the patient is unaware of (e.g., forehead muscle tension).  Relaxation – systematic relaxation of the large muscle groups.  Hypnosis – relaxation + suggestion + distraction + altering the meaning of pain.
  78. 78. Psychological Pain Methods  Acupuncture – not sure how it works. Could include:  Counter-irritation – may close the spinal gating mechanism in pain perception.  Expectancy  Reduced anxiety from belief that it will work.  Distraction  Trigger release of endorphins
  79. 79. Phantom Limb pain  Affects the majority of amputees  For most the sensation fades, but a minority experience lasting discomfort.  Theories  Neuroma  Deafferented spinal neurons  Melzack (1992) Neuromatrix innate linkage between sensation, emotion and self-recognition.  Merzenich (1998) Cortical remapping & unmasking Ramachandran (1992) phantom leg sensations often referred from the chest, phantom arm sensations from the face.
  80. 80. Phantom limb pain: during amputation under general anesthesia the spinal cord can still “experience” the insult produced by the surgical procedure and central sensitization occurs. To try to prevent it, local infiltration of anesthetics in the site of surgery. But studies show also rearrangement of cortical circuits (cortical region of the missing limb receives afferents from other site of the skin) Phantom Pain intensity as a function of Cortical Reorganization.
  81. 81. Analgesia Peripheral via prostaglandin synthesis inhibition (e.g. Asprin) Central via receptors for endogenous opioids. Bind to receptors in the periaqueductal gray, which activate descending serotoninergic fibres. These inhibit pain transmission Endogenous opioids also underlie some psychological influences. Naloxone blocks both TENS and placebo analgesia
  82. 82. PAIN TREATMENT CONTINUUM Diagnosis Oral Medications PT, Exercise, Rehabilitation Behavioral Medicine Corrective Surgery Therapeutic Nerve Blocks Oral Opiates Implantable Pain Management Devices Neurostimulation Intrathecal Pumps Neuroablation
  83. 83. Multi-Disciplinary Pain Program Models  Pain Consultation Team  Multidisciplinary Programs  Multidisciplinary Outpatient Programs  Multidisciplinary Inpatient Programs  Pain Service
  84. 84. Pain Consultation Team  Multidisciplinary group  Provides consultation services only  not ongoing treatment Anesthesiology Psychology Neurology Pharmacy Nursing Consultation Team Referral Recommendatio n
  85. 85. Multidisciplinary Clinics  Comprised of 2 or more disciplines  Goal is to provide coordinated and more comprehensive care to patients for more complex chronic pain problems  3 general subtypes  Psychoeducational clinic (mild and motivating)  Problem-based clinic (e.g. headache, LBP, FM)  Comprehensive multidisciplinary clinic  Inpatient or outpatient
  86. 86. Chronic Pain Disciplines and Roles (Core) Anesthesiology – nerve blocks Kinesiotherapy – pool therapy; activity Neurology – eval. treatment Nursing – patient care Physical Medicine – exercise; modalities Physical Therapy – exercise; modalities Psychology – eval. and treatment Occupational Therapy – UE eval and treatment
  87. 87. •Rheumatoid and Osteo-arthritis •Back pain •Menstrual Pain •Labour Pain •Peripheral Nerve Injuries •Shingles •Headache and Migraine •Cancer Pain •Trigeminal Neuralgia •Phantom Limb Pain •Sports Injuries •Sciatica •Aching Joints •Post Operative Pain •Muscular Pain •Whiplash and Neck Injury and many others                                                   
  88. 88. Decrease Inflammatory Response NSAIDs, Local Anesthetics, Steroids Decrease Conduction Gabapentin, Carbamazepine, Local Anesthetics, Opioids Prevent Centralization COX 2, Opioids, Ketamine, α-2 Agonists. Increase Inhibition TCA’s, SSRI’s, Clonidine Modify Expression Anxiolytics Mechanistic Approach To Pain Therapy
  89. 89. Summary  Chronic neuropathic pain is a disease, not a symptom  “Rational” polypharmacy is often necessary  combining peripheral and central nervous system agents enhances pain relief  Treatment goals include:  balancing efficacy, safety, and tolerability  reducing baseline pain and pain exacerbations  improving function and QOL  New agents and new uses for existing agents offer additional treatment options
  90. 90. Further Reading  Rosenzweig et al. cover pain in the second half of chapter eight.  Horne, S. & Munafo, M. (1997). Pain, theory, research and intervention. Oxford University Press  Wall, P. & Melzack, R. (1988). The challenge of Pain. Penguin.
  91. 91. REFERENCES  Review Neuropathic pain: a practical guide for the clinician ; Ian Gilron, C. Peter N. Watson, Catherine M. Cahill and Dwight E. Moulin  Dworkin RH, Backonja M, Rowbotham MC, et al. Advances in neuropathic pain. Arch Neurol 2003;60:1524-34.  Gilron I, Bailey JM, Tu D, et al. Morphine, gabapentin, or their combination for neuropathic pain. N Engl J Med 2005;352:1324-34.  Stephen Macres, Understanding Neuropathic Pain  Eisenberg E, McNicol ED, Carr DB. Efficacy and safety of opioid agonists in the treatment of neuropathic pain of nonmalignant origin. JAMA 2005;293:3043-52.
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