Chronic Pain as a Disease State
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Presented by Dr.Perry Fine at Pain Management for the Elderly Course, 2010. Scribe medical events Egypt. www.scribeofegypt.org
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Chronic Pain as a Disease State
- 1. Chronic Pain as a Disease State Perry G. Fine, MD Professor of Anesthesiology Pain Research Center School of Medicine University of Utah Salt Lake City, Utah
- 2. Disease An impairment of health or condition of abnormal functioning. 2
- 3. Adapted from: Loeser J, et al. Bonica's Management of Pain. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins. 2001;241-254. Nociception Pain Perception Suffering Pain Behavior The Complex Nature of Pain 3
- 4. Therapeutic Approaches to Pain as a Disease State Pharmacotherapy Opioids, nonopioids, adjuvant analgesics Interventional Approaches Injections, neurostimulation Psychological Support Psychotherapy, group support Lifestyle Change Exercise, weight loss Complementary and Alternative Medicine Massage, supplements Physical Medicine and Rehabilitation Assistive devices, electrotherapy Fine PG, et al. J Support Oncol. 2004;2(suppl 4):5-22; Portenoy RK, et al. In: Lowinson JH, et al, eds. Substance Abuse: A Comprehensive Textbook. 4th ed. Philadelphia, PA: Lippincott, Williams & Wilkins; 2005:863-903.
- 5. Physiology of Pain Perception • Transduction • Transmission • Modulation • Perception • Interpretation • Behavior Injury Descending Pathway Peripheral Nerve Dorsal Root Ganglion C-Fiber A-β Fiber A-δ Fiber Ascending Pathways DH Brain Spinal Cord 5 DH = dorsal horn.
- 6. A. Nociceptive Pain B. Inflammatory Pain C. Neuropathic Pain D. Noninflammatory/ Nonneuropathic Pain Noxious Peripheral Stimuli Peripheral nerve damage No known tissue or nerve damage Abnormal central processing Multiple mechanisms Brain Brain Brain Brain Inflammation Multiple Types of Pain 1. Adapted from: Woolf CJ. Ann Intern Med. 2004;140:441-451. 2. Chong MS, Bajwa ZH. J Pain Symptom Manage. 2003;25:S4-S11. • Patients may experience multiple pain states simultaneously2 6
- 7. Neuroplasticity in Pain Processing1,2 1. Woolf CJ, Salter MW. Science. 2000;288:1765-1769. 2. Basbaum AI, Jessell TM.Principles of Neural Science. 4th ed. New York, NY: McGraw-Hill. 2000;473-490. 3. Cervero F, Laird JM. Pain. 1996;68:13-23. Stimulus Intensity 100 Injury Normal Allodynia Hyperalgesia3 80 60 40 20 0 Innocuous Noxious PainSensation 7
- 8. Neuroplasticity in Spinal Cord Processing: Central Sensitization • Definition: Heightened dorsal horn excitability due to increased peripheral nociceptor activity • Features of central sensitization1: − Reduced threshold for dorsal horn neuron activation − Increased receptive field of dorsal horn neurons − Increased response of dorsal horn neurons to painful stimuli • Potential mechanisms implicated in central sensitization: − NMDA-receptor activation1 − Altered gene expression in dorsal horn neurons1 − Decreased inhibition2 − Microglial activation3 − Thalamic and somatosensory cortex changes4 NMDA = N-methyl-D-aspartic acid. 1. Mannion RJ, Woolf CJ. Clin J Pain. 2000;16:S144-S156. 2. Ossipov MH, et al. Ann N Y Acad Sci. 2000;909:12-24. 3. Wieseler-Frank J, et al. Neurosignals. 2005;14:166-174. 4. Guilbaud G, et al. Exp Brain Res. 1992;92:227-245. 8
- 9. ACC = anterior cingulate cortex. PFC = prefrontal cortex. Brain image courtesy of ATI. Apkarian AV, et al. Eur J Pain. 2005;9:463-484. PFCSomatosensory Cortex Thalamus ACC Insular Cortex Brain Regions Involved in Pain Processing Amygdala 9
- 10. Allodynia Activates Some of the Regions in the Pain Circuit S1, S2 = primary, secondary somatosensory cortices. Moisset X, Bouhassira D. Neuroimage. 2007;37:S80-S88. Baliki MN, et al. Curr Pain Headache Rep. 2007;11:171-177. Thalamus S1 S2 InsulaACC PFC 10
- 11. Neuroplasticity: Neural Reorganization Modulation Axotomy CTB = cholera toxin B. Photo courtesy of Professor S.B. McMahon. 11 C fiber terminals in laminae I/II Aβ fiber terminals in laminae III-VI
- 12. The Role of Microglia • The Journal of Neuroscience, February 28, 2007, 27(9):2357- 2368; doi:10.1523/JNEUROSCI.0138-07.2007This Article Neurobiology of Disease Extracellular Signal-Regulated Kinase-Regulated Microglia–Neuron Signaling by Prostaglandin E2 Contributes to Pain after Spinal Cord Injury • Peng Zhao, Stephen G. Waxman, and Bryan C. Hains • We recently showed that microglia become activated after experimental SCI and dynamically maintain hyperresponsiveness of spinal cord nociceptive neurons and pain-related behaviors.
- 13. Block et al. Nature Reviews Neuroscience 8, 57–69 (January 2007) | doi:10.1038/nrn2038
- 14. Brain Changes with Chronic Pain CBP = chronic back pain. Baliki MN, et al. J Neurosci. 2008;28:1398-1403. 14
- 15. Dorsal Horn BRAIN The Current Analgesic Formulary Descending Modulation Peripheral Sensitization Central Sensitization PNS Local anesthetics Topical analgesics Anticonvulsants Tricyclic antidepressants Opioids Anticonvulsants Opioids NMDA-receptor antagonists Tricyclic/SNRI antidepressants Anticonvulsants Opioids Tricyclic/SNRI antidepressants Dual mechanism opioid/mono- amine uptake inhbitors SPINAL CORD CNS 15 PNS = peripheral nervous system. SNRI = serotonin-norepinephrine reuptake inhibitor.
- 16. Peripheral Nociceptor Hyperexcitability and Sensitization Mechanisms Symptoms Targets Hyperexcitability Ectopic impulse generation; oscillations in dorsal root ganglion Spontaneous pain (shooting) Sodium channels Sensitization: Inflammation within nerves Cytokine release Spontaneous pain (ongoing) Cytokines Sensitization: Reduced activation threshold Reduced threshold to heat or cold Heat allodynia or cold allodynia TRPV1 receptor or TRPM8 receptor Reduced threshold to mechanical stimuli Static mechanical allodynia ASIC receptor Reduced threshold to histamine or norepinephrine Sympathetically maintained pain Histamine H1 receptors or α receptors ASIC = acid-sensing ion channel. TCA = tricyclic antidepressant. TNF- α = tumor necrosis factor- α. TRPM8 = transient receptor potential cation channel, subfamily M, member 8. TRPV1 = transient receptor potential vanilloid 1. Adapted from: Baron R. Nat Clin Pract Neurol. 2006;2:95-106. Mendell JR, Sahenk Z. N Engl J Med. 2003;348:1243-1255. Woolf CJ, Mannion RJ. Lancet. 1999;353:1959-1964. 16
- 17. GABA-ergic or opioidergic interneurons decreased Spontaneous pain (ongoing), dynamic mechanical allodynia, punctate mechanical hyperalgesia Amplification of C-fiber input, gating of Aβ-fiber and Aδ-fiber input Spontaneous pain (ongoing), dynamic mechanical allodynia, punctate mechanical hyperalgesia Central Dorsal Horn Hyperexcitability Mechanisms Symptoms Targets Central sensitization, increased synaptic transmission Amplification of C-fiber input, gating of Aβ-fiber and Aδ-fiber input Spontaneous pain (ongoing), dynamic mechanical allodynia, punctate mechanical hyperalgesia µ receptors, calcium channels (α2-δ), NMDA-receptors, NK1 receptors, sodium channels, intracellular cascades Intraspinal inhibitory interneurons decreased GABA-ergic or opioidergic interneurons decreased Spontaneous pain (ongoing), dynamic mechanical allodynia, punctate mechanical hyperalgesia GABAB receptors or µ receptors Changes in supraspinal descending modulation Inhibitory control (5-HT, noradrenaline) decreased Spontaneous pain (ongoing), dynamic mechanical allodynia, punctate mechanical hyperalgesia 5-HT receptors, α2 receptors α2 = alpha 2 adrenergic receptor. GABAB = gamma-aminobutyric acid receptor – subtype B. NK-1 = neurokinin. 5-HT = 5-hydroxytryptamine (serotonin) receptor. Adapted from: Baron R. Nat Clin Pract Neurol. 2006;2:95-106. Mendell JR, Sahenk Z. N Engl J Med. 2003;348:1243-1255. Woolf CJ, Mannion RJ. Lancet. 1999;353:1959-1964. 17
- 18. Pain as a Disease “When we wish to perfect our senses, neuroplasticity is a blessing; when it works in the service of pain, plasticity can be a curse” ―Norman Doidge, MD Doidge N. The Brain That Changes Itself: Stories of Personal Triumph from the Frontiers of Brain Science. New York, NY. Viking Press. 2007;177-195. 18