Biopsychosocial pain 2019
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Pain is a common yet complex biopsychosocial phenomenon that affects every aspect of a patient’s life Optimal management often requires good assessment, formulation of the problem in the patient, and combining pharmacological and non-pharmacological (psychological and social) interventions
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Biopsychosocial pain 2019
- 1. DR MARY CARDOSA PAIN SPECIALIST, HOSPITAL SELAYANG, MALAYSIA 1 UNDERSTANDING PAIN: A BIOPSYCHOSOCIAL APPROACH mary.cardosa@gmail.com
- 2. Acknowledgement • This talk was adapted from kNOw Pain, an educational program developed by Pfizer • 2
- 3. What is pain? An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage. International Association for the Study of Pain. IASP Taxonomy. Available at: http://www.iasp-pain.org/AM/Template.cfm?Section=Pain_Definitions. Accessed: July 15, 2013. International Association for the Study of Pain (IASP) 2011
- 4. Pain Is the 5th Vital Sign Phillips DM. JAMA 2000; 284(4):428-9.
- 5. Overview of Pain Costigan M et al. Annu Rev Neurosci 2009; 32:1-32; Wells N et al. In: Hughes RG (ed). Patient Safety and Quality: An Evidence-Based Handbook for Nurses. Agency for Healthcare Research and Quality; Rockville, MD: 2008; Woolf CJ et al. Ann Intern Med 2004; 140(6):441-51.
- 6. Cancer pain Pain Chronic painAcute pain Nociceptive pain Neuropathic pain Widespread pain Non-Cancer pain
- 7. Acute Pain Vs Chronic Pain • Acute pain is pain due to tissue injury e.g. trauma, surgery. • Pain goes away when the tissue injury heals. • Analgesia should be stopped when there is no more pain.
- 8. Acute Pain Vs Chronic Pain • Chronic pain is defined as ‘pain that persists for three months or more, or beyond normal tissue healing time’ • Can be due to cancer or non-cancer causes
- 9. The Pain Continuum Time to resolution Acute pain Chronic pain Chapman CR, Stillman M. In: Kruger L (ed). Pain and Touch. Academic Press; New York, NY: 1996; Cole BE. Hosp Physician 2002; 38(6):23-30; International Association for the Study of Pain. Unrelieved Pain Is a Major Global Healthcare Problem. Available at: http://www.iasp-pain.org/AM/Template.cfm?Section=Press_Release&Template=/CM/ContentDisplay.cfm&ContentID=2908. Accessed: July 24: 2013; National Pain Summit Initiative. National Pain Strategy: Pain Management for All Australians. Available at: http://www.iasp-pain.org/PainSummit/Australia_2010PainStrategy.pdf. Accessed: July 24, 2013; Turk DC, Okifuji A. In: Loeser D et al (eds.). Bonica’s Management of Pain. 3rd ed. Lippincott Williams & Wilkins; Hagerstown, MD: 2001. Insult Normal, time-limited response to ‘noxious’ experience (less than 3 months) Pain that has persisted beyond normal tissue healing time (usually more than 3 months) • Usually obvious tissue damage • Serves a protective function • Pain resolves upon healing •Usually has no protective function •Degrades health and function Acute pain may become chronic
- 10. Freynhagen R, Baron R. Curr Pain Headache Rep 2009; 13(3):185-90; Jensen TS et al. Pain 2011; 152(10):2204-5; Julius D et al. In: McMahon SB, Koltzenburg M (eds). Wall and Melzack’s Textbook of Pain. 5th ed. Elsevier; London, UK: 2006; Ross E. Expert Opin Pharmacother 2001; 2(1):1529-30; Webster LR. Am J Manag Care 2008; 14(5 Suppl 1):S116-22; Woolf CJ. Pain 2011; 152(3 Suppl):S2-15. Multiple types of pain coexist in many conditions (mixed pain) Nociceptive pain -Somatic -Visceral Neuropathic pain -Peripheral -Central Central sensitization/ dysfunctional pain Pathophysiological Classification of Pain
- 11. What is nociceptive pain? Felson DT. Arthritis Res Ther 2009; 11(1):203; International Association for the Study of Pain. IASP Taxonomy. Available at: http://www.iasp-pain.org/AM/Template.cfm?Section=Pain_Definitions. Accessed: July 15, 2013; McMahon SB, Koltzenburg M (eds). Wall and Melzack’s Textbook of Pain. 5th ed. Elsevier; London, UK: 2006; Woolf CJ. Pain 2011;152(3 Suppl):S2-15.
- 12. Nociceptive Pain Fishman SM et al (eds). Bonica’s Management of Pain. 4th ed. Lippincott, Williams and Wilkins; Philadelphia, PA: 2010. Trauma Burn pain Musculoskeletal injury Post-operative pain Infection, e.g., pharyngitis Ischemic, e.g., myocardial infarction Abdominal colic Dysmenorrhea Somatic Visceral
- 13. What is neuropathic pain? Chong MS, Bajwa ZH. J Pain Symptom Manage 2003; 25(5 Suppl):S4-11; Cruccu G et al. Eur J Neurol 2004; 11(3):153-62; Dray A. Br J Anaesth 2008; 101(1):48-58; International Association for the Study of Pain. IASP Taxonomy. Available at: http://www.iasp- pain.org/AM/Template.cfm?Section=Pain_Definitions. Accessed: July 15, 2013; McMahon SB, Koltzenburg M (eds). Wall and Melzack’s Textbook of Pain. 5th ed. Elsevier; London, UK: 2006; Woolf CJ. Pain 2011;152(3 Suppl):S2-15.
- 14. Recognizing Neuropathic Pain Common descriptors Shooting Electric shock-like Burning Tingling Numbness Postherpetic neuralgia Lumbar radicular pain Chronic post-surgical pain Post-stroke pain Diabetic peripheral neuropathy 1. Baron R et al. Lancet Neurol 2010; 9(8):807-19.
- 15. PAIN PHYSIOLOGY: HOW DO PAIN SIGNALS GET TO THE BRAIN? 15
- 16. Nociceptive afferent fiber Noxious stimuli Transmission Ascending input Spinal cord Transduction Conduction Thalamus Scholz J, Woolf CJ. Nat Neurosci 2002; 5(Suppl):1062-7. Perception Pain pathway Somatosensory cortex Descending modulation Consequences of encoding may be autonomic (e.g., elevated blood pressure) or behavioral (motor withdrawal reflex or more complex nocifensive behavior). Pain perception is not necessarily implied.
- 17. Pain Modulation Descending modulation Ascending input Spinal cord • Pain is modulated via ascending nociceptive and descending inhibitory/facilitatory spinal tracts Ascending Nociceptive Descending Inhibitory/facilitatory C fibers Aδ fibers Serotonin Norepinephrine Dopamine Brain Benarroch EE. Neurology 2008 ; 71(3):217-21; Fields HL et al. In: McMahon SB, Koltzenburg M (Eds). Wall and Melzack’s Textbook of Pain. 5th ed. Elsevier; London, UK: 2006; Scholz J, Woolf CJ. Nat Neurosci 2002; 5(Suppl):1062-7.
- 18. Pain Perception • Spinal cord transmits pain signals to specific nuclei in the thalamus, and from there to wide variety of regions in the brain – collectively known as the “pain matrix” • Pain perception can also be altered without any external stimuli (i.e., through emotion, distraction, placebo, etc.) Tracey A, Dickenson A. Cell 2012; 148(6):1308-e2. Brain matrix Perception
- 19. Biopsychosocial Model of Pain Gatchel RJ et al. Psychol Bull 2007; 133(4):581-624. PsychoSocial Bio
- 20. Pain What the patient says hurts. What must be treated. Injury Beliefs/concerns about pain Psychol. factors anxiety/anger/depression Cultural issues Language, expectations Other illnesses Coping strategies Social factors e.g. family, work Nociception is not the same as pain! Modified from Analgesic Expert Group. Therapeutic Guidelines 20075.5 BIO-PSYCHO-SOCIAL MODEL OF PAIN
- 21. Are these men feeling pain?
- 22. General principles of pain management 22
- 24. Pain History Worksheet • P = Place (Site) of pain • A = Aggravating factors • I = Intensity (Pain score) • N – Nature / Neutralizing factors Ayad AE et al. J Int Med Res 2011; 39(4):1123-41.
- 25. Pain Assessment • Make a pain diagnosis • Acute/chronic • Cancer/non-cancer • Nociceptive / neuropathic • Determine the underlying cause (if any) e.g. trauma, cancer, nerve damage, degenerative disease, diabetic neuropathy etc Forde G, Stanos S. J Fam Pract 2007; 56(8 Suppl Hot Topics):S21-30; Sokka T, Pincus T. Poster presentation at ACR 2005.
- 26. Nicholson B, Verma S. Pain Med 2004; 5(Suppl 1):S9-27. Evaluate Impact of Pain on Functioning Anxiety and depression Sleep disturbances Pain Functional impairment
- 28. Goals in Pain Management • Involve the patient in the decision-making process • Agree on realistic treatment goals before starting a treatment plan Farrar JT et al. Pain 2001; 94(2):149-58; Gilron I et al. CMAJ 2006; 175(3):265-75. Optimize pain relief Improved function Optimize pain relief Improved function Minimize adverse effects Minimize adverse effects
- 29. Multimodal Treatment of Pain Based on Biopsychosocial Approach Pharmacotherapy Psychological mx Interventional pain management RelaxationComplementary therapies Physical therapy Education Lifestyle management Sleep hygiene Gatchel RJ et al. Psychol Bull 2007; 133(4):581-624; Institute of Medicine. Relieving Pain in America: A Blueprint for Transforming Prevention, Care, Education, and Research.; National Academies Press; Washington, DC: 2011; Mayo Foundation for Medical Education and Research. Comprehensive Pain Rehabilitation Center Program Guide. Mayo Clinic; Rochester, MN: 2006. Occupational therapy
- 30. Deciding on the Best Course of Treatment for the Patient Collaborative Care Patient as the ultimate manager of his/her illness Ayad AE et al. J Int Med Res 2011; 39(4):1123-41; Saltman D et al. Med J Aust 2001; 175(Suppl):S92-6.
- 31. Many times, we overlook the psychological and social aspects of pain management 31
- 32. REDUCED (AVOIDED) ACTIVITIES UNHELPFUL BELIEFS & THOUGHTS REPEATED TREATMENT FAILURES LONG-TERM USE OF ANALGESIC, ANTI-CONSULSANT, SEDATIVE DRUGS IMPACT ON WORK, FINANCIAL DIFFICULTIES, FAMILY STRESS Pain PHYSICAL DETERIORATION (eg. loss of fitness/strength, increased weight) DEPRESSION, HELPLESSNESS, FRUSTRATION, ANGER, POOR SLEEP SIDE EFFECTS (eg. lethargy, cognitive function) Treatment framework when pain persists: A biopsychosocial perspective CNS Mechanisms: Neuroplasticity (eg.sensitization) Nociception (eg.injury, inflammation) EXCESSIVE SUFFERING & DISABILITY INPUT FROM: FAMILY; HEALTHCARE PROVIDER(S); COMMUNITY; EMPLOYER (often conflicting) M. Nicholas. 2015 Chronic Targeted medication, Relaxation/meditation, Stimulation Functional: Set realistic goals & pace up activities, exercises – despite pain Education about pain & treatments + identify & challenge unhelpful beliefs Schedule pleasant activities (not just work), improve sleep habits, anger management Cease unhelpful drugs; maintain if helping and used with self- management strategies Negotiate with other HCPs; agree on management plan Review work options, retraining, job modifications; education for family; review home roles Maintenance plan – chronic neuropathic pain will fluctuate, need to plan for these, and for dealing with other stressors
- 33. MULTIDISCIPLINARY MANAGEMENT OF PAIN PHARMACOLOGICAL THERAPY PSYCHOLOGICAL THERAPY SURGERY ASSESSMENT PHYSIOTHERAPY Occupational therapy IMPROVEMENT IN FUNCTION AND QUALITY OF LIFE Rehabilitation INTERVENTIONS PAIN
- 34. Key Messages • Pain is a common yet complex biopsychosocial phenomenon that affects every aspect of a patient’s life • Optimal management often requires good assessment, formulation of the problem in the patient, and combining pharmacological and non- pharmacological (psychological and social) interventions
Editor's Notes
- Speaker’s Notes The Task Force on Taxonomy Committee of the International Association for the Study of Pain (IASP) defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.” This definition of pain allows us to understand that pain is not only a sensory experience but also an emotion that can affect quality of life. Reference International Association for the Study of Pain. IASP Taxonomy. Available at: http://www.iasp-pain.org/AM/Template.cfm?Section=Pain_Definitions. Accessed: July 15, 2013.
- Speaker’s Notes In 2000, the Joint Commission on Accreditation of Healthcare Organizations (JCAHO) unveiled new pain management standards. Central to these new standards was the concept of pain as the fifth vital sign – something that should be regularly monitored in all patients. While there is some controversy regarding whether pain should in fact be monitored at every visit, like blood pressure, this concept highlights the fundamental importance of pain in patient care. Reference Phillips DM. JCAHO pain management standards are unveiled. Joint Commission on Accreditation of Healthcare Organizations. JAMA 2000; 284(4):428-9.
- Speaker’s Notes The physiologic function of pain is to serve as an early warning system that senses noxious stimuli to provoke a reflexive withdrawal (nociception) and to heighten sensitivity after tissue damage to reduce risk of further damage through movement (inflammation). However, continuous unrelieved pain can have a detrimental impact on both physical and psychological well-being. Unrelieved pain can lead to sympathetic activation of the pituitary-adrenal, affecting the cardiovascular , renal and gastrointestinal systems, increasing the risk of cardiac ischemia and ileus. Unrelieved pain is also frequently associated with anxiety and depression. Thus, chronic pain states, often involving neuropathic and/or central sensitization/dysfunctional pathophysiologies are considered to be maladaptive rather than protective and lessen quality of life. References Costigan M et al. Neuropathic pain: a maladaptive response of the nervous system to damage. Annu Rev Neurosci 2009; 32:1-32. Wells N et al. In: Hughes RG (ed). Patient Safety and Quality: An Evidence-Based Handbook for Nurses. Agency for Healthcare Research and Quality; Rockville, MD: 2008. Woolf CJ et al. Pain: moving from symptom control toward mechanism-specific pharmacologic management. Ann Intern Med 2004; 140(6):441-51.
- Speaker’s Notes This slide illustrates how acute and chronic pain are often classified along a pain continuum. Acute pain may be seen as a message that follows an insult to tissue, signaling the presence of a pathologic condition, thus alerting the patient to the need to either seek treatment or protect the involved area from further injury. Most episodes of acute pain are self-limiting. Acute pain becomes chronic when it persists beyond the expected period of healing, usually considered to be three months. Recurrent acute pain is not chronic pain. Chronic pain has also been defined as pain that ceases to serve a protective function, and instead degrades health and functional capability. Chronic pain conditions may be due to a single pathophysiology, that is nociceptive, neuropathic or central sensitization/dysfunctional pain only, or a may be due to a combination of more than one pathophysiological mechanisms. It is important to differentiate chronic pain from a condition with recurrent episodes of acute pain because the treatment strategies are very different for these two situations. References Chapman CR, Stillman M. In: Kruger L (ed). Pain and Touch. Academic Press; New York, NY: 1996. Cole BE. Pain Management: classifying, understanding, and treating pain. Hosp Physician 2002; 38(6):23-30. International Association for the Study of Pain. Unrelieved Pain Is a Major Global Healthcare Problem. Available at: http://www.iasp-pain.org/AM/Template.cfm?Section=Press_Release&Template=/ CM/ContentDisplay.cfm&ContentID=2908. Accessed: July 24: 2013. National Pain Summit Initiative. National Pain Strategy: Pain Management for All Australians. Available at: http://www.iasp-pain.org/PainSummit/Australia_2010PainStrategy.pdf. Accessed: July 24, 2013. Turk DC, Okifuji A. In: Loeser D et al (eds). Bonica’s Management of Pain. 3rd ed. Lippincott Williams & Wilkins; Hagerstown, MD: 2001.
- Speaker’s Notes This slide illustrates three broad categories of pain: central sensitization/dysfunctional, neuropathic and nociceptive pain. It should also be noted that many conditions feature more than one type of pain, and are thus termed ‘mixed pain’ states. Nociceptive pain is an appropriate physiologic response that occurs when specific peripheral sensory neurons (nociceptors) respond to noxious stimuli. Nociceptive pain has a protective role because it elicits reflex and behavioral responses that keep tissue damage to a minimum. Nociceptive pain may be somatic or visceral in origin. Somatic pain, such as gout, osteoarthritis and trauma-induced pain, originates with the musculoskeletal or cutaneous nociceptors and is often well localized. Visceral pain, such as dysmenorrhea or acute pancreatitis, originates in nociceptors located in the hollow organs and smooth muscles; it is often referred. Neuropathic pain has been defined by the International Association for the Study of Pain as “Pain caused by a lesion or disease of the somatosensory nervous system.” Depending on where the lesion or dysfunction occurs within the nervous system, neuropathic pain can be peripheral in origin (as in painful diabetic peripheral neuropathy and postherpetic neuralgia) or central in origin (for example, neuropathic pain associated with stroke or spinal cord injury). Central sensitization/dysfunctional pain is defined as “Hypersensitivity of the pain system such that normally innocuous inputs can activate and perceptual responses to noxious inputs are exaggerated, prolonged and spread widely”. Some common examples for this pain type are: fibromyalgia, temporomandibular joint disorder, chronic migraine/tension type headache, interstitial cystitis, irritable bowel syndrome and complex regional pain syndrome. There are cases in which more than one type of pain pathophysiology exist (mixed pain). For example, in a lumbar herniated disc patient with radiculopathy, it is common to experience both nociceptive/inflammatory pain, felt around the low back area with movement, and neuropathic pain, felt in the distribution territory of the effected root (lower extremity). References Freynhagen R, Baron R. The evaluation of neuropathic components in low back pain. Curr Pain Headache Rep 2009; 13(3):185-90. Jensen TS et al. A new definition of neuropathic pain. Pain 2011; 152(10):2204-5. Julius D et al. In: McMahon SB, Koltzenburg M (eds). Wall and Melzack’s Textbook of Pain. 5th ed. Elsevier; London, UK: 2006. Ross E. Moving towards rational pharmacological management of pain with an improved classification system of pain. Expert Opin Pharmacother 2001; 2(1):1529-30. Webster LR. Breakthrough pain in the management of chronic persistent pain syndromes. Am J Manag Care 2008; 14(5 Suppl 1):S116-22. Woolf CJ. Central sensitization: implications for the diagnosis and treatment of pain. Pain 2011; 152(3 Suppl):S2-15.
- Speaker’s Notes Nociceptive pain is a sensory experience that occurs when specific sensory neurons, called nociceptors, respond to noxious stimuli. With nociceptive pain, the painful region is typically localized to the site of injury and the pain is often described as throbbing, aching or pressure-like. Nociceptive pain is usually time limited and resolves when the damaged tissue heals (e.g., bone fractures, burns, and bruises). Somatic pain originates with the musculoskeletal or cutaneous nociceptors and is often well localized. Visceral pain originates in nociceptors located in the hollow organs and smooth muscles; it is often referred. Although nociceptive pain is generally self-limiting, it can become chronic. Treatment with conventional analgesics is usually appropriate. References Felson DT. Developments in the clinical understanding of osteoarthritis. Arthritis Res Ther 2009; 11(1):203. International Association for the Study of Pain. IASP Taxonomy. Available at: http://www.iasp-pain.org/AM/Template.cfm?Section=Pain_Definitions. Accessed: July 15, 2013. McMahon SB, Koltzenburg M (eds). Wall and Melzack’s Textbook of Pain. 5th ed. Elsevier; London, UK: 2006. Woolf CJ. Central sensitization: implications for the diagnosis and treatment of pain. Pain 2011; 152(3 Suppl):S2-15.
- Speaker’s Note: In our daily life there are many forms of acute pain, such as “somatic pain” of musculoskeletal origin due to sports injury /trauma, burn, incision (such as in post-operative pain) or infectious diseases (such as in pharingitis, otitis, etc.). It may also be a “visceral pain” due to vascular occlusion such as in myocardial ischemia, visceral nociceptive/inflammatory pain due to stretching, hypoxia or inflammation of the hollow organs such as in abdominal colic, dysmenorrhea, etc. Trigeminal or C2-C3 nerve root irritation may lead to neurovascular inflammation in acute episodic headaches such as migraine. Reference Fishman SM et al (eds). Bonica’s Management of Pain. 4th ed. Lippincott, Williams and Wilkins; Philadelphia, PA: 2010.
- Speaker’s Notes The International Association for the Study of Pain (IASP)’s definition of neuropathic pain is “Pain caused by a lesion or disease of the somatosensory nervous system”. Depending on where the lesion or disease occurs in the somatosensory system, neuropathic pain can be peripheral or central in origin. Causes of peripheral neuropathic pain include post-surgical and post-traumatic nerve injury, diabetic peripheral neuropathy, postherpetic neuralgia and neuropathic pain associated with HIV. Post-stroke pain, multiple sclerosis and spinal cord injuries are all examples of central neuropathic pain. Neuropathic pain is frequently described as a ‘shooting’, ‘electric shock-like’ or ‘burning’ pain, commonly associated with ‘tingling’ and/or ‘numbness’. Pain occurs in the neurological territory of the affected structure (nerve, root, spinal cord, brain). In peripheral neuropathic pain, it is in the territory of the affected nerve or nerve root. In central neuropathic pain, it is related to the site of the lesion in the spinal cord or brain. Neuropathic pain is almost always a chronic condition and responds poorly to conventional analgesics. References Chong MS, Bajwa ZH. Diagnosis and treatment of neuropathic pain. J Pain Symptom Manage 2003; 25(5 Suppl):S4-11. Cruccu G et al. EFNS guidelines on neuropathic pain assessment. Eur J Neurol 2004; 11(3):153-62. Dray A. Neuropathic pain: emerging treatments. Br J Anaesth 2008; 101(1):48-58. International Association for the Study of Pain. IASP Taxonomy. Available at: http://www.iasp-pain.org/AM/Template.cfm?Section=Pain_Definitions. Accessed: July 15, 2013. McMahon SB, Koltzenburg M (eds). Wall and Melzack’s Textbook of Pain. 5th ed. Elsevier; London, UK: 2006. Woolf CJ. Central sensitization: implications for the diagnosis and treatment of pain. Pain 2011; 152(3 Suppl):S2-15. .
- Speaker’s Notes Neuropathic pain has been defined as “Pain caused by a lesion or disease of the somatosensory nervous system”. It can originate from the peripheral or central somatosensensory systems. Causes of peripheral neuropathic pain include diabetic peripheral neuropathic pain, human immunodeficiency virus (HIV)-induced neuropathic pain, post-surgical and post-traumatic nerve injury, postherpetic neuralgia and radiculopathies. Post-stroke pain, multiple sclerosis and spinal cord injuries are all examples of central neuropathic pain. Neuropathic pain is frequently described as a ‘shooting’, ‘electric shock-like’ or burning’ pain, commonly associated with ‘tingling’ and/or ‘numbness’. The painful region may not necessarily be the same as the site of injury (see lumbar radicular pain image). Pain occurs in the neurological territory of the affected structure (nerve, root, spinal cord, brain). In peripheral neuropathic pain, it is in the territory of the affected nerve or nerve root. In central neuropathic pain, it is related to the site of the lesion in the spinal cord or brain. Reference Baron R et al. Neuropathic pain: diagnosis, pathophysiological mechanisms, and treatment. Lancet Neurol 2010; 9(8):807-19 .
- Speaker’s Notes This slide illustrates some central and peripheral pathways by which painful stimuli are normally processed (nociceptive pain). Transduction is the conversion of a noxious thermal, mechanical or chemical stimulus into electrical activity in the peripheral terminals of nociceptor sensory fibers. This process is mediated by specific receptor ion channels expressed only by nociceptors. Conduction is the passage of action potentials from the peripheral terminal along axons to the central terminal of nociceptors in the central nervous system. Transmission is the synaptic transfer and modulation of input from one neuron to another. Peripheral nerve fibers involved in pain include unmyelinated slowly conducting C fibers and thinly myelinated A fibers. In the superficial layers of the dorsal horn, these fibers make synaptic connection with second-order neurons that transmit the impulses through the spinal cord to the brain (ascending transmission pathway). In the brain, the thalamus and certain specific cortical areas are critical for the sensory experience of pain. Transmission and processing of pain impulses is also modulated by descending pathways. Reference Scholz J, Woolf CJ. Can we conquer pain? Nat Neurosci 2002; 5(Suppl):1062-7.
- Speaker’s Notes Ascending nociceptive pain pathways consist of nerve fibers with unmyelinated (C fibers) or thinly myelinated (Aδ fibers) axons. Aδ and C fiber nociceptors are usually activated by noxious stimuli. Activated Aδ fibers transmit sharp pain, while activated C fibers are responsible for secondary pain, which is usually described as aching or burning. Ascending nociceptive pain input is modulated by descending control mechanisms involving various monoamine neurotransmitters, such as serotonin, norepinephrine and dopamine. Descending modulation originates from prefrontal cortex, anterior cingulate cortex (ACC), insular cortex, amygdala and hipotalamus. They project down to the brainstem pain modulatory connections such as : periaquaductal grey (PAG), rostral ventral medulla (RVM) and dorsolateral pontin tegmentum (DLPT). Different monoaminergic neurotransmitters bind to different receptors in the descending pathways and thus have different effects on the perception of pain, with some inhibiting and some facilitating pain. References Benarroch EE. Descending monoaminergic pain modulation: bidirectional control and clinical relevance. Neurology 2008; 71(3):217-21. Fields HL et al. In: McMahon SB, Koltzenburg M (eds). Wall and Melzack’s Textbook of Pain. 5th ed. Elsevier; London, UK: 2006. Scholz J, Woolf CJ. Can we conquer pain? Nat Neurosci 2002; 5(Suppl):1062-7.
- Speaker’s Notes Pain is a complex, multidimensional experience involving many areas of the brain, including the thalamus; mid/rostral anterior cingulate cortex; primary and secondary somatosensory cortex; anterior, mid and posterior divisions of the insular cortex; dorsal, mid and ventral prefrontal cortices; brainstem nuclei and parts of the basal ganglia – collectively known as the “pain matrix”. Lateral systems consists of the somatosensorial cortex S1 and S2, lateral thalamus and posterior insula. They are involved in the sensory aspects of pain, such as the differentiation of the localization and intensity of pain. Medial systems consists of the anterior cingulate cortex (ACC) and anterior insular cortex, which are known to be components of the limbic system, and the medial thalamus. They are involved in the emotional, attentional, decision-making and cognitive aspects of pain perception. Thalamic nucleic transmit information to both these areas simultaneously, leading to the complex interplay between external stimuli and internal processing that results in the very personal experience we call pain. Reference Tracey A, Dickenson A. Snapshot: pain perception. Cell 2012; 148(6):1308-e2.
- Speaker’s Notes The biopsychosocial model of pain holds that pain is the result of a complex interaction between physiologic, psychological and social factors. Thus, every individual experiences pain differently as a result of their genetics, personality, past experiences, emotional state and socio-cultural viewpoint. Reference Gatchel RJ et al. The biopsychosocial approach to chronic pain: scientific advances and future directions. Psychol Bull 2007; 133(4):581-624.
- Speaker’s Notes Ask the question shown on the slide to participants to stimulate discussion.
- Speaker’s Notes A pain history and examination worksheet can be used to gather a pain history. Patients can use such a worksheet to record their pain and functional impairment. Most worksheets will include pictures of the human body (front and back) on which patients can mark the areas where they feel pain. Worksheets will cover various aspects of pain, such as: Site of pain What causes or worsens the pain? (e.g., activity) Intensity and character of pain Rate severity from 1 to 5 and evaluate changes in severity Describe the pain Check whether the pain is continuous or intermittent Associated symptoms Effect of pain on sleep Current level of depression Is the pain associated with other symptoms? Pain-related impairment in functioning? (no limitation, mild limitation or significant limitation) Relevant medical history Reference: Ayad AE et al. Expert panel consensus recommendations for the pharmacologic treatment of acute pain in the middle east region. J Int Med Res 2011; 39(4):1123-41.
- Speaker’s Notes Appropriate assessment of patients presenting with pain is crucial in order to determine whether they are suffering from a condition that requires immediate management or referral. It can also help ensure optimal treatment of pain through identification of the underlying cause of the pain and recognition of the pathophysiologic mechanism behind the pain, which can help guide treatment selection. Finally, determining baseline pain intensity enables future assessment of treatment efficacy in order to guide titration and modification of the analgesic regimen. References Forde G, Stanos S. Practical management strategies for the chronic pain patient. J Fam Pract 2007; 56(8 Suppl Hot Topics):S21-30. Sokka T, Pincus T. Pain as a Significant Predictor of Premature Mortality over 5 Years in the General Population, Independent of Age, Sex and Acutely Life-Threatening Diseases. Poster presentation at ACR 2005.
- Speaker’s Notes Although most pain disorders begin with injury or disease, their course and outcome are affected by emotional, behavioral and social factors. An individual’s emotional reaction to, and capacity to cope with, the fluctuating course of chronic pain disorders and their complications, such as physical impairment, disability, and loss of role functioning will also affect outcome. Chronic pain significantly interferes with sleep, with most studies showing a positive correlation between pain intensity and degree of sleep disturbance. Many chronic pain patients also have signs and symptoms of depression and anxiety; sleep deprivation can lead to anxiety, and depression can be both the cause and result of sleep deprivation. As lack of sleep and poor mood can both contribute to increased pain intensity, this can lead to a vicious cycle of increasing pain, fatigue and anxiety/depression. The inter-relationship between these three factors, as shown on this slide, is complex, but must be considered carefully if treatment for chronic pain is to be satisfactory. Chronic pain, sleep disturbances, and depression/anxiety must be addressed if patients are to be restored to optimal functionality. Physicians must evaluate all aspects of pain, sleep and mood in patients with chronic pain. Management and treatment should address both the pain and the comorbidities, to improve daily functioning, and enhance quality of life. Reference Nicholson B, Verma S. Comorbidities in chronic neuropathic pain. Pain Med 2004; 5(Suppl 1):S9-27.
- Speaker’s Notes Ask the question shown on the slide to participants to stimulate discussion.
- Speaker’s Notes It is important to discuss and agree on realistic treatment goals before starting a treatment plan. In cases of neuropathic pain, for example, total pain relief is usually an unrealistic goal and will result in frustration for both patient and doctor. A reduction in pain of about 30–50% is more realistic, and is clinically important to patients. With this in mind, patients need to accept reduced pain and improved function with minimum acceptable side effects as a goal of pain management. References Farrar JT et al. Clinical importance of changes in chronic pain intensity measured on an 11-point numerical pain rating scale. Pain 2001; 94(2):149-58. Gilron I et al. Neuropathic pain: a practical guide for the clinician. CMAJ 2006; 175(3):265-75.
- Speaker’s Notes The 2011 Institute of Medicine (IOM) pain report suggested that a mind-body approach should be used when caring for patients with pain. The biopsychosocial approach, combining physical and emotional factors in assessing and treating chronic pain, offers a uniquely valuable clinical perspective. This mind-body perspective is now generally accepted by pain researchers and has been found useful by clinicians in various disciplines. This animated slide lists components that might be included in such a multimodal approach to pain therapy. References Gatchel RJ et al. The biopsychosocial approach to chronic pain: scientific advances and future directions. Psychol Bull 2007; 133(4):581-624. Institute of Medicine. Relieving Pain in America: A Blueprint for Transforming Prevention, Care, Education, and Research.; National Academies Press; Washington, DC: 2011. Mayo Foundation for Medical Education and Research. Comprehensive Pain Rehabilitation Center Program Guide. Mayo Clinic; Rochester, MN: 2006.
- Speaker’s Notes It is important to have effective communication between general practitioners, their patients and their families. Patients should be given a sense of control by communicating to them that treatment is a collaborative effort and their feedback is essential regarding both the positive effects of treatment on pain severity and functioning, and the potential side effects of treatment. It is also important to systematically evaluate treatment progress by assessing pain severity and functional impairment on a regular basis, and adjusting the treatment regimen based on the results of these assessments. References Ayad AE et al. Expert panel consensus recommendations for the pharmacologic treatment of acute pain in the middle east region. J Int Med Res 2011; 39(4):1123-41. Saltman D et al. Managing osteoarthritis in general practice: a long-term approach. Med J Aust 2001; 175(Suppl):S92-6.
- Speaker’s Notes This slide can be used to summarize the main points of this presentation. The overall message of the presentation should be that by adopting straightforward principles, primary care physicians and other healthcare providers may be able to improve the care of their patients with pain.
- Speaker’s Notes Present the case to the participants.