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1 Putting Pain in Perspective: Pain Matters Mary Christenson, PT, PhD DPT 781 O Fall 2010.

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Presentation on theme: "1 Putting Pain in Perspective: Pain Matters Mary Christenson, PT, PhD DPT 781 O Fall 2010."— Presentation transcript:

1 1 Putting Pain in Perspective: Pain Matters Mary Christenson, PT, PhD DPT 781 O Fall 2010

2 2 Virtual March on Washington Launches September 1, 2010 September Pain Awareness Month is rapidly approaching! American Pain Foundation

3 3 A Story Mailis-Gagnon A, Israelson D. Beyond Pain: Making the Mind-Body Connection. University of Michigan Press; 2005:98. Mailis-Gagnon A, Israelson D. Beyond Pain: Making the Mind-Body Connection. University of Michigan Press; 2005:98. What do you want to learn in this course? What do you want to learn in this course? http://www.cvshealthresources.com/Imageb ank/Articles_images/chronic-pain.jpg

4 4 Who/What Is Affected by Persistent Pain? Individual Individual ADLs ADLs Self-esteem Self-esteem Confidence, other? Confidence, other? Family Family Friends Friends Work environment Work environment Society Society How will this present in the clinic? How will this present in the clinic?

5 5 Reflection Who treats persistent pain? Who treats persistent pain? Why is the study of pain important? Why is the study of pain important? What do you currently know about the treatment of persistent pain? What do you currently know about the treatment of persistent pain?

6 6 Pain Defined “An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.” 2 “An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.” 2

7 Statistics One out of six Americans, minimally, live with chronic pain (American Chronic Pain Association) One out of six Americans, minimally, live with chronic pain (American Chronic Pain Association) 20% globally have pain longer than 3 months 3 20% globally have pain longer than 3 months 3 ~$100 billions/year costs of persistent pain (AACPI - American Alliance of Cancer Pain Initiatives ) ~$100 billions/year costs of persistent pain (AACPI - American Alliance of Cancer Pain Initiatives ) $61.2 billion/year lost business income due to employees pain – only included musculoskeletal problems 6 $61.2 billion/year lost business income due to employees pain – only included musculoskeletal problems 6 7

8 8 Statistics (continued) ~50 million Americans have persistent pain (American Pain Foundation) ~50 million Americans have persistent pain (American Pain Foundation) Headaches are the most common type of pain (National Headache Foundation) Headaches are the most common type of pain (National Headache Foundation) Elderly : Elderly : Community-dwelling – up to 50% c/o pain Community-dwelling – up to 50% c/o pain Institutionalized – 71-83% c/o of at least one source of pain 4 Institutionalized – 71-83% c/o of at least one source of pain 4

9 9 Terminology Acute Pain Acute Pain Occurs with tissue damage or potential damage = a symptom Occurs with tissue damage or potential damage = a symptom Protects from tissue damage and or until healing has occurred Protects from tissue damage and or until healing has occurred Persistent Pain (Chronic Pain) Persistent Pain (Chronic Pain) Extends beyond normal tissue healing time, and/or Extends beyond normal tissue healing time, and/or Causes challenges greater than expected from tissue injury or medical findings, and/or Causes challenges greater than expected from tissue injury or medical findings, and/or Occurs without known tissue damage Occurs without known tissue damage

10 10 Terminology Hyperalgesia Hyperalgesia Hyperpathia Hyperpathia Allodynia Allodynia Neurogenic pain Neurogenic pain Neuropathic pain Neuropathic pain Nociceptor Nociceptor Nociception Nociception Nociceptive pain Nociceptive pain Sensitization Sensitization Peripheral Peripheral Central Central http://static.disaboom.com/content/images/articles/thumbna il/chronic-pain-with-nmd-is-und_thumbnail1.jpg

11 11 http://www.painfoundation.org/

12 12 Models of Pain Historical Historical Specificity Theory Specificity Theory Separate nerve endings for each type of sensation (temperature, touch, pain) Separate nerve endings for each type of sensation (temperature, touch, pain) Challenged: Phantom limb pain? Blockage of pain pathways? Challenged: Phantom limb pain? Blockage of pain pathways? Pattern Theory Pattern Theory Pain recognized by “sense organs” in skin Pain recognized by “sense organs” in skin Consists of signals in the CNS Consists of signals in the CNS Sensation is a learned event – no specific pathways for each sensation Sensation is a learned event – no specific pathways for each sensation

13 13 Models (continued) Gate Control Theory (Melzack and Wall, 1965) Gate Control Theory (Melzack and Wall, 1965) Physiological and psychological components of pain Physiological and psychological components of pain Nerve ending signals are modulated in the spinal cord Nerve ending signals are modulated in the spinal cord Large (non-nociceptor) and small (nociceptor) diameter afferent signals to the substantia gelatinosa (SG) and T cell Large (non-nociceptor) and small (nociceptor) diameter afferent signals to the substantia gelatinosa (SG) and T cell T cell initiates consequences of pain T cell initiates consequences of pain SG cells are inhibitory to the T cell SG cells are inhibitory to the T cell Nociceptor signals inhibit the SG neurons, therefore allowing pain signals to continue Nociceptor signals inhibit the SG neurons, therefore allowing pain signals to continue Increased signals from large diameter fibers results in increased firing of SG neurons, which ultimately decreases firing of T-cells (Result?) (Clinical application?) Increased signals from large diameter fibers results in increased firing of SG neurons, which ultimately decreases firing of T-cells (Result?) (Clinical application?) System under control of supraspinal sites that affect outcomes System under control of supraspinal sites that affect outcomes Challenges Challenges

14 14 http://www.lupusuk.org.uk/images/latestnews/lwcpfig1.gif

15 15 Gate Control Theory (continued) This theory resulted in recognition that “pain is a CNS phenomenon, that treatments for pain must be aimed not only at the peripheral nervous system but also at modulating the CNS, and that pain is multidimensional.” 2 This theory resulted in recognition that “pain is a CNS phenomenon, that treatments for pain must be aimed not only at the peripheral nervous system but also at modulating the CNS, and that pain is multidimensional.” 2

16 16 Models (continued) Biomedical Model Biomedical Model Biopsychosocial Model (conceptual model by the American College of Physicians) Biopsychosocial Model (conceptual model by the American College of Physicians) Nociception Nociception Pain Pain Pain Appraisal Pain Appraisal Pain Behaviors Pain Behaviors Social Roles for Pain and Illness Social Roles for Pain and Illness

17 17 http://www.continuingedcourses.net/active/courses/images/course033-image002.jpg Biopsychosocial Models of Pain

18 18 http://www.painxchange.com.au/images/BiopsychosocialPain.png

19 19 Peripheral Primary Afferent Nociceptors fire in response to a noxious stimulus Nociceptors fire in response to a noxious stimulus Mechanical Mechanical Thermal Thermal Chemical Chemical

20 20 Letter System Type of fiber Diameter, micrometer s Conduction velocity, m/sec General Function A-alpha13-2270-120alpha-motoneurons, muscle spindle primary endings, Golgi tendon organs, touch A-beta8-1340-70touch, kinesthesia, muscle spindle secondary endings A-gamma4-815-40touch, pressure, gamma-motoneurons A-delta1-45-15pain, crude touch, pressure, temperature B1-33-14preganglionic autonomic C0.1-10.2-2pain, touch, pressure, temperature, postganglionic autonomic Peripheral Nerve Fiber Types http://www.unmc.edu/physiology/Mann/mann12.html

21 21 Roman Numeral System Type of fiber Diameter, micromet ers Conduction velocity, m/sec General Function Ia12-2070-120muscle spindle primary endings Ib11-1966-114Golgi tendon organs II5-1220-50touch, kinesthesia, muscle spindle secondary endings III1-54-20pain, crude touch, pressure, temperature IV0.1-20.2-3pain, touch, pressure, temperature Peripheral Nerve Fiber Types http://www.unmc.edu/physiology/Mann/mann12.html II = Aβ ; III = Aδ ; IV = C

22 22 Peripheral Receptors Ia: muscle spindle Ia: muscle spindle Ib: Golgi tendon organ Ib: Golgi tendon organ II: Meissner corpuscle, Merkel’s cell, Pacinian corpuscle, Ruffini ending, hair follicle, Paciniform endings, muscle spindle II: Meissner corpuscle, Merkel’s cell, Pacinian corpuscle, Ruffini ending, hair follicle, Paciniform endings, muscle spindle III: Free nerve endings (noxious stim) III: Free nerve endings (noxious stim) IV: Free nerve endings (noxious stim) IV: Free nerve endings (noxious stim)

23 23 Free Nerve Ending

24 24 Silent Nociceptors ~1/3 of nociceptors in skin, joints or viscera do not respond to stimulus until inflammation = “silent nociceptors” ~1/3 of nociceptors in skin, joints or viscera do not respond to stimulus until inflammation = “silent nociceptors” May be activated by mediators such as prostaglandins that are released during inflammation May be activated by mediators such as prostaglandins that are released during inflammation Increases pain response Increases pain response

25 25 Peripheral Sensitization Increased responsiveness to stimuli after initial injury Increased responsiveness to stimuli after initial injury Potential mechanisms: Potential mechanisms: Lower threshold to stimulus Lower threshold to stimulus Increase in neuron activity Increase in neuron activity Increase in area of receptor fields Increase in area of receptor fields Increase in response to the same stimulus Increase in response to the same stimulus

26 26 Neuronal Activators of Pain Neuropeptides Neuropeptides Opioids Opioids Glutamate Glutamate Ion Channels Ion Channels

27 27 Non-neuronal Activators of Pain Inflammatory processes cause the release of factors that can result in activating afferent nerves Inflammatory processes cause the release of factors that can result in activating afferent nerves Serotonin released from platelets Serotonin released from platelets Bradykinin released plasma Bradykinin released plasma Prostaglandins released from arachidonic acid cascade Prostaglandins released from arachidonic acid cascade Cytokines released by macrophages Cytokines released by macrophages Others: mast cells, neutrophils, T and B cells Others: mast cells, neutrophils, T and B cells

28 28 Structures of Pain http://journals.prous.com/journals/dnp/20041703/html/dn170172/images/Block_f1.jpg

29 29 Physiology of Pain

30 30 Central Mechanisms Spinal Cord Spinal Cord Laminae I-VI make up the dorsal horn Laminae I-VI make up the dorsal horn Sensory afferents terminate (majority) on “2 nd neuron” Sensory afferents terminate (majority) on “2 nd neuron” Noxious information from skin: I, II, V (primarily) Noxious information from skin: I, II, V (primarily) Noxious information from muscles/joints: I (primarily) Noxious information from muscles/joints: I (primarily) Interneurons Interneurons Afferents from skin, joints, muscles, viscera may terminate on one neuron – referred pain? Afferents from skin, joints, muscles, viscera may terminate on one neuron – referred pain?

31 31 Dorsal Horn http://www.wdv.com/Cancer/Pain/Images/Anatomy1.gif

32 32 Central Sensitization Neurons in dorsal horn Neurons in dorsal horn High-threshold – respond to noxious stim High-threshold – respond to noxious stim Low-threshold – respond to innocuous stim Low-threshold – respond to innocuous stim Wide-dynamic-range (WDR) – respond to both Wide-dynamic-range (WDR) – respond to both Tissue injury: increased sensitivity of high- threshold and WDR neurons Tissue injury: increased sensitivity of high- threshold and WDR neurons Expansion of receptive fields in central neurons common – referred pain? Expansion of receptive fields in central neurons common – referred pain?

33 33 Sensitization Continued input from sensitized nociceptors can maintain sensitization of dorsal horn neurons Continued input from sensitized nociceptors can maintain sensitization of dorsal horn neurons Need to reduce peripheral input? Need to reduce peripheral input? Sensitization of dorsal horn neurons can also be maintained in absence of peripheral input Sensitization of dorsal horn neurons can also be maintained in absence of peripheral input Need to reduce central sensitization? Need to reduce central sensitization?

34 34 Potential Influences: Hyperalgesia (found in spinal cord) Can produce hyperalgesia Can produce hyperalgesia Glial cells Glial cells Neurotransmitters – Spinal Cord Neurotransmitters – Spinal Cord Glutamate Glutamate Substance P Substance P Can reduce hyperalgesia Can reduce hyperalgesia Adenosine Adenosine GABA GABA

35 35 Pain Sensory Pathways: Spinal Cord to Brain Spinothalamic Tract Spinothalamic Tract Transmits nociceptive pain up through the thalamus (VPL nucleus and medial thalamic nuclei) to higher centers Transmits nociceptive pain up through the thalamus (VPL nucleus and medial thalamic nuclei) to higher centers VPL to 1 o and 2 o somatosensory cortex: location, duration quality, and intensity of pain VPL to 1 o and 2 o somatosensory cortex: location, duration quality, and intensity of pain Medial thalamic to anterior cinglate, etc.: “unpleasantness” of pain Medial thalamic to anterior cinglate, etc.: “unpleasantness” of pain Spinomesencephalic and Spinoreticular Tracts Spinomesencephalic and Spinoreticular Tracts Transmits to midbrain/brainstem respectively Transmits to midbrain/brainstem respectively Integrates information with areas involved in descending inhibition, facilitation, and autonomic pain responses Integrates information with areas involved in descending inhibition, facilitation, and autonomic pain responses

36 36 Thalamus and Cortex Thalamus Thalamus Integrate information from peripheral noxious stimulation Integrate information from peripheral noxious stimulation Cortex Cortex S1 and S2: increased blood flow noted to these areas with painful stimuli S1 and S2: increased blood flow noted to these areas with painful stimuli Homunculus (more to come) Homunculus (more to come) Anterior cingulate cortex Anterior cingulate cortex Many other centers (to be continued) Many other centers (to be continued)

37 37 Brainstem Centers Contains centers that contribute facilitation and or inhibition signals Contains centers that contribute facilitation and or inhibition signals A balance between all brain/brainstem signals determines pain perception A balance between all brain/brainstem signals determines pain perception Other brain influences? Other brain influences? PAIN IS AN OUTPUT PAIN IS AN OUTPUT

38 38 Measures of Pain

39 39 Measures of Pain

40 40 Associations American Academy of Pain Management American Academy of Pain Management American Pain Foundation American Pain Foundation American Pain Society American Pain Society American Chronic Pain Association American Chronic Pain Association International Association for the Study of Pain (IASP) International Association for the Study of Pain (IASP)

41 41 References 1 Mailis-Gagnon A, Israelson D. Beyond Pain: Making the Mind-Body Connection. University of Michigan Press; 2005:98. 1 Mailis-Gagnon A, Israelson D. Beyond Pain: Making the Mind-Body Connection. University of Michigan Press; 2005:98. 2 Sluka KA, ed. Mechanisms and Management of Pain for the Physical Therapist. Seattle, WA: IASP Press; 2009. 2 Sluka KA, ed. Mechanisms and Management of Pain for the Physical Therapist. Seattle, WA: IASP Press; 2009. 3 Butler DB, Moseley L. Explain Pain. Adelaide, Australia: Notgroup Publications; 2003. 3 Butler DB, Moseley L. Explain Pain. Adelaide, Australia: Notgroup Publications; 2003. 4 Galieze L. Chronic Pain in Elderly People. Pain. 1997;70(1):3-14. 4 Galieze L. Chronic Pain in Elderly People. Pain. 1997;70(1):3-14. 5 Marchand F, Perretti M, McMahon SB. Role of the immune system in chronic pain. Nature Reviews/Neuroscience. 2005;6:521-532. 5 Marchand F, Perretti M, McMahon SB. Role of the immune system in chronic pain. Nature Reviews/Neuroscience. 2005;6:521-532. 6 JAMA. 2003;290:2443-2454. 6 JAMA. 2003;290:2443-2454.


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