Fibromyalgia disease overview

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  • Pain is common and often chronic, under-diagnosed, and undertreated2
    Pain carries a tremendous burden for patients and society2
    Presence of pain complicates diagnosis and treatment of other medical and psychiatric conditions2
    In the spectrum of clinical pain syndromes, fibromyalgia lies in the realm of dysfunctional pain or central pain amplification
    A broad spectrum of pain syndromes is seen in the clinic. Types of pain can be differentiated by the patients’ threshold to pain and by the initiating causes1
    Nociceptive pain is a normal response to a noxious stimulus such as heat or pressure with a relatively high threshold1
    In neuropathic pain and conditions of central pain amplification, there are chronic alterations or lesions in the peripheral nervous system and/or central nervous system. Neuronal damage can be due to injury, viral infection (post-herpetic neuropathy) or diabetes (diabetic peripheral neuropathy)1
    In inflammatory pain, the pain threshold is somewhat lower. A variety of immunologic mediators can give rise to inflammatory pain1
    The etiology of dysfunctional chronic pain conditions may be less clearly defined than that of neuropathic pain conditions. Often times no noxious stimuli or inflammation or neuronal damage can be identified, yet patients report extreme pain to non-noxious stimuli (allodynia) or an extreme pain to mild stimuli (hyperalgesia)1
    Reference:
    1. Woolf CJ. Pain: Moving from Symptom Control toward Mechanism-Specific Pharmacologic Management. Ann Intern Med. 2004;140:441-451.
    2. Giordano J and Schatman ME, 2008. Pain Physician;11:483-490.
  • Fibromyalgia (FM) is one of the most common chronic widespread pain
    Conditions1 with an incidence rate of 2-5% of the adult population
    FM, a chronic widespread neurologic pain condition is characterized by pain in all 4 quadrants and tenderness to stimuli
    The ACR criteria for the diagnosis of FM is used to differentiate FM from other rheumatologic conditions
    It is sensitive (88.4%) and specific (81.1%) tool that can be used to differentiate FM from other rheumatologic conditions.2
    To diagnose FM, using the ACR Diagnostic criteria:
    The patient must have chronic, widespread pain for ≥3 months
    The pain had to include all 4 quadrants of the body – that is both above and below the waist and on left and right sides of the body
    The pain must include the axial skeleton
    The patient must have pain in at least 11 of the 18 tender points identified by the ACR2
    TPs are at defined locations and using your thumb of your dominant hand, palpating with 4kg of pressure (blanching of the thumbnail) a patient with FM should feel pain at these locations at least 11/18 locations
    References:
    1. Wolfe F, Ross K, Anderson J, Russell IJ, Hebert L. The prevalence and characteristics of fibromyalgia in the general population. Arthritis Rheum. 1995;38:19-28.
    2. Wolfe F, Smythe HA, Yunus MB, et al. The American College of Rheumatology 1990 criteria for the classification of fibromyalgia. Report of the Multicenter Criteria Committee. Arthritis Rheum. 1990;33:160-172.
  • While the cause of fibromyalgia is not known, emerging evidence suggests that environmental, genetic and other factors may be involved in pain sensitivity and predispose individuals to developing FM.1
    Arnold et al demonstrated that FM and reduced pain pressure thresholds may aggregate in families1
    The aggregation odds ratio are the odds FM in a relative of a proband with FM compared with the odds of FM (in this study) in a relative of a proband with rheumatoid arthritis2
    Adjusted for the relative’s age, sex, relationship to proband, interview status, and correlation of observations within families2
    Environmental factors such as physical trauma, infections (Lyme disease, hepatitis C, parvovirus, Epstein-Barr virus), and other stressors such as work, family, or live-changing events may trigger the onset of FM2
    References:
    1. Arnold LM, Hudson JI, Hess EV, et al. Family study of fibromyalgia. Arthritis Rheum. 2004;50(3):944-952.
    2. Mease P. Fibromyalgia syndrome: review of clinical presentation, pathogenesis, outcome measures, and treatment. J Rheumatol. 2005;32(suppl 75):6-21.
    3. Arnold LM, Lu Y, Crofford LJ, et al. A Double-Blind, Multicenter Trial Comparing Duloxetine With Placebo in the Treatment of Fibromyalgia Patients With or Without Major Depressive Disorder. Arthritis Rheum. 2004;50(9):2974-2984.
  • <<Animated slide: Please advance to view entire sequence.>>
    Activation of peripheral pain receptors, or nociceptors, by noxious stimuli generates signals that travel to the dorsal horn of the spinal cord via the dorsal root ganglion2
    Within the synapse of the dorsal horn, entry of calcium causes release of glutamate and Substance P into the synaptic cleft, to affect the next neuron1,3
    From the dorsal horn, the signals are carried along the ascending pain pathway or the spinothalamic tract to the thalamus and the cortex2
    Pain can be controlled by pain-inhibiting and pain-facilitating neurons
    Descending signals originating in supraspinal centers can modulate activity in the dorsal horn by controlling spinal pain transmission2
    References:
    1. Staud R, Rodriguez ME. Mechanisms of disease: pain in fibromyalgia syndrome. Nat Clin Pract Rheumatol. 2006;2:90-98.
    2. Gottschalk A, Smith DS. New concepts in acute pain therapy: preemptive analgesia. Am Fam Physician. 2001;63:1979-1984.
    3. Henriksson KG. Fibromyalgia – from syndrome to disease. Overview of pathogenetic mechanisms. J Rehabil Med. 2003;(suppl 41):89-94.
  • While the pathogenesis of FM is not completely understood, alterations of the CNS may contribute to the chronic pain of FM2
    FM is characterized by a heightened sensitivity to pain2
    Central sensitization is a theory of the development of fibromyalgia as a consequence of functional changes in the CNS that result in hyperexcitability of the spinal cord neurons which then release excess substance P and glutamate1,4
    This may explain why in patients with FM, sensory input that would normally invoke an innocuous response, may result in pain6
    fMRI data demonstrate that response to low intensity stimuli in patients with FM is comparable to the response to high intensity stimuli in controls5
    References:
    Staud R, Rodriguez ME. Mechanisms of disease: pain in fibromyalgia syndrome. Nat Clin Pract Rheumatol. 2006;2:90-98.
    Williams DA, Clauw DJ. Understanding Fibromyalgia: Lessons from the Broader Pain Research Community. J Pain. 2009;10(8):777-791.
    Sarchielli P, Mancini ML, Floridi A, et al. Increased levels of neurotrophins are not specific for chronic migraine: evidence from primary fibromyalgia syndrome. J Pain. 2007;8:737-745.
    Vaerøy H, Helle R, Forre O, Kåas E, Terenius L. Elevated CSF levels of substance P and high incidence of Raynaud phenomenon in patients with fibromyalgia: new features for diagnosis. Pain. 1988;32:21-26.
    Gracely RH, Petzke F, Wolf JM, Clauw DJ. Functional Magnetic Resonance Imaging Evidence of Augmented Pain Processing in Fibromyalgia. Arthritis Rheum. 2002;46(5):1333-1343.
    Henriksson KG. Fibromyalgia – from syndrome to disease. Overview of pathogenetic mechanisms. J Rehabil Med. 2003;41(suppl 41):89-94.
  • <<Animated slide: Please advance to view entire sequence.>>
    Note to speaker: This slide contains an animated build to show that central sensitization involves changes
    at the level of the dorsal horn neurons. Clicking on this slide will cause subsequent components of the
    build to appear automatically.
    On this slide, pain processing is demonstrated. The peripheral nerve/nociceptive afferent fiber is stimulated and
    sends pain signals to the spinal cord. At the dorsal horn of the spinal cord, pain neurotransmitters are released
    (substance P and Glutamate), stimulating the ascending tract (spinothalamic tract).
    The ascending tract sends signals to the brain, where pain is perceived.
    The body can modulate pain signals that are sent to the brain. This is done with the descending fiber (green),
    which sends signals to the dorsal horn of the spinal cord, modulating the signals going to the brain.
    FM, a neurologic pain condition, occurs when there is an abnormality in the pain processing.
    The bottom illustration shows when minimal stimuli sends pain signals to the spinal cord.
    In FM, elevated NTs are released in response to the minimal stimuli at the dorsal horn of the spinal cord.
    The exaggerated release of NTs results in elevated pain signals sent to the brain – where the brain perceives
    elevated pain, although the stimuli is minimal.
    The descending fiber sends a decreased amount of signals to modulate the signals going to the brain.
    Overall, this demonstrates the hyperalgesia and allodynia in FM.
    Under pathological conditions:1,2
    Abnormal ectopic discharges from damaged/diseased nociceptors can induce central sensitization of spinal dorsal horn neurons
    Initially, it is activity dependent (triggered by repetitive peripheral input or ectopic discharge beyond the initial stimuli or in the absence of a known stimuli) and later it becomes sustained beyond the initial stimulus, maintained by transcriptional changes
    Central sensitization is thought to involve changes:
    In the postsynaptic dorsal horn neurons that may be triggered by increased release of transmitters from presynaptic central nociceptor terminals
    This leads to alterations in synaptic receptor density and lowering of activation threshold
    This results in amplification of the pain signal in the dorsal horn
    For a patient with FM, a normally minimally painful stimuli may cause an amplified response to normal stimuli (hyperalgesia), or normal stimuli may result in pain (allodynia)
    Note that the theory of central sensitization may be applicable to many other pain conditions
    References:
    1.Gottschalk A, Smith DS. New concepts in acute pain therapy: preemptive analgesia. Am Fam Physician. 2001;63:1979-1984.
    2.Woolf CJ. Pain: moving from symptom control toward mechanism-specific pharmacologic management. Ann Intern Med. 2004;140:441-451.
  • <<Animated slide: Please advance to view entire sequence.>>
    In the normal pain response, pain intensity increases as the stimulus intensity increases1
    Due to central sensitization, FM patients have an amplification of pain response, which presents an increased response at lower stimuli, causing the curve to shift to the left
    In FM patients, lower stimulus produces an elevated subjective pain intensity demonstrated by:
    Hyperalgesia, in which noxious stimuli cause greater and more prolonged pain
    Allodynia, in which pain results from normally painless stimuli
    References:
    Gottschalk A, Smith DS. New concepts in acute pain therapy: preemptive analgesia. Am Fam Physician. 2001;63:1979-1986.
  • Pain processing is augmented in FM patients. The pain they experience is real.1
    This slide shows the results of an fMRI study measuring the subjective pain with increasing stimulus in fibromyalgia patients against controls by measuring areas of activation in the brain
    In FM patients, some pain processing areas of the brain are activated at a much lower level of stimulus than in controls. There is overlap (as indicated by the yellow area on the fMRI) between the areas activated at low intensity stimulus in FM patients (red area) and high intensity stimulus in control subjects (green area) indicating that the pain FM patients experience is real
    The graph on the left depicts pain intensity against stimulus intensity. In FM patients, a low stimulus pressure produced a high pain level (hyperalgesia); however, in stimulus pressure controls, a similar pressure resulted in low levels of pain and a much higher stimulus pressure was required to elicit similar levels of pain
    Background Information
    fMRI was used to evaluate cerebral activation patterns during the application of painful and non-painful pressure in FM patients (n=16) and controls (n=16)
    No subjects were clinically depressed, and FM patients met the American College of Rheumatology criteria for FM. Mean age of patients was 52.6 years; range 19-69. Mean age of controls was 45.8 years; range 22-61. Patients taking opioid analgesics were excluded; other analgesics were discontinued 12 hours prior to procedures
    Each patient underwent fMRI while pressure was applied to the thumbnail bed for 5 seconds using a hard rubber probe attached to a hydraulic piston. Subjects rated the intensity and unpleasantness of sensations evoked by pressure from 0.45 kg/cm2 to the maximum tolerated, with a limit of 9 kg/cm2. Every 10 seconds, FMRI brain scans recorded areas of increased cerebral blood flow produced when pressure was applied
    13 regions of increased brain activation were revealed in the FM group, compared with 1 in the control group
    Enhanced responses were noted in multiple areas of the brain, including somatosensory primary and secondary cortex, insula, putamen, and cerebellum; this provides supporting evidence that CNS alterations may underlie FM pathophysiology
    Reference:
    1.Gracely RH, Petzke F, Wolf JM, Clauw DJ. Functional magnetic resonance imaging evidence of augmented pain processing in fibromyalgia. Arthritis Rheum. 2002;46:1333-1343.
  • Central sensitization is a leading theory of FM pathophysiology1
    Elevated pain neurotransmitters in CSF of patients with FM2-4
    Several studies showed elevated levels of glutamate and substance P
    Elevated levels suggest that this may contribute to pain amplification
    fMRI data supports FM as a disorder of central pain amplification5
    Areas activated by high intensity stimuli in control patients were activated by low intensity stimuli in patients with FM
    References:
    Staud R, Rodriguez ME. Mechanisms of disease: pain in fibromyalgia syndrome. Nat Clin Pract Rheumatol. 2006;2:90-98.
    Russell IJ, Orr MD, Littman B, Vipraio GA, Alboukrek D, Michalek JE, Lopez Y, MacKillip F. Elevated cerebrospinal fluid levels of Substance P in patients with the fibromyalgia syndrome. Arthritis Rheum. 1994;37:1593-1601.
    Bradley LA, Alberts KR, Alarcon GS, et al. Abnormal brain regional cerebral blood flow (rCBF) and cerebrospinal fluid (CSF) levels of substance P (SP) in patients and non-patients with fibromyalgia (FM). Arthritis Rheum. 1996;suppl 9:212. Abstract 1109.
    Sarchielli P, Mancini ML, Floridi A, et al. Increased levels of neurotrophins are not specific for chronic migraine: evidence from primary fibromyalgia syndrome. J Pain. 2007;8:737-745.
    Gracely, RH, Petzke F, Wolf JM, Clauw DJ. Functional Magnetic Resonance Imaging Evidence of Augmented Pain Processing in Fibromyalgia. Arthritis Rheum. 2002;46(4):1333-1343.
    Henriksson KG. Fibromyalgia – from syndrome to disease. Overview of pathogenetic mechanisms. J Rehabil Med. 2003;41(suppl 41):89-94.
    Williams DA, Clauw DJ. Understanding Fibromyalgia: Lessons from the Broader Pain Research Community. J Pain. 2009;10(8):777-791.
  • <<Animated slide: Please advance to view entire sequence.>>
    Although chronic widespread pain and tenderness are the defining features of FM, sleep disturbances, morning stiffness, and other pain-related conditions may also be present.2
    Patients often describe the pain of FM as aching, exhausting, nagging, and hurting1
    Wolfe et al demonstrated that fatigue and morning stiffness were present in >75% of FM patients6
    FM is commonly associated with non-restorative sleep which is characterized by prominent alpha wave intrusion3,5
    References:
    1.Leavitt F, Katz RS, Golden HE, Glickman PB, Layfer LF. Comparison of pain properties in fibromyalgia patients and rheumatoid arthritis patients. Arthritis Rheum. 1986;29:775-781.
    2. Wolfe F, Ross K, Anderson J, Russell IJ, Hebert L. The prevalence and characteristics of fibromyalgia in the general population. Arthritis Rheum. 1995;38:19-28.
    3.Roizenblatt S, Moldofsky H, Benedito-Silva AA, Tufik S. Alpha sleep characteristics in fibromyalgia. Arthritis Rheum. 2001;44:222-230.
    4. Staud R. Biology and therapy of fibromyalgia: pain in fibromyalgia syndrome. Arthritis Res Ther. 2006;8(3):208-214.
    5.Harding SM. Sleep in fibromyalgia patients: subjective and objective findings. Am J Med Sci. 1998;315:367-376.
    6.Wolfe F, Smythe HA, Yunus MB, et al. The American College of Rheumatology 1990 criteria for the classification of fibromyalgia. Report of the Multicenter Criteria Committee. Arthritis Rheum. 1990;33:160-172.
  • <<Animated slide: Click to proceed to animation.>>
    The pain drawing illustrates the widespread nature of a patient’s pain.1
    Although the ACR tender point examination focuses on 18 discrete points on the body, the pain of FM is widespread1
    As illustrated on this slide, pain drawings can be used to characterize the location of pain and size of painful areas. When FM patients are asked to color in areas that are painful, they typically shade in areas all over the body to indicate their widespread pain2
    References:
    Wolfe F, Smythe HA, Yunus MB, et al. The American College of Rheumatology 1990 criteria for the classification of fibromyalgia. Report of the Multicenter Criteria Committee. Arthritis Rheum. 1990;33:160-172.
    Silverman SL, Martin SA. Assessment tools and outcome measures used in the investigation of fibromyalgia. In: Wallace DJ, Clauw DJ, eds. Fibromyalgia & Other Central Pain Syndromes. Philadelphia, PA: Lippincott, Williams & Wilkins; 2005:309-319.
  • The ACR criteria for FM require that patients have a history of CWP for ≥3 months and pain in ≥11 of 18 tender point sites on digital palpation.2
    To determine the criteria for FM, Wolfe et al studied 558 patients; widespread pain, defined as:
    Axial, upper and lower segment, as well as left- and right-sided pain2
    This occurred in 97.6% of FM patients (n=293) and 69.1% of control patients (n=265)2
    Controls were age- and sex-matched patients with neck pain, low back pain, trauma-related pain, and possible SLE or RA2
    Additionally, sleep disturbances, fatigue, and morning stiffness were present in >75% of FM patients2
    The ACR criteria provide a sensitive (88.4%) and specific (81.1%) tool that can be used to differentiate FM from other rheumatologic conditions2
    Tender points are the most powerful discriminator between FM patients and controls, although tenderness is subjective and dependant upon the examiner’s strength of palpation2
    Manually done, tender point analysis requires application of 4 kg of pressure, usually with the thumb or first 2 fingers on each point to elicit a painful response2
    4 kg of pressure typically produces blanching of the thumb nail bed of the examiner’s dominant hand1
    It may be desirable to use a scale to learn the ‘feel’ of 4 kg of pressure and to practice exerting the proper amount of pressure1
    Reference:
    1. Chakrabarty S, Zoorob R. Fibromyalgia. Am Fam Physician. 2007;76(2): 247-254.
    2. Wolfe F, Smythe HA, Yunus MB, et al. The American College of Rheumatology 1990 criteria for the classification of fibromyalgia. Report of the Multicenter Criteria Committee. Arthritis Rheum. 1990;33:160-172.
  • Do a search for post 1999!
  • Fibromyalgia disease overview

    1. 1. Fibromyalgia WHPL 1
    2. 2. What is Fibromyalgia? • Pathogenesis of Fibromyalgia • Clinical Features and Diagnosis of Fibromyalgia • Management of Fibromyalgia • Summary 2
    3. 3. Categorization of Pain Conditions Nociceptive Pain Nociceptive Pain Neuropathic Pain Neuropathic Pain Inflammatory Pain Inflammatory Pain Central Pain Central Pain Amplification Amplification (ie, Burn) (ie, Herpes zoster) (ie, Rheumatoid arthritis) (ie, Fibromyalgia) Noxious stimuli Neuronal damage Inflammation Acute Pain Abnormal pain processing by CNS Chronic Pain 3
    4. 4. Fibromyalgia (FM): A Chronic Widespread Neurologic Pain Condition FM is a neurological condition associated with chronic widespread pain (CWP) and tenderness American College of Rheumatology (ACR) criteria for the diagnosis of FM: – Chronic widespread pain • Pain for ≥3 months • Pain above and below the waist • Pain on left and right sides of body and axial skeleton – Pain at ≥11 of 18 tender points when palpated with 4 kg of digital pressure . 4
    5. 5. Risk Factors for FM Genetic factors – Relatives of FM patients are at higher risk for FM • First-degree relatives are significantly more likely to have FM • Have significantly more tender points Environmental factors – – – – Physical trauma or injury Infections (Lyme disease, hepatitis C) Other stressors (eg, work, family, life-changing events) Concurrent medical illness (e.g., SLE, RA, OA, hypothyroidism, hepatitis) – Medications (steroid) Gender – Women are diagnosed with FM about 7 times as often as men – peak age 40-60 . 5
    6. 6. CONCURRENT DISEASES WITH FM •Chronic fatigue syndrome •Irritable bowel syndrome •Muscle, migraine headaches •Irritable bladder syndrome •Mood disturbances •Vulvodynia •Temporomandibular joint (TMJ) disorder 6
    7. 7. • What is Fibromyalgia? Pathogenesis of Fibromyalgia • Clinical Features and Diagnosis of Fibromyalgia • Management of Fibromyalgia 7
    8. 8. The Normal Pain Processing Pathway 3. A signal is sent via the ascending tract to the brain, and perceived as pain Pain Perceived 4. The descending tract carries modulating impulses back to the dorsal horn 2. Impulses from afferents depolarize dorsal horn neurons, then, extracellular Ca2+ diffuse into neurons causing the release of Pain Associated Neurotransmitters – Glutamate and Substance P 1. Stimulus sensed by the peripheral nerve (ie, skin) Glutamate Substance P 8
    9. 9. Central Sensitization: A Theory for Neurological Pain Amplification in FM Central sensitization is believed to be an underlying cause of the amplified pain perception that results from dysfunction in the CNS – May explain hallmark features of generalized heightened pain sensitivity • Hyperalgesia – Amplified response to painful stimuli • Allodynia - Pain resulting from normal stimuli Theory of central sensitization is supported by: – Increased levels of pain neurotransmitters • Glutamate • Substance P fMRI data demonstrates low intensity stimuli in patients with FM comparable to high intensity stimuli in controls 9
    10. 10. Central Sensitization Produces Abnormal Pain Signaling Perceived pain Ascending input After nerve injury, increased input to the dorsal horn can induce central sensitization Descending modulation Nerve dysfunction Nociceptive afferent fiber Induction of central sensitization Perceived pain (hyperalgesia/allodynia) Increased release of pain neurotransmitters glutamate and substance P Minimal stimuli Pain amplification Increased pain perception 10
    11. 11. FM: An Amplified Pain Response Subjective pain intensity 10 8 Pain in FM Hyperalgesia 6 (when a pinprick causes an intense stabbing sensation) 4 Pain amplification response Normal pain response Allodynia (hugs that feel painful) 2 0 Stimulus intensity Adapted from Gottschalk A and Smith DS. Am Fam Physician. 2001;63:1979-1986. 11
    12. 12. fMRI Study Supports the Amplification of Normal Pain Response in Patients With FM 14 Pain intensity 12 10 8 6 4 2 0 1.5 2.5 3.5 4.5 Stimulus intensity (kg/cm ) 2 Patients with FM experienced high pain with low grade stimuli FM (n=16) Subjective pain control Stimulus pressure control (n=16) Red: Activation at low intensity stimulus in patients with FM Green: Activated only at high intensity stimulus in controls Yellow: Area of overlap (ie, area activated at high intensity stimuli in control patients was activated by low intensity stimuli in patients with FM) 12
    13. 13. FM Pathophysiology: Summary Central sensitization is a leading theory of FM pathophysiology1 Elevated pain neurotransmitters in CSF of patients with FM – Several studies showed elevated levels of glutamate and substance P – Elevated levels suggest that this may contribute to pain amplification fMRI data supports FM as a disorder of central pain amplification – Areas activated by high intensity stimuli in control patients were activated by low intensity stimuli in patients with FM 13
    14. 14. • What is Fibromyalgia? • Pathogenesis of Fibromyalgia Clinical Features and Diagnosis of Fibromyalgia • Management of Fibromyalgia 14
    15. 15. Clinical Features of FM Chronic Widespread Pain • CORE criteria of FM • Pain is in all 4 quadrants of the body ≥3 months • Patient descriptors of pain include:4 • Aching, exhausting, nagging, and hurting Tenderness • Sensitivity to pressure stimuli • Hugs, handshakes are painful • Tender point exam given to assess tenderness • Hallmark features of FM4 • Hyperalgesia • Allodynia Other Symptoms • Fatigue • Pain-related conditions/symptoms • Chronic headaches/migraines, IBC, IC, TMJ, PMS • Subjective morning stiffness Other Symptoms • Neurologic symptoms • Nondermatomal paresthesias • Subjective numbness, tingling in extremities • Sleep disturbance • Non-restorative sleep, RLS 15
    16. 16. 16
    17. 17. Patients With FM Present With a Global Pain Disorder While the ACR classification criteria focuses on 18 points, patients do not usually speak of tender points1 This is a pain drawing—a patient colors all areas of the body in which they feel pain2 The diagram shows that the pain of FM is widespread1 Back Front 17
    18. 18. ACR-Recommended Manual Tender Point Survey for the Diagnosis of FM LOW CERVICAL – Anterior aspects of C5, C7 intertransverse spaces TRAPEZIUS – Upper border of trapezius, midportion OCCIPUT – At nuchal muscle insertion FOREHEAD SUPRASPINATUS – SECOND RIB SPACE – At attachment to medial border of scapula about 3 cm lateral to sternal border RIGHT FOREARM ELBOW – Muscle attachments to Lateral Epicondyle GLUTEAL – Upper outer quadrant of gluteal muscles KNEE – Medial fat pad of knee proximal to joint line LEFT THUMB Manual Tender Points Survey: • Presence of 11 tender points on palpation to a maximum of 4 kg of pressure (just enough to blanch examiners thumbnail) GREATER TROCHANTER – Muscle attachments just posterior to GT Control Points Tender Points 18
    19. 19. • What is Fibromyalgia? • Pathogenesis of Fibromyalgia • Clinical Features and Diagnosis of Fibromyalgia Summary 19
    20. 20. History of chronic, widespread pain for ≥3 months Rule out other out other conditions present with chronic widespread pain Rule conditions that may that may present with chronic Depending on widespreadMental health evaluation, sleep evaluation physician: pain (“Operator dependent”) General physical exam, neurologic exam, selected laboratory testing General physical exam, neurologic exam, selected laboratory testing (ESR, thyroid tests; avoid screening serologic tests) (ESR, thyroid tests; avoid screening serologic tests) Confirm presence of tender points (Fibromyalgia may be present, even if <11 of 18) Confirm diagnosis of fibromyalgia 20
    21. 21. Is There Any Effective Management of Fibromyalgia? All patients ● Reassurance re diagnosis ● Give explanation, including, but not solely, psychological factors ● Promote return to normal activity, exercise Most patients ● Medication trial ● Cognitive behavior therapy, counseling ● Physical rehabilitation
    22. 22. Initial Treatment of Fibromyalgia Confirm diagnosis Identify important symptom domains, their severity, and level of patient function Evaluate for comorbid medical and psychiatric disorders Assess psychosocial stressors, level of fitness, and barriers to treatment Provide education about fibromyalgia May require referral to a specialist for full evaluation; for example: To psychiatry, sleep clinic
    23. 23. Nonpharmacologic Strategies: Evidence of Efficacy Strong Evidence Modest Evidence Exercise Physical and psychological benefits May increase aerobic performance and tender point pain pressure threshold, and improve pain Efficacy not maintained if exercise stops Strength training Acupuncture Hypnotherapy EMG biofeedback Balneotherapy (medicinal bathing) Transcranial electrical stimulation Cognitive-behavioral therapy Improvements in pain, fatigue, mood, and physical function Improvement often sustained for months Weak Evidence Patient education/self-management Improves pain, sleep, fatigue, and quality of life Combination (multidisciplinary therapy) Chiropractic Manual and massage therapy Ultrasound No Evidence Tender-point injections Flexibility exercise

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