Downloaded 275 times
More Related Content
Similar to Chronic pain management
Chronic pain management
- 1. Presented by Dr. SubratKumar Nayak 2nd Year Post Graduate Trainee Moderator: Dr. Y. Arun Kumar Singh Department of Anaesthesiology & Critical Care Regional Institute of Medical Sciences, Imphal
- 2. What is PAIN? •“An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage” 5/1/2017 2Chronic Pain Management
- 3. Various Descriptors ofPain Somatic pain caused by the activation of pain receptors in either the cutaneous (the body surface) or deeper tissues (musculoskeletal tissues). Visceral pain that is caused by activation of pain receptors from infiltration, compression, extension or stretching of the thoracic, abdominal or pelvic viscera (chest, stomach and pelvic areas). Neuropathic pain caused by injury to the nervous system either as a result of a tumor compressing nerves or the spinal cord, or cancer actually infiltrating into the nerves or spinal cord. 5/1/2017 3Chronic Pain Management
- 4. Acute pain: short-lastingand manifesting in objective ways that can be easily described and observed. It may be clinically associated with diaphoresis and tachycardia. It can last for several days, increasing in intensity over time (subacute pain), or it can occur intermittently (episodic or intermittent pain). Usually related to a discreet event for onset: post op, post trauma, fracture, etc 5/1/2017 4Chronic Pain Management
- 5. Chronic pain: Long-term andtypically defined if it lasts for > three months. It is more subjective and not as easily clinically characterized as acute pain and is more psychological. This kind of pain usually affects a person's life, changing personality, their ability to function, and their overall lifestyle. Chronic pain has a psycho-social component that must be dealt with the clinical picture before depression becomes a part of multi-factorial disease. 5/1/2017 5Chronic Pain Management
- 6. 5/1/2017 6Chronic PainManagement
- 7.
- 8. 5/1/2017 8Chronic PainManagement
- 9. 5/1/2017 9Chronic PainManagement
- 10. 5/1/2017 10Chronic PainManagement
- 11. 5/1/2017 11Chronic PainManagement
- 12. 5/1/2017 12Chronic PainManagement
- 13. 5/1/2017 13Chronic PainManagement
- 14. 5/1/2017 14Chronic PainManagement
- 15. 5/1/2017 15Chronic PainManagement
- 16. Brain Regions involvedin Chronic pain 5/1/2017 16Chronic Pain Management
- 17. 5/1/2017 17Chronic PainManagement
- 18. Neuroplasticity in pain processing 5/1/201718Chronic Pain Management
- 19. What is ChronicPain? Chronic pain is pain that: – continues a month or more beyond the usual recovery period for an injury or illness or – goes on for months or years due to a chronic condition. The pain may not be constant but disrupts daily life. 5/1/2017 19Chronic Pain Management
- 20. Dimensions of ChronicPain Loneliness Hostility Social Factors Anxiety Depression Psychological Factors Pathological Process Physical Factors TIME 5/1/2017 20Chronic Pain Management
- 21. EVALUATION OF CHRONICPAIN 5/1/2017 21Chronic Pain Management
- 22.
- 23. COMMON ETIOLOGIES OF CHRONICPAIN Episodic pain syndromes: Headaches – migraine, tension, cluster… Ischemic episodes – claudication, angina, sickle cell disease Visceral pain – biliary colic, irritable bowel, pre-menstrual syndrome, renal colic Somatic pain - gout 5/1/2017 23Chronic Pain Management
- 24. Chronic pain syndromes: Somatic– low back pain ,degenerative and inflammatory arthitis, lumbosacral radiculopathy, Failed back surgery, vertebral compression fractures, bony metastases, Myofascial pain syndrome. Visceral – abdominal cancers, chronic pancreatitis. Neuropathic– CRPS, Post herpetic neuralgia, Trigeminal neuralgia,diabetic neuropathy, phantom limb pain, spinal stenosis/sciatica, spinal mets, 5/1/2017 24Chronic Pain Management
- 25. Neuralgia – anextremely painful condition consisting of recurrent episodes of intense shooting or stabbing pain along the course of the nerve. Causalgia – recurrent episodes of severe burning pain. Phantom limb pain – feelings of pain in a limb that is no longer there and has no functioning nerves. 5/1/2017 25Chronic Pain Management
- 26. ICD 11 Classification 7groups: Chronic primary pain Chronic cancer pain Chronic post traumatic & post surgical pain Chronic neuropathic pain Chronic headache & orofacial pain Chronic visceral pain Chronic musculoskeletal pain 5/1/2017 26Chronic Pain Management
- 27. Common causes oflow back pain Radiculitis or radiculopathy from a herniated disc or spinal or foraminal stenosis Facet syndrome Internal disc disruption Myofascial pain Sacroiliac joint syndrome & pyriformis syndrome Vertebral body fractures Infections Abdominal aortic aneurysm Chronic pancreatic lesions 5/1/2017 27Chronic Pain Management
- 28. Headaches 5/1/2017 28Chronic PainManagement
- 29. COMPLEX REGIONAL PAIN SYNDROMES(CRPS) •Neuropathic pain that involves upper and lower extremities. • Reflex sympathetic dystrophy and causalgia are replaced by CRPS I , CRPS II. • CRPS type I: follows minor trauma. • Preceeding events are trauma, surgery, sprain, fracture, dislocation. 5/1/2017 29Chronic Pain Management
- 30. 5/1/2017 30Chronic PainManagement
- 31. 5/1/2017 Chronic PainManagement 31
- 32. 5/1/2017 Chronic PainManagement 32
- 33. 3 phases forCRPS I 5/1/2017 33Chronic Pain Management
- 34. 5/1/2017 34Chronic PainManagement
- 35. Fibromyalgia Syndrome Etiology isunknown. 3 views of pathophysiology have emerged: Central Nervous System (neurogenic) generalized pain increase in CSF substance P decrease in serum and CSF serotonin Muscle Pathology – decreased oxygen tension and blood flow – abnormal muscle biopsies – weakness Psychopathology anxiety, depression (Loesser et al, 2001; Portenoy et al, 1996; Wall et al, 1994)
- 36. Clinical Characteristics Pain (musculoskeletaltenderness) Lightheadedness, dizziness, syncope Fatigue Chronic insomnia; sleep disturbance Cognitive deficits/short-term memory loss Depression/anxiety Numbness, dysesthesia in hands and feet (Loeser et al, 2001)
- 37. Diagnosis Based on the1990 ACR classification guidelines: • 1 historical feature + 1 physical finding • Historical feature = widespread (axial) pain of 3 months or more • Physical finding = pain in at least 3 of the 4 body segments + a finding of at least 11 tender points on digital palpation of 18 designated tender points (Merskey et al, 1994; Portenoy et al, 1996; Wall et al, 1994; Wolk M, 2002)
- 38. (Portenoy et al,1996; Wall et al, 1994)
- 39. POST HERPETIC NEURALGIA(PHN) Intractable painthat develops as a sequel of acute herpes zoster infection (AHZ). Pain from AHZ resolves usually within 3-4 weeks and if pain lasts longer than 4-6wks PHN should be suspected. In AHZ large myelinated fibers are destroyed whereas in PHN pain processing by small fibers is compromised. 5/1/2017 39Chronic Pain Management
- 40. Typically presents withunilateral pain in dermatomal distribution. Treatment: Sympathetic blockade during attack Antidepressants, anticonvulsants, opioids. TENS. 5/1/2017 40Chronic Pain Management
- 41. Trigeminal Neuralgia (TN) TICDOULOUREUX classically presents as a painful, unilateral affliction of the face, characterized by brief electric-shock-like pain, limited to the distribution of one or more divisions of the trigeminal nerve. Pain is commonly evoked by trivial stimuli, including washing, shaving, smoking, talking and brushing the teeth, but may also occur spontaneously. The pain is abrupt in onset and termination may remit for varying periods. 5/1/2017 41Chronic Pain Management
- 42. Treatment: Carbamazepine. Invasive treatment- Glycerolinjection, Radiofrequency ablation of gasserian ganglion Microsurgical decompression of trigeminal nerve. 5/1/2017 42Chronic Pain Management
- 43. Diabetic neuropathy Peripheral neuropathiesmay b present in 65% of IDDM patients. Chronic sensorimotor distal polyneuropathy is the MC type. Management: Control of blood glucose and pharmacologic therapy. Gabapentin and Pregabalin appear to be effective TCAs are also effective but not SSRIs 5/1/2017 43Chronic Pain Management
- 44. 5/1/2017 44Chronic PainManagement HIV neuropathy
- 45. 5/1/2017 Chronic PainManagement 45 Phantom Pain Occurs in as many as 80% of amputees. Treatment includes use of opioids, gabapentin, NMDA antagonist & antidepressants
- 46. MANAGEMENT of chroNicpAiN 5/1/2017 46Chronic Pain Management
- 47. Goals Improvements in nociception,not curing. Decrease pain and suffering Increase daily activity. Instill hope 5/1/2017 47Chronic Pain Management
- 48. THERAPEUTIC MODALITIES Pharmacological. Physical measures/nonpharmacological. Psychological measures. Invasive techniques. 5/1/2017 48Chronic Pain Management
- 49. 5/1/2017 49Chronic PainManagement
- 50. WHO PAIN RELIEFLADDER 5/1/2017 50Chronic Pain Management
- 51. Pain Step 1 ± Nonopioid ±Adjuvant Pain persisting or increasing Step 2 Opioid for mild to moderate pain ± Nonopioid ± Adjuvant Pain persisting or increasing Pain persisting or increasing Step 3 Opioid for moderate to severe pain ± Nonopioid ±Adjuvant Invasive treatments Opioid Delivery Quality of Life Modified WHO Analgesic Ladder Proposed 4th Step The WHO Ladder 5/1/2017 51Chronic Pain Management
- 52. PHARMACOLOGIC CONTROL About halfof hospitalized patients who have pain are under-medicated. Children are at particular risk of poor pain control methods. Medications are given as: PRN : “as needed” As a prescribed schedule 5/1/2017 52Chronic Pain Management
- 53. 5/1/2017 53Chronic PainManagement
- 54. Recommended drugs forchronic pain syndromes 5/1/2017 Chronic Pain Management 54
- 55. PHYSICAL MEASURES Exercises: Gradedexercise program prevents joint stiffness, muscle atrophy and contractures. Superficial heating modalities: Conductive – hot packs, paraffin baths, fluid therapy. Convective Radiant. 5/1/2017 55Chronic Pain Management
- 56. ULTRASOUND: for deeppain. 5/1/2017 56Chronic Pain Management
- 57. ACCUPUNCTURE: • Useful adjunctfor patients with chronic musculoskeletal disorders and headaches. • Technique – insertion of needles in discrete anatomically defined points called “MERIDIANS”. 5/1/2017 57Chronic Pain Management
- 58. Transcutaneous electrical nerve stimulation(TENS) • Used widely in chronic pain • All available trials used TENS as an adjuvant to medication, and it’s possible the effects of TENS was masked by the analgesic effect of medication 5/1/2017 58Chronic Pain Management
- 59. Physical measures Ice packs Chiropractic/osteopathicmanipulations Massage Yoga Topical agents (Ben Gay/Icy Hot – with menthol, salcylates, Capcaicin) Local injections (steroids, lidocaine) Glucosamine shown to help with osteoarthritis 5/1/2017 59Chronic Pain Management
- 60. Psychological methods Integral partof multidisciplinary approach to pain management. Self management techniques – cognitive methods, relaxation, biofeedback. Operant techniques. Group therapy. 5/1/2017 60Chronic Pain Management
- 61. Cognitive methods: Based onassumptions that a patients attitude towards pain can influence the perception of pain. Maladaptive attitudes contribute to suffering and disability. Patient is taught skills for coping with pain either individually or in group therapy. 5/1/2017 61Chronic Pain Management
- 62. Biofeedback – providesbiophysiological 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. 5/1/2017 62Chronic Pain Management
- 63. OPERANT / BEHAVIOURTHERAPY: • Based on premise that behaviour in patients with chronic pain is determined by consequences of behaviour. • Positive reinforcers aggravate the pain, negative reinforcers reduce pain behaviour. 5/1/2017 63Chronic Pain Management
- 64. INTERVENTIONAL PROCEDURES 5/1/2017 64ChronicPain Management
- 65. Role of InvasiveProcedures Intractable pain* Intractable side effects* *Symptoms that persists despite carefully individualized patient management 5/1/2017 65Chronic Pain Management
- 66. SELECTION OF BLOCK: Dependson Location of pain Its presumed mechanism Skills of treating physician. L.A ‘s can be applied locally, at peripheral nerve, somatic plexus, sympathetic ganglia or nerve root, centrally in neuraxis. 5/1/2017 66Chronic Pain Management
- 67. Somatic nerve blocks: Trigeminalnerve blocks Cervical, thoracic, lumbar paravertebral blocks Facet blocks Trans sacral nerve blocks etc. 5/1/2017 67Chronic Pain Management
- 68. 5/1/2017 68Chronic PainManagement
- 69. Sympathetic blocks: Stellate ganglionblock Celiac plexus block Thoracic, lumbar sympathetic chain block etc. 5/1/2017 69Chronic Pain Management
- 70.
- 71. EPIDURAL INJECTIONS: Lumbar interlaminarepidural injections Fluoroscopic injections Transforaminal injections Radiofrequency rhizotomy 5/1/2017 71Chronic Pain Management
- 72. 5/1/2017 72Chronic PainManagement
- 73. SPINAL INJECTIONS: Therapeutic effectsof spinal injections are a combination of primary physiologic changes that result from the procedure and the secondary results arising from the enhanced pain control that allow other treatments. 5/1/2017 73Chronic Pain Management
- 74. Spinal cord stimulation •Also called dorsal column stimulation. • Produces analgesia by directly stimulating large A beta fibers in dorsal columns of the spinal cord. • Mechanism – activation of descending modulating systems and inhibition of sympathetic outflow. 5/1/2017 74Chronic Pain Management
- 75. Indications: Sympathetically mediated pain Spinalcord lesions Phantom limb pain Failed back surgery syndrome. Technique: electrodes placed epidurally and connected to an external generator. Complications: infection, lead migration, lead breakage. 5/1/2017 75Chronic Pain Management
- 76. Intracerebral stimulation Deep brainstimulation may be used for intractable cancer pain and rarely for intractable neuropathic pain of nonmalignant origin. Electrodes are implanted stereotactically into periaqueductal and periventricular gray areas for nociceptive pain. Complications: intracranial hemorrhage and infection. 5/1/2017 76Chronic Pain Management
- 77. Discography Discogenic pain arenon specific and include non radicular back pain. Pain worsens on sitting posture. Functional discography involves insertion of catheter and injecting LA. Most feared complication is discitis 5/1/2017 77Chronic Pain Management
- 78. Intradiscal electrothermal therapy 5/1/201778Chronic Pain Management
- 79. Percutaneous Disc Decompression 5/1/201779Chronic Pain Management
- 80. 5/1/2017 80Chronic PainManagement
- 81. Minimally invasive LumbarDecompression This minimally invasive procedure is indicated in patients with low back pain & neurogenic claudication associated with MRI or CT evidence of central canal stenosis secondary to facet hypertrophy. It includes percutaneous laminotomy & thinning of the ligamentum flavum to increase the critical diameter of stenosed spinal canal.5/1/2017 81Chronic Pain Management
- 82. Vertebroplasty & Kyphoplasty Indication: Vertebralcompression fractures secondary to osteoporosis. Technique: Vertebroplasty involves injection of Polymethylmethacrylate into affected vertebral body. Kyphoplasty involves insertion of baloon before injection of cement. Complications: Pulmonary embolism, radiculopathy, spinal claudication & paraplegia. 5/1/2017 82Chronic Pain Management
- 83. Peripheral nerve stimulation Indications: treatmentof neuropathic pain ideally arising from single nerve (occipital neuralgia, supraorbital neuralgia, peripheral neuropathies) 5/1/2017 83Chronic Pain Management
- 84. Intrathecal pumps Option forindividuals in whom opioids are medications at reasonable doses or cause unacceptable side effects. Main indications are patients with cancer pain followed by pain of spinal origin with failed back spinal surgery. 5/1/2017 84Chronic Pain Management
- 85. Novel Drug Therapiesfor Treatment of Pain Central Nociception: Emerging Analgesic Targets • Excitatory amino acid and NK receptors • N-type Ca++ receptors • N-acetylcholine receptors • Adenosine (A1) receptors • Cannabinoid (CB1) receptors (Pappagallo M)
- 86. Peripheral Nociception: Emerging AnalgesicTargets • Sensory neuron specific Na+ channels (eg, PN3, NAN) • Opioid receptors • Vanilloid receptors • Serotonin receptors • Alpha-adrenergic receptors • Proton-sensitive channels (pH-sensitive) • Nerve–growth-factor receptors (*TrKA, p75) • N- or T-type Ca++ channels • Purine receptors *TrKA = tyrosine kinase (Pappagallo M)
- 87. Perioperative Management ofpatients with chronic pain 5/1/2017 Chronic Pain Management 87
- 88. Preoperative considerations Communicate with,and involve the patient in, perioperative management decisions. For opioids, continue baseline dose via appropriate route with additional supplementation for the acute event carefully titrated to the pain For antidepressants, continue low dose tricyclic antidepressants, selective serotonin reuptake inhibitors, and selective noradrenaline reuptake inhibitors; be aware of potential for serotonin syndrome For anticonvulsants, continue perioperatively; if stopping, taper the dose slowly to avoid withdrawal 5/1/2017 88Chronic Pain Management
- 89. If patient hasa spinal cord stimulator, turn this off perioperatively If patient has an intrathecal drug delivery system, continue perioperatively and supplement patient with additional analgesia for the acute event enterally and/or parenterally; be aware of potentially serious adverse effects of abrupt cessation of intrathecal medications 5/1/2017 89Chronic Pain Management
- 90. Management of Chronicpain in substance abuse disorder 5/1/2017 Chronic Pain Management 90
- 91. • Physical Dependence –Abstinence syndrome induced by administration of an antagonist or by dose reduction – Usually unimportant if abstinence is avoided – Assumed to exist after few days’ dosing but actually highly variable – Does not independently cause addiction • Addiction – Disease with pharmacologic, genetic, psychosocial elements – Fundamental features: loss of control, compulsive use, use despite harm – Diagnosed by observation of aberrant drug-related behavior 5/1/2017 91Chronic Pain Management
- 92. Tolerance Diminished drug effectfrom drug exposure Varied types: associative vs. pharmacological Tolerance to analgesia is seldom a problem in the clinical setting: Tolerance rarely “drives” dose escalation Tolerance does not cause addiction Pseudoaddiction Aberrant drug-related behaviors driven by uncontrolled pain Reduced by improved pain control 5/1/2017 92Chronic Pain Management
- 93. The prevalence ofopioid abuse in chronic pain patients ranges between 20-24% across health-care settings. Further, it has been reported that 3.3% to 11.5% of chronic pain patients with a history of SUD may develop opioid addiction or abuse, whereas only 0.19% to 0.59% of those without a prior or current history of SUD develop the same. Opioid-induced hyperalgesia is seen in Substance Use Disorder (SUD patients) 5/1/2017 93Chronic Pain Management
- 94. 5/1/2017 Chronic PainManagement 94
- 95.
- 96. 5/1/2017 Chronic PainManagement 96
- 97. REFERENCES Miller’s Anaesthesia, 8th edn. Barash’sClinical Anaesthesia, 7th edn. Raj PP: Practical Management Of Pain . Wall PD, Melzack OC: Text book of pain. ISA Journal On pain. Gowri devi M; Chronic pain Management-Psychological aspects in current concepts in pain management.CME abstract 1998. The Journal of Neuroscience, February 2007, 27(9): 2357-68. www.who.int/icd11 Addiction Science & Clinical Practice 2013; 8:21 5/1/2017 97Chronic Pain Management
- 98.
Editor's Notes
- #20 Colored portrait picture of a white woman, shoulder length brown hair with a worried look on her face . She is on the right side of the page.
- #26 Episodes of neuralgia occur suddenly and without apparent cause. Someone with causalgia may report that it feels like my arm is pressed against a hot stove. Typically follows a traumatic injury like a gun shot wound or stabbing and occurs at the site of injury. Is experienced well after the wound has healed. Phantom limb pain – example might be burning sensation in your toes after the limb and foot has been amputated. Person can experience a sense of their limb moving. Can persist for months and years. Pain can be felt as shooting, burning, or cramping (e.g., feel like hand is clenched with finger nails digging into the hand).
- #36 Fibromyalgia syndrome is not a subtype or form of arthritis. Although it is associated with widespread pain, joint swelling and inflammation are not obvious. The soft tissues that are painful in this syndrome appear to be the ligaments, muscles, bursae, tendons, and fascia. In 1990, the American College of Rheumatology established criteria for the diagnosis of fibromyalgia syndrome, including a history of widespread musculoskeletal pain of more than 3-months’ duration and pain upon palpation of specific tender points (11 of 18, with 9 bilateral). The locations of the tender points include the occiput, cervical spine, trapezius, supraspinatus, second rib, lateral epicondyle extensor muscle, gluteal region, greater trochanter, and knees (all bilateral). In view of the tenderness in these areas at stimuli not normally painful, some have viewed fibromyalgia syndrome as a disorder of “widespread allodynia.” Fibromyalgia syndrome has been reported in all age groups and in many ethnic groups. In adults, the syndrome is 4 to 7 times more common in women than in men. The highest prevalence is in women between 50 and 60 years old. Even though the syndrome may occur in association with other disorders such as systemic lupus erythematosus or rheumatoid arthritis, its presentation is not a “transition” to one of these or other disorders. Loeser JDF, Butler SH, Chapman CR, et al. Bonica’s Management of Pain. 3rd ed. Baltimore: Lippincott Williams Wilkins; 2001:581. Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, PA: FA Davis Company; 1996:145-151. Wall PD, Melzack R. Textbook of Pain. 3rd ed. Edinburgh, Scotland: Churchill Livingston; 1994:579-580.
- #37 It has been suggested that the typical patient with fibromyalgia syndrome is a middle-aged woman who complains to her doctor that “everything hurts.” In evaluating a patient, care must be taken to distinguish between a myofascial syndrome trigger point and a tender point (which occurs in fibromyalgia). Although some individuals with fibromyalgia syndrome may have an occasional trigger point upon examination, the two disorders are not synonymous. Other symptoms associated with fibromyalgia are throbbing occipital pain of muscle contraction headache, prolonged morning stiffness, chest wall pain, breast area pain, low back pain or sciatica-like radiation of pain, bursitis, tendonitis, irritable bowel, diarrhea, constipation, frequency/urgency. Loeser JDF, Butler SH, Chapman CR et al. Bonica’s Management of Pain. 3rd ed. Baltimore: Lippincott Williams Wilkins; 2001:550.
- #38 The 1990 guidelines for a diagnosis of fibromyalgia are the most widely used criteria. A diagnosis consists of one historical feature and one physical finding. The historical feature is widespread pain of 3 months or more. Pain is considered widespread when all of the following are present: pain in the left and the right sides of the body, pain above and below the waist. Additionally, axial skeletal pain must be present (cervical spine or anterior chest or thoracic spine or low back). In this definition, shoulder and buttock pain is considered as pain for each side. The physical feature is pain in 11 of 18 tender point sites on digital palpation. The 18 tender points are: occiput, low cervical, trapezius, suprespinatus, second rib, lateral epicondyle, gluteal, greater trochanter, knees. Digital palpation should be done with an approximate force of 4 kg. For a tender point to be considered “positive,” the patient must state that the touch was painful, not just tender. The presence of a second clinical disorder does not rule out the diagnosis of fibromyalgia. Merskey H, Bogduk N, eds. Classification of Chronic Pain: Descriptions of Chronic Pain Syndromes and Definitions of Chronic Pain Syndromes and Definitions of Pain Terms. 2nd ed. Seattle, WA: IASP Press; 1994:46. Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, PA: FA Davis Company; 1996:146. Wall PD, Melzack R. Textbook of Pain. 3rd ed. Edinburgh, Scotland: Churchill Livingston; 1994:580. Wolk, M. The diagnosis and treatment of fibromyalgia. http://www.systoc.com/CMEcourses/wolk (accessed 5/23/02)
- #39 Generally the treatment of fibromyalgia sydrome (FMS) is unsatisfactory, yet there are many therapeutic options that can lessen the degree of pain, improve functionality and help patients cope with the disorder. Often a great deal of relief is provided simply by explaining the nature of the syndrome and reducing the patient’s anxiety by ruling out a more serious, life-threatening condition—assuring the patient that FMS will not cause crippling or reduced life expectancy. The first, and possibly most important, step in treatment is patient education and support, both by the physician and medical staff, as well as a FMS support group, if possible. Equally important for the FMS patient is exercise, as deconditioned muscles are more prone to microtrauma, and inactivity leads to dysfunctional behavioral traits. All FMS patients need to have an ongoing home exercise program with muscle stretching, gentle strengthening and aerobic conditioning. It is important to remember that exercise for the FMS patient is health training, not sports training; should be non-impact exercise; should be done for a total of 30 minutes each day (10-minute or 15-minute sessions are fine); and strength training should be concentric and avoid eccentric muscle contractions. Pharmacologic treatments have been used with varying degrees of success in FMS patients, the most effective drugs being tricyclic antidepressants and analgesics.
- #53 Poor pain control is based on misperceptions of pain controlling medications – e.g., fear of addiction. Children, for fear of needles or lack of knowledge about pain-killer medications, may request medications less.
- #60 Capsaicin (Zostrix) – red hot chili pepper juice – used for centuries in S. America, burns for first few days then wears out substance P in pain receptors PT/chirpracter/massage/yoga/acupuncture in some studies equally effective in certain conditions like low back pain NSAIDs – beware of GI side effects and platelet effects, though the Salcylate class and Diflunisal have less of these effects. NSAIDs in studies shown to decrease narcotic use by up to 40% in things like wide-spread boney mets Relaxants – soma, flexeril, benzodiazepines
- #63 Biofeedback for the treatment of chronic pain appears to be no more effective than relaxation methods. Relaxation may work in two ways: 1) reducing muscle tension; and 2) helping the patient better manage stress and anxiety. Relaxation exercises are frequently used in preparing a pregnant women for the delivery of her child. Relaxation may also stimulate the release of endogenous opioids, as well as boosting immune function. Evidence suggests that its effects are modest but useful in combination with other methods. Mechanism by which hypnosis works for some pain conditions, particularly acute pain such as that during surgery, is not well understood. Cognitive methods of pain control appear to be as effectives as hypnosis.
- #86 Research is targeted at the isolation of novel compounds that will produce profound central antinociceptive effects by acting on the following receptors: Excitatory amino acids (EAAs) glutamate and aspartate, as well as several neuropeptides—such as substance P, calcitonin gene-related peptide, cholecystokinin, and neurokinin—are the neurotransmitters of nociception found on the C-fibers entering the dorsal horn of the spinal cord. By acting on several receptors such as N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid, kainate, the metabotropic receptors, and the neurokinin receptors, these neurotransmitters can induce central sensitization. Blockade of the N-type (neuron-specific) calcium channels within the dorsal horn represents an alternative for intrathecal analgesia with opioids or local anesthetics. An N-type calcium channel blocker (ziconotide) derived from the venom of a predatory marine snail soon may be available for clinical use. The activation of CNS adenosine A1 receptors also is pertinent to pain control, as demonstrated by intrathecal administration of adenosine in animal models. Similarly, recent studies evaluated the role of cannabinoids, not only as antiallodynic and antihyperalgesic agents, but also as potentiators of opioid analgesia. Brookoff D. Chronic Pain: A New Disease? Hosp Pract (Off Ed) 2000;35:45-52, 59.LK, Lipman AG. Recent advances in pharmacotherapy for cancer pain management.Cancer Pract. 2002;10(suppl 1):S14-S20 .
- #87 Some membrane components, recently identified and anticipated to be relevant to the various pathogeneses of pathologic pain and targets for analgesic drugs discovery, are the sensory neuron specific tetrodotoxin-resistant (TTX-R) voltage-gated sodium channels, opioid receptors, the vanilloid receptors (VRs), and the serotonin receptors. In the DRG, 2 types of TTX-R voltage-gated sodium channels have been identified: the PN3 and NAN. After peripheral-nerve or tissue injury, the abnormal processing of pain may be contributed to alterations in the sodium channel expression and function. The activation threshold of nociceptors also may be lowered by a direct modulation of heat or by mechanotransducer receptor proteins. The VR-1 receptor, for example, contributes to heat detection. Others among the emerging peripheral nociception channel and receptor targets include the following: The alpha-2 adrenergic receptors—For example, the topical application of an alpha-2 adrenergic agonist causes local inhibition of noradrenaline release by acting on the adrenergic alpha-2 autoreceptors of the sympathetic endings. The proton-sensitive channels—The H+-gated channel that is cloned is the acid-sensing ionic channel (ASIC), which is a member of the amiloride-sensitive/degenerin family and is expressed in some brain neurons, as well as in nociceptive neurons. The ASIC is transiently activated by rapid extracellular acidification (below pH 6.5) and desensitizes within a few seconds. The nerve growth factor (NGF) receptor—An example is the tyrosine kinase (TrKA) receptor for NGF. The TrKA-NGF complex is internalized and retrogradely transported to the DRG cell body, where it initiates gene transcription that promotes upregulation of channels involved in pain transmission. The N- or T-type current calcium channels—Following axonal injury, altered Ca++ signaling may contribute to hyperexcitability leading to neuropathic pain. The purine receptors—Purinoceptors on sensory nerve terminals may be acted upon by ATP released from different cell types, thereby contributing to the initiation of pain. Brookoff D. Chronic Pain: A New Disease? Hosp Pract (Off Ed) 2000;35:45-52, 59.