Ch. 44 Myofascial Pain Syndrome

Ch. 44 Myofascial Pain Syndrome R1 최 정 현 Myofascial pain (MP)  local and referred pain that arises from myofascial trigger points Trigger points (TPs)  localized, very sensitive areas in skeletal muscle  contain palpable, taut bands  painfull to palpation, reproduce the patient’s pain, and are associated with referred pain MP  It is a treatable condition that responds to physical and injection techniques, if associated conditions and postural/ergonomic factors are also addressed.  most frequently found in head, neck, shoulders, extremities and low back  more prevalent In women often associated with  chronic head and neck pain as seen with temporomandibular joint disorder  neck pain after whiplash injury  cervicogenic headache  tension-type headache TPs classified as active or latent Active patients  with a regional pain complaint Latent patient  asymptomatic patients by their local tenderness to palpation,  perhaps associated with diminished range of motion, but not associted with spontaneous pain Diagnosis carefull musculoskeletal examination seeks to identify postural, mechanical, orthopedic, or neurological abnormalities that may contribute to MP Active TPs : suspected skeletal muscle  gentle palpation across and perpendicular to the muscle fibers. TPs are detected by   identification of taut muscle bands and production of severe pain which is characteristic of the patient’s complaint. Classic referred pain and involuntary muscle contraction or a jump sign may also be elicited Referred pain may be an unreliable sign that is not usefull clinically Pain relief may occur after muscle stretching or local injection Differential diagnosis arthritis including facet syndrome discogenic pain syndromes radiculopathy neuropathy bursitis tendonitis referred visceral pain infectious and autoimmune disorders abnormal body mechanics metabolic/endocrine disease including hypothyroidism psychiatric disorders including depression fibromyalgia Pathophysiology etiology and mechanism not been established peripheral nociception occurs along with central sensitization and an autonomic component Simons et al.  primary abnormality is pathologic increase in acetylcholine release by abnormal motor endplates at rest in muscle TPs  more frequent endplate noise in myofascial TPs than adjacent muscle outside the TP Pathophysiology Needle examination recordings  TPs show low-voltage spontaneous activity and activity resembling endplate spikes  endplate noise is characteristic but not diagnostic of myofascial patient Increased acetylcholine release --> sustained depolarization of the postjunctional membrane and sustained muscle contraction Sustained maximal shortening of the sarcomere in the region of the motor endplate Chronic sarcomere shortening --> localized alterations in energy consumption and perfusion --> ischemia --> increased resting tension in the taut muscle band Muscle ischemia --> release of vasoactive substances that sensitize afferent nociceptors --> increased tenderness to palpation Pathophysiology Chronic MP  central sensitization, refferred pain to adjacent spinal levels, and persistent pain at the spinal cord and brain levels Psychological Stress and the sympathetic nervous system  perpetuate MP  Endplate potential spike activity in TPs increased with experimental psychological stress TREATMENT: MECHANlCAL The goal of treatment  to educate and empower patients to understand and manage the symptoms of MP and to regain and maintain normal function with as much independence as possible Correction of postural and ergonomic abnormalities --> standard component of patient management TREATMENT: MECHANlCAL A Study of chronic oral and masticatory muscle pain  compared four single treatments:     relaxation physial therapy transcutaneous electrical nerve stimulation (TENS) dental splinting  response was good, but similar Acupuncture treatment at points (myofascial neck pain)  more effective than treatment with either nonsteroidal antiinf1ammatory drugs (NSAIDs) or acupuncture at distant sites value of massage therapy : not been demonstrated. Ultrasound : not offer added benefit to combined exercise and massage EXERClSE AND INJECTION THERAPY Stretching exercises  cornerstone of all treatment approaches for MR  Slow, sustained muscle stretch  aims to restore normal muscle length and activity  combined with lightIy loaded daily physical activity until patients demonstrate improved pain and range of motion.  Topical cold appliation may be used to facilitate muscle stretch.  initial goal도달 후 add a graded Stabilization and muscle Strengthening program to further improve functional statusAn aerobic exercise component is included to maintain muscle and cardiovascular fitness EXERClSE AND INJECTION THERAPY Trigger point injections (TPIs)   best suited for initiation of treatment In patients intolerant of physical therapy (PT) focused on a difficult area of persistent MP identified by the therapist. The goaI of TPI   facilitate progress in PT and ultimately to support patient success in program of home Stretching exercise < injected medications > local anesthetics steroids botulinum toxin no drug (dry needling) Trigger point injections (TPIs) Injection pain and postinjection soreness vary with the drugs employed but no difference in efficacy Bupivacaine : increased injection pain and greater myotoxicity Injection pain is diminished when lidocaine or mepivacaine are diluted with water to a concentration of 0.2% to 0.25% sterile water alone : more painfull than similar injections of normal saline intensity and duration of postinjection soreness : grater after dry needling Cummings and white conclude  drug employed does not alter the outcome or offer any therapeutic benefit over dry needling elicitation of a local twitch response during injection --> best indicator of a successfull procedure Injection of botulinum toxin type A    increasingly popular but very expensive treatment for TPs in MP inhibits muscle contraction by inhibiting release of acetylcholine at the motor endplate --> sustained relaxation of muscles PHARMACOLOGIC TREATMENT NSAIDs tramadol antidepressants alpha2-adrenergic agonist and muscle relaxant (tizanidine) : MP와 FM에서 analgesia 제공 CONCURRENT MANAGEMENT 모든 방법이 실패하였을 때 physician은 other options을 고려해 봐야함.  Search for a contributing psychological component  other undiagnosed pain generators high levels of anxiety --> selected stress management techniques other underlying pain sources  lumbar and gluteal MP : discogenic, ligamentous, facet joint, sacroiliac joint pathology  thoracic TP : pancreatic cancer Ch. 45 Fibromyalgia Fibromyalgia (FM)  prevalent musculoskeletal pain disorder characerized by diffuse pain and abnormal soft tissue tenderness Associated symptoms widespread pain at multiple tender points (at the muscletendon junction and in muscles, bursae, and fat pads) reduced pain threshold fatigue sleep disturbances morning stiffness depression anxiety psychological distress subjective swelling irritable bowel syndrome headaches paresthesias prevalence : between 0.5% and 5% of the population most fieqllently seen in women between the ages of 2O and 50 years gender ratio is 10:1 favoring women no association between FM prevalence and compensation DlAGNOSIS criteria : 1. Chronic widespread pain (CWP) at least 3 months' duration, present above and below the diaphragm on both sides of the body plus axial pain 2. Painful tender points (TPs) in at least 11 out of 18 characteristic locations.  TPs are defined by mild or greater pain after palpation with an approximate force of 4 kg/cm2 (thumb pressure such that the nail bed starts to blanch) at these sites: ·Bilateral occiput, at the suboccipital muscle insertion. ·Bilateral low cervical, at anterior aspect of intertransverse spaces between C5 and C7. ·Bilateral trapezius, at midpoint of the upper border. ·Bilateral supraspinatus, at its origin above scapular spine near the border. ·Bilateral second rib,just lateral to the costochondral junctions on upper surface ·Bilateral lateral epicondyle, 2 cm distal to the epicondyle ·Bilateral gluteal, at the upper outer quadrant of the buttock. ·Bilateral greater trochanter, posterior to the trochanter. ·Bilateral knee, medial fat pad proximal to the joint line. Two other important symptoms characteristic of FM  subjective swollen feeling without objective joint swelling  paresthesia without objective neurologic findings  reflect heightened sensory perception due to central sensitization FM symptoms are often aggravated by  cold humid weather  interrupted sleep  repeated injury  mental stress  inactivity FM symptoms tend to improve with  warm dry climate  rest  modest activity  good sleep  Relxation associated with many similar conditions  irritable bowel syndrome (in 30% to 50%)  tension headaches  migraine  headaches  temporomandibular dys려nction  myofascial pain syndrome  chronic fatigue syndrome  restless legs syndrome(in one-third)  multiple chemical sensitivity  post-traumatic stress disorder Several other diseases may be associated with and aggravate symptoms of FM:  systemic lupus  rheumatoid arthritis  Sjogren’s syndrome  Osteoarthritis  spinal stenosis  neuropathy  hypothyroidism  growth hormone deficiency(in about one-third of patients) PATHOPHYSIOLOGY strong association between FM and sleep disturbance Normal sleep  four nondream stage (non-REM sleep)  dream stage (REM sleep) many FM patients  alpha-delta EEG panern : not get into the restorative stages 3 and 4 of non-REM sleep  due to alpha wave (7.5 to 11 Hz) intrusion during delta wave (0.5 to 2 Hz) sleep  experimental induction of alpha-delta sleep in healthy individuals  induce symptoms suggestive of FM (muscle aching, stiffness, and tenderness) Nonrestorative sleep  increased pain and fatigue pharmamlogic correction of the sleep abnormality may improve both symptoms PATHOPHYSIOLOGY often associated with diseases 1. autoimmune basis : rheumatoid arthritis, systemic lupus  possible immune system alteration시사 2. endocrine abnormality diminished responsiveness ofthe hypothalamic-pituitary system growth hormone deficient 3. underlying psychological disturbance 30% of FM patients -->clinical depression PATHOPHYSIOLOGY muscle pathology  most common findings : disuse or deconditioning  주로 central nervous system (CNS) pathophysiology임 을 시사(rather than peripheral) Abnormal central neurophysiology  most accepted pathologic mechanism in FM pathological nociceptive processing within the CNS  substance P and nerve growth factor, neuropeptides의 cerebrospinal fluid levels 증가: enhance nociceptive neurotransmission Activation of N-methyl-D-aspartate (NMDA) receptors : important part in central senitization MANAGEMENT goals of patient management  accurate diagnosis  patient education and empowerment  symptom control for pain, fatigue, and sleep  management of associated psychological, endocrine, and autonomic disorders  Treatment of any peripheral pain generators  improved physical conditioning and function patient education by Bennett Key components          . validate the patient’s symptoms and explain nature of FM syndrome ·Emphasize nondestructive and treatable nature of FM symptoms ·Set realistic goals: improving function without complete symptom eradication. ·Discuss all treatment options and enlist patient in selection of plan ·Stress importance of gentle, life-long aerobic exercise and pacing activity. ·Educate patient on principles of sleep hygiene. ·Teach coping skills: meditation and relaxation techniques. ·Improve patient assertiveness and active role in FM management plan ·Refer patients to educational resources, including on-line selfhelp material. NONPHARMACOLOGIC PATlENT MANAGEMENT Cognitive-behavioral Strategies  teach patients how their thoughts and behaviors influence symptoms  how they an potentially control their symptoms  significant changes in tender points, pain scores, coping scores, or pain behaviors. EXERClSE THERAPY FM patients : good candidate for rehabilitative physical therapy  too rigorous program may be deleterious  carefully planned individual exercise program is required  aerobic exercise produces significant benefits  improvements in pain scores and tender points  Strength training may also have had benefits on some FM symptoms PHARMACOLOGIC TREATHENT OF PAlN AND ASSOCIATED SYHPTOMS nonsteroidal anti-inflammatory drugs(NSAIDs) or acetaminophen  addressing peripheral pain generators tricyclic antidepressants (TCAs)    most common drug tratment for FM improve sleep, fatigue, pain, and well-being in that order but not improve tender points selective serotonin reuptake inhibitors (SSRIs)   less impressive analgesic effcts helphll for emotional components and mood disorder combination of fluoxetine and amitriptyline --> superior to either agent alone serotonin-epinephrine dual reuptake inhibitors (SNRIs)    quite similar to TCAs but other receptor improve on side-effect profile and increase patient tolerance when compared to TCA PHARMACOLOGIC TREATHENT OF PAlN AND ASSOCIATED SYHPTOMS Venalafaxin   5-HT system at low doses NE effects apparent at higher doses tizanidine   alpha2-adrenergic agonist and muscle relaxant with antinociceptive and antispasmodic actions effectively for FM-related pain and for sleep disturbance Low-dose (started at 5 to 1O mg) TCA therapy at bedtime  most common sleep therapy for FM patient with sleep disturbance Cyclobenzaprine   TCA-analogue muscle relaxant effects on sleep and evening fatigue For patients intolerant of TCAs   short-acting imidazopyridine hypnotics(zolpidem and zaleplon) unlike benzodiazepines, not interfere with stage 3 and stage 4 sleep, or with memory PHARMACOLOGIC TREATHENT OF PAlN AND ASSOCIATED SYHPTOMS most common sleep disorder in FM patients --> restless leg syndrome  characterigd by crawling sensations ofthe legs and an     uncontrollable urge to stretch L-dopa/carbidopa at dinner donazepam at bedtime이 효과적 other dopamine agonists (pergolide, pramixepole, and tolixepole) and bedtime methadone역시 효과적 Sleep apnea환자에서는 sedative피해야 Fatigue  often resistant to drug therapy  SSRI와 5-HT3 antagonist(tropisetron)이 증상개선.