MYOFASCIAL PAINFocus on the Upper Extremity
Benson Daitz MD & Brian M. Shelley MD
UNM Family & Community Medicine
Resident School, April 2018
FINANCIAL DISCLOSURES
•None.
OBJECTIVES: MPS
After this session, participants will be able to:
•Define myofascial pain syndrome (MPS)
• Identify common presentations of MPS in the upper extremity
•Perform a trigger point injection in a myofascial trigger point.
MYOFASCIAL PAIN SYNDROME (MPS)
• Characterized by the development of myofascial trigger points (TrP or MTrP) that are locally tender when active.
• Refer pain through specific patterns to other areas of the body.
• Due to many causes like trauma, arthritis, deconditioning.
• Trigger points are usually associated with a taut band, a ropey thickening of the muscle tissue.
• Diagnosis depends on history, exam, and specialized manual palpation.
• Local twitch response may be seen in palpation and treatment
• Fascia also very important.
JANET TRAVELL MD
•A TrP is a “hyperirritable spot, usually within a taut band of skeletal muscles or in the muscle’s fascia, that is painful on compression and that can give rise to characteristic phenomena.”
MPS: Mechanism (Travell)
•The “integrated hypothesis” includes:•Spine•Muscle•NMJ
•Abnormalities at the neuro-muscular junction:↑ ACh production, depolarization↑ Sustained shortening of sarcomeres↑ Energy demand, release of sensitizing
substances, leading to…↑ ACh production (BTXA blocks release)
SHAH
• Compared to carefully matched controls, people with neck pain secondary to active TrPs had significantly elevated local levels of • endogenous substance P (SP)• calcitonin gene-related peptide (CGRP)• bradykinin (BK)• serotonin/5-hydroxytryptamine (5-HT)• norepinephrine (NE)• tumor necrosis factor alpha (TNF-α)• interleukin 1-beta (IL-1β)
Shah JP, Danoff JV, Desai M, et al. Biochemicals associated with pain and inflammation are elevated in sites near to and remote from active myofascial trigger points. Arch Phys Med Rehabil (2008);89:16-23.
SHAH
•At motor endplate (distal axon):•↑CGRP → ↑Ach → ↓AchE activity•Leads to increased ACh receptors and activity, and persistent focal muscle fiber contraction•TrPs have spontaneous electrical activity (SEA), or dysfunctional endplate potential of extrafusal (skeletal) muscle fibers
Travell
Shah
•Muscle pain can activate nociceptive-specific neurons in the brainstem and spinal cord, via biochemical and neuronal pathways.•Active TrPs are a source of ongoing peripheral nociception that may induce central sensitization, via “afferent bombardment” of dorsal horn neurons, and biochemical milieu.
SHAH
•Central sensitization comes about via increased excitatory and decreased inhibitory processes, and activation of previously “silent synapses” and wide-dynamic range (WDR) neurons in the dorsal horn.
•There is also a biochemical basis for central sensitization:•Muscle nociceptors → •↑L-glutamate/SP (pre-synaptic) → •↑ alpha-amino-3-hydroxy-5-methyl-4-
isoxazolepropionic acid (AMPA) (post-synaptic) → •↑ previously dormant N-methyl-D-aspartate (NMDA)
receptors
SHAH
•Stimulated WDR neurons can ascend the spinothalamic tract, activating the limbic system (anterior cingulate gyrus, insula, and amygdala)•Modulates pain and the emotional/affective components
of pain•Elicitaton of the LTR has been shown to result in rapid
reduction of SP and CGRP in the areas of active TrPs.•This may be due to increased local blood flow or
inflammatory responses• It is possible to identify taut bands via ultrasound, which
appear as focal hypoechoic (darker) areas with “heterogenous echotexture.”
Precipitating Factors of TrPs
•Anatomic variations•Posture•Work•Stress•Degenerative conditions• Injuries, trauma•Medical conditions
• Idiopathic
Differential Diagnosis
• Not mutually exclusive
• Similar to precipitating factors
• General Medical Conditions• Arthropathies• Tendinopathies• Spinal disk disease (and/or stenosis, radiculopathy, FBSS)• Nutritional Deficiencies• Deconditioning• Neuropathy (from DM)• Migraine• Fibromyalgia
• Psychological Conditions• Anxiety• Depression• Somatization
Differential Diagnosis in the Upper Extremity
• ALL AREAS• Radiculopathy • Arthritis• Neuropathy• Myelopathy• Thoracic outlet syndrome
• SHOULDER• Subacromial bursitis• Bicipital tendinitis• Impingement syndrome• Adhesive capsulitis• Rotator cuff pathology
• ELBOW• Lateral epicondylitis• Medial epicondylitis• Cubital tunnel syndrome
• WRIST/HAND• Carpal tunnel syndrome• De Quervain's
tenosynovitis
Classic Anatomic Diagram Of Neck
Muscles
Compare: Sternocleidomastoid (only)
“Key” Trigger Points
COMMON TRIGGER POINTS IN
UPPER EXTREMITY SYNDOMES:
Trapezius
Levator scapulae
Scalenes
Infraspinatus
Pectoralis
Deltoid
Biceps
Triceps
ECRL/B
Extensor digitorum
FCR
But all muscles shown below are clinically relevant.
Can find diagrams at: www.triggerpoints.net
Trapezius
Palpation
• Trapezius TrP #2:• Use dominant hand fingertips to find TrP
• Notice variation in resistance/texture
• Notice taut bands/orientation
• Notice local twitch response, if present
• Notice referral pattern, if present
Trapezius
Levator Scapulae
SCALENES
Rhomboid
Pectoralis Major
Latissimus Dorsi
Serratus Anterior
Serratus Posterior Superior
Subscapularis
Supraspinatus
Infraspinatus
DELTOID
Biceps Brachii (Note: more distal, less “area”)
TRICEPS
BRACHIORADIALIS
SUPINATOR
Pronator teres
PRONATOR QUADRATUS (HWANG)
EXTENSORS
Extensor digitorum (communis)
Flexor muscles
Flexor pollicis longus
TPI
Trigger Point Injection (TPI)
TPI: One way to do this
•1% lidocaine, without epinephrine•27 G needle, 1.25” long•3 cc syringe• Inject 0.25-0.50 cc per site• Inject 4-10 sites per session, in same region•First time: just a few (~4)
Effect of TPI
• Muscular level: TPI often induces a local twitch response (contraction and release), which is what often leads to positive therapeutic outcome.
• Mechanical disruption by the needle seems to be the level at which TPI works, since dry needling and anesthetic are both effective in deactivating trigger point (Travell and Simons, vol. 1, p. 152).
• The LTR possibly interrupts the dysfunctional spinal and NMJ cycles, as well (Botox works at NMJ).
• Dr. Shelley’s opinion: lidocaine adds to the process by breaking the pain cycle, even temporarily, allowing for more movement of the muscle.
• Thin needles• 27 G for most injections• 30 G for the face• 22-25 G for deep sites (3.5 “ needle)
• No make up, no ink• No steroids• As few TPIs as possible• As little injectate as possible• Err on superficiality (might even be treating fascia sometimes)• Proximal>>distal• Think hard before injecting distal to the elbow and knees• Think even harder before injecting distal to the wrists and
ankles• Aim to inject over bony structures when possible:
• Ribs• Vertebral bodies• Scapulae….
SAFETY
Infraspinatus… safe?
DEMO and PRACTICE
Thank You
RESOURCES
BOOKS• Travell JG, Simons DG. Myofascial Pain and
Dysfunction: The Trigger Point Manual, 2nd ed.Baltimore: Williams & Wilkins, 1999.
• Ferguson LW, Gerwin R. Clinical Mastery in the Treatment of Myofascial Pain. Philadelphia: Lippincott Williams & Wilkins, 2004.
• Davies C. Trigger Point Therapy Workbook (2nd Ed.). Oakland: New Harbinger, 2004. (Good for patients.)
DIGITAL• MyoRehab site: http://www.triggerpoints.net/• Various apps out there