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