Journal of the K. S. C. N. Vol. 3, No. 2 myofascial pain syndrome Gun-Sei Oh, M.D., Hee-Jung Song M.D. Department of Neurology, Eulji University, Scho

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1 Journal of the K. S. C. N. Vol. 3, No. 2 myofascial pain syndrome Gun-Sei Oh, M.D., Hee-Jung Song M.D. Department of Neurology, Eulji University, School of Medicine, Daejeon, Korea - Abstract - Pain and tenderness are characteristically referred from myofascial trigger points(mtrps) located in muscle remote from the site of the pain. Pain from MTrPs can be identified by careful history taking and skillful physical examination, and it is quickly responsive to physical and medical management in the absence of serious perpetuating factors. Skeletal muscle makes up nearly half of body weight. Each of the approximately 500 skeletal muscles is subject to acute and chronic strain. Each muscle can develop myofascial trigger points and has its own characteristic pattern of referred pain. Perpetuating factors can increase irritability of muscles, leading to the propagation of trigger points and increasing the distribution and severity of pain. One current source of confusion is use of the term myofascial pain syndrome(mps) for two different concepts. Sometimes, MPS is used in a general sense that applies to a regional muscle pain syndrome of any soft tissue origin. Historically, the term MPS has been used in the restricted sense of that syndrome which is caused by TrPs within a muscle belly(not scar, ligamentous, or periosteal TrPs). Key Words : Myofascial pain syndrome, Trigger points 198 Journal of the K. S. C. N. 2001

2 Table 1. Comparisons Between Central Trigger Points (TsPs) and Attachment Trigger Points Finding Most Likely Cause Central TrPs In motor endplate zone Dysfunctional endplates Nodule Contraction knots Local and referred pain Nociceptors sensitized by local energy crisis Taut band beyond nodule Contraction Knot Tension Attachment TrPs In attachment zone Taut band tension Palpable induration Inflammatory reaction Local and referred pain Nociceptors sensitized by persistent taut band tension Taut band at attachment TrP Contraction knots in central TrP 199

3 200 Journal of the K. S. C. N. 2001

4 Figure 1. Synaptically ineffective connections(dotted line) between sensory neurons in the spinal cord. 201

5 Figure 2. Pathogenesis of myofascial trigger points. TrP=trigger point. 202 Journal of the K. S. C. N. 2001

6 Figure 3. Changes in local twitch responses after spinal cord transection. 203

7 Figure 4. Comparison of surface electromyographic response to fatiguing exercise of normal muscle(black lines) and muscle with active myofascial trigger points(red lines(. The averaged maplitude(open circles) and mean power frequency(solid circles) of the elec - tromyographic record from the muscle with trigger points start out as if the muscle is already fatigued and show that hte muscle reaches exhaustion more quickly(and is slower to recover) thean normal muscle. These changes are accompaned by accelerated fatigue and weakness of the muscle with trigger points. 204 Journal of the K. S. C. N. 2001

8 Figure 5. Motor activation of the upper trapezius muscle in response to painful pressure applied to a trigger point in the long head of the ipsilateral triceps brachii muscle. The bar marks the period of painful pressure applied to the triceps trigger point. The marked increase in surface electromyographic activity(referred spasm) corresponds to the period of mechanical stimulation of the trigger point.(redrawn with permission from the data of Barbara J. Headley, PT.) 205

Figure 6. Typical recording of the spontaneous electrical activity(sea)and spikes recorded from an active locus of a trigger point at two dif - ferent sweep speeds.

9 Figure 6. Typical recording of the spontaneous electrical activity(sea)and spikes recorded from an active locus of a trigger point at two dif - ferent sweep speeds. A, recording at the same slow sweep speed of 100 msec/div used by Hubbard and Berkoff to report this electri - cal activity. Only spikes of unknown initial polarity are identifiable. B, a similar amplification but a ten-times higher sweep speed of 10 msec per division that was used in subsequent studies by others who also gave observed the olw amplitude noise component as well as the polarity of initial deflection of the spikes from active loci. This additional information is the spikes from active loci. This additional information is of critical importance for understanding the source and nature of these of these potentials. 206 Journal of the K. S. C. N. 2001

Figure 7. Schematic of a trigger point complex of a muscle in longitudinal section. The schematic identifies three regions that can exhibit abnormal tender-ness(red).

10 Figure 7. Schematic of a trigger point complex of a muscle in longitudinal section. The schematic identifies three regions that can exhibit abnormal tender-ness(red). It also illustrates contraction knots that most likely: make a trigger point feel nodular, cause the taut band, and mark the site of an active locus. A, the central trigger point(ctrp) which is found in the endplate zone, contains numer - ous electrically active loci, and contains numerous contraction knots. The local tenderness of the CTrP is identified by a red oval. A taut band of muscle fibers extends from the trigger point to the attachment at each end of the involved fibers. The sustained tension that the taut band exerts on the attachment tissues can induce a localized enthesopathy that in identified as an attachment trigger point(atrp). The local tenderness of the enthesopathy at the ATrP in identified by a red circlewith a black border. B, this enlarged view of part of the central trigger point shows the distribution of five contraction knots. The vertical lines in each muscle fiber iden - tify the relative spacing of its striations. The space between two striations corresponds to the length of one sarcomere. Each contrac - tion knot identifies a segment of muscle fiber experiencing maximal contracture of its sarcomeres. The sarcomeres within one of these enlarged segments(contraction knot) of a these enlarged segments(contraction knot) of a muscle fiber are markedly shorter and wider than the sarcomeres of the neighboring normal muscle fibers which are free of contraction knots. In fibers with these contraction knots(note the lower three individual knots), the sarcomeres in the part of the muscle fiber that extends beyond both ends of the contraction knot are elongated and narrow compared to normal sarcomeres. At the top of this enlarged view is a pair of contraction knots separated by an interval of empty sarcolemma between them that is devoid of contractile elements. This con - figuration suggests that the sustained maximal tension of the contractile elements in an individual contraction knot could have caused mechanical failure of the contractile elements in the middle of the knot. If that happened, the two halves would retract, leaving an interval of empty sarcolemma between them. In patients, the CTrP would feel nodular as compared to the adjacent mus - cle tissue, because it contains numerous swollen contraction knots that take up additional space and are much more firm and tense than uninvolved muscle fibers. 207

Figure 8. Schematic of the enerth crisis hypothesis which postu - lates a viciouw cycle(red arrows) of events that appears to contribute significantly to myofascial trigger points.

11 Figure 8. Schematic of the enerth crisis hypothesis which postu - lates a viciouw cycle(red arrows) of events that appears to contribute significantly to myofascial trigger points. The function of the sarcoplasmic reticulum(sr) is to store and release ionized calcium that induces activity of the contractile elements, which causes sarcomere shortening. An initiating event such as trauma or a marked increase in the endplate release of acetylcholine can result in excessive release of calcium from the SR(black arrow). This calcium produces maximal con - tracture of a segment of muscle which creates a maxi - mal energy demand and chokes off local circulation. The ischemia interrupts energy supply which causes failure of the calcium pump of the sarcoplasmic reticu - lum. completing the cycle. Figure 9. Tissue oxygen saturation values recorded by an oxygen probe that progressed in 0.7 mm steps through normal muscle and then into a tender, tense induration-muskelharten(another name for a TrP)-in three patients with Myogelosis. Arrow marks hte palpa - ble border of the induration. The dashed line indicates the mean oxygen saturation of adjacent normal muscle. The area marked in red identifies the severe oxygen deficiency recorded as the probe approached the center of the induration. Note the comparable region of increased oxygen saturation surrounding the central region of hypoxia.(data reproduced with permission from Bruckle W, Suckfull M, Fleckenstein W, et al. Gewebe-pO2-Messung in der verspannten Ruckenmuskulatur [m. erector spinae]. Zeitschrift fur Rheumatologie 49: , 208 Journal of the K. S. C. N. 2001

12 Figure 10. Integrated hypothesis. The primary dysfunction hypothesixed here is an abnormal increase(by several orders of magnitude) in the production and release of acetylcholine packets from the motor nerve terminal under resting conditions. The greatly increased number of miniature endplate potentials produces endplate noise and sustained deplolarization of the postjunctional membrane of the muscle fiber. This sustained depolarization could cause a continuous release and uptake of calcium ions from local sar - coplasmic reticulum(sr) and produce sustained shortening(contracture) of sarcomeres. Each of these four highlighted changes Would increase energy demand. The sustained muscle fiber shortening compresses local blood vessels, thereby reducing the nutrient and oxygen supplies that normally meet the energy demands of this region. The increased energy demand in the face of an impaired energy supply would produce a local energy crisis, which leads to release of sensitizing substances that could inter - act with autonomic and sensory(some nociceptive) nerves traversing that region. Subsequent release of neuroactive substances could in turn contribute to excessive acetylcholine release from the nerve terminal, completing what then becomes a self sustain - ing vicious cycle. Table 2. Recommended Criteria for Identifying a Latent Trigger Point or an Active Trigger Point Essential Criteria 1. Taut band palpable (if muscle accessible). 2. Exquisite spot tenderness of a nodule in a taut band. 3. Patients recognition of current pain complaint by pressure on the tender nodule (identifies an active trigger point). 4. Painful limit to full stretch range of motion. Confirmatory Observations 1. Visual or tactile identification of local twitch response. 2. Imaging of a local twitch response induced by needle penetration of tender nodule. 3. Pain or altered sensation (in the distribution expected from a trigger point in that muscle) on compression of tender nodule. 4. Electromyographic demonstration of spontaneous electrical activity characteristic of active loci in the tender nodule of a taut band. 209

13 Table 3. Common Referral Diagnoses Received When Overlooked TrPs were Actually the Cause of Patients Symptoms Initial Diagnosis Some Likely Trigger point Trigger Poin Manual Sources Chap. #(Volume 1) Angina Pectoris (atypical) Appendicitis Atypical Angina Atypical Facial Neuralgia Atypical Migraine Back Pain, Middle Back Pain, Low (Bicipital) Tendinitis Chronic Abdominal Wall Pain Dysmenorrhea Earache (enigmatic) Epicondylitis Frozen Shoulder Myofascial Pain Dysfunction Occipital Headache Postherpetic Neuralgia Radiculopathy, C Scapulocostal Syndrome Subacromial Bursitis Temporomandibular Joint Disorder Tennis Elbow Tension Headache Thoracic Outlet Syndrome Tietz s Syndrome Pectoralis major Lower rectus abdominis Pectoralis major Masseter Temporalis Sternal division of sternocleidomastoid Upper trapexius Sternocleidomastoid Temporalis Posterior cervical Upper rectus abdominis Thoracic paraspinals Lower rectus abdominis Thoracolumbar paraspinals see Volume 2 muscles Long head of biceps brachii Abdominal muscles Lower rectus abdominis Deep masseter Wrist extensors Supinator Triceps brachii Subscapularis Masticatory muscles Posterior cervicals Serratus anterior Intercostals Pectoralis minor Scalenes Scalenes Middle trapezius Levator scapulae Middle deltoid Masseter Lateral pterygoid Finger extensors Supinator Sternocleidomastoid Masticatory muscles Posterior cervicals Suboccipital muscles Upper trapezius Scalenes Subscapularis Pectoralis minor and major Latissimus dorsi Teres major Pectoralis major enthesopathy Internal intercostals , Journal of the K. S. C. N. 2001

14 Table 4. Clinical Features Distinguishing Myofascial Pain due to Trigger Points (TrPs) from Fibromyalgia Myofascial pain (TrPs) Fibromyalgia 1 female : 1 male 4-9 females : 1 male Local or Regional pain Widespread, general pain Focal tenderness Widespread tenderness Muscle feels tense(taut bands) Muscle feels soft and doughy Restricted range of motion Hypermobile Examine for trigger points Examine for tender points Immediate response to injection of TrPs Delayed and poorer response to injection of TrPs 20% also have fibromyalgia 72% also have active TrPs 01. Simons DG., Travell JG., Simons, LS. Travell & Simons Myofascial Pain and Dysfunction : The Trigger point manual, volume 1. upper half of body, Second Edition, Baltimore : Williams & Wilkins Simons DG. Myofascial pain syndrome : one term but two concepts : a new understanding [Editorial]. J Musculoske Pain : 3(1) : Simons DG. Myofascial pain syndrome due to trigger points. In : Goodgold J, ed : Rehabilitation Medicine. St Louis : Mosby, 1998 : Sola AE, Rodenberger ML, Gettys BB. Incidence of hypersensitive areas in posterior shoulder muscles. Am J phys Med 1955 ; 34: Fishbain DA, Goldberg M, Meagher BR, et al. Male and female chronic pain patients categorized by DSM-III psychiatric diagnostic criteria. Pain. 1986:26:

15 Figure 11. Predicted importance of supraspinal, vascular, and myofascial inputs to brain-stem neurons in various forms of migraine and tension-type headache. Some examples of the innumerbable modulations of the vas - cular-supraspinal-myogenic model of migraine and other headaches. S: supraspinal net effect(usually facilitation during headache); M: myofascial nocicep - tive input; V: vascular nociceptive input. Thickness of arrows represents relative intensity of input. a; migraine aura without headache: despite strong vascu - lar input there is no pain because of small S and M. B; migraine with aura: because of stronger supraspinal or myofascial input the subject now suffers from headache. c; migraine without aura:the vascular input is not as strong as in migraine with aura, byt the headache is no less intense because of a stronger supraspinal facilitation or the combined effects of V and M. The latter case is likely to suffer alternating migrainous or tension-type headaches depending on small shifts in the relative magnitude of M and V. d; tension-type headache: M is greater than V, and S is medium or large.(reprinted with permission from Olesen J. Clinical and pathophysiological obser - vaplained by integration of vascular, supraspinal and myofascial inputs. Pain 1991;46: ) 06. Fricton JR. Myofascial pain, chapter 9. In : Bailliere s Clinical Rheumatology : Fibromyalgia and Myofascial Pain Syndromes, Vol.8, No. 4, Edited by Masi AT. B a i l l i e r e Tindall(Sannders), Philadelphia, 1999; Skootsky SA, Jaeger B, oye RK. Prevalence of myofascial pain in general internal medicine practice. West J Med 1989;151; Gerwin RD. A study of 96 subjects examined both for fibromyalgia and myofaocial pain [abstract]. J Musculoske Pain. 1995:3(Supp(2): Perl. ER. Sensitization of nociceptors and its relation to sensation. In Bonica JJ and Albe-Fessard, editors : Advances in pain research and therapy, vol. 1, New York, 1976, Raven Press. 10. Frost. A Diclofenac versus lidocaine as injection therapy in myofascial pain. scand J rheumatol. 1986:15: Foreman RD, Blair RW, and Weber RN. viscerosomatic convergence onto T2-T4 spinoreticular, spinoreticular - spinothalam:c, and spinothalamic Tract neurons in the cat. Exp Neurol. 1984:85: Milne RJ, et al. Convergence of cutaneous and pelvic visceral nociceptive inputs onto primate spinothalamic neurons. Pain. 1981:11: Procacci P. et al. Cutaneous pain threshold changes after sympathetic block in reflex dystrophies. Pain. 1975:1: Roberts JT. The effect of occlusive arterial diseases of extremities on the blood supply of nerves : experimental and clinical studies on the role of the vasa nervorum. Am Heart J. 1948;35: Simons DG. Referred phenomena of myofascial trigger points. In : VecchietL, Albe-Fessard D, Lindblom u, et al, eds. Pain Research and clinical Management, Vol.7, New Trends in Referred Pain and Hyperalgesia. New York : Elsevier, 1993: Simons DG. Neurophysiological basis of pain caused by trigger points. Amer Pain Soc J 1994:3: Mense S. Considerations concerning the neurological basis of muscle pain. Can J physiol pharmacol. 1991:69(5): Mense S. Nociception from skeletal musile in relation ta clinical muscle pain. Pain. 1993:54: Mense S. Referral of muscle pain : new aspects. Amer pain Soc J 1994:3: Hong C-Z. Pathophysiology of Myofascial Trigger Point. J Formos Med Assoc. 1996;95: Travell JG, Simons DG. Myofascial Pain and Dysfunction : the trigger Point manual, vol 1. Baltimore : Williams & Wilkins, Travell JG, Simons DG. Myofascial Pain and Dysfunction : the trigger Point manual, vol 2. Baltimore : Williams & Wilkins, Hong C-Z. Myofascial trigger point infection. Crit Rev phys Rehab Med 1993:5: Hong C-Z. Consideration and recommendation of myofascial trigger point injection. J Musculoskelet Pain. 1994:2: Hong C-Z. Trigger point injection : dry needling vs lidocaine injection. Am J phys Med Rehabil. 1994:73: Hong C-Z, Simons DG. Response to standard treatment for pectoralis minor myofascial pain syndrome after whiplash. J Musculoskelet Pain. 1993;1: Hong C-Z, Simons DG, Statham L. Electromyographic analysis of local twitch responses of human extensor digitorum communis muscle during ischemic compression over the arm. Arch phys Med Rehabil. 1986:67: Hong C-Z,. Persistence of local twitch response with loss of conduction to and from the spinal cord. Arch phys Med Rehabil. 1994:75: Weeks VD, Travell J. How to give painless injections. AMA Scientific Exhibits 1957, Grune & Straton, New York, 1957(pp,318322). 212 Journal of the K. S. C. N. 2001

16 30. Kimura J. Electrodiagnosis in Diseases of Nerve and Muscle, vol. 2. F.A. Davis, philadelphia Simons DG, Stolv WC. Microscopic features and transient contraction of palpable bands in canine muscle. Am H phys Med. 1976:55; Russell IJ. Neurochemical pathogenesis of fibromyalgia syndrome. J Musculoske Pain. 1996:4(1/2) : Sorensen J, Bengtsson A, Backman E, et al. Pain analysis in patients with fibromyalgia. Effects of intravenous morphine, lidocaine, and Ketamine. Scand J Rheumatol. 1995:24(6): Lowe JC, Cullum ME, Graf LH Jr, et al. Mutations in the c- erb A beta l gene : do they underlie euthyroid fibromyalgia? Medical Hypothesis 1997;48(2): Bennett RM. The Contribution of muscle to the generation of fibromyalgia symptomatology. J Musculoske Pain. 1996:4(1/2): Olesen J. Clinical and pathophysiological observations in migraine and tension-type headache explained by integration of vascular, supraspinal and myofascial input. P a i n 1991;46;

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