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162 Section 3 / Nonpharmacological Pain Therapy the sarcolemma. Increased calcium concentrations result in
sus-tained muscle fiber contraction. This hypothesis was later refined to include a dysfunctional motor endplate occurring secondary to muscle injury, and resulting in excessive release of acetylcholine (ACh). Sustained maximal contraction of the muscle fibers in the vicinity of the dysfunctional endplate causes increased metabolic demand and decreased concentrations of adenosine triphosphate (ATP). The calcium pump that returns calcium to the sarcoplas-mic reticulum is ATP dependent, as is the uncrosslinking of actin and myosin; thus, calcium concentrations and contractile activity remain increased.
Gerwin et al. (2004) further expanded the integrated hypothe-sis by stating that the most likely cause leading to development of the taut band is altered activity of the motor endplate or neu-romuscular junction. Muscle injury alters the normal equilibrium between the release and breakdown of ACh and its removal by acetylcholinesterase from acetylcholine receptors in the postsynap-tic membrane. Substances such as CGRP and SP, released during muscle injury, facilitate increased release of ACh, inhibition of breakdown, and upregulation of acetylcholine receptors. A persis-tent muscle fiber contraction develops leading to the development of the taut band and subsequent MTrP.
Central Modulation—A New Hypothesis
A new hypothesis, proposed by Hocking (2010), to explain the pathogenesis of MTrPs examines the role of the central nervous system and its modulatory mechanisms. Hocking, a practicing vet-erinarian in Australia, submits that most clinically relevant MTrPs in dogs (those that restrict stride and distort posture) are found in the flexor muscles, in contrast to Gerwin et al.’s (2004) con-clusion that taut bands and subsequent MTrPs are the result of a dysfunctional motor endplate. Hocking proposes that their ori-gin is rather a chronic expression of an intrinsic ␣-motoneuron property: the plateau potential or sustained partial depolarization.
␣-motoneurons are large lower motor neurons with cell bodies located in the brainstem and spinal cord and whose axons provide motor innervation of skeletal muscles.
Hocking identifies two classifications of MTrPs, “antecedent”
MTrPs formed in nociceptive withdrawal reflex agonist muscles, and “consequent” MTrPs formed in nociceptive withdrawal reflex antagonist muscles, generally extensor muscles. Sustained stim-ulation of peripheral nociceptors and ensuing central sensitization result in persistent efferent␣-motoneuron activation of agonist mus-cles and simultaneous inhibition of antagonist musmus-cles. Facilitation of C fiber withdrawal reflexes, due to central sensitization, predis-poses to antecedent MTrPs formation, while consequent MTrPs are proposed to be due to tonic reticulospinal or reticulotrigeminal facil-itation or plateau potentials in the␣-motoneurons innervating these muscles. Hocking submits that consequent MTrPs develop from changes in patient posture brought about by pain and/or impair-ment, counteraction of C fiber withdrawal reflex reciprocal inhibi-tion of antagonist muscles, and counteracinhibi-tion of postural changes induced by antecedent MTrPs.
Muscle-related Mechanisms of MTrP Development
Low-level muscle contractions, uneven intramuscular pressure distribution, direct trauma, unaccustomed eccentric contractions, eccentric contraction in unconditioned muscle, and maximal or submaximal concentric contractions can lead to muscle injury and
subsequent development of MTrPs (Gerwin et al., 2004; Dommer-holt & Huijbregts, 2011).
Low-level Muscle Contractions
Hagg (2003) postulated that myalgia was related to submaximal repetitive activity resulting in selective overloading of the ear-liest recruited and last derecruited motor units (Dommerholt &
Huijbregts, 2011). This is referred to as the “Cinderella Hypothe-sis.” Muscle forces generated at submaximal levels, also known as low-level muscle contractions, do not allow the recruited smaller type I fibers to rest and, thus, they become overworked. The result is metabolically overloaded muscle units with loss of cellular calcium homeostasis, subsequent activation of autogenic destructive pro-cesses, and myalgia. Hocking’s (2010) hypothesis describes low-level muscle contractions as a response to C fiber nociceptor input.
Uneven Intramuscular Pressure Distribution
Otten (1988) confirmed, based on mathematical modeling applied to a frog gastrocnemius muscle, that during static low-level muscle contractions capillary pressures increase dramatically, especially near the muscle insertions. Increased intramuscular pressures lead to excessive capillary pressure, decreased circulation, ischemia, and hypoxia. The pathological changes brought about by increased pressure could lead to the formation of MTrPs and support Simon and Travell’s Integrated Trigger Point Hypothesis.
Direct Trauma
Direct trauma to the muscle and muscle fibers may generate injury to the sarcoplasmic reticulum and/or the sarcolemma resulting in increased calcium concentrations, sustained contraction, and devel-opment of taut bands.
Eccentric and (Sub) Maximal Concentric Contractions
Eccentric muscle contraction is defined as muscle lengthening under tension. Eccentric muscle contraction is defined as muscle lengthening under tension, as opposed to concentric muscle con-traction, during which the muscle shortens. Numerous studies in people indicate that mechanisms applicable to the development of MTrPs occur with muscle damage from eccentric exercise, exercise in unconditioned muscle, or maximal or submaximal concentric exercise (Gerwin et al., 2004; Dommerholt et al., 2006; Dommer-holt & Huijbregts, 2011). Steiss and Levine (2005) suggests that eccentric contractions may be an explanation for muscle damage in the canine athlete. Muscle damage linked to these types of contrac-tions is due to contraction-induced capillary constriccontrac-tions, hypop-erfusion, ischemia, and hypoxia. These changes result in a local acidic environment, release of protons (H+), potassium ions (K+), CGRP, bradykinin (BK), and SP, leading to activation of muscle nociceptors (Gerwin et al., 2004; Dommerholt & Huijbregts, 2011).
PAIN INITIATION IN MYOFASCIAL PAIN SYNDROME The inflammatory model of muscle pain has been well studied, but no models of inflammation-induced MTrPs are known (Mense
& Gerwin, 2010). Serum creatine phosphokinase (CPK) is not increased, thus global muscle inflammation does not appear to play a role in MTrP development. However, the ultrastructural muscle
14 / Myofascial Pain Syndrome in Dogs 163 fiber derangements brought about by the aberrant muscle
contrac-tions result in profound biochemical changes localized at the trigger point zone including: decreased pH and increased concentrations of BK, CGRP, SP, tumor necrosis factor-␣(TNF-␣), interleukin-1
(IL-1), serotonin, and norepinephrine (Shah et al., 2005). Sub-stance P and CGRP are primarily produced in the dorsal root gan-glion and transmitted antidromically down the neural process. The increased release of these substances results in prolonged nocicep-tive activation (Shah et al., 2008).
PERPETUATING FACTORS IN MYOFASCIAL PAIN Gerwin states in the fourth chapter of Travell and Simons’ Myofas-cial Pain and Dysfunction, “the clinical importance of factors that perpetuate myofascial trigger points is generally underestimated.”
The clinician must be acutely aware of perpetuating factors and how they affect the development of MTrPs. Gerwin also states “attention to perpetuating factors often spells the difference between success-ful and failed therapy.”
Mechanical Stresses
Mechanical stresses are by far the most common perpetuating fac-tors for MTrPs in dogs. Acute traumatic events may activate MTrPs, but are not responsible for perpetuating them. Sudden activation of MTrPs may occur after acute muscle strain, joint strain, fractures, direct muscle trauma, or excessive or unusual exercise. Such MTrPs are generally easy to treat once the soft tissue injury has healed.
More commonly in dogs, MTrPs are both activated and perpetuated by chronic muscle overload. Postural changes in the dog resulting from orthopedic injury, postoperative surgical trauma and pain, neuropathy, joint dysfunction, and pain related to osteoarthritis cre-ate muscle overload. Many of the same muscle-relcre-ated mechanisms that lead to the development of MTrPs also maintain them.
A canine patient with chronic osteoarthritis has compensatory postural changes that activate and perpetuate MTrPs in numer-ous muscles. Moderate to severe osteoarthritis of the coxofemoral joints activates and perpetuates MTrPs in the functional unit mus-cles of the coxofemoral joint, mainly flexors (including iliopsoas) and adductors. The cranial shift in weight overloads muscles in the thoracic limbs, namely the m. infraspinatus, m. deltoideus, and the long head of the m. triceps brachii. Repeated lateral flexion of the spine, which assists in ambulation by advancing the pelvis and pelvic limb while limiting coxofemoral flexion and extension, results in overloading of the miliocostalis lumborum. A dog with a non-weight-bearing pelvic limb adopts hopping actions during ambulation of the weight-bearing limb, and this results in unaccus-tomed eccentric contractions of the coxofemoral and stifle extensors in an attempt to limit flexion. Lumbar paraspinal muscles become overloaded, as they must now assist with ambulation in addition to spinal stabilization. The m. iliopsoas, which is actually two separate muscles, the m. psoas major and m. iliacus that join shortly before their insertion on the medial proximal femur, develops MTrPs, becomes shorter in length, and kyphosis can develop.
Nutritional Factors
In humans, deficiencies of vitamin B12(cobalamin) and folic acid have been described as perpetuating factors for MPS (Simons et al., 1999; Mense & Gerwin, 2010; Dommerholt & Huijbregts, 2011).
There are no references in the veterinary literature pertaining to
deficiencies of these substances causing pain of any type; however, cobalamin deficiency causes malaise and failure to thrive. Both substances currently have clinical application as markers for small bowel disease and the Gastrointestinal Laboratory at Texas A&M University offers assays for each. Cobalamin deficiency in the dog can occur with exocrine pancreatic insufficiency.
Iron insufficiency has been identified as a perpetuating factor for MTrPs in people; however, the relationship between the two is not clearly understood. In dogs, iron deficiency is recognized as a cause of anemia, and may be due to inadequate intake, malabsorp-tion, and/or iron loss via chronic hemorrhage (Shell, 2006). The relationship of iron deficiency to MTrPs in animals is unknown.
Metabolic Factors
Hypothyroidism is the most common endocrine disorder in dogs, and is associated with a variety of clinical signs; however, the veterinary literature does not mention pain as a consequence of hypothyroidism. In humans, muscle pain, stiffness, weakness, and cramps and pain on exertion are reported with hypothyroidism (Simons et al., 1999).
Nerve Impingement
In people, peripheral nerve entrapments and radiculopathies can result in the development and perpetuation of MTrPs. Myofascial trigger points tend to be formed in the muscles of the extremities innervated by nerves arising at the same spinal cord segment as the entrapped nerve. This could be a potential cause of MTrPs in animals.
Visceral–somatic Pain Representations
Gerwin (2002) states that visceral pain can activate and perpetuate MTrPs in the area of referred pain. Neurons in the dorsal horn of the spinal cord receive input from the viscera and from receptors in the skin and deeper soft tissues. As a result of this overlap, visceral nociceptive activation of the dorsal horn neurons may result in muscle pain, and may be a cause of MTrPs in animals. Visceral disease should be ruled out when MTrPs are found.
DIAGNOSIS OF MTrPS Manual Identification of MTrPs
Due to the lack of objective laboratory or diagnostic imaging tech-niques to confirm the existence of MTrPs, a diagnosis based upon palpation has been questioned frequently in the medical literature.
However, Gerwin et al. (1997) and Bron et al. (2007) demon-strated good interindividual reliability of palpation skills for locat-ing MTrPs. Currently, clinical examination with palpation is the only method of diagnosis in veterinary patients. Palpation skills require initial expert guidance and instruction followed by frequent clinical application.
An excellent knowledge of anatomy is required, as well as an understanding of the actions of each muscle to be examined. Clin-ical knowledge of “functional muscle units,” defined as a unit of muscles that exercise action upon a given joint or joints, is criti-cal. Muscle dysfunction leads to joint dysfunction and vice versa.
When muscle dysfunction occurs MTrPs can develop (Dommerholt
& Huijbregts, 2011).
164 Section 3 / Nonpharmacological Pain Therapy
Figure 14.1. Flat palpation—examination with finger pressure across muscle fibers while compressing against firm underlying structure such as bone.
Clinical (Myofascial) Examination
There are three basic palpation techniques employed in a myofascial examination as defined by Simons and Travell (1999).
Flat Palpation: Examination by finger pressure that proceeds across the muscle fibers at a right angle to their length while com-pressing them against a firm underlying structure, such as a bone.
This technique could be used for the m. infraspinatus (Figure 14.1).
Pincer Palpation: Examination of a part of a muscle by holding it in a pincer grasp between the thumb and fingers. Groups of muscle fibers are rolled between the tips of the digits to detect taut bands.
This technique could be used for the m. triceps, m. sartorius, and m. tensor fascia latae (Figure 14.2).
Snapping Palpation: A fingertip is placed against the tense band of muscle at right angles to the direction of the band, and suddenly
Figure 14.2. Pincer palpation—examination of muscle by holding it in a pincer grasp between thumb and fingers.
Figure 14.3. Snapping palpation—examination of muscle by pincer grasp while rapidly drawing back and rolling muscle fibers under fingers.
pressed down while the examiner draws the finger back, rolling the underlying fibers under the finger. The motion is similar to that used to pluck a guitar string, except that the finger does not slide over the skin but moves the skin with it. To most effectively elicit an LTR, the taut band is palpated and snapped at the MTrP, with the muscle positioned to eliminate slack (Figure 14.3). Snapping palpation can be performed on the same muscles described for pincer palpation.
The patient can be examined in either the standing position or in lateral recumbency. However, taut bands are easier to appreciate in the recumbent patient with the muscle in a more relaxed state.
In each position, an assistant is needed to provide gentle patient restraint, because examination can induce a jump sign. Education of the client prior to the myofascial examination is needed to avoid concern when pain is elicited.
Palpation of a muscle containing a taut band reveals a discrete hardness of the muscle in the area of the band. The taut band will parallel the direction of the muscle fibers and, when located, its length is examined to locate the hyperirritable MTrP. Patient response to palpation aids in localization of the MTrP rather than appreciation of a knot or swelling.
Simons et al. (1999) define the jump sign in people as “a general pain response of the patient who winces, may cry out, and may withdraw in response to pressure applied on the trigger point.”
This definition also applies to canine patients that show varying degrees of withdrawal or wincing but less commonly vocalize.
Adequate digital pressure is needed to localize the taut band and MTrP; however, pressure must not be excessive in order to avoid generating significant patient reaction not due to localization of MTrPs. The jump sign is not to be confused with the LTR. In the canine patient, the LTR is rarely observed during examination as factors such as hair coat and muscle location limit observation.
In people, MTrPs are classified as either “active” or “latent.”
Active MTrPs produce pain spontaneously, whereas the latent MTrP produces pain only with stimulation. Other than the clinical pres-ence of pain, the two types of MTrPs are similar in that they both cause muscle weakness and reduced range of motion. In the canine
14 / Myofascial Pain Syndrome in Dogs 165 patient, it is impossible to determine which MTrPs are active or
latent. Hocking (2010) states that in dogs, “all MTrPs feel similar, palpation elicits similar pain reactions, and appropriate stimulation induces a similar local twitch response.”
Objective Criteria for Diagnosis of MTrPs
No objective criteria exist that can validate the clinical criteria used to diagnose MTrPs (Mense & Gerwin, 2010). However, recent advances in ultrasound and magnetic resonance imaging of MTrPs may have clinical application in human and veterinary patients (Sikdar et al., 2009; Chen et al., 2010).
TREATMENT OF MTrPS
Treatment of MTrPs in dogs consists of noninvasive and invasive therapies. Currently, there are no studies to validate the effective-ness of any therapy in dogs, and reported results remain strictly anecdotal. In people, numerous studies exist regarding noninvasive and invasive MTrP therapy; however, in many the diagnosis of MPS may lack validity. Tough et al. (2007), after an extensive literature review, reported variability in criteria used to diagnose MPS and MTrPs in people.
Noninvasive MTrP Therapy Therapeutic Lasers
Currently, lasers are a popular modality for the treatment of pain in the veterinary patient. Class IIIa (3a) lasers provide a maximum output power of 5 milliwatts (mW), Class IIIb lasers provide output power up to 500 mW, and Class IV lasers provide output power greater than 500 mW, and one currently marketed veterinary model claims a maximum output power of 15 W. The amount of laser energy delivered during a treatment session is reported in Joules (J), and one Joule is equal to 1 W/s. The dose is reported as the energy per session in Joules divided by the area (cm2) where the energy is directed; therefore, the therapeutic laser dose is indicated in J/cm2.
Studies regarding myofascial pain and MTrPs in people are lim-ited to Class III lasers. This is due, in part, to the inability to calculate an accurate therapeutic dose when using a Class IV laser.
Class IV lasers cannot be directly focused on a defined area due to the risk of thermal injury, and must be constantly moved over a region during treatment.
Treatment with Class IIIa and Class IIIb lasers is more commonly referred to in the literature as low-level laser therapy (LLT). LLT has been widely used in the treatment of MTrPs in people. Several double-blind placebo-controlled studies report positive effects of LLT on MTrPs (Hakguder et al., 2003; Gur et al., 2004; Ilbuldu et al., 2004). However, other studies report no therapeutic benefit (Altan et al., 2005; Dundar et al., 2007). Proper therapeutic dosages for treatment are not known, and conflicting information exists in humans and in animal models. Hakguder et al. (2003) suggested that inadequate dosage may be the cause of the unpredictability in the reported efficacy of laser therapy. However, Gur et al. (2004) reported efficacy with a lower dosage, and in a recently published paper using the rabbit as an animal model, Chen et al. (2010) reported better treatment outcomes with energy of 5.4 J per session versus 14.4 J per session.
Electrotherapies
Several references exist that discuss the use of transcutaneous elec-trical nerve stimulation (TENS) in the management of pain in dogs;
however, no specific mention of its use in myofascial pain was found (Steiss & Levine, 2005; Mlacnik et al., 2006; Canapp, 2007). Hou et al. (2002) reported that TENS combined with other physical modalities appeared to have an immediate effect with regard to decreasing myofascial pain in people. However, Dommerholt and Huijbregts (2011) concluded that insufficient evidence is available to determine the effectiveness of TENS in myofascial pain.
Therapeutic Ultrasound
In a randomized controlled study, Aguilera et al. (2009) reported an immediate reduction in MTrP sensitivity with therapeutic ultra-sound in humans. Draper et al (2010) used therapeutic ultraultra-sound to decrease stiffness of latent MTrPs in the m. trapezius in humans. In that study, a 3 mHz therapeutic ultrasound was used at 1.4 W/cm2 for 5 minutes in a circular motion on an area twice the size of the 7 cm2ultrasound head. In contrast, previous studies by Gam et al.
(1998) and Lee et al. (1997) reported that therapeutic ultrasound was no more effective than placebo. Gam et al. (1998) surveyed patients up to 6 months after treatment by means of a patient questionnaire, and the studies reporting benefits from therapeutic ultrasound were based on immediate response only.
Physical/manual Therapies
Mense and Gerwin (2010) concluded that data are either inade-quate or conflicting regarding most manual therapies for treatment of MPS. Dommerholt and Huijbregts (2011), referring to physical and manual therapies, state that current evidence did not exceed the moderate level. They additionally assert that most trials examined multimodal treatment programs, so positive effects cannot exclu-sively be credited to a particular therapy.
Ischemic compression, also known as trigger point pressure release, is a commonly described manual therapy for the treatment of MTrPs in humans. Studies in humans show that ischemic com-pression may be of benefit in treatment of MTrPs associated with shoulder pain, neck pain, headaches, and carpal tunnel syndrome (Hou et al., 2002; Hains et al., 2010a, 2010b; Montanez-Aguilera et al., 2010). Numerous descriptions of the technique can be found in the academic medical literature as well as in the lay literature regarding massage therapy. Digital compression of the MTrP for 60–90 seconds with increasing pressure is the most commonly described method. In dogs the taut band is identified and examined for the exquisitely tender MTrP, then digital pressure is applied to the point of patient recognition. After 15–20 seconds, pressure may gradually be increased in most patients. Providing a gentle stretch to the muscle while applying pressure may assist in release of the MTrP.
Invasive MTrP Therapy
Several types of invasive MTrP therapy have been described in peo-ple, including trigger point dry needling with an acupuncture needle and MTrP injections with local anesthetics and other substances. In the author’s experience, trigger point injection is not well accepted by many canine patients compared with dry needling. A hypodermic needle is much larger than an acupuncture needle, and the injection of lidocaine is painful, possibly explaining canine objection to this technique. Numerous substances have been used in trigger point
166 Section 3 / Nonpharmacological Pain Therapy injections in people. Local anesthetics, corticosteroids, and
vita-min B12are most commonly described. Iwama and Akama (2000), in a randomized, double-blinded trial, reported a water-diluted 1%
lidocaine mixture (1:3) resulted in better efficacy and less pain on injection. Iwama et al. (2001) later determined that water-diluted 0.25% lidocaine and water-water-diluted 0.25% mepivacaine were less painful on injection than saline-diluted 0.25% lidocaine and water-diluted 0.25% bupivacaine. The study additionally concluded that water-diluted (1:3) concentrations of 0.2–0.25% lidocaine or mepivacaine were the most effective dilutions for trigger point injections.
Confusion exists in the literature as to what constitutes myofas-cial trigger point dry needling. Myofasmyofas-cial trigger point dry needling is the insertion of an acupuncture needle into an MTrP within a taut band identified during clinical examination. It is not the insertion of a needle into a traditional acupuncture point, super-ficially over an MTrP, or into a prespecified location.
A systematic review of the literature by Furlan et al. (2005) sug-gested that myofascial trigger point dry needling appeared to be a useful adjunct to other therapies for lower back pain in humans. A more recent review and meta-analysis by Tough et al. (2009) con-cluded that there was at least limited evidence that supported the efficacy of myofascial trigger point dry needling in humans; how-ever, the reviewers commented that additional studies are needed.
In more recent studies in humans, Fernandez-Carnero et al. (2010) showed dry needling of MTrPs in the m. masseter to be effec-tive in the treatment of myofascial temporomandibular disorders.
Srbely et al. (2010) demonstrated short-term antinociceptive effects using dry needling of MTrPs. This effect was limited to mus-cles innervated by the same spinal cord segment. When an MTrP in the m. infraspinatus was needled, pain thresholds to pressure were increased in MTrPs in the m. supraspinatus (segments C5 and C6) while no change in pain threshold to pressure was found in MTrPs in the m. gluteus medius (segments L4, L5, and S1).
Tsai et al. (2010) demonstrated that pressure point thresholds in active MTrPs located in the upper m. trapezius were increased with dry needling of MTrPs located in the m. extensor carpi radialis longus. Improvement in the range of motion of the neck was an additional finding. Osborne and Gatt (2010) were able to man-age pain and improve the active joint range of motion (ROM) in acute shoulder injury during intense competition by performing dry needling of MTrPs in the scapulohumeral muscles of elite female athletes.
The clinician who undertakes invasive therapy for the treatment of MTrPs needs not only a thorough knowledge of anatomy, but also must develop the kinesthetic skills to accurately place the needle into the MTrP. Employing the examination techniques previously described, the taut band is identified and its length examined to localize the MTrP. The acupuncture needle (Seirin J Type No. 5 [0.25] with insertion tube) is rapidly inserted, with the aid of the insertion tube, into the superficial tissues and then directed into the deep tissues and muscle to the taut band (Figure 14.4). An appreciation of an increase in resistance as the needle enters the taut band develops with experience. If needle placement is accurate, a LTR may be appreciated in the taut band (Figure 14.5). The needle is moved in and out of the MTrP, slowly, until no further LTRs are appreciated. In dogs, the LTR confirms the presence of an MTrP, but does not distinguish between an active MTrP and a latent MTrP.
Figure 14.4. The taut band is identified and its length examined to localize the MTrP. The acupuncture needle (Seirin J Type No. 5 [0.25] with insertion tube) is rapidly inserted, with the aid of the insertion tube, into the superficial tissues and then directed into the deep tissues and muscle to the taut band.
Figure 14.5. An increase in resistance, as the needle enters the taut band, is expected. If needle placement is accurate, an LTR may be appreciated in the taut band. The needle is moved in and out of the MTrP, slowly, until no further LTRs are appreciated.
Two landmark studies by Shah et al. (2005; 2008) have helped to validate invasive MTrP dry needling and the therapeutic importance of the LTR. After induction of the LTR by the needle entering the MTrP, local concentrations of biochemical mediators such as SP and CGRP decreased. This may explain the observed decrease in pain in people after release of the MTrP. In the later study, not only were there similarities in the biochemical milieu of the active MTrPs, but increased concentrations of analytes were found in remote muscle