Trigger points and the Integrative Neuromuscular Acu Reflex point System

Trigger-point therapy was developed in modern times as a clinical technique for myofascial pain syndrome. A British physician was working as a young research assistant under Sir Thomas Lewis at University College Hospital in 1938, John Kellgren—later to become professor of rheumatology at Manchester University in the United Kingdom—observed that the pain in myalgia, or what is currently known as myofascial pain syndrome, originates in small, circumscribed, exquisitely tender points in muscle. He found that he could reproduce this spontaneously occurring pain by applying sustained pressure to these points and could alleviate it by injecting those points with procaine hydrochloride (Novocain). He also observed that this pain is not generally felt at the tender point itself but is referred to an area of the body some distance from it.1 Kellgren's work prompted Janet Travell to study patients with muscu-loskeletal pain. She soon discovered that this referred pain is triggered by neural hyperactivity at the points in muscle and its surrounding fascia, Kellgren had referred to as "tender points"; she gave them the name trigger points. She introduced the terms myofascial pain and zones of pain referral and also named the disorder myofascial pain syndrome.

Later Travell and David G. Simons published their two-volume work, Myofascial Pain and Dysfunction: The Trigger Point Manual, which is now the classic clinical manual in trigger-point medicine. Although this book is authoritative in its field, Simons's observation2 is noteworthy:

"Despite the fact that an increasing number of clinicians and scientists believe that most common enigmatic unexplained musculoskeletal pain comes from trigger points, mainstream medicine has yet to accept or incorporate them as an integral part of its teaching, research and practice.

We are now becoming aware of several factors that may account for this slow progress.

Although the core of trigger points lies in skeletal muscle, all branches of the nervous system and several endocrine systems interact with them. In other words, trigger points are very complex."

Three factors appear to be critical:

"1. There is no generally accepted account of the pathophysiology of trigger points, which prevents the establishment of authoritative diagnostic criteria, and this in turn inhibits research.

2. At present, there is no recognized laboratory test or imaging technique to serve as an objective standard for diagnosing trigger points. Diagnosis can be made only through physical examination and patient history.

3. In the absence of an established gold-standard diagnostic test, appropriate specific diagnostic tests and appropriate diagnostic criteria remain controversial and unresolved. This is in part because clinicians depend heavily on the history as well as the physical examination, but interrater reliability studies to date have addressed only the physical examination. These interrater reliability studies make it clear that for many clinicians it takes training and much experience to develop adequate skills for diagnostic reliability and therapeutic competence. Agreement on diagnostic criteria is also confounded by the many variations in structure and accessibility of some 500 individual muscles; no one examination applies to all muscles"2 (p. 16)

Although these observations are still applicable today, an increasing number of clinicians of different medical disciplines are now successfully treating myofascial pain syndrome by using dry needling.

Another important clinical observation should be mentioned. In Myofascial Pain and Dysfunction: The Trigger Point Manual, Volume 1, Travell and Simons stated,

"In comparative studies,3,4 dry needling was found to be as effective as injecting an anesthetic solution such as procaine or lidocaine in terms of immediate inactivation of the trigger point. In the Hong study3 of the response of trapezius muscle trigger points to 0.5% lidocaine or to dry needling, both groups experienced essentially the same amount of improvement immediately and 2 weeks later. However, within 2-8 hours, 42% of the lidocaine-injected patients and 100% of the dry-needled patients developed local soreness. The soreness of the patients treated by dry needling had significantly greater intensity and duration than the soreness of lidocaine-injected patients." (pp. 151-152)

These results indicate that the critical therapeutic factor in both cases is mechanical disruption by the needle. This is consistent with the understanding that disruption of the trigger-point knots of contraction by needling will terminate the local energy crisis and the sensitization of nearby nerves that it causes.

In the study by Hong3 mentioned in this quotation, both the subjects who received lidocaine injections and those who received dry needling may have been subjected to the same size of syringe needles. In clinical practice, fewer patients experience postneedling soreness when finer acupuncture needles are used.

ETIOLOGY OF TRIGGER POINTS

Simons2 suggested three major etiologic features of trigger points that explain the most widely recognized characteristics of their clinical pathophysiologic mechanisms. These features are related to one another in a positive feedback cycle that is self-perpetuating once it starts but can be interrupted at several points in the cycle in a number of ways. Although the understanding of the pathways between them are not well established,5-8 substantial evidence supports this hypothesis. The three features are as follows:

• Increased acetylcholine release at the neuromus-cular junction (motor plate)

• Increased tension of muscle fibers passing through the trigger point that produces a palpable taut band

• The presence of sensitizing substances in the muscle tissue of the trigger point that can produce pain A brief description of these three features is provided below. The author believes that this account of the physiologic mechanisms of trigger points also describes the most common clinical features of most, if not all, acu-reflex points.

Acetylcholine Release

Research on the basic physiology of trigger points has revealed increased electrical activity at the motor endplate. This endplate "noise" is associated with greatly increased release of acetylcholine transmitter. Other pathophysiologic processes may also be responsible for these effects. For example, if an immune reaction were to block the normally prompt inactivation of acetylcholine by cholinesterase within the synaptic cleft, the acetylcholine receptors in the postjunctional membrane would continue to produce excessive levels of minute endplate potentials (endplate noise).

Calcitonin gene-related peptide inhibits the expression of cholinesterase in vertebrate experi-ments.5 Such a process allows more acetylcholine to affect receptors in the postjunctional membrane, producing a result comparable to that caused by an increased release of acetylcholine. In addition, the peptide can induce expression of the acetylcholine receptor, which would also increase the number of minute endplate potentials.

Increased Fiber Tension

The specific mechanisms responsible for taut bands are still under investigation. Clinically, they are considered an essential feature of trigger points, and successful results have been achieved by needling them. Histologic studies have revealed increased tension in affected muscle fibers and evidence of disrupted contractile elements.5 Local regions of hypercontracted fibers are observed as contraction knots or contraction discs that increase tension in those fibers. Shortened sarcomeres with adjacent regions of compensatory lengthening of the sarcomeres in those fibers are observed. Such a structure would further increase tension in the fiber because of the elastic resistance of sarcomeres to passive stretch, especially when elongated beyond their resting length. These observations help explain the increased physical tension and tissue distress in muscles that harbor trigger points. More research is needed to clarify the source of the increased tension that constitutes palpable taut bands.

Sensitizing Substances in Trigger Points

Researchers have demonstrated measurable quantities of sensitizing substances at trigger points. Shah and colleagues6 made a study of the tissue milieu in the trigger points of nine subjects: three normal, three with latent trigger points, and three with active trigger points. They used a novel acupuncture-size microdi-alysis needle to sample both normal tissue and trigger points in upper trapezius muscles. The acupuncture needle contained in-and-out delivery tubes that ended at a dialyzer membrane set 0.2 mm from the open tip of the needle. The results are summarized in Table 10-1. These data convincingly indicate the physical and histopathologic milieu of a trigger point in the muscle, as distinct from normal tissue.

The significant difference in the levels of these substances between normal muscle tissue and trigger-point sites indicates that trigger points have demonstrable and complex histopathologic features. The significant histochemical difference found between latent and active trigger points provides a measurable clinical distinction between the

Physiologic Comparison of Relative Amounts of m „ „ „ Algogenic Substances TABLE 10-1 c

Sampled by Microdialysis from Latent and Active

Trigger Points

Measurement Active Trigger Points

Compared with Latent Trigger Points and Normal Muscles

T P < 0.08 T P < 0.08 T P < 0.08 T P < 0.08 T P < 0.08

two types of point. All of this has advanced the understanding of the physiologic process of triggerpoint formation and treatment.

INTERACTIONS OF MYOFASCIAL TRIGGER POINTS

The neuromuscular dysfunction of skeletal muscle seems to be the major clinical manifestation of trigger points, but their pathophysiologic processes are incredibly complex. In the context of pain and other internal problems, trigger points interact with all major components of the central nervous system, the endocrine system, and immune system. A muscle containing active trigger points becomes shorter and weaker. The affected muscle resists stretching, and any attempt to extend it results in pain. The physiologic processes of the muscle may change when trigger points develop. Changes such as gooseflesh, localized sweating, and intense coldness of the distal part of a limb have been observed. All these observations show that the development of trigger points in the muscles is not an isolated histologic structure.

How these points are interrelated to human physiologic systems and homeostasis is still not adequately understood. For example, trigger points often exist in clusters involving regional function. Lewit8 recognized the tendency of trigger points to appear in chains of functionally related muscles, particularly the deep stabilizers of the lower torso and especially in the diaphragm and pelvic floor muscles. The importance of the core stabilizer muscles is now becoming recognized, but the diaphragm is often overlooked.9 The surprising observation that trigger points in these core muscles are commonly found to be an important part of headache is a reminder that core systems are involved, as well as the trigger points of individual muscles. Evidence from research indicates the importance of treating core systems while working on peripheral problems such as those in the limbs.9

TRIGGER-POINT NOCICEPTORS

Myofascial pain syndrome develops as a result of the activation and sensitization of nocicep-tors at trigger-point sites in muscle. Two types of

Pressure pain threshold pH

Substance P Calcitonin gene-related peptide Bradykinin Serotonin Norepinephrine Tumor necrosis factor-a Interleukin-1ß

nociceptors are relevant in this discussion: cutaneous and muscular. In the skin there are high-threshold Ad-mechanothermal nociceptors and C-polymodal nociceptors. In muscle the corresponding nociceptors are group III and group IV, respectively.

Needling into the skin surface causes activation of cutaneous Ad-mechanothermal nocicep-tors, which in turn causes a transient pain and then activation of cutaneous C-polymodal nociceptors, which gives rise to a persistent, dull, aching, and sometimes burning or stinging pain. It is possible that the effect of trauma on muscle is similarly to activate Ad-mechanothermal (group III) and C-polymodal (group IV) nociceptors.

Because the persistent dull, aching type of pain present in myofascial pain syndrome is similar in every respect to the pain that arises when cutaneous nociceptors of C-afferent fibers are activated, however, it seems reasonable to relate that pain to the activation of C-afferent (group IV) nociceptors at trigger-point sites in muscle. This view is supported by the observation that the pain in this disorder may be eliminated by stimulating the cutaneous and subcutaneous Ad-mechanothermal nerve fibers with dry needles.

Although muscular trauma is the main etiologic factor for the development of passive and active trigger points, pathologic conditions of internal viscera may also cause the development of trigger points in skeletal muscles. Also, a muscle may suffer a direct injury and become acutely, chronically, or recurrently overloaded with sensitized trigger points. In addition, muscles may be subjected to repeated microtrauma such as the repetitive strain injury as found in patients with certain occupations. Some of these trauma or injuries can be prevented if attention is paid to regular maintenance of muscle health.

MYOFASCIAL TRIGGER-POINT SITES

Trigger points appear usually at sites associated with certain neural configurations, as discussed in previous chapters. They are often found in muscle bellies, especially in the region of muscular motor points where the nerves enter the muscles. Trigger points are also formed at muscle insertion sites because of physical stress and the rich innervation of dense connective tissues. Some trigger points, such as those in the sternocleidomastoid muscle, develop in the free borders of muscles where nerves penetrate the deep fascia and come up to the surface to give off branches.

Palpable taut bands are often detected in painful muscles, especially in the neck and upper back. These taut bands often harbor trigger points. Temporary pain relief is reported by patients when these trigger points in the taut bands are needled.

SOME MYOFASCIAL PAIN PATTERNS CAUSED BY TRIGGER POINTS

Some pain patterns caused by common trigger points are depicted in Figure 10-1. Keen attention should be paid to the relationship between the location of the trigger points, the types of pain that they are related to, and their neural innervation. Pain patterns are discussed as follows on a regional basis for convenience.

• Pain patterns in the head and face involve four muscles: the sternocleidomastoid, splenius capi-tis, temporalis, and masseter (Table 10-2).

• Pain patterns in the neck, shoulder, and upper limbs involve eight muscles: the scalene, trapezius, levator scapulae, infraspinatus, supraspinatus, sub-scapularis, deltoid, and pectoralis (Table 10-3).

• Pain patterns in the lumbar spine, hip, and lower limb involve 13 muscles: the gluteus maximus, gluteus medius, gluteus minimus, piriformis, vastus lateralis, vastus intermedius, vastus medialis, biceps femoris, gastrocnemius, soleus, per-oneus longus, extensor digitorum longus, and tibialis anterior (Table 10-4).

The patterns of trigger points and those of homeostatic acu-reflex points match very well. Observant readers will see that the homeostatic acu-reflex point system provides a logical understanding of trigger-point pain patterns (Figs. 10-2 to 10-5).

Myofascial pain that is related to or caused by trigger points is a type of soft tissue pain. It is characterized by the development of sensitive or tender locations within muscles or other soft tissue, such as fascia, ligaments, or tendons, and these are known as trigger points.

Travell and Simons defined a myofascial trigger point (MTrP) as a "hyperirritable locus within a taut band of skeletal muscle, located in the muscle tissue or its associated fascia".10 Sensitive MTrPs may arise a few days after an acute strain of a muscle, or their onset may be gradual, a cumulative effect of repeated overuse of a muscle. Some MTrPs are related to acute or chronic visceral diseases, such as those that can develop in the pectoral muscles as a result of heart disease, or in the abdominal muscles after gastroenteritis

Ulnar Pain After Trapezius Dry Needling
Sternomastoid Splenius capitis Temporalis Masseter Lower trapezius

Upper trapezius Levator scapulae Posterior cervical Adductor pollicis First interosseus

Infraspinatus

Dry Needle Serratus Anterior

Supraspinatus

Scaleni

Infraspinatus

Supraspinatus

Scaleni

Masseter ReflexDry Needling Soleus Muscle

Short

Tibialis Long Gastro- Soleus Peroneus Abductor hallucis extensors anticus extensors cnemius longus

Subscapularis
Deltoid

Pectorals

Middle finger Extensor extensor carpi Supinators radialis

Pectorals

Peroneus Reflex

Pectoralis major

Serratus anterior

Pectoralis major

Serratus anterior

Longissimus

Vastus Biceps medialus femoris

Gluteus minimus

Vastus medialis

Vastus medialis

or diarrhea. Constant mental tension, experienced as anxiety or stress, can cause prolonged contraction of the skeletal muscles, which results in the development of MTrPs. In addition, poor physical fitness or posture, emotional stress, or nutritional deficiency can perpetuate MTrPs. Some female patients complain of more painful MTrPs just before or during menstruation. Athletes experience more muscle tightness and consequently more sensitive MTrPs during and after training in cold weather.

Clinical symptoms related to MTrPs may include a deep ache or pain, stiffness of the muscles, and

Text continued on p. 159

TABLE 10-2 Pain Patterns of Major Trigger Points in the Head and Neck Muscles

Muscle

Origin

Insertion

Innervation

Main Function

Patterns of Referred Pain from Trigger Points of the Muscle

Sternocleidomastoid*

Splenius capitis

Temporalis

Masseterf

Lateral surface of mastoid process of temporal bone; lateral half of the superior nuchal line of occipital bone

Inferior half of liga-mentum nuchae and spinous processes of superior six thoracic vertebrae Floor of temporal fossa and deep surface of temporal fascia

Inferior border and medial surface of zygomatic arch Superficial parts, including superficial and intermediate layers

Sternal head: attached to the anterior surface of manubrium of sternum and lateral to jugular notch via a rounded tendon Clavicular head: superior surface of medial third of clavicle Lateral aspect of mastoid process and lateral third of superior nuchal line

Tip and medial surface of coronoid process and anterior border of ramus of mandible

Lateral surface of ramus of mandible and its coro-noid process

Spinal root of accessory nerve (XI) and branches of cervical plexus (C2-C3)

Dorsal rami of C2-C4

Deep temporal branches of mandibular nerve (V3)

Mandibular nerve (V3) via masseteric nerve that enters its deep surface

Unilateral action: laterally flexes the neck, rotates the face to contralateral side Bilateral action: flexes the neck, facilitates inhalation

Laterally flexes and rotates head and neck to same side; extends head and neck when acting bilaterally

Elevates mandible, closing jaws; its posterior fibers revert mandible after protrusion

Elevates and protrudes mandible to closing jaws; deep fibers revert it

Superficial and deep layers have somewhat different functions

Sternal division: vertex; occiput; across the neck; over the eye, throat, and sternum Autonomic symptoms: eye and sinuses Clavicular division: frontal headache and earache; dizziness Vertex of the head, occiput, and diffusely through the cranium, back of the orbit, sometimes down to the lower neck and shoulder

Temporal region (temporal headache), eyebrow, upper teeth; occasionally maxillary teeth and temporo-mandibular joint Superficial layer: Eyebrow, maxilla, anterior mandible, and upper or lower molar teeth

Deep layer: region of temporo-mandibular joint and deep in the ear

*Sternal and clavicular divisions have different function.

Superficial and deep layers have a different angulation of fiber direction.

TABLE 10-3 Major Pain Patterns from Trigger Points of the Neck, Shoulder, and Upper Limb

Muscle

Origin (Proximal or Medial Attachment)

Insertion (Distal or Innervation Lateral Attachment)

Main Function

Patterns of Referred Pain from Trigger Points of the Muscle

Scalene

Scalenus posterior Scalenus medius Scalenus anterior

Trapezius

Levator scapulae

Supraspinatus

Posterior tubercles of transverse processes of C4-C6 vertebrae

Posterior tubercles of transverse processes of C2-C7 vertebrae

Anterior tubercles of transverse processes of C3-C6 vertebrae

Medial third of superior nuchal line; external occipital protuberance, ligamentum nuchae, spinous processes of C7-T12 vertebrae, lumbar and sacral spinous processes

External border of second rib

Cervical nerves of C7-C8

Superior surface of first rib, posterior to groove for subclavian artery Scalene tubercle on the inner border of first rib and ridge on the upper surface of first rib Lateral third of clavicle, acromion, and spine of scapula

Posterior tubercles of transverse processes of C1-C4

Supraspinous fossa of scapula

Superior part of medial border of scapula

Superior facet on greater tubercle of humerus

Cervical nerves of C3-C8

Cervical nerves of C4-C6

Spinal root of accessory nerve (XI) and C3 and C4

Dorsal scapular nerve (C5) and cervical plexus (C3-C4) Suprascapular nerve (C4, C5, and C6)

Flexes neck laterally; elevates second rib during forced inspiration Flexes neck laterally; elevates first rib during forced inspiration

Assists in elevating first rib; laterally flexes and rotates cervical part of the vertebral column

Scapula is elevated by superior fibers, retracted by middle fibers, and depressed by inferior fibers Superior and inferior fibers act together in superior rotation of scapula Elevates scapula and tilts its glenoid cavity inferiorly by rotating scapula Helps deltoid muscle abduct arm and acts with rotator cuff muscles

Referred pain can radiate from all three scaleni Upper vertebral of scapula

Down the front and back of arm and radial forearm; may extend to thumb and index finger Pectoral region

Upper fibers: posterolateral^ along neck, behind ear to temple

Lower fibers: posterior side of neck and adjacent mastoid area; suprascapular and interscapular region

Concentrates in angle of neck and along vertebral border of scapula

Mid-deltoid region; may extend down the arm, lateral epicondyle, and wrist

TABLE 10-3 Major Pain Patterns from Trigger Points of the Neck, Shoulder, and Upper Limb—Cont'd

Muscle

Origin (Proximal or Medial Attachment)

Insertion (Distal or Lateral Attachment)

Innervation

Main Function

Patterns of Referred Pain from Trigger Points of the Muscle

Infraspinatus

Subscapularis

Deltoid

Pectoral

Pectoralis major

Pectoralis minor

Infraspinous fossa of scapula

Subscapular fossa

Lateral third of clavicle, acromion and spine of scapula

Middle facet on greater tubercle of humerus

Lesser tubercle of humerus

Deltoid tuberosity of humerus

Clavicular head:

anterior surface of the medial half of clavicle Sternocostal head: anterior surface of sternum, superior six costal cartilages, and aponeurosis of external oblique muscle Ribs 3 to 5 near their costal cartilages

Lateral lip of intertubercular groove of humerus

Suprascapular nerve (C5 and

Upper and lower subscapular nerves (C5, C6, and C7) Axillary nerve (C5 and C6)

Medial border and superior surface of coracoid process of scapula

Medial pectoral nerve (CS and T1)

Laterally rotates arm; helps hold humeral head in glenoid cavity of scapula

Medially rotates and adducts arm; helps hold humeral head in glenoid cavity Anterior fibers: flexes and medially rotates arm Middle fibers: abducts arm Posterior fibers: extends and laterally rotates

Deeply in anterior deltoid and shoulder joint; down the front and lateral aspect of arm and forearm; suboccipital and posterior cervical areas Posterior deltoid area, medially over scapula, down posterior arm, wrist

Local region of affected deltoid muscle

Lateral and medial pectoral nerves Clavicle head: C5

and C6 Sternocostal head: C7, C8, and T1

Adducts and medially rotates humerus Acting alone: clavicular head flexes humerus; sternocostal head extends humerus

Stabilizes scapula by drawing it inferiorly and anteriorly against thoracic wall

Anterior chest and breast, down ulnar aspect of arm to fourth and fifth fingers

Front chest, front shoulder, down the ulnar side of arm, forearm, and fingers

TABLE 10-4 Major Pain Patterns from Trigger Points of Lower Limb Muscles

Muscle

Origin (Proximal or Medial Attachment)

Insertion (Distal or Lateral Attachment)

Innervation

Main Function

Patterns of Referred Pain from Trigger Points of the Muscle

Gluteus maximus

Gluteus medius

Gluteus minimus

Piriformis

Vastus lateralis

External surface of ala of ilium, iliac crest, dorsal surface of sacrum and coccyx, and sacrotuberous ligament

Lateral surface of ilium between anterior and posterior gluteus lines

Lateral surface of ilium between anterior and inferior gluteus lines

Anterior surface of sacrum and sacrotuberous ligament

Greater trochanter and lateral lip of linea aspera of femur

Vastus medialis Intertrochanteric line and medial lip of linea aspera of femur

Most fibers end in ili-otibial tract; some fibers insert on gluteal tuberosity of femur Lateral surface of greater trochanter of femur

Anterior surface of greater trochanter of femur

Inferior gluteal nerve (L5, S1, and S2)

Extends thigh and assists in its lateral rotation; steadies thigh and assists in raising trunk from flexed position Superior gluteal nerve Abducts and medially (L5 and S1) rotates thigh; steadies pelvis

Superior gluteal nerve Abducts and medially (L5 and S1) rotates thigh; steadies pelvis

Superior border of greater trochanter of femur

Base of patella and, via patella ligament, to tibial tuberosity

Base of patella and, via patella ligament, to tibial tuberosity

Branches from ventral rami of S1 and S2

Femoral nerve (L2, L3, and L4)

Femoral nerve (L2, L3, and L4)

Laterally rotates extended thigh and abducts flexed thigh; steadies femoral head in acetabulum Extends leg at knee joint

Extends leg at knee joint

Medial, lateral, and inferior buttock

Along the posterior crest of ilium, to sacrum, to posterior and lateral buttock, and to upper thigh Anterior fibers: lower lateral buttock; down the lateral thigh, knee, and leg to the ankle Posterior fibers: similar as for anterior fibers, but a more posterior or medial pattern Sacroiliac region, posterior hip region, proximal two thirds of posterior thigh

Along lateral thigh from pelvis and greater trochanter to lateral knee region Anteromedial aspect of knee; upper anteromedial aspect of thigh

TABLE 10-4 Major Pain Patterns from Trigger Points of Lower Limb Muscles—Cont'd

Muscle

Origin (Proximal or Medial Attachment)

Insertion (Distal or Lateral Attachment)

Innervation

Main Function

Patterns of Referred Pain from Trigger Points of the Muscle

Vastus intermedius

Biceps femoris

Gastrocnemius

Soleus

Fibularis (Peroneus) longus

Anterior and lateral surfaces of body of femur

Long head: ischial tuberosity Short head: lateral lip of linea aspera and lateral supracondy-lar line

Lateral head: lateral aspect of lateral condyle of femur

Medial head: popliteal surface of femur, superior to medial condyle

Posterior aspect of head of fibula; superior fourth of posterior surface of fibula; soleal line; and medial border of tibia

Head and superior two thirds of lateral surface of tibia

Extensor digitorum Lateral condyle of tibia, superior longus (Fig. 10-17)

Tibialis anterior three fourths of anterior surface of fibula, and interosseous membrane Lateral condyle and superior half of lateral surface of tibia

Base of patella and, via patella ligament, to tibial tuberosity Lateral side of head of fibula; tendon is split at this site by fibular collateral ligament of knee joint

Posterior surface of calcaneus via tendo calcaneus

Posterior surface of calcaneus via tendo calcaneus

Base of first metatar-sal bone and medial cuneiform bone Middle and distal phalanges of lateral four digits

Medial and inferior surface of medial cuneiform bone and base of first metatarsal bone

Femoral nerve (L2, L3, and L4)

Long head: tibial division of sciatic nerve (L5, S1, and S2) Short head: common fibular division of sciatic nerve (L5, S1, and S2) Tibial nerve (S1 and S2)

Extends leg at knee joint

Flexes and rotates leg laterally; long head extends thigh

Plantarflexes foot, raises heel during walking, and flexes knee joint

Tibial nerve (S1 and S2)

Superficial fibular (peroneal) nerve (L5, S1, and S2) Deep fibular (peroneal) nerve (L5 and S1)

Deep fibular (peroneal) nerve (L4 and L5)

Plantarflexes foot and steadies leg on foot

Everts and weakly plantarflexes foot

Extends lateral four digits and dorsiflexes foot

Dorsiflexes and inverts foot

Middle portion of anterior thigh

Back of the knee, may extend to up pos-terolateral area of thigh and up to the lower buttock

Over posterior ankle, calf, and back of knee and up to posterior thigh and midbelly of the muscle Posterior and plantar surfaces of heel; over back of calf; distal Achilles tendon; sacroiliac joint Above, below, and posterior to the lateral malleolus On the muscle proper, dorsolateral aspect of foot, to the tips of middle three toes Anteromedial aspect of ankle and on the dorsal and medial surfaces of great toe

Epicranius, occipitofrontal, frontal belly

Corrugator supercilii Orbicularis oculi Depressor supercilii Levator labii superioris alaeque nasi Levator labii superioris Infra-orbital nerve Nasalis Levator anguli oris

Orbicularis oris Parotid duct Buccinator Masseter, deep part Orbicularis oris Mentalis Depressor labii inferioris Depressor anguli oris Digastric, anterior belly Masseter, superficial part

Stylohyoid Hyoid bone Hypoglossal nerve [XII]

Inferior constrictor

Pericranium

Temporalis

Epicranial aponeurosis Zygomatic arch

Pericranium

Temporalis

Posterior Occipital Trigger Point

Inferior constrictor

Vagus nerve [X]

Common carotid artery

Figure 10-2 Facial and masticatory muscles. Facial trigger points usually develop in these muscles.

Temporomandibular joint, joint capsule, lateral ligament

Epicranius, occipitofrontalis, occipital belly

Cartilaginous external acoustic meatus

Ramus of mandible Styloid process Superficial temporal artery Sternocleidomastoid Digastric, posterior belly

Internal jugular vein

Vagus nerve [X]

Common carotid artery

Figure 10-2 Facial and masticatory muscles. Facial trigger points usually develop in these muscles.

Buccinator lymph node Facial lymph nodes

Digastric, anterior belly

Submandibular lymph nodes

Submental lymph nodes Lateral cervical lymph nodes, superior deep nodes Omohyoid, superior belly Lateral cervical lymph nodes, inferior deep nodes Jugulo-omohyoid lymph node Common carotid artery Internal jugular vein

Inferior Deep Cervical Lymph Node

Lateral cervical lymph node, inferior deep lymph node

Scalenus anterior

Omohyoid, inferior belly Figure 10-3 Neck muscles where the trigger points may appear.

Brachial plexus, supraclavicular part

Lateral cervical lymph node, inferior deep lymph node

Scalenus anterior

Omohyoid, inferior belly Figure 10-3 Neck muscles where the trigger points may appear.

Superficial parotid lymph nodes

Mastoid lymph nodes

Jugulodigastric lymph nodes

Occipital lymph nodes Sternocleidomastoid Splenius capitis Lateral cervical lymph nodes, superficial nodes Levator scapulae Accessory nerve [XI] Scalenus medius Trapezius Scalenus posterior

Brachial plexus, supraclavicular part

Sternocleidomastoid Pectoralis major, clavicular part Internal intercostal Deltoid Coracobrachial

Biceps brachii, short head

Pectoralis major

Pectoralis minor Rib II

Latissimus dorsi

Serratus anterior

Pectoralis major, abdominal part

(Sternalis, var.)

Subclavius

Axillary vein

Pectoralis minor

(Sternalis, var.)

Pectoralis Trigger Points

Brachial plexus, infraclavicular part

Axillary artery

Serratus anterior

Serratus anterior External oblique

Pectoralis major, sternocostal head Figure 10-4 Muscles of the thorax where the trigger points develop but should be needled with caution.

Brachial plexus, infraclavicular part

Axillary artery

Serratus anterior External oblique

Pectoralis major, sternocostal head Figure 10-4 Muscles of the thorax where the trigger points develop but should be needled with caution.

Iliopsoas

{Iliacus-Psoas major

Tensor fasciae latae Sartorius

Quadriceps femoris

Vastus lateralis Rectus femoris

Vastus medialis-

Pectineus Adductor longus

Gracilis

Semitendinosus-

Semimembranosus<

-Gluteus medius Gluteus maximus

-Biceps femoris

Fibularis [peroneus] longus Tibialis anterior Extensor digitorum longus

Extensor hallucis longus

_ Gastrocnemius, medial head

Soleus

Gastrocnemius

Soleus

Calcaneal tendon

Figure 10-5 Muscles of the lower limb where some of the trigger points hide in deep tissues. A, Anterior view. B, Posterior view.

restriction of movement. The pain can be referred from the MTrPs to other areas, and the referred pain area may not even include the MTrPs; that is, the patient may feel pain only in the area of the referred pain, not in the MTrPs themselves. The pattern of pain referral is usually consistent for each muscle, and so the location of the relevant MTrPs can easily be determined. The author's primary homeostatic acu-reflex point system provides a road map for locating hidden MTrPs.

PALPATION

Palpation is the clinical technique used to locate MTrPs. A trigger point may be manifested as a taut band of varying size in a flat muscle such as the trapezius, infraspinatus, or rhomboideus muscle. The clinician can draw fingers across the patient's fibers to feel the taut band below the skin. When the taut band is identified, the clinician's thumb and the index finger can be used to gently lift the muscle off the underlying tissue and encircle it so as to find the most sensitive area on the band. The pain reported by the patient can then be reproduced by pressing the sensitive area for a few seconds.

In muscles that are thick, such as the gluteus maximus, or deep, such as the piriformis, the trigger points may not be accessible to palpation. The clinician may use the thumb or two fingertips to press the muscle to locate the sensitive area.

TWITCH RESPONSE

The development of MTrPs leads to tight or painful muscles and can reduce or even completely inhibit the response to neural control of muscle contraction. In athletes, any muscles that are overtrained respond more slowly to neural control, which impairs their physical performance.

Sometimes the tight fibers of the muscles relax suddenly when physical palpation or needling is applied to the sensitive area. This appears as a brief twitch under the skin. This sudden muscular relaxation, the local twitch response (LTR), produces enormous relief of muscular tension. Thus achieving LTR is considered by many clinicians to be a therapeutic goal of the treatment session.

To elicit the LTR, the needle should precisely touch or penetrate the sensitive tissue of the contracture within the muscle. In some muscles, the LTR is immediate. If straightforward needling does not elicit the desired response, the clinician can grasp the needling area with thumb and index finger while manipulating the needle with the other hand. Manipulation can be in a gentle piston-like motion up and down, while the needle is either rotated in alternate directions or withdrawn only as far as the subcutaneous layer and reinserted at a slightly different angle. This last procedure may be more painful than some patients can tolerate.

There are differing opinions about LTR as a therapeutic goal. Because LTR immediately provides enormous relief of tension, some clinicians believe that it is a necessity for healing muscle tightness. Others believe that relief from pain and tension can still be achieved with simple needling, without manipulating and producing LTR. Good clinical results have also been achieved by other needling techniques such as distant needling, scalp needling, and other styles of needling, often without producing noticeable LTR. In addition, the relief of soft tissue pain involves several distinct variables of muscle physiologic conditions, such as contracture, inflammation, blood and lymphatic microcirculation, trophic conditions, tissue adhesion, joint mechanics, and scar tissue. It seems that acute muscular injuries involve mostly fiber contracture and inflammation, whereas chronic muscle problems are affected by all the factors just mentioned. Thus the LTR does provide enormous and immediate relief for acute muscle pain, but it takes more time to achieve noticeable relief for chronic muscle pain, and the LTR may not be important for every session as long as the needling-induced lesion is made in the sensitive or painful area of the muscle. Patients who do not experience any LTR may nonetheless report relief of their pain a few hours or a day later.

The author believes that both views are based on clinical experience and that more research is therefore needed to illuminate the differences between them. Before clear data are available, however, a practitioner should probably know a variety of needling techniques so as to be able to select the proper technique for a particular condition to achieve the best results.

As described in previous chapters, homeo-static acu-reflex points gradually arise in symmetric, systemic, and predictable patterns. The pattern and sequence of this sensitization is universal in human beings. This universal sensitizing sequence also reflects the particular anatomic features of each homeostatic acu-reflex point. The development of the homeostatic acu-reflex point system is also related to the functional biomechanics of the human musculoskeletal system. For example, most of the 24 primary homeostatic acu-reflex points are related to the mechanical balance of the musculo-skeletal core system, including the neck, upper spine, lumbar spine, and hips. These points are also related to visceral homeostasis. Acute muscle injuries or chronic mechanical imbalance sensitize both the primary homeostatic acu-reflex points and newly evolved trigger points. All the sensitized points are symptomatic points, and they arise usually as local and unilateral points.

TREATMENT AND PROGNOSIS

Direct needling into sensitive trigger points or sensitive tissue usually produces fast relief of the contracture of the affected muscle or muscles. In addition to local needling, systemic treatment is recommended according to the Integrative Neuromuscular Acu-reflex Point System (INMARPS). After a needling session, gentle physical therapy can help retrain the muscles for restoration of physiologic and functional homeostasis.

The prognosis of the treatment depends on both the healing potential of the body and the medical history of the injury. The method of evaluation of the healing potential was introduced in Chapter 9. In healthy patients or those with acute conditions, long-lasting relief can be achieved with a few treatments. Because MTrPs cannot dissipate perma nently, they will, in the majority of cases, revert to being latent MTrPs after treatment and may become active again in some months as a result of patient behavior and central sensitization. The author and colleagues have developed vacuum therapy, in which an area of negative pressure is created inside the muscles or around the trigger points. This negative pressure inside the tissue physically stretches the muscle fibers, reduces the adhesion between the tissue layers (micro-explosion), improves the blood and lymphatic microcirculation, and restores the biomechanical balance. Vacuum therapy greatly improves the effects of needling.

References

1. Kellgren JH: Observations on referred pain arising from muscle, Clin Sci 3:175-190, 1938.

2. Simons DG: New aspects of myofascial trigger points: etiological and clinical. In Pongratz DE, Mense S, Spaeth M, editors: Soft tissue pain syndromes, clinical diagnosis and pathogenesis, Binghamton, NY, 2004, Haworth Press, pp 15-21.

3. Hong CZ: Lidocaine injection versus dry needling to myo-fascial trigger point: the importance of the local twitch response, Am J Med Rehabil 73:256-263, 1994.

4. Jaeger B, Skootsky SA: Double blind, controlled study of different myofascial trigger point injection techniques [Abstract], Pain 4(Suppl):S292, 1987.

5. Mense S, Simons DG, Russel IJ: Muscle pain: its nature, diagnosis, and treatment, Philadelphia, 2001, Lippincott Williams & Wilkins.

6. Shah JP, Phillips T, Danoff J, et al: Novel microanalytical technique distinguishes three clinically distinct groups:

(1) subjects without pain and without a myofascial trigger point; (2) subjects without pain with a myofascial trigger point; (3) subjects with pain and a myofascial trigger point [Abstract], Am J Phys Med Rehabil 83:231, 2004.

7. Lewit K: Incidence and possible role of myofascial trigger points in migraine [Abstract], J Musculoskel Pain 12(Suppl 9):31, 2004.

8. Akuthota V, Nadler SR: Core strengthening, Arch Phys Med Rehabil 85(Suppl 1):S86-S92, 2004.

9. Heiderscheit B, Sherry M: What effect do core strength and stability have on injury prevention and recovery? In MacAuley D, Best T, editors: Evidence-based sports medicine, London, 2007, Blackwell, pp 59-72.

10. Travell JG, Simons DG: Myofascial pain and dysfunction: the trigger point manual (vol 1), ed 2, Baltimore, 1999, Williams & Wilkins, p 5.

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Essentials of Human Physiology

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