Trigger Points Introduction
(Excerpts from Trigger
Point Manual [1])
TABLE OF
CONTENTS
1 CLINICAL CHARACTERISTICS OF
MYOFASCIAL TRIGGER POINTS. 1
2 Theoretical Thinking (Possible
Explanations of Trigger Point Phenomena) 3
3 Trigger Point Examination. 4
4 Alternative Treatment Techniques. 5
5 Literature Review.. 5
1.1 Introduction
1.1.1
A Myofascial TP is a hyperirritable
focal point within a taut band of skeletal muscle fibers. On compression, it
can evoke typical referred pain and autonomic phenomena. A Myofascial TP is
located in skeletal muscle and its associated fascia distinguished from a TP in
other tissues such as skin, ligament and periosteum.
1.1.2
Trigger Points can be either active or
latent. Active Trigger Points cause pain, restriction of movement and muscular
weakness. Latent trigger points cause restriction of movement and muscular
weakness but DO NOT cause pain. Latent
TPs can remain in muscle tissue for years after apparent injury recovery yet
remain clinically silent until activated by minor overstretching, overuse or
chilling of the muscle when an acute attack of pain ensues. Both Active and
Latent TPs cause dysfunction but only active TPs cause pain.
1.1.3
Healthy muscle tissue does not contain
TPs, which means there are no taut bands, focal tenderness or pressure induced
pain referral and local twitch responses.
1.1.4
Although both sexes and all ages can
develop TPs sedentary, middle-aged women who engage in novel, repetitive or
over activity are very vulnerable [2].
Excepting later years, women are more prone to trigger points than men are. Sola[3]
Solberg [4]
Agerberg
[5]
1.1.5
Women are also more likely than men to
seek medical assistance for TP related pain. Kraft [6]
The dental field reports more female than male patients with TPs and in three
studies report 79%-84% of the TP pain related patients were women. [7]
[8]
[9]
1.1.6
Children can also develop trigger
points. Bales
[10]
1.1.7
The frequency of Active TPs increases
with age and level of activity into the most active middle years with
diminishing TP prevalence in later years where chief symptoms are the stiffness
and restricted motion of latent TPs. Travell [11]
1.1.8
Postural muscles (Neck, Shoulder &
Pelvic Girdles) and masticatory muscles are most likely to develop TPs.
1.1.9
Common muscles, which develop TPs, are
the upper Trapezius, scalene, Sternocleidomastoid, Levator scapulae and
quadratus lumborum.
1.2
DIFFERENTIAL DIAGNOSIS
1.2.1
Introduction
1.2.1.1
These clinical characteristics are
listed in the order one is likely to discover them during examination and
provides an operational definition of Myofascial Trigger Points.
1.2.1.2
Finding a site of local tenderness
{Number 5) is essential to the diagnosis, but non-specific. Numbers 6 and 7, a
local twitch response and pain reproduction, when present, is specific and
diagnostic of a Myofascial TP. The more of the remaining findings that
are present, the more certain is the diagnosis, which may be recorded as
Myofascitis of specific muscles for administrative or insurance purposes.
1.2.2 Criteria
1.2.2.1
History of sudden onset during or
shortly following acute overload
1.2.2.1.1
A history of sudden onset during or shortly following acute
overload stress, or a history of gradual onset with chronic overload of the
affected muscle;
1.2.2.2
Characteristic patterns of pain
1.2.2.2.1
Characteristic patterns of pain that are referred from
myofascial TPs, patterns that are specific to individual muscles;
1.2.2.3
Weakness and restriction
1.2.2.3.1
Weakness and restriction in the stretch range of motion of the
affected muscle
1.2.2.4
A taut, palpable band
1.2.2.4.1
A taut, palpable band in the affected muscle
1.2.2.5
Exquisite, focal tenderness
1.2.2.5.1
Exquisite, focal tenderness to digital pressure (the TP), in
the band of taut muscle fibers
1.2.2.6
Local twitch response
1.2.2.6.1
A local twitch response elicited through snapping palpation or
needling of the tender spot (TP)
1.2.2.7
Reproduction of the patient's pain
1.2.2.7.1
The reproduction of the patient's pain complaint by pressure
on, or needling of, the tender spot (TP)
1.2.2.8
Elimination of symptoms
1.2.2.8.1
The elimination of symptoms by therapy directed specifically
to the affected muscles
2
Theoretical Thinking (Possible Explanations of Trigger Point
Phenomena)
2.1
Summary
2.1.1
Acute Muscle Strain
2.1.1.1
The contractile elements in a portion
of the muscle are overloaded resulting in tissue damage which includes tearing of
the sarcoplasmic reticulum. This releases stored calcium. Because the
sarcoplasmic reticulum is damaged, it cannot reabsorb calcium ions. Sustained
contraction is the result of this lack of calcium ion re-absorption. Chronic
stress and excessive fatigue combined with continued contraction of the muscle
may result in further damage to the muscle cell repeating this process.
2.1.2
Sustained Muscle Contraction
2.1.2.1
The ATP energy supply combined with
excess calcium results in sustained Contracture of the muscle fibers producing
a region of uncontrolled metabolism within the muscle tissue. Severe local
vasoconstriction may result because of a TP mediated reflex response via the
central nervous system and sympathetic nervous system fibers.
2.1.3
Increased Metabolism with Decreased
Circulation
2.1.3.1
Metabolic demand is increased when
muscle fibers continually contracted but circulatory supply is decreased by
sympathetic nervous system mediated vasoconstriction. The muscle fibers passing
through this region become taut and are strongly shortened independent of
propagated action potentials. These taut fibers may be what is palpated as a
band in the muscle.
2.1.4
Questions and Problems
2.1.4.1
The tautness of the bands, when
examined clinically suggests that at least half the total fiber length is contracted.
The mechanism with which the Contracture of the sarcomeres might propagate
along each fibre is not clear since muscle cells that may not have sarcoplasmic
reticulum damage are also contracted.
2.1.4.2
Excess calcium should diffuse through
the tissues within hours or days and lose its effectiveness. This would make it
difficult to explain how active and latent trigger points persist for a much
longer period.
2.1.5
Explanation for sustained contraction
2.1.5.1
Total depletion of ATP could lead to
conditions similar to other disease processes which cause muscle Contracture
with electrical silence such as McArdle's Disease, Carnatine Deficiency, and Rigor Mortis. The processes of these diseases may explain
this sustained contraction.
2.1.5.2
ATP depletion results in the myosin
heads not releasing from the actin filaments and thus the sarcomeres become
rigid at that length. For this explanation a central region of this ATP deficit
contracture must be surrounded by a region of runaway metabolism to insure that
the ATP was not replenished.
2.1.6
Nerve sensitising substances Released
2.1.6.1
Serotonin, kinins and prostaglandin
may be released in the TP zone by several mechanisms. Tissue injury may result
in some blood extravasation as observed by Awad [12].
2.1.6.2
More research is needed to determine
whether the initial phase of increased metabolism with reduced circulation
would create a local accumulation of metabolic products resulting in the
release of prostaglandins and or other sensitising substances.
2.1.7
Dystrophic Changes
2.1.7.1
Dystrophic changes have been reported [13]
similar to those induced experimentally by muscle ischemia [14].
Prolonged regional ischemia of critical intensity combined with runaway energy
demands may result in these dystrophic changes.
3.1 Flat Palpation
3.1.1
Using the padded aspect of the fingers
or thumb and proceeding at a right angle across the muscle fibers while
pressing them against the underlying tissue or bone.
3.1.2
When trigger points exist taut bands,
exquisite, focal tenderness (Trigger Points), and a twitch response will be
detected.
3.2 Pincer Palpation
3.2.1
The muscle or muscles are rolled
between the tips of the digits to detect taut bands of fibers, to detect
exquisite, focal tenderness (Trigger Points), and to elicit local twitch
responses.
3.3 Snapping Palpation
3.3.1
Locate a taut band of muscle and place
fingertip at right angles. Begin moving your fingers back and forth to roll the
underlying fibers under the finger. This is just as plucking a guitar string
except contact with the surface is maintained. The purpose of this method is to
elicit a local twitch response and is most effective when done near or on the
trigger point with the muscle at a neutral length or slightly lengthened.
4.1 Ischemic Compression
4.1.1
Progressively stronger pressure is
applied with the digits or elbow until the trigger point tenderness subsides.
At first the tissues blanch and then become hyperaemic (Flushed) on release of
the pressure.
5
Literature Review
5.1
Characteristics of Patient Population
5.1.1 Sola reports that among 200 asymptomatic 17 to 35 year old subjects,
54% of the women and 45% of the men had latent trigger points in the
shoulder-girdle muscles. However, of the 100 subjects in each group,
practically equal numbers, 13 female and 12 male subjects, experienced referred
pain in response to pressure on the TPS.
5.1.2 Solberg reports that, a group of 739 college students were studied
for evidence of masticatory apparatus dysfunction. A significantly greater
number of female than male students had headaches and were aware of
temporomandibular joint sounds, indicative of the Myofascial pain-dysfunction
syndrome associated with TPs. Other questions relating to masticatory pain and
dysfunction were answered without evidence of sex distinction. Twice as many
women as men had tenderness of the lateral Pterygoid muscle.
5.1.3 Agerberg studied 194 persons, who comprised a random sampling of
70-year-old male and female residents of a town in Sweden, who showed no
appreciable sex difference in the frequency of pain and dysfunction of the
masticatory system.
5.1.4 Kraft reported on 91 patients who were referred to a Physical
Medicine and Rehabilitation Service and who were diagnosed as suffering from
"fibrositis syndrome, 69 were women and 22 were men.
5.1.5 Bales observed Infants with point tenderness of the rectus abdominis
muscle and colic, both of which were relieved by sweeping a stream of
vapocoolant over the muscle, which helps to inactivate myofascial TPs. When
children were examined for them, myofascial TPs were found to be a common
source of Musculoskeletal pain in childhood.
5.1.6 Travell reported in a personal communication with Sola AB who found
that laborers, who exercise their muscles heavily every day, are less likely to
develop active TPs than are sedentary workers who tend to indulge in occasional
orgies of vigorous physical activity. Travell reports similar experience.
5.2
Metabolism of Trigger Points
5.2.1 Awad observed blood extrvasation in the TP zone which included large
number of platelets that are a source of serotonin. This is not only a
sensitising agent, but also causes local ischemia. He also observed
degranulating mast cells, which release histamine.
[1] Travell
Janet G., Simons David G.(1983).Myofascial pain and dysfunction-the trigger
point manual .428 E. Preston Street Baltimore, Md 21202, U.S.A:Williams &
Wilkins.
[2] Travell
Janet G., Simons David G.(1983).Myofascial pain and dysfunction-the trigger
point manual .428 E. Preston Street Baltimore, Md 21202, U.S.A:Williams &
Wilkins. Page 13
[3] Sola AB,
Rodenberger ML, Gettys BB: Incidence of hypersensitive areas in posterior
shoulder muscles. Am J. Phys Med 34:585-590, 1955.
[4] Solberg WK.
Woo MW, Houston IB: Prevalence of mandibular dysfunction in young adults. 1 Am
Dent Assoc 98:25-34. 1979.
[5] Agerberg G,
bsterberg T: Maximal mandibular movements and symptoms of mandibular
dysfunction in 70-year-old men and women. Swed Dent J 67:147-163.1974.
[6] Kraft GH,
Johnson EW, LaBan MM: The fibrositis syndrome. Arch Phys Med Rehabil 49:155-
162, 1968.
[7] Butler IH,
Folke LEA, Bandt CL: A descriptive survey of signs and symptoms associated with
the myofascial pain-dysfunction syndrome. ] Am Dent Assoc 90:635-639, 1975.
[8] Cohen SR:
Follow-up evaluation of 105 patients with myofascial pain-dysfunction syndrome.
J Am Dent Assoc 97:825-828, 1978.
[9] Sharav Y,
Tzukert A, Refaeli B; Muscle pain index in relation to pain, dysfunction, and
diz- ziness associated with the myofascial pain-dys- function syndrome. Oral
Surg 46;742-747, 1978.
[10] Bales T,
Grunwaldt E: Myofascial pain in childhood. J Pediatr 53:198-209, 1958.
[11] Travell
Janet G., Simons David G.(1983).Myofascial pain and dysfunction-the trigger
point manual .428 E. Preston Street Baltimore, Md 21202, U.S.A:Williams &
Wilkins. Page 13
[12] Awad EA:
Interstitial myofibrositis: hypothesis of the mechanism. Arch Phys Med
54:440-453, 1973.
[13] Miehlkc K,
Schulze G, Eger W: Klinischc und experimcntelle Untersuchungen zum Fibrositis
syndrom. Z Rheumaforsch 19:310-330, 1980.
[14] Stenger RI.
Spiro D. Scully RE, Shannon IM: Ultrastructural and physiologic alterations in
ischemic skeletal muscle. Amer J Patho140:1-20. 1962.
