TRIGGER POINT BOOK, fizjoterapia, Terapia Manualna, Fizjoterapia w sporcie
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BOOK
MYOFASCIAL SYNDROMES
DIAGNOSIS
Patients with chronic myofascial pain are people who have suffered more than just pain for many months or longer. The severity and
chronicity of their "untreatable" pain has often reduced their physical activity, limited participation in social activities, impaired sleep,
induced a major or minor degree of depression, caused loss of role in the family, led to loss of employment, and deprived them of control
of their lives. Many have been depersonalized by the ultimate indignity-the conviction that their pain is not "real," but psychogenic. Well-
meaning practitioners sometimes have also convinced the patients' families and friends that the pain is not real, leaving many patients
nowhere to turn for help. The patients come to the clinician seeking relief from their suffering, which they may present only in terms of
pain.
When examining the patient who has presented with chronic enigmatic pain, the diagnostician must first conduct a thorough, time-
consuming history and physical examination to identify what conditions are contributing to the patient's pain and to determine whether
there is a significant myofascial component. If it appears likely that the patient does have chronic myofascial pain syndrome, the
diagnostic task becomes twofold. In addition to identifying which TrPs, in which muscles, are causing what portion of the patient's total
pain complaint, the examiner must determine what perpetuating factors converted the initial acute myofascial pain syndrome to a chronic
one. Myofascial TrPs may be perpetuated by mechanical (structural or postural) factors, by systemic factors, by associated medical
conditions, and by psychological stress.
The central nervous system powerfully modulates pain input from the muscles in ways that can explain referred pain and altered
sensation from TrPs. In phase 1 (constant pain from severely active TrPs), patients may already have such intense pain that they do not
perceive an increase and cannot distinguish what makes it worse. Phase 2 (pain from less irritable TrPs that is perceived only on
movement and not at rest) is ideal for educating the patient as to which muscles and movements are responsible for the pain, and how to
manage it. In phase 3 (latent TrPs that are causing no pain), the patient still has some residual dysfunction and is vulnerable to reactivation
of the latent TrPs.
Myofascial Physical Examination
Specific myofascial examination of the muscles is undertaken following a complete general physical examination.
When searching for active TrPs that are responsible for the patient's pain, it is essential to know the precise location of the pain and to
know which specific muscles can refer pain to that location. Muscles that could be causing the pain are tested for restriction of passive
stretch range of motion and for pain at the shortened end of active range of motion, as compared with uninvolved contralateral muscles.
Suspected muscles are also tested for mild to moderate weakness either by conventional isometric strength testing or during a lengthening
contraction. Such weakness is not associated with atrophy of the muscle.
The muscles showing abnormalities in these tests are the ones most likely to have the taut bands and spot tenderness of the TrP. The taut
bands are located by palpation and then tested for a local twitch response and reproduction of the patient's pain complaint by digital
pressure on the TrP. One must try to distinguish active TrPs from latent ones, which can also respond positively to the tests described but
are not responsible for a pain complaint. Active TrPs are more irritable than latent TrPs and show greater responses on examination. If
inactivation of the suspected TrP does not relieve the pain, it may either have been a latent TrP or it may not have been the only active TrP
referring pain to that area.
Examination for mechanical perpetuating factors requires careful observation of the patient's postures, body symmetry, and movement
patterns. Common mechanical factors that can influence many muscles are the round-shouldered, head-forward posture with loss of
normal lumbar lordosis, and body asymmetries including a lower limb-length inequality and a small hemi-pelvis. Tightness of the
iliopsoas and hamstring muscles can also seriously disrupt balanced posture.
DIFFERENTIAL DIAGNOSIS
Two variants of myofascial pain syndromes should be recognized: the myofascial pain modulation disorder, which leads to diagnostic
confusion, and the post-traumatic hyperirritability syndrome, which complicates management. In addition, either fibromyalgia or articular
dysfunction can confusingly mimic a chronic myofascial pain syndrome. Each requires an additional specific examination technique and
its own treatment approach.
Myofascial Pain Modulation Disorder
It appears that the aberrant referral patterns are caused by a distortion of sensory modulation in the central nervous system. Many of these
patients had previously experienced trauma or painful impact at the focus of pain, but often not of such severity that it would be expected
to cause structural damage to the central nervous system. The mechanism behind this sensory nervous system dysfunction is not clear, but
possible mechanisms are being explored in current neurosensory research.
Post-traumatic Hyperirritability Syndrome
This syndrome follows a major trauma, such as an automobile accident, a fall, or a severe blow to the body that is apparently sufficient to
injure the sensory modulation mechanisms of the spinal cord or brain stem. The patients have constant pain, which may be exacerbated by
the vibration of a moving vehicle, by the slamming of a door, by a loud noise (a firecracker at close range), by jarring (bumping into
something or being jostled), by mild thumps (a pat on the back), by severe pain (a TrP injection), by prolonged physical activity, and by
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emotional stress (such as anger). Recovery from such stimulation is slow. Even with mild exacerbations, it may take the patient many
minutes or hours to return to the baseline pain level. Severe exacerbation of pain may require days, weeks, or longer to return to baseline.
These patients almost always give a history of having coped well in life prior to their injury, having paid no more attention to pain than
did their friends and family. They were no more sensitive to these stimuli than other persons. From the moment of the initial trauma,
however, pain suddenly became the focus of life. They must pay close attention to the avoidance of strong sensory stimuli; they must limit
activity because even mild to moderate muscular stress or fatigue intensifies the pain. Efforts to increase exercise tolerance may be self-
defeating. Such patients, who suffer greatly, are poorly understood and, through no fault of their own, are difficult to help.
In these patients, the sensory nervous system behaves much as the motor system does when the spinal cord has lost supraspinal
inhibition. In the latter, a strong sensory input of almost any kind can activate non-specific motor activity for an extended period of time.
Similarly, in these patients, a strong sensory input can increase the excitability of the nociceptive system for long periods. In addition,
these patients may show lability of the autonomic nervous system with skin temperature changes and swelling that resolve with
inactivation of regional TrPs. Since routine medical examination of these suffering patients fails to show any organic cause for their
symptoms, they are often relegated to "crock" status.
Any additional fall or motor vehicle accident that would ordinarily be considered minor can severely exacerbate the hyperirritability
syndrome for years. Unfortunately, with successive traumas, the individual may become increasingly vulnerable to subsequent trauma. A
frequent finding is a series of motor vehicle accidents over a period of several years.
Fibromyalgia
Patients with fibromyalgia are predominantly female (73-88%). Men and women are nearly equally likely to have myofascial pain
syndromes. The patient with an acute myofascial pain syndrome typically can identify the onset precisely as to time and place. Usually the
muscle was subjected to momentary overload, e.g. an automobile accident, a near fall, a sudden and vigorous movement (sports activity),
moving a heavy box, reaching over to pick something up from the floor, or getting into an automobile, although there may be a lag of
several hours to a day after the initiating event before pain appears. Patients with chronic myofascial pain may have difficulty identifying
the onset so clearly. These patients are likely to have more than a single myofascial pain syndrome. In contrast, the symptoms of
fibromyalgia typically develop insidiously; these patients usually can identify no specific moment in time when their symptoms began.
Thus, the onset of myofascial pain characteristically relates much more strongly to muscular activity and specific movements than does
fibromyalgia.
The orientation of the patient examination is quite different for the two conditions. For the diagnosis of myofascial pain, the clinician
painstakingly identifies precisely the distribution of each pain complaint, looks for dysfunctional postures and asymmetries, and examines
the muscles to determine which ones show a restricted stretch range of motion. Restriction of motion is not a part of the diagnosis of
fibromyalgia.
The myofascial examination includes palpation of the suspected muscles for tender spots in taut bands, which, when compressed, refer
pain to the area of the patient's pain complaint and, when snapped transversely, produce a local twitch response. To examine for
fibromyalgia, the prescribed tender point locations are examined only for tenderness; a relationship between the location of the tender
points and the distribution of the patient's pain is not an issue.
On palpation, the diffusely tender muscles of patients with fibromyalgia feel soft and doughy (except in specific areas, if they ateo have
TrPs in taut bands), whereas the muscles of patients with myofascial pain feel tense and are non-tender except at TrPs and in reference
zones.
Muscles that exhibit TrPs also exhibit some weakness without atrophy, but they are not particularly fatigable. Generalized severe fatigue,
rather than weakness, is characteristic of fibromyalgia.
The chronicity of myofascial pain syndromes is caused by perpetuating factors that usually are correctable; the chronicity of fibromyalgia
is inherent to the disease. This distinction is not evident at initial evaluation.
Some features are confusingly common to both conditions. Disturbed, non-restful sleep may occur in either, but is not required for
diagnosis. Over half of the designated tender point locations are also common muscle TrP sites. By definition, a latent or an active TrP at
one of those tender point sites would be counted as a tender point. Recent studies indicate that taut bands may be found not only in patients
with myofascial pain and in patients with fibromyalgia, but also in "normal" subjects. This finding may have unexplored implications as to
the relationship between the taut band and its TrP. Many patients with fibromyalgia also have active myofascial TrPs.
At this time, no specific cause of either fibromyalgia or myofascial TrPs has been established. However, clinically, myofascial pain caused
by TrPs is primarily a focal dysfunction of muscle, whereas fibromyalgia is a systemic disease that also affects the muscles.
Articular Dysfunction
We think of articular dysfunction either as joint hypomobility (including loss of joint play) that requires manual. movement,
mobilization, or manipulation to restore normal function, or as hypermobility that requires stabilization. The term somatic dysfunction is
now commonly used and includes skeletal dysfunctions that are often treated by mobilization and manipulation, as well as myofascial
dysfunctions that are frequently treated with myofascial release techniques.
An understanding of the interface between myofascial pain syndrome and articular dysfunction is one of the great voids in our current
knowledge of manual medicine.
TREATMENT
A chronic myofascial pain syndrome became chronic because of perpetuating factors that were unrecognized or were inadequately
managed. An identifying characteristic of a chronic myofascial pain syndrome is the initially unsatisfactory response to specific
myofascial therapy. Relief is usually only temporary, lasting a few hours or days. However, with correction of the perpetuating factors, the
involved muscles become increasingly responsive to therapy. Occasionally, severe perpetuating factors render the TrPs so irritable that
even the most gentle attempts at therapy cause more distress than relief. As progress is made in resolving the perpetuating factors, the
involved muscles become increasingly treatable.
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If one starts by correcting obvious mechanical perpetuating factors, myofascial TrP therapies that were previously ineffective are then
likely to provide significant relief and to encourage the patient. Each component myofascial pain syndrome should be analyzed and
managed as a single-muscle syndrome in the context of other TrPs in the same region. For patients with chronic pain, a home program of
stretch exercises is extremely important, probably even more so than for patients with a myofascial pain syndrome of only one or two
muscles.
Setting specific goals as described by Materson34 is critical for patients with chronic myofascial pain. The primary goal is to teach
patients how to recognize specific TrP syndromes, how to employ appropriate body positioning, and which stretch techniques to use for
relief. This puts the patients in control. If they want more relief, they know how to obtain it. If they prefer to trade a given level of pain for
the time and effort required to relieve it, that is their decision. They learn that control of the pain is in their hands. They come to
understand what constitutes abuse of their muscles (that will aggravate the pain) and what measures will reduce unnecessary overload of
the muscles. They learn to converse with and listen to their muscles.
Mechanical Perpetuating Factors
If the clinician selects for initial treatment a myofascial pain syndrome that is a major source of pain, is likely to respond to TrP therapy,
and has a mechanical perpetuating factor that is readily correctable (such as sitting posture or lower limb-length inequality), the patient
will see immediate benefits and will develop confidence in the treatment. Additional mechanical perpetuating factors relevant to the
patient's pain should also be corrected promptly.
Faulty posture is a mechanical perpetuating factor that is becoming increasingly common and serious with the proliferation of computer
terminals and computerized work stations.
Postural training should be one of the first parts, if not the first part, of the treatment program.
Faulty posture can aggravate TrPs in many regions of the body and can also increase the tenderness of fibromyalgia tender points.
In the seated individual, the "slumped posture," or fatigue posture, is characterized by a flattened lumbar spine (loss of normal lordosis),
sometimes by an increased dorsal kyphosis, by protracted scapulae, and usually by a flattened cervical spine with the head forward. This
posture leads to multiple muscle and joint problems in the trunk, upper limbs, neck, and head, as well as limited respiratory function.
For the seated slumped position, the patient can improve postural alignment by consciously raising the top of the head upward, keeping it
slightly forward. This simple maneuver lifts the chest to an optimum position for respiratory function. A comparable alignment can be
accomplished by "putting a hollow" in the low back. Since this erect posture (sitting "tall") cannot be actively held for long periods, the
individual can achieve this without effort by positioning the buttocks against the back of the chair and then placing a small roll behind the
lumbar spine (waist level). "Reaching" upward with the top of the head can be done several times a day as an exercise. The principle of
raising the top of the head away from the shoulders should also be applied when leaning forward to bathe or eat, thereby avoiding rolling
the shoulder up and forward and dropping the head.
For good seated posture, one's feet must reach the floor; when a person's legs are short or a seat is too high, a flexible footrest (small firm
pillow, bean bag, or sand bag] may be used to support the feet. A hard telephone book is less desirable, but can be temporarily useful. The
arms should be supported on armrests that are high enough to allow the individual to sit erect with the elbows supported. Forearm support
extensions can be adapted for desk work when typing. When one sits on a sofa or at a desk, arm support can be provided by using a lap
board placed on a pillow.
An alternate sitting position is one of sitting toward the front edge of a chair seat, placing one foot back under the chair and the other foot
forward. This balanced position promotes an erect posture with a natural, but not excessive, lumbar curve. Another way to promote good
sitting alignment with little effort is to place a pad at the back of the chair seat, directly under the ischial tuberosities (not under the thighs).
The padding tilts the pelvis forward slightly to induce normal lumbar lordosis, which, in turn, facilitates good upper body alignment.
Having two ways of sitting with good posture can be particularly useful for someone working at a desk. Frequent changes of position are
needed to promote health of the muscles and intervertebral discs.
Most important is patient awareness of the problem, understanding of its significance, and willingness to practice sitting and standing
erect. Following appropriate postural training (both "static" and dynamic), the patient can take responsibility for the management of the
pain that results from chronic postural strain and many activities of daily living. As patients exercise increasing control, they improve both
physically and emotionally.
Description of the myofascial syndromes
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o
semispinalis capitis
o
semispinalis cervicis
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o
multifundi
•
o
rectus capitis p. et a.
o
obliquus capitis
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
o
carpi radialis longus
o
extensor carpi radialis brevis
o
extensor carpi ulnaris
o
brachioradialis
•
•
•
•
o
flexor carpi radialis
o
flexor carpi ulnaris
o
flexor digitorum superficialis
o
flexor digitorum profundus
o
flexor policis longus
o
pronator teres
•
•
o
interossei
o
adductor digiti minimi
•
•
•
•
•
•
o
iliocostalis
o
semispinalis
o
multifundi
o
rotatores
•
o
obliquus abdominis
o
transversus abdominis
o
rectus abdominis
o
pyramidalis
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•
•
o
Bulbospongiosus
o
Ischiocavernosus
o
Transversus Perinei
o
Sphincter Ani
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o
Levator Ani
o
Coccygeus
o
Obturator Internus
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•
•
•
o
Gemelli
o
Quadratus Femoris
o
Obturator Internus
o
Obturator Externus
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•
•
Quadriceps Femoris Group
o
o
o
o
•
o
Adductor Longus
o
Adductor Brevis
o
Adductor Magnus
o
Gracilis
•
o
Biceps Femoris
o
Semitendinosus
o
Semimembranosus
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•
•
o
Peroneus Longus
o
Peroneus Brevis
o
Peroneus Tertius
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•
•
•
o
Extensor Digitorum Longus
o
Extensor Hallucis Longus
•
o
Flexor Digitorum Longus
o
Flexor Hallucis Longus
•
o
Extensor Digitorum Brevis
o
Extensor Hallucis Brevis
o
Abductor Hallucis
o
Flexor Digitorum Brevis
o
Abductor Digiti Minimi
•
o
Quadratus Plantae
o
Lumbricals
o
Flexor Hallucis Brevis
o
Adductor Hallucis
o
Flexor Digiti Minimi Brevis
o
Interossei
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