Myofascial Pain Syndrome

Myofascial Pain Syndrome is a condition that is often confused with fibromyalgia . In contrast to this, however, sufferers complain of localized pain and the hardened trigger points can be felt. Severe musculoskeletal pain is the most important feature of the myofascial pain syndrome.

What is myofascial pain syndrome?

In the USA, however, an increasing number of examinations and investigations have been carried out by the attending physicians in order to be able to assist those affected. Above all, the delineation of the chronic pain of the myofascial pain syndrome to fibromyalgia proves to be problematic.

Because the most important feature of both diseases are severe pain in the musculoskeletal system, the cause of which can not be found in joints, muscle diseases , periosteum or neurological problems.

Myofascial Pain Syndrome causes

To date, medical research does not know which causes underlie the myofascial pain syndrome and whether genetic dispositions play a role. However, risk factors and probable triggers could be determined, the interaction of which promotes the occurrence of the disease.

These risk factors include mental stress , malnutrition , hormonal imbalances and muscle weakness . These factors lead to an overload of the muscle and the resulting permanent contraction of the muscle strands over a longer period. A persistent hardened trigger point arises.

The primary and secondary forms of the myofascial pain syndrome are further differentiated: the secondary form is a concomitant disease of various primary diseases such as osteoarthritis or neurological diseases. The cause of the primary myofascial pain syndrome is overloading of the musculature due to poor posture, bad workloads or excessive training in case of insufficient fitness.

Then the muscles are already over-stimulated by low loads, whereupon they react with inflammation . The differentiation of the forms is irrelevant for patients, because the symptoms are identical. Only for the adequate treatment of the disease, the cause of the myofascial pain syndrome must be found.

Diseases

  • arthrosis
  • Neurological diseases
  • hormonal imbalances

Myofascial Pain Syndrome Symptoms and course

People with myofascial pain syndrome complain of localized, severe muscular pain . These pains can occur in any part of the body, but by definition they must be confined to a so-called quadrant of the body. The majority of patients complains of shoulder pain , leg pain , hip pain , but also aches and butches are often affected.

The symptoms of myofascial pain syndrome are many-sided, they can show up in various other symptoms. In addition, the pain is transmitted through the local release of messenger substances on surrounding body parts, so that the person affected by the myofascial pain syndrome itself can no longer name where it has pain.

diagnosis

This is already a problem of the myofascial pain syndrome: The diagnosis is difficult, especially since the disease does not make itself felt with impaired blood and laboratory values. However, the unremarkable blood levels provide initial evidence of the disease and a way to exclude other causes.

If a patient complains of diffuse pain, the attending physician must first examine the musculoskeletal system for trigger points. These show as palpable, pressure-sensitive hardening of the muscle belly, which causes pain in the surrounding body parts when touched. In addition, limited mobility of the muscles in this area and increased twitching when applying pressure are noted.

Hardened muscles and increased twitching when pressure is applied to the clear delineation of fibromyalgia and myofascial pain syndrome.

Myofascial Pain Syndrome Treatment and therapy

Since the myofascial pain syndrome is usually diagnosed only after its chronification, patients have to accept that the disease can not be cured. The aim of the treatment is to alleviate the symptoms by relaxing the muscles and improving circulation in the affected area of ​​the body. Doctors can prescribe painkillers and muscle relaxants.

However, these are not a panacea. In addition to the medical treatment, regular warmth treatments, massages and stretching exercises should be performed, accompanied by a trained physiotherapist . However, this therapy is only suitable for mild cases.

In severe forms of myofascial pain syndrome, manual trigger point therapy is initiated. The therapist, usually an osteopath, places needles in the trigger point during acupuncture and at the same time stretches the affected muscle strand. If this therapy does not work, the injection of saline solutions, local anesthetics or botulinum toxin remains in the trigger point.

The secondary myofascial pain syndrome is treated according to the underlying disease. Every therapy of the myofascial pain syndrome requires the active cooperation of the patient. Self-help groups and psychotherapeutic support help those affected to come to terms with their illness and to shape their lives with the myofascial pain syndrome.

Myofascial Pain Syndrome prevention

Since medical research has not found any cause of the myofascial pain syndrome to date, there are no suggestions for prevention. However, the avoidance of risk factors and a regular fitness adapted to the fitness state seem sensible. More important than the prevention of the disease is the mental stability of patients with myofascial pain syndrome to enable them to live happily with the disease.

ABSTRACT

Myofascial pain syndrome is compounded by sensory, motor and autonomic symptoms that are generated by myofascial trigger points that are exquisite in sensitivity and irritability. These trigger points are located in a palpable taut band in muscle or fascia, which produces a local twitch response of muscle fibers for a specific type of palpation and if there is enough hyperirritability results in pain, tenderness and autonomic phenomena and dysfunction that would appear usually in distant areas from its site of origin. 

With a high prevalence in the general population, Myofascial Pain Syndrome is responsible for disability and dysfunction in work areas and daily life activities. It presents precipitating factors, such mechanical, structural, postural, nutritional and endocrine, and involves a specific pathophysiology, involving multiple pro-inflammatory factors and neuro-vasoactive substances. 

Diagnosis is mainly clinical, and there are several treatments to prevent chronicity and development, which usually involves easy and economic access to treatments, which may give the patient a solution to chronic pain, often underdiagnosed and undertreated, if it has adequate knowledge about this entity

INTRODUCTION

Myofascial Pain Syndrome by trigger points (DMF) is an entity described by Drs. Janet Travell and David Simons in 1992 corresponds to a regional non-inflammatory muscular pathology that can occur in any striated muscle of the body. Its main characteristic is the presence of a hypersensitive area called trigger point, which is present in a palpable tense band of muscle tissue and has the ability to refer pain to distant areas. This last quality makes its diagnosis difficult and may be the reason for failed treatments.

At least 30% of the population has some symptom in the locomotor system in which pain of muscular origin is of significant importance. Muscle injuries often meet criteria for Myofascial Pain Syndrome (SMF). It is a regional, acute or chronic, primary or secondary muscular process, very prevalent and disabling, but quite unknown, underdiagnosed and undertreated, probably because it is not accompanied by structural alterations detectable with complementary imaging or analytical tests and often because it is associated to other musculoskeletal processes  .

The musculoskeletal processes are the most frequent cause of pain, both acute and chronic and the main cause of disability in the working-age population; its consequences in terms of dysfunction, disability and costs are high. However, it is a treatable condition that responds favorably to timely and adequate treatment, focused not only on the management of pain, but also in the attention of structural, postural, ergonomic and metabolic conditions that alter muscle function3. 

So it is very important for the general practitioner to handle this diagnosis, and its adequate treatment and thus be able to provide patients with the adequate care of a condition that may be incapacitating in their work environment, and even in basic activities of daily life .

Epidemiology

In pain units, it is estimated that between 30 and 85% of patients come for Myofascial Pain Syndrome. In Mexico, the prevalence of musculoskeletal pain is 19.6% in the southeastern region. The international prevalence is from 13.5 to 47%. The definition of musculoskeletal pain, the different conditions included and the age of the populations studied are factors that cause variation in reported prevalences. Myofascial pain syndrome affects 85% of the population at some time in their life and affects any part of the body in 30 to 93% of the population.

The lack of unified coded based on studies multicenter interncionales3 diagnoses and the absence of a diagnostic test criteria difficult to calculate its actual prevalence.

In a cross-sectional study where records were reviewed of patients seen in the polyclinic of Temporomandibular Disorders and Orofacial Pain at the University of La Frontera, Temuco-Chile, from June 2010 to December 2012 it was concluded that the prevalence of DMF is high in patients who consult for orofacial pain and temporomandibular disorders, being 80.99%.

A prevalence of 44% in the American population has been described, being the most frequent age of presentation between 27.5 and 50 years. The latter does not coincide with the results found, since the most frequent age of presentation is 15 years, but supports the idea that DMF would not be associated with the age of presentation of the pathology, and may debut at any time.

The presence of DMF has been associated with other painful conditions such as tension-type headache, with a greater association with the upper trapezius muscle and even the pathophysiology of this primary headache has been questioned. 

Similarly, high prevalences of DMF have been found in patients with mechanical neck pain, whiplash injuries, cervicogenic headache and fibromyalgia5, which makes the study of DMF even more important considering the large number of work absences and disability that occurs in the patients.

Precipitating factors

The most common precipitating factors are of traumatic origin. After the acute phase of a macrotrauma, when the pain should have diminished if it persists, the presence of a pain of myofascial origin should be suspected. Other very important causes that trigger these phenomena are postural abnormalities, which are assumed during work activities or even activities of daily life (positions at bedtime, when reading, writing, etc). Mechanical factors, related to skeletal abnormalities, can secondarily produce muscle alterations in an attempt to correct the underlying skeletal abnormality 

SDM is more prevalent in the head, neck, shoulders, hips and lower back because the muscles of these regions work permanently against gravity to maintain posture or repetitively during daily activities. It is also common in people who have been involved in a motor vehicle accident .

A third are the psychological factors. Prolonged periods of stress or depression can produce underlying changes on some muscle groups, triggering myofascial pain. Another important factor is the sleep disturbances that due to the loss of an adequate relaxation of the muscle causes it to maintain a permanent activity, which translates into hyperirritability and consequently pain .

There is a last category that in some cases are not taken into account. This type of alterations are for example nutritional deficiencies, especially of some vitamins (B 1, B 12, C and folic acid), as well as some minerals: Calcium, Potassium, Iron and Magnesium. It must also take into account factors such endocrine, including alterations in the metabolism of thyroid .

These predisposing factors can become perpetuating factors of pain and therefore it is very important to correct it to eliminate a potential cause of development or perpetuation of pain.

Trigger points

Studies with electromyography suggest that the trigger point arises when the nociceptor and the motor plate coincide. A study was carried out with the aim of correlating the entry sites of the branches of the accessory nerve in the trapezius muscle with motor plates and the myofascial trigger points, 12 cadavers were taken to which the accessory spinal nerve was dissected to observe the exact point where the branches of this penetrated the muscular belly, 8 points were identified, which in all cases corresponded to the clinical description of the myofascial trigger points and were common to all the corpses.

This area of ​​referred pain is the feature that distinguishes myofascial pain syndrome from fibromyalgia. This pain can be reproduced reliably by feeling the trigger point, despite the fact that it is located some distance from its origin. This referred pain rarely coincides with dermatological or neuronal distributions, but follows a consistent pattern 

Painful points may develop after an initial injury inflicted on the muscle fibers. This injury can consist of a traumatic incident or repetitive microtrauma of the muscles. The trigger point causes pain and stress in the muscle or muscle fibers. As stress increases, the muscles become fatigued and become more susceptible to the activation of additional trigger points. The activation of one of these painful points occurs when a series of predisposing factors is combined with a triggering event. This theory is known as “theory of the harmful association” .

Pathophysiology

Tissue damage is produced which releases neurovasoactive substances and in this way the local nociceptors are rapidly sensitized. Thus, the first sequel to peripheral sensitization is muscle spasm; if the sensitization is very marked, then the muscle fibers begin to discharge action potentials spontaneously and therefore the pain is added to the sensation of muscular spasm. 

Under normal circumstances this injury recovers quickly and the nociceptors return to their normal threshold of sensitivity. However, for reasons still unknown today, in some patients local sensitization expands to neighboring nociceptors and in this way the lesion begins to become chronic.

Travell and Simons, in their integrated hypothesis, attributed the dysfunction of the motor plate as a possible etiology of PG, at which point motor neurons contact their corresponding muscle fibers. This dysfunction seems due to an abnormal depolarization of the motor plate by presynaptic, synaptic and postsynaptic mechanisms (excessive release of acetylcholine, defects of the enzyme acetylcholinesterase and increased activity of the nicotinic receptor of ACh, respectively). 

The ACh released in the synaptic space rapidly activates the nicotinic receptors of the ACh of the postsynaptic muscular membrane, leading to a potential for muscle action and contraction maintained in resting conditions with persistent shortening of the sarcomeres.

The resulting muscle contraction can alter arterial flow and the supply of oxygen, calcium and other nutrients necessary to induce muscle relaxation and meet the highest demands of local energy and ischemia.

The local energy demands, due to the effect of the sustained release of ACh, depolarization and sustained contraction, produce a rapid local depletion of adenosine triphosphate, which implies a metabolic failure that Simons has called energy crisis .

On the other hand, relative ischemia, which can be an important factor, if not the dominant one, in the development of the taut band, and the shortening and continued spasm of the contractile unit can damage and distort the affected tissues. Under these conditions, the synthesis and release of inflammatory substances (TNFa, bradykinin, protons, noradrenaline, serotonin, IL-1b, histamine, potassium, prostaglandins, leukotrienes, somatostatin, substance P, peptide related to the calcitonin gene (GCRP ), some of these substances act as inhibitors of acetylcholinesterase, which results in increased acetylcholine in the motor plate.

This is given in an acidic environment, which activates muscle nociceptors and increases activity in the motor plate . This phenomenon is known as peripheral sensitization and causes muscle spasm. The continued stimulation of the nociceptors can activate neighboring nociceptors and even second or third order neurons, causing central sensitization that may be responsible for the referred pain.

Painful stimuli coming from a chronic form of various structures, such as joints, viscera, nerves and muscle tissue with myofascial trigger points, converge on the dorsal root ganglion and activate healthy neural networks that release substance P and PGRC and initiate the formation of points Myofascial trigger in your muscles. These neurotransmitters diffuse to nearby neurons sensitizing and become more efficient in the transmission of painful stimuli .

It presents three basic components:

1. Palpable band, usually can not be seen at the eye examination. It represents a segmental spasm of a small portion of the muscle and is found if an adequate exploration of the affected muscle is performed .

2. Presence of trigger point (PG). It is a focus of irritability in the muscle when it is deformed by pressure, stretching or contraction, which produces a local pain, a referred pain and occasionally autonomic phenomena. In routine clinical practice we can find :

to. Active PG. They are painful without stimulation. Always sensitive, the patient feels them as a point of constant pain. The pain increases when the muscle is palpated, when it is pressed, when it is mobilized and when it is stretched .

b. Latent PG or satellites. They develop within the reference zone of the original active PG. They do not cause pain during normal activities. They are only painful on palpation .

3. Referred pain pattern, specific and proper for each muscle. It is a pain that comes from a trigger point, but feels distant from the origin of it, simulating the irradiation of a pain produced by nerve compression, so they are known as pseudoradiculares, but does not cause pain in the classical distribution of a root or a nerve and does not exhibit associated motor or sensory deficits 

Diagnosis

Clinical history: Patients with active PG complain of persistent local or regional pain, of mild to severe intensity, which the patient recognizes when the PG is compressed and generally limits the mobility of the muscle in question. The muscles used to maintain body posture are often affected, mainly the muscles of the neck, shoulders and pelvic girdle. The pain may be constant, although it is usually related to muscle activity. The PGs of each muscle have their own characteristic pain pattern and, thus, the distribution of pain can help identify the muscles responsible. It does not follow a dermatomer or radicular distribution.

Latent TrPs characteristically cause an increase in muscle tension and limitation of mobility, which patients are generally not aware of or simply accept .

Patients complain of few systemic symptoms. The SMF in the region of the head and neck can be accompanied by imbalance, dizziness, tension headache, tinnitus, temporomandibular pain, eye symptoms and torticollis. Pain in the upper extremities is often referred to and pain in the shoulders may resemble visceral pain or mimic tendonitis or bursitis. In the lower extremities, TrPs can affect the quadriceps or calf muscles and can lead to a limitation of mobility in the knee and ankle .

They can be associated with autonomic symptoms such as sweating, tearing, reddening of the skin and vasomotor and thermal changes. Functional disability may also appear with decreased work tolerance, alterations in muscle coordination, joint stiffness, fatigue and weakness. Other associated neurological symptoms are paresthesias, dysesthesias, blurred vision, shaking and tremor. In more evolved stages may appear alterations in sleep, mood changes and stress.

Physical examination: a meticulous medical, neurological and musculoskeletal examination must be performed. Pain prevents a muscle with a PG from reaching full mobility and also limits its strength, endurance, or both. The most frequent finding is the palpation in the painful muscle of a taut, rope-like band that follows the direction of the muscle fibers, in which a well-localized painful nodule is palpated. 

The location of the GP is based on the sensation of the doctor, assisted by the expressions of pain of the patient and the visual or palpable observation of a transient local response of shaking of the fibers of the taut band. The digital pressure of about 4 kg for about 5 s in active or latent TrPs can produce a characteristic referred pain pattern of each muscle.

A very characteristic sign is the patient’s reaction to the firm palpation of the PG, known as a jump sign, it is an involuntary reflex or shuddering of the patient, disproportionate to the applied pressure .

There are usually no neurological deficits or alterations in hematological, biochemical or urinary laboratory tests, unless there are concomitant diseases such as nutritional or metabolic alterations. Electromyography will reveal the increase in spontaneous electrical activity in the TrPs. X-rays or MRI do not reveal any pathological changes in the affected muscle or connective tissue. 

Ultrasonography may be useful in being able to visualize the spasmodic response when stimulating PG, as well as thermography, by showing areas of increased skin temperature in the PG region. The algometers are used to quantify the pressure sensitivity in a muscle point. They are applied perpendicular to the area of ​​maximum sensitivity..

Treatment

Prevention: Exercise is essential, since a strong muscle is much less prone to contractures. To avoid back pain is advisable to exercise or, in any case, stay physically active, avoid sedentary lifestyle, adopt a brave mental attitude to pain and comply with postural hygiene rules designed to perform daily activities so that the back support the lowest possible load .

Early treatment is important to avoid compensation for other muscles of the functional unit. Initially, treatment will focus on reducing pain and inactivating PG, for which different modalities of physical therapies combined with myofascial and massage release techniques have been used .

The second stage should focus on the recovery of range of motion, correction of biomechanical deficits and muscle strengthening according to the findings of the physical examination of each patient to restore the balance between the muscles that work as a unit functional .

In a third phase, the patient must continue with an exercise program at home. Patients with Myofascial Pain Syndrome should be educated about the factors that can contribute to the generation of their pain and loss of mobility, as well as specific strategies for the maintenance of postures and appropriate use of body mechanics during work and activities of daily life. An ergonomic evaluation should be carried out in the workplace when it is suspected that this is a pain generator to recommend the necessary furniture modifications together with recommendations for postures, frequent work breaks and stretching exercises .

Among the most used and widespread treatments are:

1. Spray and stretch: This technique involves the application of several cold cycles by means of a spray of ethyl chloride in the area of ​​referred pain, followed by passive elongation of the involved muscles .

2. Postisometric relaxation: Consists of contracting the tense muscle against resistance from its maximum painless length of 3 to 10 seconds and then encouraging its elongation3.

3. Release by pressure: Formerly known as ischemic compression, it consists in the application of progressive pressure for 15 seconds in the PG until resistance and discomfort of the patient are found.

4. Infiltration of the PG: It seems to be the most effective method to inactivate the PG, either with local anesthetics or with a dry needle3. In a systematic review published in 2001 of 23 randomized clinical trials of the treatment of Myofascial Pain Syndrome with PG infiltration, it was concluded that the nature of the injected substance does not mark differences in the results and that the infiltration of a substance does not obtain therapeutic benefits, compared with dry puncture, supported by high-quality clinical trials12. However, post-infiltration pain generated by dry infiltration is more intense and lasting than that experienced by patients treated with lidocaine .

Most authors do not recommend the use of corticosteroid infiltration3. It does not add an associated beneficial effect and on the contrary it can even produce cumulative damage to the muscle fiber; therefore, it would only be indicated if the patient has an associated inflammatory pathology (eg, adhesive capsulitis, tendonitis, etc.).

5. Recent studies suggest that botulinum toxin has analgesic effects independently of its action as an agent that causes chemical denervation on the muscle. This analgesic action seems to be mediated by the inhibition of glutamate release and the reduction in the production of substance P. The injection of botulinum toxin for the treatment of low back pain in which there is an associated muscular component is a treatment of proven efficacy. In the Myofascial Pain Syndrome of the pyramidal syndrome, its injection in said muscle is more effective than the injection with placebo or with local anesthetics with corticosteroids. The same occurs in chronic facial pain and in that originating in the anterior scalene and in the iliopsoas.

In conclusion, its efficacy has been demonstrated in painful syndromes associated with spasticity, while in those with increased muscle activity (eg, tension headache), its activity is limited .

6. Drugs: Most experts recommend the oral use of analgesics, non-steroidal anti-inflammatory drugs, muscle relaxants, anticonvulsants and antidepressants as adjuvant treatment to infiltration and physiotherapy. They have not been shown clear benefits in the treatment of mechanical neck pain with any drugs especially 3. Patches of procaine or lidocaine placed on superficial PGs have been used. A quantity of anesthetic paste (similar to the volume of a hazelnut) is placed on the area to be treated and enclosed in an occlusive dressing. After 45 minutes the anesthetic is absorbed percutaneously and, if it has reached the PG, it can achieve inactivation. It is recommended to add later stretch. It has also been suggested that patches of larger dimensions associated with antiepileptic drugs may also improve chronic back pain.

7. The ozone on contact with the tissues generates, at the intramuscular level, an anti-inflammatory effect due to the increase in the production of antioxidant enzymes that leads to a state of adaptation to oxidative stress, neutralizing the formation of unstable reactive oxygen compounds. The analgesic effect of ozone decreases the defense muscular contracture, which is reflexively activated to protect the area of ​​the herniated disc. This action is related to the inhibition of the synthesis of prostaglandins and proinflammatory cytokines and increases the release of immunosuppressive cytokines. Localized oxygenation and analgesia allow vasodilation and muscle relaxation, favoring oxidation of lactate, neutralizing acidosis, increasing the synthesis of ATP.

8. In a non-probabilistic, controlled experimental, double-blind study with 43 patients. The experimental group of 22 subjects who underwent lumbar paravertebral ozone and in PG together with pharmacological and rehabilitative treatment, in the management of patients with lumbar pain and chronic lumbociatalgia, compared with only pharmacological treatment and Rehabilitation, in the control group of 21 patients ; It was found to be more effective, with statistical significance (p <0.05) to reduce the intensity of pain (90.5%), functional disability (90.5%), and increased the degrees of trunk flexion (85.7%). % versus 40, 70 and 75%) respectively, at four weeks after the start of treatment .

9. Eletroacupuncture (EA) involves the passage of an electrical current through the needle and is supposed to be more effective in pain relief than manual acupuncture. Studies investigating the mechanisms of action of AD have revealed that endogenous opioid peptides in the central nervous system mediate the analgesic effects produced by this treatment. Therefore, EA is applied at the acupuncture points to stimulate muscle nociceptors, which activate the endogenous atinociceptive system. The WHO approved more than 40 disorders that can benefit from acupuncture treatment.

In a study with 20 women, with a BMI ranging from 19 to 25 kg / m, ranging from 18 to 40 years with regular menstrual cycles controlled by oral contraceptive, with local pain or referred pain for more than six months and at least a myofascial trigger point in the upper trapezius. Participants received a total of nine EA sessions. more than five weeks. A mixed current of 2 Hz and 100 Hz was applied alternately every 5 seconds for 30 minutes. 

The results were measured pain intensity by the analogue visual scale (VAS), pressure pain threshold (PPT) measured by an algometer, by electromyography (EMG) and the quality of life measured by the SF-36 questionnaire. There was a significant improvement in pain intensity and PPT occurred after treatment (p <0.0001). EMG of the right trapezius during contraction increased significantly, suggesting improvement of muscle function; quality of life improved, related to the physical components of the SF-36 (p <0.05). The EA showed to be a reliable method for the relief of Myofascial Pain Syndrome.

Myofascial Pain Syndrome
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