Myofascial Pain Syndrome Mps Biology Essay

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There are a group of people with idiopathic back and leg pain for whom no correlated underlying disease can be found1. The complaint is of muscular tenderness and pain. The problem may be isolated to the lumbar spine or be a part of the larger syndrome called Myofascial pain2.

Definition

Myofascial pain syndrome (MPS) are very common, it is a painful part of nearly everyone's life at one time or another3 and recognized by clinicians as one of the most common cause of pain and dysfunction of the musculoskeletal system4. MPS is a myalgic condition in which muscle and musculotendinous pain are the primary symptoms5.

Myofascial pain syndrome is caused by Myofascial trigger points (TrPs) and has sensory, motor, and autonomic symptoms6. Simon et al defined MPS as regional pain syndrome of any soft tissue origin.

MPS from TrP is common as a cause of acute muscle pain and of chronic pain. Many symptoms can be related to MPS including backache, tension-type headache, shoulder pain, tennis elbow, pelvic floor pain, and levator ani syndrome, and many other different presentations.5

MPS is characterized by pain on movement and pain on palpation of a specific affected area of the muscle7. It is often located in the neck, back, shoulders8 and in the masticatory muscles3.

TrPs who produces local and referred pain9, tenderness, motor dysfunction, and autonomic phenomena are tender spots in discrete taut bands of hardened muscle3. Taut bands may contain a degree of nodularity, particularly at the region of greatest hardness, which is also usually the region of greatest tenderness. The nodularity is not always palpable and it is not required for the diagnosis of Trp5. A trigger point is composed of numerous so-called contraction knots. A single contraction knot appears as a segment of a muscle fiber with extremely contracted sarcomeres and an increased diameter. The TrP hypothesis assumes that in myofascial pain motor endplates release excessive acetylcholine, which is verified histopathologically by the shortenong of sarcomere9. Mense in 2010 showed that taut band is made up of a series of contracted muscle fibers, made up of multiple foci of intensely contracted sarcomeres thought to be located at or near the motor endplate zone. The intensity of the contraction of the TrP results in a sensory phenomenon of localized, exquisite pain that is always associated with the taut band5.

Alvarez et al differentiated Trigger points as active or latent, depending on their clinical characteristics. Pain at rest is caused by active TrP. It is tender to palpation with a pain pattern that is comparable to the patients pain complaint. The pain is often radiating. Referred pain is a very important characteristic of a trigger point. It differentiates a trigger point from a tender point. Tender point is pain localized to the site of palpation10. A latent trigger point does not causes pain at rest, but may restrict movement or cause muscle weakness11.

The etiology of myofascial pelvic pain is controverted in most cases. A variety of etiologies are possible, including organ pathology, neuromuscular disorders, and psychological causes12.

Trigger points are the hallmark of myofascial pain. Trigger points have several features in common, including10,13:

One or more trigger points may be present

They are located within a tight band of muscle

They cause local pain and a referred pain

Pain or tenderness may occur in the lack of stimulation or only when pressure is applied

A local twitch response occurs when strong pressure is applied (strummed) across the point. However, it is not always palpable

Over time, muscles with trigger points become weak, tender, and shortened14. This, in turn, can cause surrounding muscle groups to also contract and develop trigger points, thereby worsening myofascial pain and related symptoms.

Myofascial trigger points are thought to develop when acute trauma or the repetitive micro traumas that occur with daily activity and exercise cause high intensity stimulation of the motor end plate of the pelvic floor muscles4. As an example, anxiety may predispose some patients to continuously contract their muscles. Short-term or chronic pain can similarly cause a patient to unconsciously contract muscles. Poor posture and joint misalignment, leg length discrepancy, and dysfunction of joints, are orthopedic abnormalities that increase the strain of the muscles. Additional potential causes of myofascial trigger points are chronic repetitive contraction of muscles, repetitive minor trauma from straining, sudden severe strain sustained during physical activities, such as sports or dance, direct physical trauma, local inflammation, referred pain from other attaching muscle groups or viscera or nerves, poor posture/ergonomics.

Other studies showed that prolonged muscle contraction, spasm, and inappropriately high muscle tone are thought to diminish blood supply and increase oxygen demand of the muscles of the pelvic floor15,16. Ischemic muscle may secrete vasoactive and neuroactive substances, which further sensitize muscle nociceptors, alter receptor field properties, and convert wide-band mechanoreceptors to nociceptors, resulting in pain and perpetuating this cycle17. Changes in the central processing of painful stimuli may also play a role. Such changes may lower the pain threshold, allow nonpainful stimuli to cause pain (allodynia), and increase the field, degree, or duration of pain (hyperalgesia).

Travel and Simons related the etiology of myofascial TrPs to a focal muscular dysfunction which can exert a strong influence on all major parts of the nervous system, and can lead to spinal level neuroplastic changes that help to convert an acute pain problem into a chronic one3.

Laskin pointed out the key elements of the theory of MPS. He believed that muscle spasm is the primary factor responsible for the signs and symptoms of the MPS. Spasm can be initiated in one of three ways: muscular overextension, muscular overcontraction, or muscle fatigue18.

Studies to support muscular fatigue as the direct cause of pain have been performed by Christenson who found that prolonged voluntary loading can produce the signs and symptoms of the MPS19.

Histopathologic investigations have attempted to correlate myofascial pain and dysfunction with the direct overloading of muscles or with indirect disturbances of the blood supply. Yavelow hypothesizes that prolonged isometric contraction interferes with local circulation and ionic interchange across cell membranes, thus depriving cells of glycogen and oxygen and increasing the lactic acid concentration20.

Newtons adds that intense gamma firing, related to increased reticular stimulation by stress, initiates the excessive isometric contraction rendering protective reflexes ineffective in correcting motor activity upon sensory input. The alpha and gamma systems are further abused by prolonged isometric contraction which in turn cuts off circulation to the muscles, and the spindles become unresponsive to further stretching21.

Travells points out that when the muscles are subjected to noxious stimulation of various sorts (mechanical, emotional, metabolic,) they act in one way, they develop spasm and shorten. .A muscle spasm is unable to relax voluntarily and it resists passive lengthening: this condition results in poor neuromuscular coordination3.

There is general agreement according to Bron that any kind of muscle overuse or direct trauma to the muscle can lead to the development of TrPs. Muscle overload is thought to be the result of sustained or repetitive low-level muscle contractions, eccentric muscle contractions, and maximal or submaximal concentric muscle contractions. Although muscle damage is not required for the development of TrP, there may be a disruption of the cell membrane, damage to the sarcoplasmic reticulum with a subsequent release of high amounts of calcium-ions, and disruption of cytoskeletal proteins, such as desmin, titin, and dystrophin. Ragged red (RR) fibers and increased numbers of cytochrome-c-oxidase (COX) negative fibers are common in patients with myalgia, which are suggestive of an impaired oxidative metabolism6,22.

Muscle overuse is the result of muscle contractions that surpass muscle capacity. The capillary blood flow of the muscle is temporarily obstructed during muscle contractions. The blood flow is recovered when the muscle is relaxed. In dynamic rhythmic contractions, intramuscular blood flow is improved by this contraction-relaxation rhythm, also known as the muscular pump. During continued muscle contractions, though, muscle metabolism is highly dependent upon oxygen and glucose, which are in short supply.

Even contractions performed at only 10 % and 25 % of capacity or maximum voluntary contraction may produce intramuscular pressures high enough to impair the intramuscular blood circulation.

Otten, proved that the augmented pressure gradients during low-level exertions may lead to the development of pain6 and finally to the formation of TrPs.

Since oxygen and glucose are necessary for the synthesis of adenosine triphosphate (ATP), which provides the energy required for muscle contractions, persistent contractions may cause a local energy crisis due to the lack of oxygen. To sustain an satisfactory supply of ATP, the muscle can switch within a few seconds to anaerobic glycolysis. During the early phase of glycolysis, one glucose molecule is broken down into two pyruvic molecules liberating enough energy to form two ATP molecules. Under aerobic circumstances, oxygen interact with pyruvic acid producing a high amount of ATP (16 molecules per pyruvic acid molecule), water and carbon dioxide. Under anaerobic circumstances, though most of the pyruvic acid made during glycolysis is transformed into lactic acid, thereby increasing the intramuscular acidity (pH). Most of the lactic acid disperses out of the muscle into the bloodstream; post-exercise lactic acid is washed out within 30 minutes after exercise. Unfortunately, when the capillary circulation is restricted, as in MPS, this process is not accomplished.

Researchers at the US National Institutes of Health found that in the direct environment of active TrPs, the pH may be well below 5, which is more than sufficient to excite muscle nociceptors, including acid-sensing ion channels (eg, ASIC 1 and 3), and the transient receptor potential vanilloid receptor TRPV123,24. Small increases of the H+ concentration, as seen with inflammation, heavy muscle work, and ischemia, are sufficient to excite muscle group IV endings, contributing to mechanical hyperalgesia and central sensitization25. Furthermore, a low pH downregulates acetylcholinesterase (AChE), increases the efficacy of acetylcholine (ACh), and maintains the sarcomere (super-) contraction. It also triggers the release of several nociceptive substances, such as calcitonin gene-related peptide (CGRP)25, which can enhance the release of ACh from the motor endplate and simultaneously decrease the effectiveness of AChE in the synaptic cleft. CGRP also upregulates the ACh-receptors (AChR) at the muscle and thereby creates more docking stations for ACh. Miniature endplate activity depends on the state of the AChR and on the local concentration of ACh, which is the result of ACh-release, reuptake, and breakdown by AChE6.

Relaxation within the muscle cells occurs when myosinactin cross-bridges detach. After ATP is attached to the myosin molecule, the link between myosin and actin weakens, and the myosin head detaches from actin. In other words, the cross-bridge between myosin and actin breaks. Simultaneously, the Ca2+ ion detaches from the troponin molecule, which blocks tropomyosin. Under normal physiological circumstances, large amounts of free calcium-ions will reenter the sarcoplasmic reticulum by the Ca2+ pump (Calcium ATPase), which places a high demand on ATP during relaxation. In case of severe energy depletion, the sarcomeres may stay contracted, until enough ATP is available to resolve the intracellular Ca2+ accumulation.

High concentrations of intracellular Ca2+ are associated with sustained sarcomere contraction and muscle damage. Ca2+ accumulation due to sustained motor unit activity has been suggested to play a causative role in the development of muscle disorders and TrPs26.

In a preliminary study using Doppler ultrasound, Sikdar et al have shown that blood flow waveforms show significant differences between active TrPs, latent TrPs and normal sites. The flow waveforms near active sites showed increased systolic velocities and flow reversal with negative diastolic velocities27. They identified 2 contributing factors, namely an increase in the volume of the vascular compartment, and an increased outflow resistance. Increased outflow resistance could be due to muscle contractures at the TrP that compress the capillary or venous bed.

Release of acetylcholine from the motor nerve terminal, the binding of acetylcholine to its

endplate region receptor, and the release of calcium into the cytosol to activate muscle contraction,

are points where contractile activity can be modulated. Release of acetylcholine from the motor

nerve terminal is calcium-dependent, and modulated by adenosine and by sympathetic activity

(mediated through alpha and beta adrenergic receptors). Release of acetylcholine is also enhanced

by calcitonin gene-related peptide (CGRP). CGRP also up-regulates acetylcholine receptors

(AChR), creating more binding sites at the motor endplate, and inhibits acetylcholine esterase

(AChE). Sympathetic modulation of cytosolic calcium concentration is also mediated through

activation or inhibition of a second messenger system utilizing cyclic adenosine monophosphate

(cAMP). A feedback mechanism is also at work in which high cytosolic calcium concentration

inhibits release of acetylcholine from the motor nerve terminal. Abbreviations: A2 and A2A are

adenosine receptors, ACh: acetylcholine, AChE: acetylcholine esterase. AChR: acetylcholine

receptor, RyR: Ryanodine receptor, Ca2+: calcium, CGRP: Calcitonin gene-related-peptide5

This chart shows the relationship of a muscle injury, such as a single muscle overload or a

repetitive overload, to the development of the taut band, the motor abnormality in myofascial

pain syndrome. The physiologic changes in this chart cascade downward from muscle injury to

ischemia, to release of CRGP and so on, to prolonged muscle fiber contraction and development of

the taut band5

This chart shows the relationship of muscle injury to the sensory manifestations of

trigger point pain, namely the activation of peripheral nociceptors and the initiation of central

sensitization5

Clinical presentation

In a recent article showed trigger points (TPs) are defined as hyperirritable spots located within the taut band of skeletal muscle that are painful to compression and give rise to characteristic referred pain patterns and autonomic symptoms28. Trigger points may simultaneously exist in muscle, tendon, ligament, fascia or fibrous articular capsules.

Trigger points often give rise to characteristic pattern of referred pain distant from the point of contact. The pain provoked is diffuse and radiates to an area representing the symptomatic site. In the majority of cases, digital pressure on the painful point will reproduce the symptoms of the chief complaint, or even worsen the level of reported pain. Inactivation of TPs, however, may eradicate the patients pain. When TPs are localized in a palpable group of contracted muscle fibers, they may feel like a hypersensitive band. That group of fibers is called a taut band3.

Diagnosis

The reliability of MTrP diagnosis has long been a controversial point in the medical literature, because there had been no laboratory or imaging technique that was capable of confirming the clinical diagnosis. Diagnosis is only possible by clinical history and examination.

Nonetheless, the literature was critical of the capability to make a diagnosis of MTrP pain until recently. Part of the problem was certainly the failure to comprehend the nature of referred pain, an issue put to rest with the advances in the understanding of pain neurophysiology. Quite a lot of attempts to prove the clinical efficacy of manual physical examination prior to 1997 failed. In 1997 Gerwin et al. established the first paper to interrater the reliability in trigger point. The furthermost consistent findings in that study were localized tenderness, existence of a taut band, and pain recognition.

These features became the recommended features required for recognizing a trigger point. That study also indicated that not all muscles are similarly easy to examine, and not all features of the trigger point, such as the local twitch response, are equally easy to identify.

The efficacy of physical examination in sensing MTrPs has been confirmed by consequent studies. The reliability has been demonstrated to an accuracy of a square centimeter or so within a single muscle (Sciotti et al. 2001), signifying that examiners could individually identify the same taut band region. Referred pain and the jump sign had the highest degree of agreement among the blinded examiners. Identification of a nodule in a taut band and eliciting a twitch response had the two lowest degrees of agreement. In clinical practice, feedback from patients allows assessment of reproducing clinically relevant pain elicited by palpation.

Treatment

The management of MPS include several procedures:

Postural and ergonomic factors

The most serious element in the active management of myofascial pain syndromes is the correction of predisposing factors. These delay the ability of the muscle to fully recuperate and are the most common cause of treatment failures.

Stretching

The muscles involved in MPS are shortened due to focal contractions of sarcomeric units. It is believed that these focal contractions result in continued ATP consumption, and that the restoration of a full muscle

stretch length breaks the link between the energy crisis and the contraction of the sarcomeric units. Effective stretching is achieved through the method of spray and stretch. This includes the cutaneous application, beside the axis of the muscle, of ethyl chloride spray while passively stretching the muscle. Other techniques to improve effective stretching consist of trigger point to pressure release, reciprocal inhibition, deep stroking massage and post-isometric relaxation.

Strengthening

Muscles TrPs become weak due to the inhibitory effects of pain. Slowly progressive strengthening of the muscle is required to restore full function and decrease the risk of reappearance and the preservation of satellite trigger points.

TrPs injections

Injection of TrPs is considered to be the most effective to inactivate it. Using a fine needle to inactivate all the foci inside a trigger-point locus is a supposed to be a critical element of effective trigger-point therapy (see Figure ). Precise localization of the Trp is established if a local twitch response is gained; yet this may not be obvious when needling deeply lying muscles. Efficacious elimination of the TrP usually results in a relaxation of the taut band. While dry needling is effective, the use of a local anesthetic (1% lidocaine or 1% procaine) aids to confirm the accurateness of the injection and delivers instant satisfaction for patients. There is no proof that the injection of corticosteroids offers any enhanced effect. A useful role for botulinum toxin in TrP injections has not so far been convincingly demonstrated, but may have a role in treatment of resistant cases.

Medications

At present there is no proof that any form of drug treatment eliminates MTrP. Non-steroidal anti-inflammatory drugs (NSAIDs) and other analgesics habitually offer moderate symptomatic relief. Tricyclic antidepressant drugs, which control pain at the central level, are frequently of benefit, particularly in those patients with a related sleep disturbance. Tizanidine (a muscle relaxant, ameliorates pain by activating a2-adrenergic receptors) is a useful adjunct in difficult to treat MPS yet there is no proof of its effectiveness.

Psychological techniques

Severe MPS that are not responding to treatment, it is not uncommon for patients to become anxious and depressed. These mood disorders need to be known and suitably treated. Persistent muscle tension worsens

the pain of MTrPs. In such refractory cases it is often essential to use additional management techniques, such as EMG biofeedback, cognitive behavioral therapy, and hypnotic/meditation relaxation techniques.29

Introduction

Back pain is the second most common reason for clinician visits in the United States30. Up to 84% of adults have low back pain at a certain time of their lives30,31.

The range of illness and morbidity correlated to low back pain is wide-ranging. For many, back pain are self-limited and resolve spontaneously. For others, back pain is recurrent or chronic, causing an important pain that interferes with quality of life. Rarely, acute back pain is related to serious medical illness, including infection, malignancy, or other systemic disease.

Risk factors

Risk factors include smoking, obesity, older age, female gender, physically strenuous work, sedentary work, psychologically strenuous work, low educational attainment, job dissatisfaction and psychological factors such as somatization disorder, anxiety, and depression3135.

A prospective study conducted in England found that physical activity outside the workplace was not associated with back pain, but that poor physical health in both men and women, and heavier weight in women, amplified the risk of new back pain35. The same study found that jobs comprising lifting, pulling, or pushing heavy objects, and jobs comprising long periods of standing or walking, were related with a higher incidence of low back pain, particularly among women36.

CLINICAL EVALUATION Low back pain is often related to disc degeneration, which is the primary objective for many diagnostic approaches. Pain can also be due to muscles or ligaments so it is also an important entity.

Even if the differential diagnosis of low back pain is wide, the majority of patients seen in primary care will have a non-specific low back pain, meaning that there is no neoplastic, infectious, or primarily inflammatory cause37. Less than 5% of patients with low back pain will have serious systemic pathology. Even though patients are often told a precise diagnosis for their back pain, reproducibility of these diagnoses (ie, muscle spasm, sacroiliac pain, trigger points) among providers is poor3841.

Diagnosis

Laboratory tests (CBC, ESR, and possibly CRP) are useful in for patients who may have spinal infection or malignancy, it should be considered in patients with low back pain who have not improved within four weeks.

Lumbar x-rays, CT, and MRI scans are often abnormal in asymptomatic patients. Abnormalities of these tests in patients with low back pain must be interpreted with caution.

Plain radiographs is used for infection, fracture, malignancy, spondylolisthesis, degenerative changes, disc space narrowing, and prior surgery and it is not used for diagnosis of an herniated disc. An ESR (or CRP) may be a useful screening test to determine which patients with risk factors for systemic illness should proceed to a radiologic study.

An MRI or CT should be done when the clinical investigation suggests emergent conditions (cauda equina syndrome, infection, tumor, fracture with neurologic impingement, or other mass lesions or defects); in patients with at least 4 to 6 weeks of radicular symptoms or a several month history of neurogenic claudication who would be appropriate surgical candidates for disc disease or spinal stenosis respectively.

MRI is considered the best initial test for most patients with low back pain who require advanced imaging. CT scan gives a better view of the bony structures.

A myelogram is not often needed for patients with low back pain. It may be suitable in patients with multiple disc abnormalities, multilevel radiculopathies, extruded free disc fragments, a disc fragment in the lateral recess, or previous lumbar surgery.

Electromyography (EMG) is most useful in assessing patients with radiculopathy who may be surgical candidates and who have poor correlation between their radicular symptoms and neuroimaging, and in patients with multilevel disease evident on neuroimaging.

Radionuclide bone scans are not useful in evaluating patients with back pain. The value of discography is controversial in the diagnosis of herniated disc as a cause of chronic low back pain.

DIFFERENTIAL DIAGNOSIS

Treatement

Referral, generally to a neurosurgeon or orthopedist, is indicated when patient have one of the following:

? Cauda equina syndrome: bowel and bladder dysfunction (urinary retention), bilateral leg numness and weakness and saddle anesthesia. It is a surgical emergency.

? Spinal cord compression: acute neurologic deficits in a cancer patient or with patients at risk of spinal metastases, and requires evaluation for surgical decompression or radiation therapy, with specific management determined by the underlying pathology.

? Progressive or severe neurologic deficit

Patients may similarly be referred to a neurologist or physiatrist if one of the following is present:

? Neuromotor deficit, persistent after four to six weeks of conservative therapy.

? Sciatica, sensory deficit, or reflex loss persistent after four to six weeks in a patient with positive straight leg raising sign, constant clinical findings, and favorable psychosocial circumstances.

Bennet mentioned that cute low back pain has many causes. Several are actually serious, such as cancer metastases, massive disk herniations (e.g. cauda equina syndrome), osteomyelitis, pancreatic cancer, aortic aneurysms and vertebral fractures. Though, the most common cause of acute back pain is lumbosacral strain. 95% of cases resolves in 3 months. If the pain does not resolve, a chronic low back pain syndrome will develop and is usually accompanied by an active myofascial trigger points42. Simons describes 15 torso and pelvic muscles that can be involved in low back pain3. The most common muscle group involved is the quadratus lumborum ; pain originating from TrPs in these muscles is felt as a band in the low back with intermittent radiation in a sciatic distribution or into the testicles. Active quadratus lumborum TrPs often result in difficulties with straightening up. TrPs related to the iliopsoas are similarly a common cause of chronic low back pain. The characteristic distribution of iliopsoas pain is a vertical band in the low back region and the upper portion of the anterior thigh. TrPs at the origin of the gluteus medius from the iliac crest are the cause for low back pain in the sacral and buttock with a radiation of pain to the outer hip region29.

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