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14 Articles in Volume 12, Issue #2
Chronic Pain in the Elderly: Special Challenges
Chronic Pain School
Diagnosis and Management Of Myofascial Pain Syndrome
ECG Screening Prior to Initiating Methadone: Is it Really Necessary?
HCG and Testosterone
How to Manage Unmotivated Pain Patients
March 2012 Pain Research Updates
Methadone for Pain Management
PPM Editorial Board Discusses Methadone Prescription Safety Measures
PPM Launches Online Opioid Calculator
Spontaneous Low Back Pain, Radiculopathy, And Weakness in a 28-Year-Old
Tapering a Patient Off Opioids
The Comorbidity of Chronic Pain and Mental Health Disorders: How to Manage Both
What Are Best Safety Practices For Use of Methadone In the Treatment Of Pain?

Diagnosis and Management Of Myofascial Pain Syndrome

Investigating—and eliminating—the underlying causes of active trigger points is key for clinicians to effectively manage patients with myofascial pain syndrome, a common cause of chronic musculoskeletal pain.
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Myofascial pain syndrome (MPS) is a common musculoskeletal disorder caused by myofascial trigger points.This painful disorder can affect any of the skeletal muscles in the body and the prevalence varies by medical specialty—it accounts for 21% of orthopedic clinic visits, 30% of general medicine visits, and approximately 85% to 93% of pain management clinic visits.2 MPS has become a major cause of time lost from work, resulting in a loss of millions of dollars from the economy.3

The pathophysiology of MPS is not completely understood. It is currently hypothesized that trigger points, the most common feature of MPS, contain areas of sensitized low-threshold nociceptors (free nerve endings) with dysfunctional motor end plates. These motor end plates connect to a group of sensitized sensory neurons in charge of transmitting pain information from the spinal cord to the brain.3

The affected muscle with the trigger point is associated with motor dysfunction and usually contains a palpable taut band or nodularity within the muscle belly. The taut band is considered to be a sustained band of contracted muscle due to increased concentrations of acetylcholine (ACh)—a neurotransmitter—in the synaptic cleft, changes in the ACh receptor activity, and/or changes in acetylcholinesterase activity.4

Electrodiagnostic studies suggest that a pathologic increase in ACh contributes to an increase in motor end plate activity as well. This constant state of muscle contraction and hyperactivity of motor end plates can increase the amount of energy consumption and affect the delicate supply and demand of nutrients and oxygen to the affected muscle. The high demand of resources needed by the affected muscle can eventually lead to hypoperfusion, ischemia, hypoxia, and finally, muscle damage.2 Localized muscle ischemia and muscle damage can trigger the release of neurovasoreactive substances such as prostaglandins, bradykinin, serotonin, adenosine triphosphate, potassium, and protons (H+), which can then activate the muscle nociceptors responsible for myofascial pain.4

Signs and Symptoms
Patients with MPS usually report regionalized aching, and diffuse, persistent pain in certain muscles and joints. The pain intensity can vary from mild to severe and is usually related to muscle activity. Patients may even have a history of dropping things due to pain-induced muscle weakness.3 Symptoms may begin after trauma or injury to the affected area or can be of gradual onset.2 The most commonly affected areas are the muscles in the neck and shoulders (ie, trapezius, scalene, and sternocleidomastoid muscles) and pelvic girdle.1

Trigger points, one of the main characteristics of MPS, are considered to be hyperirritable, circumscribed spots located in a palpable taut band of skeletal muscle (Table).5 These points are painful on compression and can produce referred pain, referred tenderness, and even autonomic phenomena.1 Referred pain and tenderness occur when pain is referred to remote sites from compression of a myofascial trigger point.5 For example, pain from compression of trigger points in the scalene muscles of the neck may be felt in the hand. Myofascial trigger points of different muscles are associated with their own characteristic pain pattern; thus, the unique distribution of pain can help the clinician to correctly determine which muscles are affected by MPS.2

Myofascial trigger points are different than the tender points found in fibromyalgia, in which pain occurs only at the site of palpation and is commonly associated with fatigue and sleep disturbances. Associated autonomic phenomena such as sweating, abnormal tearing, abnormal salivation, increased vasomotor response, and increased pilomotor response, can also potentially occur in extreme cases of MPS. It is believed that an autonomic phenomenon is a result of multiple sensitive nociceptors located in the region of trigger points. Nociceptors are activated upon compression of a trigger point, which can potentially overstimulate sensory neurons.5 Other associated neurologic symptoms include paresthesias, numbness, blurred vision, trembling, dizziness, and tinnitus.2

MPS trigger points can be classified as active or latent depending on their clinical characteristics. An active trigger point causes spontaneous pain and is tender to palpation with referred radiating pain.1 Latent trigger points are tender but not spontaneously painful. They usually are found in asymptomatic patients and can cause stiffness and limit range of motion (ROM).A number of studies suggest that latent trigger points can be commonly found in the shoulder-girdle muscles of 45% to 55% of asymptomatic young adults.2 Latent trigger points can be a result of active trigger points that have been suppressed with treatment.5 They also can develop into active trigger points as a result of psychological stress, muscle tension, and physical factors such as poor posture.

Another classic sign of MPS includes visible or palpable local twitch responses (LTRs) in the affected muscle. LTRs are brisk contractions of the muscle fibers within or around the taut band. Additionally, limitation of movement and, initially, muscle weakness without atrophy can be seen in patients.The pain induced by engaging the affected muscle is the underlying cause of limited ROM and reduced muscle strength. The prolonged muscle inactivity can then, eventually, lead to muscle atrophy.5

A thorough physical examination for MPS should entail a meticulous neurologic and musculoskeletal examination. Upon examination, a trigger point can be located by palpating a firm, hypersensitive nodule that elicits radiating pain when local pressure is applied to it.1 The referred pain also can be associated with sensory disturbances such as parasthesias, dysesthesia, and localized extreme skin tenderness. Observations can be confirmed with electromyography (EMG). An active group of nociceptors in the tender nodules can show evidence of spontaneous electrical activity on EMG. Also, the clinician can further localize trigger points by noting lowered skin resistance to electrical current in these areas compared with the surrounding tissues.3

Currently, no laboratory test or imaging technique has been completely established for diagnosing trigger points for MPS. However, lab tests can be helpful in looking for predisposing conditions, such as vitamin deficiencies, hypothyroidism, and hypoglycemia. Trigger points are sometimes associated with an increase in blood flow, which can be detected by infrared or liquid crystal thermography. Other imaging studies are useful in order to rule out other causes of musculoskeletal pain. Ultrasonography with needle penetration also has been used to visualize LTRs associated with MPS.3

Last updated on: March 19, 2012
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