Lumbar Myofascial Pain Syndrome

Lumbar Myofascial Pain Syndrome

The muscles of the back work together as a functional unit to stabilize and allow coordinated movement of the low back and allow maintaining an upright position.

Trauma to an individual muscle can result in dysfunction of the entire functional unit. The rhomboids, latissimus dorsi, iliocostalis quadratus lumborum, multifidus, and psoas muscles are frequent sites of myofascial pain syndrome.

The points of origin and attachments of these muscles are particularly susceptible to trauma and the subsequent development of myofascial trigger points. Injection of these trigger points serves as a diagnostic and therapeutic maneuver.

The muscles of the back are particularly susceptible to the development of myofascial pain syndrome. Flexion/extension injuries to the back or repeated microtrauma secondary to improper lifting and bending may result in the development of myofascial pain in the muscles of the back. Myofascial pain syndrome is a chronic pain syndrome that affects a focal or regional portion of the body. The sine qua non of myofascial pain syndrome is the finding of myofascial trigger points on physical examination. Although these trigger points are generally localized to the regional part of the body affected, the pain of myofascial pain syndrome often is referred to other areas. This referred pain often is misdiagnosed or attributed to other organ systems, leading to extensive evaluations and ineffective treatment. Patients with myofascial pain syndrome involving the muscles of the low back often have referred pain into the hips, sacroiliac joint, and buttocks.

What are the Symptoms of Lumbar Myofascial Pain Syndrome

The trigger point is the pathognomonic lesion of myofascial pain and is thought to be the result of microtrauma to the affected muscles. This pathological lesion is characterized by a local point of exquisite tenderness in affected muscle. Mechanical stimulation of the trigger point by palpation or stretching produces not only intense local pain, but also referred pain. In addition to this local and referred pain, an involuntary withdrawal of the stimulated muscle often occurs that is called a jump sign . This jump sign also is characteristic of myofascial pain syndrome.

Taut bands of muscle fibers often are identified when myofascial trigger points are palpated. Despite this consistent physical finding in patients with myofascial pain syndrome, the pathophysiology of the myofascial trigger point remains elusive, although many theories have been advanced. Common to all these theories is the belief that trigger points are the result of microtrauma to the affected muscle. This microtrauma may occur as a single injury to the affected muscle or as the result of repetitive microtrauma or chronic deconditioning of the agonist and antagonist muscle unit.

In addition to muscle trauma, a variety of other factors seem to predispose to development of myofascial pain syndrome. The weekend athlete who subjects his or her body to unaccustomed physical activity often develops myofascial pain syndrome. Poor posture while sitting at a computer keyboard or watching television has been implicated as a predisposing factor to the development of myofascial pain syndrome. Previous injuries may result in abnormal muscle function and predispose to the subsequent development of myofascial pain syndrome. All these predisposing factors may be intensified if the patient also has poor nutritional status or coexisting psychological or behavioral abnormalities, including chronic stress and depression. The muscles of the low back seem to be particularly susceptible to stress-induced myofascial pain syndrome.

Stiffness and fatigue often coexist with the pain of myofascial pain syndrome, increasing the functional disability associated with this disease and complicating its treatment. Myofascial pain syndrome may occur as a primary disease state or may occur in conjunction with other painful conditions, including radiculopathy and chronic regional pain syndromes. Psychological or behavioral abnormalities, including depression, frequently coexist with the muscle abnormalities associated with myofascial pain syndrome. Treatment of these psychological and behavioral abnormalities must be an integral part of any successful treatment plan for myofascial pain syndrome.

How is Lumbar Myofascial Pain Syndrome diagnosed?

No specific test exists for lumbar myofascial pain syndrome. Testing is aimed primarily at identifying occult pathology or other diseases that may mimic myofascial pain syndrome (see discussion of differential diagnosis).

Plain radiographs help delineate bony abnormality of the lumbar spine, including arthritis, fracture, congenital abnormalities (e.g., trefoil spinal canal), and tumor.

All patients with recent onset of myofascial pain syndrome should undergo magnetic resonance imaging (MRI) of the lumbar spine to rule out occult pathological processes.

Screening laboratory tests, consisting of complete blood count, erythrocyte sedimentation rate, antinuclear antibody testing, and automated blood chemistry testing, should be performed to rule out occult inflammatory arthritis, infection, and tumor.

Differential Diagnosis

Lumbar myofascial pain syndrome is a clinical diagnosis of exclusion that is supported by a combination of clinical history, physical examination, radiography, and MRI. Pain syndromes that may mimic lumbar myofascial pain syndrome include lumbar strain, inflammatory arthritis, and disorders of the lumbar spinal cord, roots, plexus, and nerves.

Congenital abnormalities, such as arteriovenous malformations, trefoil spinal canal, and spondylolisthesis, also may mimic the clinical presentation of lumbar myofascial pain syndrome.


Lumbar myofascial pain syndrome is best treated with a multimodality approach. Physical therapy, including correction of functional abnormalities (e.g., poor posture, improper chair or computer height) and the use of heat modalities and deep sedative massage, combined with nonsteroidal antiinflammatory drugs (NSAIDs) and skeletal muscle relaxants, represents a reasonable starting point. If these treatments fail to provide rapid symptomatic relief, local trigger point injection of anesthetic and steroid into the myofascial trigger point area is a reasonable next step. Dry needling of these trigger points may also provide symptomatic relief.

Underlying diffuse muscle pain and sleep disturbance and depression are best treated with a tricyclic antidepressant compound, such as nortriptyline, which can be started at a single bedtime dose of 25 mg. Clonazepam may also help treat associated sleep disturbance and anxiety.

When performing trigger point injections, careful preparation of the patient before injection helps optimize results. Trigger point injections are directed at the primary trigger point, rather than the area of referred pain. It should be explained to the patient that the goal of trigger point injection is to block the trigger of the persistent pain and, it is hoped, provide long-lasting relief. It is important that the patient understands that for most patients with myofascial pain syndrome, more than one treatment modality is required to provide optimal pain relief.

The use of the prone or lateral position when identifying and marking trigger points and when performing the actual trigger point injection helps decrease the incidence of vasovagal reactions. The skin overlying the trigger point to be injected should always be prepared with antiseptic solution before injection to avoid infection.

After the goals of trigger point injection are explained to the patient and proper preparation of the patient has been carried out, the trigger point to be injected is reidentified by palpation with a sterile gloved finger.

A syringe containing 10 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone to be injected is attached to a 25-gauge needle of a length adequate to reach the trigger point. For the deeper muscles of posture in the low back, a 3½-inch needle is required.

A volume of 0.5 to 1 mL of solution is injected into each trigger point. The patient should be informed that a series of two to five treatment sessions may be required to abolish the trigger point completely.


The proximity to the spinal cord and exiting nerve roots makes it imperative that this procedure be performed only by clinicians well versed in the regional anatomy and experienced in performing interventional pain management techniques. Many patients report a transient increase in pain after injection of trigger points.

If long needles are used, pneumothorax or damage to the retroperitoneal organs, including the kidneys, also may occur.

Clinical Pearls

Trigger point injections are an extremely safe procedure if careful attention is paid to the clinically relevant anatomy in the areas to be injected. Care must be taken to use sterile technique to avoid infection and universal precautions to avoid risk to the operator.

Most side effects of trigger point injection are related to needle-induced trauma to the injection site and underlying tissues. The incidence of ecchymosis and hematoma formation can be decreased if pressure is placed on the injection site immediately after trigger point injection. The avoidance of overly long needles helps decrease the incidence of trauma to underlying structures. Special care must be taken to avoid pneumothorax when injecting trigger points in proximity to the underlying pleural space.

Antidepressant compounds are the primary pharmacological treatment for myofascial pain syndrome. Tricyclic antidepressants are thought to be more effective than selective serotonin reuptake inhibitors in the treatment of this painful condition.

The precise mechanism of action of antidepressant compounds in the treatment of myofascial pain syndrome is unknown. Some investigators believe that the primary effect of this class of drugs is to treat the underlying depression that is present in many patients with myofascial pain syndrome.

Drugs such as amitriptyline and nortriptyline represent good first choices and should be given as a single bedtime dose, starting with 10–25 mg and titrating upward as side effects allow.


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