A 45-year-old patient presents to the pain clinic complaining of lower back pain and insisting that he needs to be “run through the CT scanner.” He was in his usual state of health until experiencing back pain 6 weeks ago when he spent a weekend planting trees at his mother-in-law’s house (in other words, seriously overdoing it). Although the initial pain subsided after 2 weeks, he had recurrence of the same pain 2 weeks ago when he slipped and fell on the sidewalk. Since then, the pain has steadily escalated in intensity to its current level. It is a constant nonradicular pain that he describes as tightness and an aching sensation mostly localized in the left low back. There is no sensory or motor deficit associated with this. He denies any bowel or bladder dysfunction. He also denies any constitutional symptoms such as fever, night sweats, chills, and loss of weight or appetite. There is no increase of pain with Valsalva maneuver. Pain worsens with increased levels of activity, especially with lateral flexion, extension, and rotation at the lumbar spine. His physical exam was within normal limits, except for left paraspinal muscle spasm associated with a trigger point.

When a patient presents with low back pain, there is often immediate focus on obtaining imaging studies to establish a diagnosis. However, indiscriminate expensive imaging studies can add greatly to total health care expenses both in terms of the acute episode of back pain and in the long-term management of a chronic condition. A careful history and physical exam will usually exclude diagnoses that may require immediate operative treatment from those that can be safely and efficiently managed with other modalities. If imaging is sought, many practitioners advocate just a basic x-ray (if low back, flexion and extension are also recommended).

It is crucial to remember that myofascial pain is one of the most common reasons for low back pain. There is a primary or idiopathic etiology, as well as a secondary etiology, stemming from radiculopathy, disc or facet syndrome, dystonia, or postural imbalance such as a leg length discrepancy. The failure to recognize this can result in apparent treatment failures.

The presence of trigger points is the classic hallmark of myofascial pain. Because trigger points are not visualized on any imaging studies or laboratory
tests, they are identified only by careful palpation. Trigger points may be appreciated as bands or knots within involved muscles. Palpation of trigger points produces pain concordant with the patients’ usual pain. The pain from the trigger point is centrifugally referred in the affected muscle along the myofascial plane. The most common muscles affected are those in the neck, shoulder girdle, and low back.

Muscles are sprained when placed under constant stress. A sprain usually affects a few fibers in the body of the muscle. The initial inflammation settles within 1 to 2 weeks. If sensitization of the dorsal horn occurs at the corresponding level in the spinal cord, there is an increase in tone within the whole muscle. Chronically, the taut band remains as a painless “latent” trigger point. This makes the muscle vulnerable to further injury because the latent trigger point makes the muscle less pliable. In some patients, the sensitization leads to a self-perpetuating loop that keeps the trigger points active for many months after the original injury.

Treatment of myofascial pain syndrome varies. It includes trigger point injections, spray and stretch, transcutaneous electrical nerve stimulation, ultrasound therapy, dry needling, massage therapy, and elimination of causative and perpetuating factors. The major goal of trigger point therapy is to relieve both pain and the tightness of the involved muscles. An interesting feature of trigger point injections is that they are useful as both a diagnostic and a therapeutic tool.

Trigger point injections should always be done in conjunction with a physical therapy program that focuses on stretching, strengthening, and improving the range of motion. The mechanism of trigger point inactivation by injection is unknown. Simons and Travell suggested several possible mechanisms: (i) mechanical disruption of the trigger point, (ii) depolarization block of the nerve fibers by the released intracellular potassium, (iii) washout of the neurosensitizing inflammatory mediators by injected fluid or local hemorrhage, (iv) interruption of the central feedback mechanism, and (v) focal necrosis of the trigger point by the injected drug.