Fibrositis/fibromyalgia: a form of myofascial trigger points?

The diagnostic criteria for fibrositis and primary fibromyalgia are similar to those for myofascial pain syndromes due to trigger points. Tender points in muscles are likely to be myofascial trigger points; nonmuscular tender points clearly are not myofascial trigger points, but may be areas of tenderness referred from such trigger points. Myofascial trigger points refer pain to a distance and restrict range of motion of the muscle. They are associated with a palpable taut band that exhibits a local twitch response of the muscle, and they are responsive to treatment. Persistence of myofascial trigger points is due to perpetuating factors that can usually be corrected. Although their number is unknown, it is likely that some patients who are diagnosed as having fibrositis/fibromyalgia have multiple myofascial trigger points aggravated by a powerful perpetuating factor and also have a systemic disease process independent of the myofascial trigger points. Since myofascial pain syndromes are treatable, these patients would benefit greatly by identification and relief of the myofascial component of their pain.

Lesions of rat skeletal muscle after local block of acetylcholinesterase and neuromuscular stimulation.

In skeletal muscle, a local increase of acetylcholine (ACh) in a few end plates has been hypothesized to cause the formation of contraction knots that can be found in myofascial trigger points. To test this hypothesis in rats, small amounts of an acetylcholinesterase inhibitor [diisopropylfluorophosphate (DFP)] were injected into the proximal half of the gastrocnemius muscle, and the muscle nerve was electrically stimulated for 30-60 min for induction of muscle twitches. The distal half of the muscle, which performed the same contractions, served as a control to assess the effects of the twitches without DFP. Sections of the muscle were evaluated for morphological changes in relation to the location of blocked end plates. Compared with the distal half of the muscle, the DFP-injected proximal half exhibited significantly higher numbers of abnormally contracted fibers (local contractures), torn fibers, and longitudinal stripes. DFP-injected animals in which the muscle nerve was not stimulated and that were allowed to survive for 24 h exhibited the same lesions but in smaller numbers. The data indicate that an increased concentration of ACh in a few end plates causes damage to muscle fibers. The results support the assumption that a dysfunctional end plate exhibiting increased release of ACh may be the starting point for regional abnormal contractions, which are thought to be essential for the formation of myofascial trigger points.

Appearance of new receptive fields in rat dorsal horn neurons following noxious stimulation of skeletal muscle: a model for referral of muscle pain?

To test the hypothesis that painful stimuli to skeletal muscle lead to a widespread unmasking of synaptic connections in dorsal horn neurons, intramuscular injections of bradykinin (BKN) were made outside the receptive fields (RFs) of these cells in the rat. Following BKN injections, new RFs all of which were located in the deep tissues and had high mechanical thresholds appeared in 9 out of 21 (42.8%) nociceptive dorsal horn neurons which originally had a single RF in deep tissues or in the skin. The appearance of new RFs may lead to a mislocation of the source of pain if in fact the impulse activity of a nociceptive dorsal horn neuron contains information on the site of the stimulus.

Myofascial origins of low back pain. 3. Pelvic and lower extremity muscles.

Gluteal, pelvic, and lower extremity muscles are common sites of origin of myofascial low back pain. Trigger points (TPs) in the gluteus maximus and medius muscles refer pain locally to the gluteal and sacral regions, while those in the gluteus minimus are likely to refer pain down the lower extremity as far as the ankle on the same side. TPs in intrapelvic muscles refer pain chiefly to the pelvic region. Besides producing referred myofascial pain, TPs in the piriformis muscle can cause symptoms of entrapment of the peroneal portion or all of the sciatic nerve. TPs in the soleus muscle may refer pain to the sacroiliac joint.

Myofascial origins of low back pain. 1. Principles of diagnosis and treatment.

Myofascial trigger points (TPs) are frequently overlooked sources of acute and chronic low back pain. An active myofascial TP is suspected by its focal tenderness to palpation and by restricted stretch range of motion. The restricted lengthening of the muscle is due to the tense band of muscle fibers in which the TP is located. The presence of a TP is confirmed by a local twitch response and by reproduction of its known pattern of referred pain, which matches the distribution of the patient's pain. Only an active TP causes a clinical pain complaint; a latent TP does not. The pain can be relieved by the stretch-and-spray procedure, ischemic compression, or precise injection of the TP with procaine solution. Relief is usually long lasting only if mechanical and systemic perpetuating factors are corrected.

Myofascial origins of low back pain. 2. Torso muscles.

Trigger points (TPs) in muscles of the lower torso associated with the spine are an important cause of low back pain. The quadratus lumborum is the muscle most commonly involved, but TPs located there are often overlooked because of inadequate physical examination techniques. TPs in the lower rectus abdominis refer pain horizontally across the low back, and those in the iliopsoas refer pain in a vertical pattern, parallel to the lumbosacral spine. The pain pattern of TPs in the serratus posterior inferior is noted in the region of the muscle itself.

Myofascial trigger points and sensitization: an updated pain model for tension-type headache.

Present pain models for tension-type headache suggest that nociceptive inputs from peripheral tender muscles can lead to central sensitization and chronic tension-type headache (CTTH) conditions. Such models support that possible peripheral mechanisms leading to pericranial tenderness include activation or sensitization of nociceptive nerve endings by liberation of chemical mediators (bradikinin, serotonin, substance P). However, a study has found that non-specific tender points in CTTH subjects were not responsible for liberation of algogenic substances in the periphery. Assuming that liberation of algogenic substances is important, the question arising is: if tender muscle points are not the primary sites of on-going neurogenic inflammation, which structure can be responsible for liberation of chemical mediators in the periphery? A recent study has found higher levels of algogenic substances, and lower pH levels, in active myofascial trigger point (TrPs) compared with control tender points. Clinical studies have demonstrated that referred pain elicited by head and neck muscles contribute to head pain patterns in CTTH. Based on available data, an updated pain model for CTTH is proposed in which headache can at least partly be explained by referred pain from TrPs in the posterior cervical, head and shoulder muscles. In this updated pain model, TrPs would be the primary hyperalgesic zones responsible for the development of central sensitization in CTTH.

Symptomatology and clinical pathophysiology of myofascial pain.

Myofascial pain syndromes, fibromyalgia, and articular dysfunctions may all be contributing to our patients' ubiquitous musculoskeletal pain problems that generally are poorly understood and poorly managed. Thepectoralis minor myofascial pain syndrome, for example, results from trigger points (TrPs) activated by stress overload of the muscle. Symptoms of pain referred to the shoulder and ulnar aspect of the arm and forearm, and of pain on reaching around and behind the body, are characteristic. Findings include restricted stretch range of motion and some weakness of the muscle, taut bands of muscle fibers, and focal trigger point tenderness of each taut band on palpation. Snapping palpation at the TrP elicits a local twitch response (LTR). The increased muscle tension of a pectoralis minor syndrome commonly entraps the lower trunk of the brachial plexus, producing symptoms of a cervical radiculopathy.

Myofascial pain syndromes: where are we? Where are we going?

In recent years, research activity related to myofascial pain syndromes due to trigger points (TrPs) has blossomed. This paper introduces and relates the presentations made in a symposium entitled "Myofascial Pain Syndromes: Where are we? Where are we going?" at the 47th Annual Assembly of the American Academy of Physical Medicine and Rehabilitation in Kansas City October 2, 1985. It summarizes a number of recent research advances and key research issues related to myofascial pain syndromes: 1. Thermography appears valuable for imaging the reflex thermal tracks of previously identified TrPs. 2. Three new devices are reported to measure reliably the pressure threshold for pain of TrPs and tender points (TePs). 3. Fibrositis/fibromyalgia and myofascial pain syndromes may or may not be separate entities. The question needs to be resolved. 4. New evidence strongly supports previous indications that a TrP is a region of increased energy consumption with an inadequate oxygen supply. 5. A foundation has been established for investigating the sensitizing agent(s) responsible for the increased sensitivity of TrPs and muscular TePs. 6. At least four mechanisms can account for the pain referred by TrPs in muscles. The convergence-projection mechanism appears to be consistently present in visceral pain pathways and to be likely in mammalian muscle nociceptive pathways.

Myofascial trigger points: a need for understanding.

The muscle pain syndromes caused by myofascial trigger points are beset with a cloud of confusing terminology and confusing concepts. This paper introduces the presentations made at a symposium entitled "Myofascial Trigger Points: Multidisciplinary Facets," at the 55th Annual Session of the American Congress of Rehabilitation Medicine in New Orleans on November 17, 1978. Following a summary of discussions at the end of the symposium, the "Commentary" proposes a set of neurophysiologic mechanisms that may account for most of the clinical phenomena associated with myofascial trigger points.

Do endplate noise and spikes arise from normal motor endplates?

The concept that the endplate noise and endplate spike components of motor endplate potentials represent normal endplate potentials seems to be flawed. The morphology of the normal miniature endplate potentials described in the physiology literature is different from the morphology of the noise-like component of endplate potentials. This noise-like component is identified as normal in current electromyographic literature. There is strong experimental evidence that one source of the endplate noise component is grossly increased release (up to three orders of magnitude) of acetylcholine from the nerve terminal of that neuromuscular junction. The spikes can be accounted for by release of additional acetylcholine in response to mechanical stimulation by the electromyographic needle. Other possibilities exist.

Myofascial pain: relief by post-isometric relaxation.

The post-isometric relaxation technique begins by placing the muscle in a stretched position. Then an isometric contraction is exerted against minimal resistance. Relaxation and then gentle stretch follow as the muscle releases. This technique was applied to tight, tender muscles that are commonly associated with musculoskeletal pain and was systematically tested on 351 muscle groups in 244 patients. The method produced immediate pain relief in 94%, lasting pain relief in 63%, as well as lasting relief of point tenderness in 23% of the sites treated. Patients who practiced autotherapy on a home program were more likely to realize lasting relief. Pain was relieved in both the muscle itself and at tender insertion points. The technique is useful in addition to, or in place of, local anesthetic injection or dry needling. These results confirm other observations that the increased tension of the affected muscles and the resulting pain and dysfunction are both relieved by restoring the full stretch length of the muscle.