Fibromyalgia Trigger Points
Not only is fibromyalgia characterized by the presence of multiple characteristic tender points – specific areas of the body that hurt when relatively minor degrees of pressure are applied – but its sufferers also frequently have to deal with areas of painful cramping and knotting in muscle and connective tissue, known as trigger points. Due to their often overlapping anatomic locations and physical characteristics, many individuals – even physicians – incorrectly assume that fibromyalgia tender points and trigger points are the same thing, when in fact, they are not. The medical and scientific literature has historically added to the confusion, with many researchers incorrectly using the two terms interchangeably. Furthermore, because fibromyalgia frequently co-occurs with other disorders of the musculoskeletal and central nervous systems, it is possible for fibromyalgia patients to experience both tender points and trigger points. Therefore, an understanding of the defining characteristics of each is important from a therapeutic standpoint.
The presence of tender points was one of the two main diagnostic criteria for fibromyalgia, as specified in the American College of Rheumatology (ACR) 1990 guidelines. Tender points can be present on any of 18 symmetrically-distributed locations across the body, including: the lower neck (both front and back), upper chest, inside upper arm, inner knee, upper thigh, upper buttock, upper back, and shoulders. Based on these original criteria, tender points are determined by applying light pressure with the fingertip to each of the 18 locations; if intense pain is felt at a particular site, it is considered an “active” tender point. Tender points are generally centered in the muscle itself and characterized by pain that remains more or less localized to the affected area.
On the other hand, trigger points tend to affect both the muscle and connective tissue, and result in a persistent, deep, muscular pain that radiates outward to other areas. What sets trigger points apart from fibromyalgia tender points is the characteristic cramping, hard, and knot-like feel that they give to the affected muscle (Schneider, 1995). The presence of multiple trigger points is characteristic of a condition known as myofascial pain syndrome. Fascia refers to the connective tissue that surrounds muscles. Under normal circumstances, fascia is able to contract and relax in a fluid, painless manner. However, when the connective tissue becomes damaged, the fascia tightens up, giving the trigger point its characteristic knot-like feel.
It is well-accepted among researchers that fibromyalgia and other widespread musculoskeletal pain conditions – including myofascial pain syndrome – have a number of overlapping symptoms and features (Macfarlane, 1999; Bennett, 2004), and often mimic each other in presentation (Gerwin, 1995), which can lead to diagnostic difficulties (Giamberardino et al., 2011). Although study findings differ with regard to the number of fibromyalgia patients who have trigger points and the extent to which they are present, evidence does exist to suggest that many fibromyalgia patients have active myofascial trigger points (Ge et al., 2009; Bengtsson et al., 1986).
A recent publication from an historically productive research group led by Hong-You Ge has caused considerable debate among fibromyalgia researchers, while at the same time suggested new avenues for exploration in terms of fibromyalgia causation. In 2011, Ge and colleagues published findings of a study in which they asked fibromyalgia patients and healthy control subjects (30 in each group) to use an anatomical map (i.e., picture of the body) and on it record areas of spontaneous pain as well as the intensity of the pain. Next, during a clinical examination, the presence of active myofascial trigger points were determined for all fibromyalgia patients. Among the 30 fibromyalgia patients, a total of 308 active myofascial trigger points were detected. Trigger points were considered to be “active” if, when pressed firmly for a period of five seconds, they reproduced the patients’ spontaneous pain symptoms. If no reproduction was made, the trigger point was considered to be “latent.” In summary, the researchers found that the intensity of the spontaneous pain was significantly related to the total amount of pain produced by the manual identification of the trigger points. In addition, the pattern of pain that resulted was similar to that which the patients reported at the beginning of the study. Their findings led the researchers to propose that fibromyalgia pain may be due in large part to pain that is caused by myofascial trigger points (Ge et al., 2011). These provocative findings have resulted in subsequent discussion and commentary from leading fibromyalgia researchers.
In a recent editorial by Robert M. Bennett and Don L. Goldenberg, spurred by the findings of Ge et al. (2011), Dr. Bennett acknowledges the widely-accepted view that fibromyalgia results from an inability to properly process pain signals. However, in light of the findings from Ge and colleagues, Dr. Bennett also argues that other sources of pain (such as myofascial trigger points) may fit into this widely accepted model of fibromyalgia causation and therefore merit continued research. On the other side of the spectrum, Dr. Goldenberg points out a number of limitations to the study performed by Ge et al. (2011), including the fundamental lack of consensus regarding a definition for myofascial trigger points in the existing scientific literature, methodological limitations in the study design, and statistical and study design flaws in supporting research cited by the authors. In addition, Dr. Goldenberg points out the lack of comorbid symptoms in patients with myofascial trigger points compared to those with fibromyalgia, and the lack of studies to support existing claims that certain therapies are beneficial to trigger points but not to tender points. In closing, Dr. Goldenberg points out the lack of evidence to allow for definitive distinction between a trigger point and a tender points, either clinically or on the biological level (Bennett and Goldenberg, 2011).
Despite these disparate points of view, the findings of Ge and colleagues nevertheless underscore the importance of continued research into the causes of fibromyalgia pain, and pose interesting questions in the comparison of myofascial pain syndrome and fibromyalgia. Of interest, the findings of Ge and colleagues groundbreaking study have recently been replicated by a group of researchers in Spain, who also found that widespread pain sensitivity in fibromyalgia patients was directly related to increased numbers of active myofascial trigger points (Alonso-Blanco et al., 2011).