Anatomy of Fibromyalgia

In order to better understand how massage can help in cases of Fibromyalgia (FM), a short discussion of anatomy and pathology is appropriate.

Muscles are surrounded by fascia. This connective tissue plays an important role in the determination of the extent of muscle stretch and contraction. It is very important to understand that fascia also provides pathways for nerves and blood vessels. In cases of FM, due to the prolonged pathological hypertonus in muscles, fascia becomes tense causing compression of muscle fibers, nerve tissue and blood vessels. This kind of irritation first initiates, and later brings about the development of, fibromyositis. The condition of constant muscle tension in FM cases creates an overload (strain) on muscles and tendons. Strain always leads to the development of inflammation.

The persistence of this inflammatory condition prompts calcium deposits in muscles and tendon attachments to the periosteum — in other words, fibromyositis. A chronic inflammatory condition of the skeleto-muscular system causes secondary changes in neurotransmitter levels and activities in the central nervous system. The changes appear after the patient starts to experience chronic pain. In such a case, the initial trigger is in the skeletal muscles where local, pathological abnormalities were developed.

Authors of many studies have detected significant depletions of adenosine tri-phosphate (ATP) concentration, as well as other high-energy phosphates in the skeletal muscles of FM patients (Bengtsson et al., 1986, Larsson et al., 1988, Bennett, 1991, Park et al., 1998). ATP is a major energy source for muscular contraction. When a nervous command arrives through a motor neuron to a skeletal muscle to produce a contraction, ATP molecules are used. This energy causes the actin and myosin to attach to, and slide past, one another during muscular contractions. When a muscle needs to relax, it again uses ATP molecules to detach myosin from actin. It is important to remember that constant (chronic) muscular hypertonus uses and exhausts the stores of ATP.

Imagine a situation where the concentration of ATP is decreased. The motor commands arrive from the central nervous system to the muscles, and muscular contraction is achieved using available ATP. However, when the muscle needs to relax, ATP is in short supply, as most of it has been used in the contraction. In such a case, some of the muscle fibers remain in the contracted state, even during periods of relaxation. New nervous commands arrive, and again, all available ATP is used to produce a contraction. This is how tension starts to build. The more tension builds up in skeletal muscles, the more tension we can find in the fascia, aponeurosis and other soft tissues. Tension causes a decrease in elasticity, and it starts to affect microcirculation. A mismatch between motor nervous commands and insufficient arterial blood supply initiates changes in the local pH, followed by the activation of pain receptors. It’s at this time the patient starts to feel pain.

After several weeks or months (depending on the individual) of such bombardment of the central nervous system with chronic pain, changes in neurotransmitter activities and concentrations become apparent. The level of substance P (a neurotransmitter responsible for the slow or chronic pain conduction through the spinal cord) increases and the level of serotonin decreases. Serotonin is a very important neurotransmitter, mediating basic bodily functions such as smooth muscle contraction (especially digestive system musculature) and blood coagulation. Additionally, serotonin acts as a neurotransmitter in the brain. It is responsible for our wakeful state and excitement. Patients with clinical depression, which frequently accompanies FM, show a significant decrease in the concentration of serotonin in the brain. All examined FM patients exhibit an increase in the concentration of substance P in the spinal cord, which in most cases is the result of a decreased pH level in muscles.

Important findings supporting this theory are pathological changes found in the muscle cell mitochondria (Bennett, 1991), as well as a decrease in magnesium concentration (Abrahams and Flechas, 1992). Mitochondria are the power plants of the cell, synthesizing ATP (magnesium is a mediator in ATP synthesis). Numerous mitochondria are found within each cell. When ATP is depleted in the skeletal muscles of FM patients, an “energy crisis” (Eisenger, 1992) is created, triggering the entire clinical picture.