What is myofascial pain? (Proceedings)


What is myofascial pain? (Proceedings)

Aug 01, 2009

Medical practitioners are adept at recognizing and treating the pain associated with internal organ pathology, osteoarthritis, and musculoskeletal injuries, but are less familiar with the chronic pain and dysfunction that arise from myofascial pain syndromes. Anyone who has suffered from tension headaches, tennis elbow or recurrent back pain has experienced some form of myofascial pain.

Eminent researcher David Simons quotes "Muscle is an orphan organ. No medical specialty claims it. As a consequence, no medical specialty is concerned with promoting funded research into the muscular causes of pain, and medical students and physical therapists rarely receive adequate primary training in how to recognize and treat myofascial trigger points." In spite of volumes of scientific literature, studies have demonstrated that primary care physicians are largely ignorant of the diagnosis and treatment of myofascial pain. Students of anatomy are taught to ignore the tough white connective tissue that interferes with visualization of underlying structures, depriving them of the opportunity to appreciate the complex structure and function of fascial tissues.

The term "myofascial" is derived from the root "myo" meaning muscle, and "fascia" defined as a sheet or band of fibrous connective tissue enveloping, separating or binding together muscle, organs or other structures of the body. Myofascial pain is the conscious perception of the stimulation of pain fibers within muscle or fibrous connective tissue that is provoked by the presence of muscle trigger points, or by fascial restrictions that bind, compress or pull on pain sensitive structures. This presentation will focus on the structural and physiologic characteristics of myofascial tissues and relate them to the patho-physiology of muscle trigger points, fascial restrictions and their treatment.

Connective tissue structure and function

The fascial system is an extensive continuous network that imparts organization and form to the body. All other tissues are supported upon (epithelial), invaginated into (glandular epithelium), or imbedded within (muscles, blood vessels and nerves) connective tissue. Connective tissue is composed of cellular (fibroblasts) and extracellular (fibers and ground substance) elements. The functions of connective tissue include mechanical support, independent movement of skin and muscles, transfer of tensile forces, shock absorption, growth and repair, immunological defense (inflammation), transport of nutrients and metabolites, communication, and control of metabolic processes.

Fibroblasts secrete the extracellular matrix. Their long cytoplasmic processes are interconnected and linked in continuous bodywide network. Because of their interconnectedness, it is hypothesized that fibroblasts contribute to a body-wide signaling network.1 Fibroblasts are responsible for growth and repair by producing collagen and secreting the extracellular matrix. Mechanical stimuli, such as stretch, compression, shear and tensile forces determine the location and rate of production of connective tissue components. Fibroblasts respond to mechanical stimuli via a process called mechano-transduction. Mechano-transduction is the process of converting mechanical deformation of a fibroblast's cytoskeletal structure into chemical or electrical signals. The signals alter molecular structure and function inside the cell, activating signaling pathways and altering genetic expression. Mechanical stimuli profoundly affect cell function and behavior.

Ground substance is a gel-like substance that consists of proteoglycan aggregates capable of binding water and electrolytes. Ground substance exhibits the property of thixotropy; the tendency to become more fluid-like when disturbed. Conversely, when static, ground substance becomes more viscous. Increased viscosity limits the degree to which nutrients, oxygen and metabolites are able to diffuse through ground substance, depriving surrounding cells and tissues of vital substances.

Collagen fibers provide the structural framework of connectives tissue. They provide a balance between resistance to tensile forces and mobility of the tissue. Collagen fibers respond to mechanical stimuli by orienting along the lines of stress. Motion deprivation results in random fiber orientation and increased cross-linking between fibers. Consequently, tissue mobility and extensibility are reduced. Thickened, immobile collagen fibers are more susceptible to injury, are painful when stretched and may compress, bind and restrict muscular, vascular and neural elements within them.

Fascial structures are rich in sensory mechanoreceptors, free nerve endings, autonomic innervation and smooth muscle cells. The exact functions of these elements have not been determined, but are the subject of ongoing research. Free nerve endings have a role in pain perception, thus it is likely that pathologic processes within fascia can and does give rise to pain. Fascial contraction independent of motor fiber influence has been observed and is potentially a function of smooth muscle cells. Fascial contraction may play a role in maintaining proper tension in structures such as the lumbar fascia. Mechanoreceptors have a postulated role in kinesthesia, coordination of motor and local autonomic functions and influence of local fluid dynamics.

Painful fascial restrictions are a response to trauma that may be in the form of an acute injury, repetitive micro-stresses, or habitual postural strain or to prolonged immobilization. The fascia loses its flexibility, ground substance becomes more viscous and collagen cross-links proliferate. Elastic properties of elastin diminish. The loss of resiliency affects the quality and quantity of movement; restricted fascia places tension on adjacent structures. Over time structural alignment, biomechanics and strength are affected. Compensatory movement patterns are established to avoid painful and restricted motions. Function and performance subsequently diminish.

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