We do not know exactly why myofascial trigger points occur and there are many theories about how and why they form. In Part One, we discussed a couple of muscle theories. In Part Two we will discuss theories that involve the fascia, a connective tissue layer covering the muscles, and nerve networks.
Excess Hyaluronic Acid Hypothesis
Hyaluronic acid is an important substance found throughout the body. Some of its functions include retaining moisture in the skin and eye, lubricating our joints, and helping with wound healing. In the muscles, it lines one of the fascial layers that cover the muscles, allowing muscle fibers to glide smoothly as we move. Muscle overuse or trauma triggers an overproduction of hyaluronic acid, which has the opposite effect, causing the fascia to become dense and sticky.
This dense and sticky fascia is also thought to excessively stimulate the nerves carrying sensory information from the fascia, which then gets translated to pain, hypersensitivity, numbness, etc. So excess hyaluronic acid not only causes a physical stiffness within the muscles and fascia, but overstimulates the nerves.
Overstimulated Nerves Hypothesis
The overstimulated nerve hypothesis, aka central sensitization, suggests these painful muscle areas are caused by our brain and spinal cord becoming more sensitive to pain signals. This increased sensitivity is often kick-started by a problem in the same area of the body, such as a mechanical muscle imbalance or lack of good blood flow to the area. As the nervous system receives continuous signals bringing attention to the problem, they become overstimulated and hypersensitive.
Like a smoke alarm that is so sensitive the toaster sets it off, this hypersensitive nervous system then sends signals back to the area of the body with the problem and sets off an inflammatory response, or an immune response to fight off or heal damaged tissue, even though there is no real damage in the area. This response is called neurogenic inflammation.
These inflammatory signals sustain a vicious feedback loop that promotes hypersensitivity. We may feel more pain than usual, experience pain from something that normally would not cause discomfort or even feel pain in a different spot than where the problem is. Although we do not yet know exactly how these inflammatory signals cause trigger points, these inflammatory signals have been found in higher concentrations in trigger points than surrounding healthy muscle.
Although our understanding of what causes myofascial trigger points is still growing, the different theories involving muscles, fascia and nerves highlight the complex relationship between physical and nerve-related factors that can contribute to myofascial pain. In Part Three we will discuss how sleep and stress can contribute to myofascial pain and why it is so important to address these factors when trying to resolve myofascial pain.
References:
Shah J. Myofascial Trigger Points Then and Now: A Historical and Scientific Perspective. PMR 2015. 7:746-761.
Srbely J. New Trends in the Treatment and Management of Myofascial Pain Syndrome. Curr Pain Headache Rep. 2010. 14:346-352.
Shah J. Uncovering the biochemical milieu of myofascial trigger points using in vivo microdialysis: An application of muscle pain concepts to myofascial pain syndrome. J Bodywork and Movement Ther 2008. 12:371-384.