While trigger points may develop as a result of trauma, injury, or overuse, there may be other mechanisms at play
Identifying and treating myofascial trigger points can be uniquely effective therapeutically. However, trigger points rarely develop in isolation and may return if the underlying cause is not identified and addressed.
Long-standing trigger points may lead to secondary (and even tertiary) changes in the nervous system (sensitization) and to trigger point formation elsewhere remote from the original problem. While trigger points may develop as a result of trauma, injury, or overuse, there may be other mechanisms at play.
The fact that trigger points are so ubiquitous in the population as a whole (from babies to the elderly) needs to be explored. So far, models have focused on the “where” and “how” but not the “why.” Our mechanical systems are imbued with self-awareness, self-healing, and self-regulation, so what is the body trying to achieve and why?
We are born with a number of protective mechanisms prewired into our nervous system. When we touch something hot, we quickly withdraw our hand; when we smell something unpleasant we turn or move away. As a rule, the body reacts to noxious stimuli by “switching off” or pulling away from the stressor. Mechanical pain is relayed back to the brain via a number of mechanoreceptors: the brain then responds by initiating movements for maximal efficiency. Muscle groups are then arranged hierarchically into functional units of agonist, antagonist, fixator, and synergist.
In myofascial dysfunction, “switch-off” mechanisms work to avoid the noxious stimuli. We are forced to recruit synergists, fixators, and agonists, often in a less efficient manner, to perform our daily tasks. This is fine in the short term, but over time it can lead to neuroplastic changes in the spinal cord and brain (sensitization). These mechanisms often include reflexes maintained locally in the spinal cord, and centrally in the brain.
Muscular conflict can be palpated around a region of pain as a result of these protective mechanisms. It is worth noting that, as humans, we often “push through” these barriers to carry on with our complex lives.
This “switching-off” mechanism is universal throughout the body
On a cellular level the “switch-off” phenomenon has been observed in a diverse range of diseases and conditions. In cancer, for example, some of the latest ideas center around the fields of the “immune-neural cortex” and “immune oncology.” In these fields the cancer cells have been observed to suppress or “switch off” our immune surveillance mechanisms by creating an immunosuppressive microenvironment around them: they fool our “immune checkpoints” and self-tolerance systems.
Chronic viral infections, such as hepatitis, have a similar effect on the immune system. The latest HIV research, for example, suggests that the virus acts as a chronic noxious stimulus: this not only fools the immune surveillance mechanisms into “switching off” but, over time, also makes T-cells both hyperactive and unresponsive (or silent) at the same time.
The immune and nervous systems operate as a continuum. In the musculoskeletal system we are able to observe both the “switching-off” and the hyperactivation in the peripheral (spinal cord) and the somatosensory and motor cortices.
Pain is a big stimulus
With regard to myofascial trigger points, the stressor is acute or chronic pain, either in a joint or in the myofascial matrix. In both cases the body “switches off” around the stimulus. This switching is maintained both locally and centrally.
The phenomenon is observable in muscles around a fracture site, a slipped disc, or, for example, a frozen shoulder. Painful stimuli are often mediated by inflammation and its noxious exudates, which is part of a well-demonstrated cascade.
When our feedback mechanisms are altered, the brain is forced to adapt and compensate. Pain is a highly motivating symptom for the nervous system: it is our alarm bell that something is wrong.
Research into central sensitization has introduced the concept of polymodal receptors. Kawakita et al. (2002) suggested that these “sensitized neural structures,” may be proto-trigger points, or “trigger points in situ.” In this scenario the brain switches on “trigger points on demand” where needed as part of the myofascial protective mechanism.
As therapists we need to think like detectives. We need to find the tissues that are causing the symptoms and then reflect and observe how the body has adapted over time to compensate. This requires a holistic view of the client's body, organs, bones, and supporting tissues, as well as their posture, nutrition, occupation, psychological state, and general wellbeing.
This trigger point therapy blog is intended to be used for information purposes only and is not intended to be used for medical diagnosis or treatment or to substitute for a medical diagnosis and/or treatment rendered or prescribed by a physician or competent healthcare professional. This information is designed as educational material, but should not be taken as a recommendation for treatment of any particular person or patient. Always consult your physician if you think you need treatment or if you feel unwell.
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