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3 Cards in this Set
- Front
- Back
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Trigger Point Characteristics |
Pain, often exquisite, is present at a discrete point. A nodule is embedded within a taut band in the muscle. Pressure reproduces the pain symptoms, with radiations in a specific and reproducible distribution (map), often remote from the pressure point. Pain cannot be explained by findings from a neurological examination. They make the host muscle shorter and fatter and reduce its efficiency: this can lead to pressure on nerves and blood vessels. They may also cause impaired range of motion, muscle weakness, and loss of coordination. |
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Physiology of Trigger Points |
When a trigger point forms, it has been demonstrated that there is a sustained sarcomere hypercontraction (Borg-Stein 2002). This leads to shortening, protein degradation, and myofiber and mitochondrial swelling. These findings are consistent with metabolic stress and ATP depletion. Trigger points manifest in regions where sarcomeres and extrafusal motor endplates become overactive. Microscopy has demonstrated that actin and myosin myofilaments (sitting within a taut band) stop sliding over one another and get stuck. The "cell stress" triggers the increased release of myokines, inflammatory cytokines, and neurotransmitters that also contribute myofascial trigger points and myofascial pain syndrome. Histological investigation indicates abnormal calcium and ACh levels, and a shortage of ATP in the vicinity of the trigger point. Grinnel et al. (2003) demonstrated that stretching and/or hypertonicity of muscles causes a pulling of integrin protein peptides at the motor nerve terminal, triggering excessive ACh release without the need for calcium. Other abnormal chemicals present in the milieu of "active" trigger points include Prostaglandins, Substance P, Cytokines, Bradykinin (BK), Hydrogen (H+), Calcitonin gene-related peptide (CGRP), Tumor necrosis factor (TNF-a), Interleukins IL-1 beta, IL-6, and IL-8 Serotonin, Norepinephrine. These chemicals have many interactions are are part of various feedback loops. For instance, bradykinin is known to activate and sensitize muscle pain fibers (nociceptors). This may help to explain some of the inflammatory hyperalgesia, tenderness, pain, and lowered pain thresholds seen in patients with chronic trigger points. If this situation is allowed to continue over a significant period of time, there is eventually a change of pH leading to cellular oxidative stress. This leads to hypertonia, weakness, shortening, and fibrosis (muscle stiffness) of the muscle, along with reflex inhibition of other muscle groups. Under microscopy, these fibers have been described as "ragged red". Treatment is thus aimed at interfering with and attenuating this cycle. |
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How Does It Work |
With NMT, somatic inputs (trigger points, pain responses, joint position and other somatic stimuli) can be blended in specific and co-ordinated sequences (or programmes). The brain interprets these somatic inputs at the level of the spinal cord (locally) and somato-sensory cortex (distally); it responds by changing the somato-motor output, (changing the reciprocal inhibition and facilitation patterns) resulting in a plethora of changes such as increased strength and power, reduced pain and disability and increased function. Clinically, after each NMT session, patients describe a sense of joints being “oiled inside” or feeling that “normal” muscular control has been regained. With regard to somatic dysfunction, NMT is readily used to reinvigorate and release protective joint postures (such as with spondylolisthesis) and/or treat protective spasm around joint problems (such as an arthritic hip). |
