Pathophysiology of Trigger Points

By Pressure Positive December 23, 2015 Leave a comment Go to comments

Pathophysiology of Trigger Points

Posted by Judith Winer on Dec 17, 2015

Cycle of misery: trigger point formation hypothesis – these individual links in the chain do not always occur in this order. (Sourced from: Starlanyl & Sharkey 2013.)

Sadly, too many therapists remain out of the loop, when it comes to understanding trigger points. In the case of some (mostly PT's, but others included) there is still a tremendous cynicism. This is generally because these therapists have received a negatively biased education, and have somehow avoided the opportunities to learn and explore trigger point therapy first hand.

For anyone willing to take the time to piece it all together, there is plenty of freely available research to support trigger point therapy. Mainstream acceptance of trigger point therapy has grown rapidly in recent years. We're committed to playing our part to push for the introduction of trigger point therapy as a standard teaching requirement for all manual therapists. 

In todays trigger point blog we take a deeper look at where trigger points come from.

The Integrated Trigger Point Hypothesis (ITPH)

The ITPH is the current theory/working hypothesis. It explains most of the trigger point phenomena, and is based on the best electrodiagnostic and histopathological evidence to date. First introduced by Travell and Simons in 1981 as the “energy crisis theory” (Simons et al. 1998), the ITPH has been expanded over the years by many others in the field.

Trigger points manifest in the region where sarcomeres and extrafusal motor endplates become overactive. Microscopy has demonstrated that actin and myosin myofilaments (sitting within a taught band) stop sliding over one another and get stuck. Reitinger et al. (1996) reported “pathological alterations” in mitochondria within these myofilaments, as well as an increase in the width of A bands and a decrease in the width of I bands. The affected sarcomere(s) becomes permanently “switched on,” leading to a contraction and “wind-up.” The swollen, contracted actin and myosin filaments may actually get stuck in the Z band because of the gel- like titin molecules ratcheting the fibers in place and preventing detachment (Dommerholt et al. 2006).

Recent electrophysiological investigations have revealed that the electrical activity of “active trigger points” arises from dysfunctional extrafusal motor endplate zones rather than from (as previously thought) muscle spindles. Electrical discharge frequencies of 10–1000 times normal have been demonstrated in the “endplate zone” in horses, rabbits, and humans (Simons et al. 2002, Dommerholt et al. 2006).

Histological investigation indicates abnormal calcium and ACh levels, and a shortage of ATP in the vicinity of the trigger point. It is worth noting that 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 (Shah et al. 2003):

Prostaglandins Substance P; Cytokines Bradykinin (BK); Hydrogen (H+); Calcitonin gene-related peptide (CGRP); Tumor necrosis factor (TNF-α); Interleukins IL-1 beta, IL-6, and IL-8; Serotonin; Norepinephrine.

These chemicals have many interactions and 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.

Vicious Cycle of Energy Crisis

Sustained dysfunction and sarcomere contraction leads to local intracellular and extracellular chemical changes including:

• Localized ischemia/hypoxia

• Increased metabolic needs

• Increased energy (required to sustain contraction)

• Failed reuptake of calcium ions into the sarcoplasmic reticulum

• Localized inflammation (to facilitate repair)

• Compression or watershed effect on local vessels

• Energy crisis

• Production of inflammatory agents (which sensitize local autonomic and nociceptive fibers) 

If this situation is allowed to continue over a significant period of time, the above changes lead to a vicious cycle. Calcium is unable to be taken into the actin and myosin myofilaments, leading to sarcomere “failure.”

Bengtsson et al. (1986), Hong (1996), and Simons et al. (1998) have all proposed variations of the energy crisis theory. This theory suggests that the body attempts to resolve sarcomere and endplate failure (outlined above) by changing the blood supply to the sarcomere (vasodilation).

One further result of this anomalous situation is the migration of localized acute and chronic inflammatory cells. Inflammation is a cascade: this cascade mechanism starts to occur around the dysfunctional sarcomere. Inflammation brings with it sensitizing substances, such as bradykinin and substance P, a peptide present in nerve cells, which not only increases the contractions of gastrointestinal smooth muscle, but also causes vasodilation.

This has the effect of stimulating both local (small) pain fibers and local autonomic fibers, which in turn leads to increased ACh production and hence a vicious cycle. Eventually, the brain sends a signal to the muscle in which the trigger point manifests to cause it to rest. 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 vicious cycle.

For therapists interested in taking trigger point therapy to the next level, see NAT home study courses. Always affordable, powerful, and immediately practical!

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