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Induction of muscle cramps by nociceptive stimulation of latent myofascial trigger points

PainSci » bibliography » Ge et al 2008
Tags: muscle pain, etiology, neurology, muscle, pain problems, pro

PainSci commentary on Ge 2008: ?This page is one of thousands in the bibliography. It is not a general article: it is focused on a single scientific paper, and it may provide only just enough context for the summary to make sense. Links to other papers and more general information are provided wherever possible.

It’s possible that trigger points irritate muscles enough to cause cramping. In this experiment, 14 brave volunteers allowed injection of an irritant into their trigger points to see if it would cause cramping. It did!

Latent trigger points were identified with electromyography, and EMG was also used to monitor for cramps before, during, and after the injection of glutamate. For comparison, they also injected saline solution, and injected a control point in healthy muscle.

Injection of both glutamate and saline caused more pain in trigger points than the control points, and glutamate hurt more than saline solution. Glutamate caused cramping in nearly everyone (92%) when injected into trigger points. Saline solution and control points caused no cramping at all.

The authors reasonably concluded that “latent MTrPs could be involved in the genesis of muscle cramps.”

~ Paul Ingraham

original abstract Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.

The aim of this present study is to test the hypothesis that nociceptive stimulation of latent myofascial trigger points (MTrPs) increases the occurrence of local muscle cramps. Nociceptive muscle stimulation was obtained by a bolus injection of glutamate (0.1 ml, 0.5 M) into a latent MTrP and a control point (a non-MTrP) located in the right or left gastrocnemius medialis muscles in 14 healthy subjects. A bolus of isotonic saline (0.9%, 0.1 ml) injection served as a control. The injections were guided by intramuscular electromyography (EMG) showing resting spontaneous electrical activity at a latent MTrP and no such activity at a non-MTrP. Intramuscular and surface EMG activities in the gastrocnemius medialis muscle were recorded pre-, during-, and post-injection for a period of 8 min to monitor the occurrence of muscle cramps, which are characterized by a brief episodic burst of high levels of EMG activity. The results showed that glutamate and isotonic saline injections into the latent MTrPs induced higher peak pain intensity than into the non-MTrPs (both P < 0.05). Glutamate injection induced higher peak pain intensity than isotonic saline injection into either latent MTrPs or non-MTrPs (both P < 0.05). Muscle camps were observed in 92.86% of the subjects following glutamate injection into the latent MTrPs, but not into the non-MTrPs (P < 0.001). No muscle cramps were recorded following isotonic saline injection into either the latent MTrPs or the non-MTrPs. These results suggest that latent MTrPs could be involved in the genesis of muscle cramps. Focal increase in nociceptive sensitivity at MTrPs constitutes one of the mechanisms underlying muscle cramps.

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