What do you do about latent trigger points?
By definition there are active and latent trigger points. They both exist in a taut band of tissue, are hypersensitive on palpation (pressure stress), display a local twitch on needling and palpation and have spontaneous electrical activity at rest (on EMG), but only active trigger points produce symptoms that the client is familiar with. In undergraduate days the active trigger point was a holy grail in regards to the requirement of ‘thou shalt reproduce the patient’s pain'. Like other holy grails, there didn’t seem to be many around, for me at least.
So if a latent trigger point isn’t producing pain, is it of clinical significance? I am guessing that some would say no and others yes. Hey that’s the world we live in, but see what you think after considering these two papers.
The first one is titled “Sustained Nociceptive Mechanical Stimulation of Latent Myofascial Trigger Point Induces Central Sensitization in Healthy Subjects”, authored by Yi-Meng Xu, Hong-You Ge, and Lars Arendt-Nielsen in Denmark. The Journal of Pain, Vol 11, No 12 (December), 2010: pp 1348-1355.
The abstract reads: The aim of the study is to test if sustained nociceptive mechanical stimulation (SNMS) of latent myofascial trigger points (MTrPs) induces widespread mechanical hyperalgesia. SNMS was obtained by inserting and retaining an intramuscular electromyographic (EMG) needle within a latent MTrP or a nonMTrP in the finger extensor muscle for 8 minutes in 12 healthy subjects. Pain intensity (VAS) and referred pain area induced by SNMS were recorded. Pressure pain threshold (PPT) was measured immediately before and after, and 10, 20, and 30 minutes after SNMS at the midpoint of the contralateral tibialis anterior muscle.
When compared to nonMTrPs, maximal VAS and the area under VAS curve (VASauc) were significantly higher and larger during SNMS of latent MTrPs (both P less than 0.05).
There was a significant decrease in PPT, at 10, 20, and 30 minutes post SNMS of latent MTrPs (all P less than 0.05), but not for non trigger points (see picture: reproduced with permission of authors).
Muscle cramps following SNMS of latent MTrPs, were positively associated with VASauc (r = 0.72, P = 0.009) and referred pain area (r = 0.60, P = 0.03).
They concluded that painful stimulation of latent MTrPs in healthy subjects can initiate widespread central sensitization, but not in non trigger point muscle. So potentially a stress (mechanical, thermal, or chemical) that overloads a latent trigger point, could initiate central changes.
One of the characteristics of central sensitisation involves increasing spatial fields. Taking this a step further, it would therefore seem clinically relevant to identify all trigger points in the anatomical area of pain, and decide using a process of clinical reasoning, if those trigger points not reproductive of a client’s familiar pain i.e. latent trigger points, require treatment. It would seem plausible, that as spatial fields increase with central sensitisation, latent trigger points in the area could potentially become involved in the pain picture.
It is important to acknowledge that in the clinical realm, when managing clients with central sensitisation, other factors like emotions, attitudes and beliefs and social factors, often play a more significant role in pain perception, than the tissue involved, over the passage of time.
The second paper is “Latent myofascial trigger points: their effects on muscle activation and movement efficiency”, authors Karen Lucas, Barbara Polus, Peter Rich from RMIT, Journal of Bodywork and Movement Therapies (2004) 8, 160–166.
They looked at the efficiency of shoulder elevation (plane of scapular) of healthy subjects and those with latent trigger points by examining the EMG of key shoulder girdle muscles, then used dry needling and stretching as an intervention in ½ of the group and sham US as the control intervention in the other ½.
From their abstract, “One aspect of function is the timing of muscle activation… the effects of pain-free latent myofascial trigger points (LTrPs) in the scapular rotator muscle group were investigated. Surface electromyography was used to identify the muscle activation pattern (MAP) of the upper and lower trapezius, serratus anterior, infraspinatus and middle deltoid during scapular plane elevation. Repeated measures ANOVA was used to compare the control group (n=14) and the LTrP group (n=28). The LTrP group was then randomly assigned to either placebo intervention or true treatment to investigate the effect of removing the LTrPs. The data established that LTrPs in the scapular rotator muscles changes the MAP of this muscle group and of muscles further distal in the shoulder girdle kinetic chain. Treatment to remove LTrPs normalised the MAP.”
Because of the altered pattern of recruitment, some muscles remained switched on for longer and recruitment sequencing was different with respect to arm movement.
They concluded that “LTrPs in the scapular rotator muscles do alter the timing and decrease the consistency of the MAP” and that “these findings occurred in the absence of pain and may have implications in the areas of shoulder impingement syndrome, rotator cuff overuse and in training optimal movement efficiency of the upper limb.”
Latent (adj.) is defined as “a quality or state, existing but not yet developed or manifest; hidden or concealed” . While not physically hidden or concealed from the palpating fingers, perhaps their functional influence is hidden in plain sight.
Putting these papers together, builds a case for increased consideration of the role latent trigger points may have in the development or maintenance of central sensitisation and influencing normal, efficient movement patterns. The latter point about inefficient motor patterns is of interest for therapists treating sports persons aiming for optimal movement patterns, or clinicians dealing with overuse and chronic injuries.
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All the best,
Doug Cary FACP
Specialist Musculoskeletal Physiotherapist (awarded by Australian College of Physiotherapy, 2009)
PhD Candidate Curtin University
Clinical Director AAP Education
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