We've all heard of trigger points, right? Those things that hurt when you press on them or when someone else presses on them. Right? So far, so good. They are spots, or points, fair enough; and they hurt when provoked, i.e., they "trigger" discomfort. I can accept all this so far. We have something physical, a sore spot, and we have some action, provocation that makes said spot hurt.
It all gets rather smushed together, this (ectodermal) phenomenon called "pain" being generated somehow, then "felt" or perceived as being associated with some (mesodermal) part of the body, with a motor deficit or malfunction of some sort, such that when a certain movement is attempted it is thwarted by a pain signal. I suspect it was the interference with motor output that made it somehow acceptable to leap to the conclusion that muscle was somehow to blame. But it isn't, not necessarily. Correlation is not causation. After all, muscle is just doing whatever the CNS tells it to do. Really. Muscle is just a puppet of the nervous system. It has no "behaviour" other than doing whatever the nervous system decides it needs (non-conscious) or wants (conscious) to do.
Now, why in the first place trigger points were ever blamed on muscle is probably, in retrospect, just sloppy, convenient, heuristic thinking. I can accept that stuff like that goes on all the time. Why such sloppy, convenient and heuristic thinking is allowed to continue when better explanations have come to exist, I don't understand, and sort of resent actually..
First of all, supposed "trigger points" are found/discerned/their existence implied from outside a patient by another person poking at them. Let's bear in mind that there is a thick layer of blubber, even on skinny people, between a patient's "muscle" and a practitioner's finger poke. Let us not automatically mentally subtract the outer layer as inconsequential, the way trigger point diagrams would have us do.
That layer, known as cutis/subcutis, usually a good half inch thick, contains:
1. a huge amount of neural structure, i.e.
- Cutaneous nerves with all their rami to the surface
- All the neural receptors needed to signal the state of the environment to the brain
- All the neural structure required to regulate blood flow in the skin organ which according to Gray's Anatomy, is ten times that required to maintain the skin organ itself.
3. Plenty of smooth muscle tissue, responding not to the will of a person but rather to brainstem exigencies/dictates, e.g. shivering/goosebumps, vascular lumen contraction via sympathetics, vascular lumen enlargement via efferent neuropeptide leakage by afferent sensory neurons, plenty of opportunity for nociceptive afferents to be bothered by sympathetic efferents and vice versa.
Could it be, therefore, that "trigger points" are no more than areas of secondary hyperalgesia? Tell me how it is possible to diagnose "trigger points" in striated muscle, through a half inch of protective cutis subcutis full of all sorts of autonomic behaviour and potential afferent crankiness, plus a dense layer or two of fascial containment around said muscle? I just don't buy it. And I can't buy any diagram that shows red striped muscle with a red "x" on it, indicating a sore spot, with no skin over it or neural structure depicted in the area. I.e., Travell and Simons. To me, all this blaming a muscle for pain is a good example of looking backward through a telescope. It can be done, I suppose, but it doesn't help anyone see or conceptualize anything better. (I realize this all sounds like heresy. So shoot me. But please read on.)
Several years ago, Quintner and Cohen pointed out some of the logical problems inherent in the 'myofascial' idea surrounding the phenomena of "trigger points", making what I still think is a really good stab at deconstructing the nonsense in which they (still) remain embedded. See their article, "Referred Pain of Peripheral Nerve Origin: an Alternative to the "Myofascial Pain" Construct." I think it's a great article, one of a kind, but still, I wish they had gone further and pointed out or at least mentioned that no tissue other than neural tissue (i.e., neurons, direct ectodermal derivatives) can directly signal the brain (also direct ectodermal derivative) to provoke it into mounting a pain output/perception for our conscious awareness to,.. um, be aware of, consider. In other words, quite apart from the "trigger point" issue, is there really any such thing as "myofascial pain"? I would argue that no, there isn't. Only neural tissue can send sensory-discriminative information to the brain, and only the brain can mount that sort of cognitive-evaluative-motivational-affective-sensory-discriminative display known as "pain". Other kinds of tissue in the body are usually innocent victims, not guilty culprits. (I can hear people thinking, "But what about inflammation? The immune system?" Yes, the immune system can bother the nervous system, terribly, but ultimately, the internal regulation system controls the immune system, so there you go. The only exception I can think of is a channelopathy or other genetic or epigenetic pathology. For regular garden-variety mechanical pain? Not so much. Please read on.)
ALTERNATE EXPLANATIONS THAT MAKE WAY MORE SENSE
A few years ago I started reading about tunnel syndromes. There are more than enough of these described in this book (see below) that I think I'll go with the idea that most of the "pain" (in the mechanical sense) experienced as being located in the body, is likely due to one or more neural entrapments, not misbehaving mesoderm being some sort of causal factor.
In the book, Tunnel Syndromes, (Marko M. Pecina , Andrew D. Markiewitz , Jelena Krmpotic-Nemanic, 2001) over 50 different neural tunnel syndromes are described and illustrated. The non-invasive treatment recommended in this book is kinda pathetic, really, but they probably don't realize what manual therapy can do with mechanical pain, and each tunnel syndrome is fully described and its diagnosis differentiated. Here is what the authors say:
1. Tunnel syndromes can occur with no apparent “cause” (e.g., a tumor pressing into a nerve, etc.) - many are “idiopathic”
2. Function of a nerve can be dramatically altered without needing to be compromised in terms of space: diverse factors can adversely affect nerves function, such as:
- inflammatory changes that thicken a neural wall/reduce blood supply,
- edema 2° to hormonal changes from pregnancy, menopause, birth control pills, myxedema from hypothyroidism,
- anatomical variation (anastomoses, other soft tissue variations not visible on x-ray), or
- repetitive movement.
4. Ischemic changes will first affect sensory fibers; if they continue motor fibers will be affected.
5. Pain (i.e., nociceptive input, nociception) is the most common symptom.
(I would add, pain on provocation, or secondary hyperalgesia, fits in here too, since nerves themselves
a) can "hurt" because of being innervated by nervi nervorum, and
b) come all the way out to skin by way of cutaneous rami sheathed in skin ligaments.)
So, in addition to repetitive movement, how about not enough movement, or variety of movement?
I would urge everyone to get a copy of Rempel D, Lundborg G, Dahlin L;
J Bone Joint Surg Am. 1999;81:1600-10.
Check out the wonderful diagram of the microanatomy of peripheral nerve it contains (posted above).
Lundborg, back in the 80's, worked out the microanatomy, how the vascular supply inside a nerve worked, what assisted it to function (um, movement), what happened to it if it became impaired, the sorts of mini-compartment syndrome effect this could have; he measured all sorts of finicky pressure gradients within a given nerve, and so on. Without lymphatics (although this idea of no lymphatics inside nerves is itself disputed by some), sometimes venous drainage alone can't take care of all the neural needs by itself, in there. Inside a tunnel. Who needs to worry about external compression on a nerve if it can develop problems all on its own inside its own tunnel? From blood flow backed up? I.e., increased volume? Lately Coderre has hypothesized a link between mini-compartment syndrome of blood flow in nerves and CRPS.
Why did Lundborg bother studying all this nerve stuff? Because he was learning how to do nerve grafts, and was trying to figure out what he had to do to keep his grafts from failing. What must have been blatantly obvious to him was that nerves have/are special kind of tissue(s) and require just the right conditions to grow together again.
Why should we as manual therapists care about any of this? Because by knowing about it, by knowing about nerves and the kinds of trouble they can get themselves into, how they can become nociceptive "drivers" themselves, we can drop off a lot of cumbersome and useless hypothetical baggage that forces us to consider and develop extraneous ideas about what tissue we think we are treating when we treat "trigger point" "pain" in people.
If we can get onto the correct tissue conceptually, then we stand a better chance of getting on the right tissue perceptually, too.
As always, it doesn't hurt to remember that the nervous system is only 2% of the body but uses up 20% of available energy, signals itself constantly at an average speed of 120 meters per second, constitutes 72 kilometers of nerve in a single human, and if every neuron were laid end to end, it would be more like 100,000 km.; that if a neuron's soma were the size of a tennis ball, its axon would be a half mile long and the size of a garden hose. The other 98% of the tissue comprising the human body doesn't know, doesn't much care, lives fast, dies young, replaces itself without much fuss. In other words, don't blame mesodermal derivatives for things over which they have absolutely no control. They're just passing through something called a human life, controlled for the length of a life span by something called a nervous system. Treat that instead - it can respond to what you do. From skin cell to sense of self. Continuous and indivisible from a signalling point of view. The other stuff can't.
|Two different sources on tunnel syndromes, same information re: mechanism|
Note the second source, re: "Ischaemic changes will first affect sensory fibres"
Take it to the bank. ;-)
Well said! I don't diagnose trigger points by palpation, though, and I don't really believe people who say they do. I do it by asking the client to tell me when I hit something really tender. (Or, alternatively, by noticing when they rocket up and smack off the ceiling.) And I find the Travell & Simon referral patterns really useful in guessing where to poke. (Which doesn't, of course, mean that it's "in the muscle")
Sometimes I'll find a tight strand (which I think must be a cutaneous nerve, since they lie parallel beneath the surface, and well above/more superficial than striped muscle) which is not "tender" - and I will treat "it" so I can feel softening. Things that are unusually palpable/abnormal-ish and things that are "tender" don't necessarily overlap perfectly. Nowadays I just attend to anything that doesn't feel "right", tender or not. And those x's in those books? There are a lot of cutaneous nerves overlapping with them, perfectly.
In Travell's second edition of Vol. 1 I think (I'm going off my memory) that they said that trigger points tended to occur at the neuromuscular junction and that they have found damaged end plates at the sites. (I'm having deja vu. Have we been through this before?)
I can accept that the explanation for what are the phenomena we call trigger points may not be what has been assumed. And when you point out that it the nerve that senses pain, it seems so obvious when you put it that way, though that wasn't the way we thought of it before. But what do you make of the damaged end plates? Their thinking was that it allowed an uncontrolled release of acetylcholine & sustained contracture of the muscle fibers. It does make sense to me it's the nerve, not the muscle fiber, that has the pain.
I'm trying to understand. I *have* found the Xs on the TP chart to be useful. It is quite a common occurrence, pressure on them feels good and often makes the pain go away, at least for awhile. Is there a problem with that? If better understanding can take it a step further, I'm all for it, but at the moment it seems like interesting ideas but does it make a difference?
And, while I accept that skin is always in the way and perhaps we've ignored it and overlooked the cutaneous nerves, which may be playing a role we were unaware of, we certainly can palpate some structures through the skin, just like I can palpate through a thick cloth. I may misinterpret what I feel - and time in gross anatomy class certainly helped me come to that realization - but we can feel things. Help me out here.
Probably the verb of treatment (i.e., the non-verbal treatment behaviour) doesn't need much changing. Human primate social grooming is human primate social grooming.
What needs upgrade IMO, is the treatment construct itself, to make it congruent with pain science.
Pictures of muscles with x's on them are useful, as I suppose acupuncture charts are, but hello, there are a bunch of nerves just under and within the skin organ that continue to be overlooked, ignored, in both cases. And I don't think it's very smart to ignore a bunch of sensitive anatomy, i.e. the innervated skin organ and rely on patternicity, on conceptualizations.
Maybe what you are palpating/can feel is inside the skin organ itself. All the half inch thick skin organ, more like trying to palpate through two stacked rubber yoga mats, a bit softer maybe and much more responsive.
I think something that has been deemed "abnormal" at neuromuscular junctions has been conflated into being the "cause" of a treatment construct called "trigger points." Logically that would need to be unpacked. Because correlation is not causation. And because it's more likely that neural dysfunction gives rise to neuromuscular junction abnormality AND nociception, secondary hyperalgesia etc., rather than the other way round.
Couldn't read the full article via your link but found a readable copy of the rempel article at at http://ergo.berkeley.edu/docs/1999rempeljbjs.pdf . Thanks for great article
Thank you Mark.
I've stumbled onto your post via Todd Hargrove's (which was via Paul Ingraham's Save yourself site) and haven't had time to go through your old posts yet so apologies if i'm flogging a pre-butchered steak here but what's your thoughts/feelings on nerve receptor types and their implications for treatment modalities? We currently know and believe that nerves can be stimulated by a wide variety of means including but not exclusive to mechanical, electrical, chemical, and thermal depending on the property of the neuron itself and also the receptor type[s] inherent to the nerve. As clinician's/therapists/people we use neural stimulation of various types to alter other's brain/body activity and, hopefully, achieve a more healthy state, even if we/they don't know the mechanism and theory behind the stimulation. (some people rub a sore joint and it feels better, others put chemical irritant (tigerbalm/capsaicum/ebalm etc) and it feels better, other's mechanically mobilise joints and it feels better, others put on a heat pack and it feels better etc) and yet i don't see/read much on the interweb about thoughts on how we utilise the different receptors behind it all. As much as i'm against the decorticated body explanations that occurred historically (trigger points are in the muscle!) i'm also a little wary that the pendulum is swinging towards a disembodied cortex explanation. 'no tissue other than neural tissue (i.e., neurons, direct ectodermal derivatives) can directly signal the brain' seems to be implying that the brain (a really complex and enormous bunch of neural tissue) can only be stimulated when neural tissue is stimulated (or the axiom neural tissue is stimulated when neural tissue is stimulated). We know people have brain/neurons, we know people have bodies, we know they relate to each other and that sometime the way they relate creates a conscious perception of pain, if we are looking at what mediates/determines this would it not be dependant upon the receptor type inputs? Sorry this is a bit rushed (and most probably not as well worded as i hoped) but i'm between clients and needing to put the idea down on the page.
Hi Mark H,
1. "'no tissue other than neural tissue (i.e., neurons, direct ectodermal derivatives) can directly signal the brain' seems to be implying that the brain (a really complex and enormous bunch of neural tissue) can only be stimulated when neural tissue is stimulated (or the axiom neural tissue is stimulated when neural tissue is stimulated)."
That is the case. Other than neuroendocrine feedback, the only way the brain has a clue what's happening in the body is by data collection via neural tissue. I do not know of any other way the brain receives information except through nerves, usually via transduction at the receptor level (but sometimes ectopic firing), sufficient to mount action potentials sufficient and necessary to provoke a crossing of neurotransmitter across a synapse.
2. "We currently know and believe that nerves can be stimulated by a wide variety of means including but not exclusive to mechanical, electrical, chemical, and thermal depending on the property of the neuron itself and also the receptor type[s] inherent to the nerve. "
Huh? If you know of another way, let me know.
3. "what's your thoughts/feelings on nerve receptor types and their implications for treatment modalities?"
What modalities are you thinking of?
What do you make of Sikdar and Shah's work where they use ultrasound vibration sonoelastography to image a trigger point? Shah et al describe them as "focal, hypoechoic regions on 2D ultrasound" and they determined, based on this visual evidence, that TrPs are eliptical in shape with a size of 0.16+/- 0.11 cm square.
Shah also goes on in another study to show what is going on inside the TrP by collecting fluid from the TrP. The title is "An in vivo microanalytical technique for measuring the local biochemical milieu of human skeletal muscle"
These two papers would seem to indicate that the phenomenon of trigger points do exist in skeletal muscle and have increased levels of substances known to provoke pain signals from nociceptors.
Thank you for your reply and for your links to the papers. I see that Jay Shah was involved in both studies. I wrote about my impressions of my only encounter with him, in this blogpost. http://humanantigravitysuit.blogspot.com/2011/07/letter-to-biomechanically-minded.html .
One of the papers you linked to discussed the use of ultrasound to visualize areas of "trigger point" dysfunction, supposedly within skeletal muscle, related to the idea of "trigger points." The problem I had with this paper was that I could not, from the paper, determine how the authors knew for a fact that they were visualizing into skeletal muscle, and not the superficial layer, which on humans is quite thick. It sounded like they were visualizing smooth muscle, i.e., vasculature, a lot of which exists in a thermodynamically busy layer like cutis subcutis. A researcher in the university I'm affiliated with is doing some basic ultrasound visualizing of supraspinatus anatomy, so perhaps I will learn more about how it is done/determined. Still, I can't tell from the paper you provided, or at least I wasn't persuaded, the authors weren't clear, on how they knew for a fact they were seeing a physiological dysfunction in "muscle". I was glad to see they described the limitations of the study including small sample size, low interrater reliability, etc.
The other paper used microsamples from tissue, supposedly "muscle" tissue, drawn from supposed "trigger points" found by palpation, in humans, and compared them to samples drawn from rat muscle. Before I'd buy the idea that something called "trigger points" are found in skeletal muscle because the same substances were found in rat muscle and samples drawn from humans (from something, some tissue in there) then compared, I'd want to see in the paper a discussion of human cutis/subcutis, its thickness, the barrier to muscle it represents in terms of thickness, and histologically and functionally and anatomically, in humans, because in humans it is a lot thicker than in rats. I'd want an idea of how it was circumvented AS a barrier and not just ignored, because IMO it is confounder to the entire concept. I fail to understand why, when the fact of custis/subcutis being a barrier has never been addressed in a paper about trigger points, considered then eliminated methodologically, why I would be expected to hove to the concept at all, especially about their being in muscle or from muscle. No mention whatsoever. Why is it left out?
So, I thank you but I'm not yet convinced, still don't buy the idea.
I've been a practicing PT for about a year now and am interested in the topic of myofascial pain/dysfunction (among others). I've recently read a number of posts by yourself and others on the topic of TPs and am trying to wrap my head around it all.
The criticism seems to be mainly focused on Travell & Simmons, their mapping of TP's and referral patterns, their treatment approach (spray & stretch), the terrible inter-tester reliability of being able to consistently identify/locate them (the absurdity of TP maps), and the fact that there are a number of overlying layers that seem to have been forgotten or omitted.
To my frustration, most of the posts I've read have failed to explain why taut bands of muscle or "knots" can be palpated, why these taut bands hurt to press on, and what we can do about them clinically.
In fact, I am confused about whether the presence of these painful taut bands is being refuted. Have we all agreed these taut bands exist - whatever you want to call them - and are arguing over why they exist and what to do about them? Or are we arguing over their very existence? Everyone seems very hung up on the terminology ("trigger points") and the theoretical model, but what about the phenomena itself?
Every single day in the clinic I am able to palpate taut bands of muscle - "knots", "TPs", or whatever you want to call them - that hurt when you push on them. One common example that comes to mind is infraspinatus - this muscle seems to be notorious for tight knots that hurt and refer pain into the shoulder. Now, I wont call them TPs, and I wont claim that they're always in the same location, nor will I claim that they are the only cause of pain. I will also admit that it possible that overlying structures may be responsible for the pain. However, having said all of that, it seems pretty obvious to me that there is a knot in the muscle and it hurts - regardless of the underlying cause and terminology.
Can we agree on this much?
If so, the question becomes, 1. why is this happening, 2. what can we do about it, and 3. what do you want to call them.
I have no allegiance to TP theory, so for arguments sake lets throw that out. And Im perfectly content to agree that the muscle is the canary in the mine (i.e. a symptom of the problem rather than the problem). I also find it relatively easy to believe that a nerve, in fact, is the underlying problem and the tight band is a manifestation of this dysfunction. That still begs the question, however, of why and what to do. Based on nerve entrapment/tunnel issues I suppose the logical conclusion would be to treat the entrapment. Ok, so how? Manual therapy to address interfaces? Neural flossing? Is it possible that myofascial structures may be partly responsible for nerve entrapment? If so, what do we do about them? Do we try to "mobilize" or "loosen" these structures? How? Myofascial release? Needling? From what I've gathered you're not a big advocate for either.
I've recently become interested in dry needling techniques to address myofascial restrictions and pain because I've witnessed immediate improvements in muscle tone, ROM, and pain symptoms. We can argue over why there is an improvement - "resetting the system", triggering inflammatory cascade, placebo, etc - but at the end of the day if it improves both signs of restriction and symptoms of pain, why not use it?
Anyways, i'll wrap this up. The long and the short of it: in my clinical experience i've been able to find "knots" in muscles, and have identified they hurt. Now I just want to know what to do about them.
>>> "the question becomes, 1. why is this happening, 2. what can we do about it, and 3. what do you want to call them."
The first question, "1. why is this happening" is probably the most important. If we can stop poking at sore spots long enough to think about them, that is.
Like anything else that goes wrong in the structural frame of the body, and is associated with pain, it's like the end result, not the "cause". End result of what? I expect the answer will turn out to be some sort of small fibre dysfunction or atrophy, perhaps, or a "sick nerve"/neuritis type of problem. Complete with secondary hyperalgesia.
>>2. what can we do about it
We can ignore them, and teach the patient things they can do for themselves to help their nerves be restored back to health. If we want to treat them, fine - nerves respond to movement, be it active or passive. Treat the nerves. Forget about muscles.
>> 3. what do you want to call them.
Sore spots. Those do exist. That works for me. I also call sore spots "cranky spots" and "crabby spots." I certainly do treat them, but I don't delude myself they are from or in muscle. They resolve completely when nerves are considered and treated, so I think they never existed in the first place.
Thank you for your comment.
Thanks for your response Diane.
"Sore spots. Those do exist...I certainly do treat them"
Care to expand on how you treat them? If you don't mind me asking?
I don't mind.
I locate one, then pull the skin sideways until it goes away completely, and softening occurs. Then I hold it there for a few minutes. Then I let it go, slowly. Pretty simple. Movement usually has improved, directly following.
Thank you for the insightful take on a very complex issue. I'm glad you also touched on the tunnel syndromes. In treatment in situations like carpal tunnel syndrome, I have always found that treatment of the neck region always works. I believe that the nerves, blood supply and lymphatic system working properly 'up-channel' will lead to proper function 'downstream' relieving the patient's symptoms. This is also why I think there are so many failed carpal tunnel surgeries. Just a thought. Again, thanks for your thoughts on the trigger points, very insightful indeed.
"I locate one, then pull the skin sideways until it goes away completely, and softening occurs. Then I hold it there for a few minutes. Then I let it go, slowly. Pretty simple. Movement usually has improved, directly following"
Thank you so much for your interesting article.
I do have "trigger points" on my upper right back, outer side of my right arm and pain on my anterior right wrist. They seem to appear when I do a wrong movement or lifting something. I have them for years now but not all the time. I use a hard tennis ball against a wall and keep moving it until I find the sore spot. Once I found it, I move the ball around slowly and apply more pressure. Sometimes I feel a release. It might take a day or longer to feel ok again. Then I stop using the ball.
I used to think the wrist was the problem but I kept having pain in my back and arm as well so I started thinking something else was going on.
My question is:
Is there anything that I can do to prevent them from coming back in the first place
(exercise, stretching...) or do you think it is a some kind of chronic condition?
Varying your movement input is usually a good idea. By that I mean,
a) whatever you do one one side of your body, try to do the same on the other side (a bit tricky, I realize, if you are dominant-handed, and most of us are..)
b) don't do any one thing, statically, for very long, without taking a break
c) motion is lotion - try to explore the edges of your range of movement, every joint, every day, at least once. That will help keep your nerves fed.
Thank you so much for your fast answer.
Is there any books or literature available that will show me exercises I can do to "explore the edges of your range of movement, every joint"?
Look up exercises on youtube - look for Feldenkrais movement videos, Hannah somatics.. all the kinds that make you think. Think about what you are doing. Deliberate slow deep breathing, moving deliberately, slowly, gently, fearlessly, all the while respecting the boundaries of your own movement.
Find just one new thing/video, and practice that one. Until you have it perfectly. Then try a new one. Anyone can do this. You can do this.
Neil Pearson, Lifeisnow.com, is a PT/yoga therapist with lots of experience in helping people in pain move again, without fear. Because fear makes you tense up, doesn't it? Check out some of his work.
Point well explained!
Thank you so much for this article. Love to see other massage therapists reasoning!
I have recently started my massage therapy business and came across this article.
Realy appreciate taking the time to educate us on this.
By no means, massage therapy is an exciting topic to write about, but you did an excellent job keeping it entertaining and not boring. Thanks a ton.
I have been reading in preparation for a dry needling course and I have always been skeptical about the theories surrounding TrP's, their origin and how they are governed. It is an evolving line of study and it seems to change like the wind.
That has always been my gripe is that we have gone from ischemic muscle to overdriven muscle spindles to faulty end plates and excessive release of AcH. An every continuing education course from John Barnes to the dry needling gurus to the DN with IMS promises to cure all that enter your building.
Some one mentioned Shah and his work with dialysis in realtime in the TrP while inserting a DN into the Trp and the instantaneous changes in the elevated levels of biochemicals in the TrP . . .only problem is other studies show healthy tissue behaving the same way and having the same levels of "noxious" chemicals.
Dysfunctional endplates . . .maybe, but not many controls in those studies that are well managed.
Where does that leave us. As you said, the muscle is not the villain and is more the hostage and an innocent bystander to the whole process. Studies show that you can inject saline into deep structures and cause the exact same referred pain in the exact same "Trp" . . .so it is probably CNS in origin and should be treated as such.
I want to know, placing a needle into a body, then driving said needle into a trigger point deep within the body and you are hitting a Trp based on a Twitch respone or cramp. . . pnumothorax please . . .
and somewhere in every article you review . . ."the exact mechanism and causal factors of MF TrP are not entirely understood" . . .but we know how to treat them . . .even though the experts in a study could not find them . . .but we know how to treat them
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