Table of Contents
You Mean Zac Didn’t go to a PRI Course?
Yes. From time to time I occasionally take a gander at what else is out there in PT land. It was probably about time I check out this whole dry needling thing and see what the fuss is about.
I took the Spinal Manipulation Institute’s version based on some recommendations from a few colleagues I trust. Ray Butts was MC’ing for the weekend.
I know needling is quite the controversial topic, but I was amazed at the sheer quantity of evidence supporting this modality. Like, an insane amount. I am not sure what the “haterz” found their criticisms on, so please comment if you have some ammo (I am a noob to this after all).
And Ray’s lecture on dry needling mechanisms? Oooohhh lawwwwd. Easily one of the best foundational science lectures I have ever heard. Period. The passion this group has not only for science but the physical therapy profession is inspiring. They made me excited to be a PT. Perhaps even inspired me to contemplate the PhD route.
All that said, I am unsure as to where needling will fit into my practice. The assessment that would point you toward needling someone was sorely lacking. I’ve noticed this problem to be quite common in manual therapy courses. It’s pretty much you hurt here/have this diagnosis, then use this protocol.
My second big gripe it how long it takes. Ray advocated we leave the needles in situ for 8-30 minutes. That is a long-ass time, especially when I have much faster treatments at my disposal.
Moreover, a lot of the research shows several visits needed before meaningful change occurs.
The difference maker for me would have to be that the treatment effects are so good that spending that much time is worth it. If that’s the case, I may find a place for it in my PRI-brain.
Do I think you should attend their course? Let’s just say I plan on taking DN-2 at some point. I really enjoy the way they presented the material; and if you need a manual technique it’s not a bad place to go. Needling may have some power that perhaps other techniques may lack.
Want to know what that power is? Then you better keep reading.
Dry Needling vs. Acupuncture
I know what you are thinking. You are channeling your inner Frank Costello right this second:
The big differences are assessment and intent. SMI supports a medical assessment and treatment making anatomical sense. These two qualities are not always seen in the acupuncture realm.
In fact, it is this difference that actually makes medical acupuncturists safer than traditional acupuncturists. The literature shows double the adverse events comparing the two in some cases. Knowledge of anatomy is critical.
That said, SMI draws heavily from the acupuncture literature. And if rationale and style are the two big differences, I am totally cool with that.
Ray likened it to PT manipulation versus chiropractic adjustment. The psychomotor qualities are quite similar, but the purported mechanisms are often quite different. Either way, the literature is valuable.
What Exactly are we Needling?
Who knows? Likely, we are not going after trigger points in the traditional sense. The research has been pretty clear at debunking both our ability to “find” them (the error rate is 3.3-6.6 cm) and the classic Travell and Simons referral patterns.
What does exist is an inflammatory mess within the purported area. The longer inflammatory mediators are present, the more likely C-fibers will fire. Increased C-fiber firing increases area nociceptor and central receptor quantity, and eventual interneuronal death via substance P production.
And guess what? If you stick a needle in the area and achieve a localized twitch response (LTR), the inflammatory mediator concentration immediately changes.
You can call this area a trigger point, sore spot, or an AIGS. We are simply arguing semantics. It’s all the same (I’ll call them MTrPs from here on).
Let’s just agree on how to diagnose them. Here are the evidence-based assessment pieces for MTrPs as of this writing:
- There is a sore spot.
- The pain produced is familiar to the patient.
The Inner Workings
So how are needles going to help with all this jazz? Many ways.
Endogenous opioids play a huge role here. When this system kicks in, there is decreased immune molecule activity, reduced intracellular sodium, and increased potassium. This change increases resting membrane potential from -70 mV to -150 mV. That change makes it pretty tough for nociceptors to produce action potentials.
Everyone loves the nervous system, but some aneural cells also stimulate opioid production. Both keratinocytes and fibroblasts have been shown to produce opioids, which may be why many skin-level therapies are effective for pain.
Another purported mechanism occurs through adenosine production. When a needle is inserted, ATP production increases. When ATP is initially produced and binds with P2X receptors, pain is produced. This binding creates the desirable de qi response; that deep ache one feels when needled.
From there, ATP breaks down to ADP (which binds with P2Y receptors to produce pain) and finally adenosine. Once adenosine is produced, it can block nociception at the spinal cord level.
That’s not the only central mechanism with needling. Much of the literature has demonstrated that folks with active MTrPs on one side show many more latent MTrPs on the contralateral side. Does this not look an awful lot like mirror pain? A central phenomenon?
Moreover, if you look at decreasing limbic and paralimbic area activity, needling has been shown to dominate tactile stimulation. A needle might be a great way to shut down an amygdala hijack.
The Dunning Difference
The way SMI teaches needling is quite a bit different from your Kinetacores and Myopains from my understanding. The latter two are all about LTRs.
It is thought that the LTR helps remove accumulated acetylcholine in the neuromuscular junction. This molecule eventually cascades to increased calcium within the muscle, which can contribute to hyperactivity at the extrafusal motor endplate. Remove acetylcholine = remove hypertonicity = remove inflammatory markers.
However, this maneuver is not the show. Over the long term needling, with or without a LTR, has similar effects.
SMI likes to wind the needle. This technique has been shown to reorganize collagen fibers, stimulate keratinocytic and fibroblastic opioids via mechanotransduction, and increase ATP production.
This Ain’t Your Average Headache Lecture
I don’t want to spoil all the fun, but Ray changed my perception on headaches quite a bit; at least how big of an impact we can have.
Migraines were the big eye opener here. The symptoms of migraines both with and without aura have many parallels to cervicogenic headaches.
It may be the case that many diagnosed migraines are actually cervicogenic headaches, or at the very least have a cervicogenic trigger.
Which means guess what? We can help these people. The big tests to rule out a cervicogenic component:
- Lateral glides
- C1-C2 rotation – usually decreased in this population
If you do end up treating these folks (which per SMI involves needling and upper cervical manipulations), usually you will see improvements occur in the following order:
Frequency → duration → intensity
- “We’re going to have to start thinking outside of the box or we’ll be in the rehab museum.”
- “Let ‘em ride the lightning.”
- “Are you tracking on that?”
- “We don’t believe in vertebral subluxation but we can learn from those articles.”
- “You want to hang out and party with the median nerve, not tap it.”
- “As with many decisions of the APTA, it’s a decision of indecision.”
- “We don’t needle nipples. That’s not my bag.”
- “They probably need more needling than your average cat.”
- “We won’t do any fetal needling ya know what I mean?”
- “If you really want to piss off OTs, this will do it.”
- “That Butts guy is full of poop.”