Multifidus mediated pain

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can someone explain to me the pathophysiology of the multifidus being a pain generator? Do you look for atrophy on MRI? I know some of the new devices are targeting this muscle
A lot of this is marketing, but I suspect most PT providers will tell you that weak lumbar paraspinal muscles are associated with CLBP. I think that statement is something we all support. The jump in logic is that this is a cause and not a symptom of CLBP, but much like CGRP was initially a biomarker for migraines, people are now targeting these things to "fix them"

Changes in the cross-sectional area of multifidus and psoas in patients with unilateral back pain: the relationship to pain and disability - PubMed - Example of older data looking at CSA as a metric for weak muscles to suggest targeting multifidus plus others for exercise training

Structural Changes of Lumbar Muscles in Non-specific Low Back Pain: A Systematic Review - PubMed - Review of the literature looking at the relationship of multifidus atrophy with CLBP. You can see atrophy/fatty infiltration on MRIs. I compare the psoas fat to the multifidus fat myself, but it's a subjective measure.

An implantable restorative-neurostimulator for refractory... : PAIN - Mainstay Medical shows off their work with functional electrical stimulators targeting the multifidus muscle with motor stimulation programs to encourage regrowth. This is published later than the next paper, but it was probably started up and going before these second data.

Percutaneous Peripheral Nerve Stimulation for Chronic Low Back Pain: Prospective Case Series With 1 Year of Sustained Relief Following Short‐Term Implant - This is where we start jumping the shark to some extent and people start saying "me too" with their device and dropping 60 day leads to cause "multifidus contraction" but the Mainstay and SPR systems are very different in what they're doing and how they're doing it, despite both claiming a similar basis from the earlier atrophy data.

The other PNS companies feel like they can do it too and you can target the medial branch with sensory or motor programs with them. Now it's a bit of handwaving all around.

I do it. I felt slimey for it initially but beat dropping an SCS in. Results have been good. Durability and effectiveness isn't 100% for people. I haven't used a durable implant system for it yet but plan to in the next 12 months.
 
A lot of this is marketing, but I suspect most PT providers will tell you that weak lumbar paraspinal muscles are associated with CLBP. I think that statement is something we all support. The jump in logic is that this is a cause and not a symptom of CLBP, but much like CGRP was initially a biomarker for migraines, people are now targeting these things to "fix them"

Changes in the cross-sectional area of multifidus and psoas in patients with unilateral back pain: the relationship to pain and disability - PubMed - Example of older data looking at CSA as a metric for weak muscles to suggest targeting multifidus plus others for exercise training

Structural Changes of Lumbar Muscles in Non-specific Low Back Pain: A Systematic Review - PubMed - Review of the literature looking at the relationship of multifidus atrophy with CLBP. You can see atrophy/fatty infiltration on MRIs. I compare the psoas fat to the multifidus fat myself, but it's a subjective measure.

An implantable restorative-neurostimulator for refractory... : PAIN - Mainstay Medical shows off their work with functional electrical stimulators targeting the multifidus muscle with motor stimulation programs to encourage regrowth. This is published later than the next paper, but it was probably started up and going before these second data.

Percutaneous Peripheral Nerve Stimulation for Chronic Low Back Pain: Prospective Case Series With 1 Year of Sustained Relief Following Short‐Term Implant - This is where we start jumping the shark to some extent and people start saying "me too" with their device and dropping 60 day leads to cause "multifidus contraction" but the Mainstay and SPR systems are very different in what they're doing and how they're doing it, despite both claiming a similar basis from the earlier atrophy data.

The other PNS companies feel like they can do it too and you can target the medial branch with sensory or motor programs with them. Now it's a bit of handwaving all around.

I do it. I felt slimey for it initially but beat dropping an SCS in. Results have been good. Durability and effectiveness isn't 100% for people. I haven't used a durable implant system for it yet but plan to in the next 12 months.
Do any studies show before and after hypertrophic changes?
 
Before you go stimulating the multifidus, you may want to shoot PRP in there first.

Neither will work BTW.

Edit - I should say, I personally do not see the utility of it despite many ppl claiming great results.
 
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Never ever have I seen someone which back pain and immediately thought “oh, this patient might have multifidus atrophy”. 😁😁
 
Never ever have I seen someone which back pain and immediately thought “oh, this patient might have multifidus atrophy”. 😁😁
There are more things in heaven and earth....oh whatever. If you don't think about it, you won't see it, but in all honesty, it's a nonspecific indicator for CLBP that may be reactive or causative.

It's an easy enough thing to target, and I do feel more strongly for doing it over RFA in patients that are younger.

Start with a simple 60 day trial with SPR and see how you like it if your site of service allows that.
 
There are more things in heaven and earth....oh whatever. If you don't think about it, you won't see it, but in all honesty, it's a nonspecific indicator for CLBP that may be reactive or causative.

It's an easy enough thing to target, and I do feel more strongly for doing it over RFA in patients that are younger.

Start with a simple 60 day trial with SPR and see how you like it if your site of service allows that.
N = 1 for me and it failed. She has a few mm of lead in her back BTW. It fractured.

Why is it better than RFA for younger pts?

Which young pts have multifidus atrophy that PT wouldn't treat?

I don't get it.
 
N = 1 for me and it failed. She has a few mm of lead in her back BTW. It fractured.

Why is it better than RFA for younger pts?

Which young pts have multifidus atrophy that PT wouldn't treat?

I don't get it.
You might could have done it wrong, but they made the lead better so it should fracture less. What you're describing is that initial exposure bias, where your first experience ruins you even though it's fraught with things that you can get better at. The data are reasonable and the risk is low.

I don't philosophically like the idea of repeated ablations for younger patients. Drop head for example with cervical RFA is a fear. My hope is 60 days of perc PNS to the multifidus, jump start them with PT, and then nothing else.
 
A lot of this is marketing, but I suspect most PT providers will tell you that weak lumbar paraspinal muscles are associated with CLBP. I think that statement is something we all support. The jump in logic is that this is a cause and not a symptom of CLBP, but much like CGRP was initially a biomarker for migraines, people are now targeting these things to "fix them"

Changes in the cross-sectional area of multifidus and psoas in patients with unilateral back pain: the relationship to pain and disability - PubMed - Example of older data looking at CSA as a metric for weak muscles to suggest targeting multifidus plus others for exercise training

Structural Changes of Lumbar Muscles in Non-specific Low Back Pain: A Systematic Review - PubMed - Review of the literature looking at the relationship of multifidus atrophy with CLBP. You can see atrophy/fatty infiltration on MRIs. I compare the psoas fat to the multifidus fat myself, but it's a subjective measure.

An implantable restorative-neurostimulator for refractory... : PAIN - Mainstay Medical shows off their work with functional electrical stimulators targeting the multifidus muscle with motor stimulation programs to encourage regrowth. This is published later than the next paper, but it was probably started up and going before these second data.

Percutaneous Peripheral Nerve Stimulation for Chronic Low Back Pain: Prospective Case Series With 1 Year of Sustained Relief Following Short‐Term Implant - This is where we start jumping the shark to some extent and people start saying "me too" with their device and dropping 60 day leads to cause "multifidus contraction" but the Mainstay and SPR systems are very different in what they're doing and how they're doing it, despite both claiming a similar basis from the earlier atrophy data.

The other PNS companies feel like they can do it too and you can target the medial branch with sensory or motor programs with them. Now it's a bit of handwaving all around.

I do it. I felt slimey for it initially but beat dropping an SCS in. Results have been good. Durability and effectiveness isn't 100% for people. I haven't used a durable implant system for it yet but plan to in the next 12 months.
so are you just trialing these patients and not implanting them? Are you using this sort of like SPRINT pns? Where you remove it and the durability lasts?

I know some people implant these devices. Atrophy mks sense, but why not just trial, then do PT and strengthen and then remove?

I dont know too much about this, so just trying to learn...
 
so are you just trialing these patients and not implanting them? Are you using this sort of like SPRINT pns? Where you remove it and the durability lasts?

I know some people implant these devices. Atrophy mks sense, but why not just trial, then do PT and strengthen and then remove?

I dont know too much about this, so just trying to learn...
Right, it's the 64555 trial code for PNS with SPR sprint running a motor stim program as 60 day trial. There are providers using the Stimrouter platform for it as a durable therapy but I'm not excited about that due to the MRI conditionality and the lead explant is no fun.

Reactiv-8 requires a whole another process as there is no official trial, just an implant. They provide assistance with the prior auth.

The few I'm looking at for durable implants are patients that did well with it in for the "SPR trial" but lost efficacy after removal or soon after.
 
You might could have done it wrong, but they made the lead better so it should fracture less. What you're describing is that initial exposure bias, where your first experience ruins you even though it's fraught with things that you can get better at. The data are reasonable and the risk is low.

I don't philosophically like the idea of repeated ablations for younger patients. Drop head for example with cervical RFA is a fear. My hope is 60 days of perc PNS to the multifidus, jump start them with PT, and then nothing else.
Have you put one of these in a young neck? I don't get what is special about a young person that's different than an older person.
 
Have you put one of these in a young neck? I don't get what is special about a young person that's different than an older person.
I have. Neck results are oddly better than low back for my cohort. Mostly that was for occipital neuralgia, but also one for axial neck pain.

As far as I know, RFA doesn't have the ability to be curative as the nerves recover and can theoretically be harmful with worsening motor deficits over decades of repeated use. I don't mind doing it in people where I'm looking at 15-20 years of this but I worry about making a youngish 30-40 yo into an old person that can't look at me without holding up their head with their hands.

I've seen them and they haunt me, so if 60 day PNS can prevent or delay a few years of ablations, I'm for it.
 
I have. Neck results are oddly better than low back for my cohort. Mostly that was for occipital neuralgia, but also one for axial neck pain.

As far as I know, RFA doesn't have the ability to be curative as the nerves recover and can theoretically be harmful with worsening motor deficits over decades of repeated use. I don't mind doing it in people where I'm looking at 15-20 years of this but I worry about making a youngish 30-40 yo into an old person that can't look at me without holding up their head with their hands.

I've seen them and they haunt me, so if 60 day PNS can prevent or delay a few years of ablations, I'm for it.
So you are saying a 60 day PNS trial is curative.? DO you work/speak for the company?
 
Weak Multifidus and Paraspinals absolutely can be a cause for low back pain due to weak core muscles and compensatory mechanisms. Solution? Back extensions or Supermans, 3 sets, 10 reps, twice a day. Anyone trying to sell you on Activ8tion or PNS or anything else is an absolute idiot. I loved the rep telling me about Activ8tion. I just said "I tell my patients to work out."
 
So you are saying a 60 day PNS trial is curative.? DO you work/speak for the company?
No, I said RFA wasn't curative. You may have assumed I think PNS was curative but I primarily think of PNS as not destructive.

To me it is a bridge to PT which is I do think can be curative for nonspecific CLBP. I tell patient's I'm trying to electrically rehabilitate the nerves, but they'll have to do more of the lifting as the therapy gets on board.

I do think SPR's marketing of "preserve the nerve" is cute and all, but this ain't magic.

And no, I don't work/speak for the companies but I do talk on these topics.
 
No, I said RFA wasn't curative. You may have assumed I think PNS was curative but I primarily think of PNS as not destructive.

To me it is a bridge to PT which is I do think can be curative for nonspecific CLBP. I tell patient's I'm trying to electrically rehabilitate the nerves, but they'll have to do more of the lifting as the therapy gets on board.

I do think SPR's marketing of "preserve the nerve" is cute and all, but this ain't magic.

And no, I don't work/speak for the companies but I do talk on these topics.
And done.
End scene.

Expensive bridge to PT for NSLBP.
 
No, I said RFA wasn't curative. You may have assumed I think PNS was curative but I primarily think of PNS as not destructive.

To me it is a bridge to PT which is I do think can be curative for nonspecific CLBP. I tell patient's I'm trying to electrically rehabilitate the nerves, but they'll have to do more of the lifting as the therapy gets on board.

I do think SPR's marketing of "preserve the nerve" is cute and all, but this ain't magic.

And no, I don't work/speak for the companies but I do talk on these topics.
How many of these pts do you see a year?
 
Right, it's the 64555 trial code for PNS with SPR sprint running a motor stim program as 60 day trial. There are providers using the Stimrouter platform for it as a durable therapy but I'm not excited about that due to the MRI conditionality and the lead explant is no fun.

Reactiv-8 requires a whole another process as there is no official trial, just an implant. They provide assistance with the prior auth.

The few I'm looking at for durable implants are patients that did well with it in for the "SPR trial" but lost efficacy after removal or soon after.
I think Reactiv8 is a great idea. I have no experience if it works - I just like the idea.

I don't like that you can't trial before an implant, so to me - trialing with SPRINT makes some sense if you are thinking of going that route. For some really stupid reason, the Reactiv8 reps HATE the idea of using SPRINT as a trial. So my answer is - then come up with a trial system, dummy.
 
To me it is a bridge to PT which is I do think can be curative for nonspecific CLBP. I tell patient's I'm trying to electrically rehabilitate the nerves, but they'll have to do more of the lifting as the therapy gets on board.

Dude...In good faith and with respect I'm compelled to reply this post is silly.

What is a "bridge to PT?"

Rehabilitation of a what nerve? The medial branch?
 
I think Reactiv8 is a great idea. I have no experience if it works - I just like the idea.

I don't like that you can't trial before an implant, so to me - trialing with SPRINT makes some sense if you are thinking of going that route. For some really stupid reason, the Reactiv8 reps HATE the idea of using SPRINT as a trial. So my answer is - then come up with a trial system, dummy.
I see the logic but I'm not sure it works.

Isn't SPRINT marketed as neuromodulation of the medial branches and Reactiv8 directly stimulating the multifidi muscles?

Two different targets and two different mechanisms of action.
 
I see the logic but I'm not sure it works.

Isn't SPRINT marketed as neuromodulation of the medial branches and Reactiv8 directly stimulating the multifidi muscles?

Two different targets and two different mechanisms of action.
Yeah probably.

But what is the alternative? Implant with NO objective data it will help?

I can’t do that.
 
How come everyone is giving their philosophy and opinion and nobody is talking about the evidence? One of these aforementioned things has a blinded prospective RCT…
 
I see the logic but I'm not sure it works.

Isn't SPRINT marketed as neuromodulation of the medial branches and Reactiv8 directly stimulating the multifidi muscles?

Two different targets and two different mechanisms of action.
Throw em both in then!
/s
 
I see the logic but I'm not sure it works.

Isn't SPRINT marketed as neuromodulation of the medial branches and Reactiv8 directly stimulating the multifidi muscles?

Two different targets and two different mechanisms of action.
I do think they're doing different things but I haven't used Reactiv8 yet. The pain relief curves have oddly different kinetics as Reactiv8 builds up slowly over weeks to months while SPR's stimulation you can see benefit in the recovery unit or it can build over 2 - 4 weeks.

I do prefer cheaper ways to engage them in PT and am a fan of life coaching, but I'd rather offer this as an off ramp than just wash my hands of the case. At ~5 - 10k for a unilateral vs bilateral system, the margin isn't huge for PNS with SPR.

Personally, I find it to be a technically unrewarding case as I am feel like I'm doing a fluoro or ultrasound guided trigger point with a wire, but the results are positive, so I offer it. I just don't intellectually believe in PNS for CLBP as I do for true neuralgias, but I offer it to patients and they like it over other options.

Mainstay has a good RCT for the indication we referenced above

SPR has multiple RCTs for other indications and a decent prospective trial on it
 
I do not find the mechanism for either plausible for longterm pain relief.
Tooth fairy science best explains it.
What do you think about 4 year data from the Reactiv8 trial? I know it’s a sponsored RCT but the results are impressive. To my knowledge there’s nothing else we do that is better at year 3 and 4 than year 1.
 
What do you think about 4 year data from the Reactiv8 trial? I know it’s a sponsored RCT but the results are impressive. To my knowledge there’s nothing else we do that is better at year 3 and 4 than year 1.
And how does this work?
Industry sponsored study is a commercial.
 
How come everyone is giving their philosophy and opinion and nobody is talking about the evidence? One of these aforementioned things has a blinded prospective RCT…
because i didnt review the study.

- i just did. it is a blinded study, and all people got the leads placed. study design appears okay...

- interestingly, those who had the lead placed but not stimulated got benefit from the injection. 33% reduction in VAS.

the study reports as clinically significant because the ones getting active stim got 45% reduction in VAS.

also, 31% improvement ODI vs 43%. pretty high for placebo effect...

- treatment blinded until 120 days, 4 months.

remind me - how long do RFAs last for?


here are the exclusion criteria:
Furthermore, candidates were excluded if they had prior lumbar spine surgery below T8 or spinal fusion at any level; a pathology seen on MRI that was clearly identified as the likely cause of CLBP and that was amenable to surgery; leg pain worse than back pain, or radiculopathy below the knee; neurological deficit possibly associated with the back pain; the source of pain was the sacroiliac joint as determined by the investigator; any surgical correction procedure for scoliosis at any time, or a current clinical diagnosis of moderate to severe scoliosis (Cobb angle ≥25°); any comorbid pain conditions (for interference with pain assessment); any previous rhizotomy or rhizolysis procedure on the dorsal root ganglion or medial branch at or below T8 within the prior year; any anesthetic block or injection of epidural steroids at or below T8 in the 30 days before the baseline visit; current baseline opioid use of more than 120 mg of morphine equivalent per day; any pain-related disability compensation or litigation issues; and evidence of an active disruptive psychological or psychiatric disorder or other known condition significant enough to impact perception of pain, compliance with intervention, and/or ability to evaluate treatment outcome (eg, active depression) as determined by a psychologist or psychiatrist.

which essentially eliminates almost everyone i see.
 
because i didnt review the study.

- i just did. it is a blinded study, and all people got the leads placed. study design appears okay...

- interestingly, those who had the lead placed but not stimulated got benefit from the injection. 33% reduction in VAS.

the study reports as clinically significant because the ones getting active stim got 45% reduction in VAS.

also, 31% improvement ODI vs 43%. pretty high for placebo effect...

- treatment blinded until 120 days, 4 months.

remind me - how long do RFAs last for?


here are the exclusion criteria:


which essentially eliminates almost everyone i see.
Glad you took the time to look it over. Very strong placebo effect the first 3-6 months appeared. But then there seems to be a clear benefit to me. But to those like Steve who don’t believe anything industry related except the scs of choice I got nothing for you.
 
Glad you took the time to look it over. Very strong placebo effect the first 3-6 months appeared. But then there seems to be a clear benefit to me. But to those like Steve who don’t believe anything industry related except the scs of choice I got nothing for you.
- interestingly, those who had the lead placed but not stimulated got benefit from the injection. 33% reduction in VAS.

the study reports as clinically significant because the ones getting active stim got 45% reduction in VAS.

What is your criteria for success?
For MBB or SCS it is 80% relief.
For joints- 50%.

Sham was 33%, active was only 45%. 12% better than sham. This is what we consider failure of an intervention.
What if stents opened a vessel only 45%? (poor comparitor)
Add that it is the best the company could do to sell us this crap. Failure.
 
- interestingly, those who had the lead placed but not stimulated got benefit from the injection. 33% reduction in VAS.

the study reports as clinically significant because the ones getting active stim got 45% reduction in VAS.

What is your criteria for success?
For MBB or SCS it is 80% relief.
For joints- 50%.

Sham was 33%, active was only 45%. 12% better than sham. This is what we consider failure of an intervention.
What if stents opened a vessel only 45%? (poor comparitor)
Add that it is the best the company could do to sell us this crap. Failure.
I feel the major strength of this study is the improvement over time. That’s the opposite of what we see with everything else.

Major flaws of the study and therapy noted.

this is a better conversation than individual philosophies, in my opinion.
 
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