February 20, 2024 • 32 mins
Persistent weakness and lack of volitional muscle control are huge problems after injury and surgery. It’s not uncommon after major surgeries, like ACL reconstruction, to have chronic weakness and asymmetry in strength.
In this episode, I talk to Dave Sherman about a recent research study he published looking at why this may happen, and then what we can do about it as clinicians.
Full show notes: https://mikereinold.com/arthrogenic-muscle-inhibition-with-dave-sherman
Full show notes: https://mikereinold.com/arthrogenic-muscle-inhibition-with-dave-sherman
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Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
(00:00):
On this episode of the sportsphysical therapy----podcast, I'm
joined by Dave Sherman.
After graduating PT school fromBoston university, Dave received
a PhD from the university ofToledo.
And is now doing postdoctoralresearch work in the area of
arthrogenic muscle inhibition.
In this podcast, we're going totalk about AMI and his recent
research publication on neuraldrive and motor unit
(00:21):
characteristics after ACLreconstruction.
But don't worry we're going todiscuss what the clinician can
do with this information as wellHey, Dave, welcome to the
podcast.
Really excited to have you.
(00:43):
Thanks, Mike.
I'm glad to be here.
Not everybody knows this.
Some people do know this aboutpodcasts, but Dave and I've been
talking for months and he's hada lot of exciting things going
on in his life that's beenkeeping him all busy.
But we've been really excited totry to get together and have
this podcast episode.
So it's, it's, it's great tofinally have you on.
Um, I, I've been following alittle bit of your research
lately and you've been producingsome really good stuff.
(01:04):
Um, why don't we start by, youknow, maybe filling the
listeners in a little bit ifthey're unfamiliar with.
Somebody to work, but when yougive them a brief information,
just like on your background,what you're currently up to,
where you're at.
Um, I think that'd be a greatstart.
Yeah, definitely.
So I'm a physical therapist andathletic trainer.
I trained at Boston University,uh, graduated now with my DPT
almost 10 years ago and then,uh, moved down to Fort Worth,
(01:28):
Texas.
We worked, uh, we worked, mywife and I, she is also a sports
PT.
She did a residency at TexasHealth Sports Medicine, Ben
Hogan at the time.
I was fortunate enough toconvince them to give me a job
so they could keep her around.
Uh, we stayed there for aboutfive years.
Um, you know, five years later,2018, we're looking around and,
(01:48):
um, I kind of had this, thisresearch bug.
I was frustrated with some ofmy, uh, clinical outcomes at the
time.
I thought, you know, we weredoing well applying the science
and, um, and still I was fallingshort of my patient's
expectations and decided, okay,there's something more to this
that I should go back and lookinto.
Did kind of a nationwide searchand ended up in Toledo with a
(02:10):
PhD program that was wellaligned with a mentor, um, and
like the questions, uh, lookingat the questions that I wanted
to answer.
So I just wrapped up that PhDafter five years, um, or five,
sorry, four years in Toledo andI've been in Boston, back in
Boston ever since.
So currently a postdoc at BostonUniversity in the division of
(02:33):
rheumatology that's in theschool of medicine and I study,
um, essentially arthrogenicmuscle inhibition in knee
osteoarthritis, which isamazing, which obviously has
tons of carry over to otherpathologies and stuff.
But I think that's, that's sucha great way to do it.
Um, you know.
There's a ton I want to talkabout, obviously, to your
expertise, um, but I do knowthat sometimes people have this
(02:56):
question, so I thought you'd bea great person to ask this too,
but like, what, what made you goback to get your PhD after you
were treating PT?
I know you kind of alluded to ita little bit there, but like,
like, I know a lot of PTs are,Maybe considering that, or maybe
they don't completely understandthat process, but that's like in
their, their thought process.
But why don't you tell us alittle bit about that and like
what went into trying to go, goback to school?
(03:16):
You know, did you really loveschool that much?
Like what was it that you wantedto go get your PhD?
Yeah, uh, well, that's funny.
So in PT school, I think I wasthe only one in my class that
actually liked the evidencebased practice course, you know,
just thought it was like moreinteresting than everyone else.
That's awesome.
So that was something.
And, uh, and so it was alwaysseemed like a possibility.
(03:37):
Oh, maybe there's something tothis research thing.
And then at Texas Health.
Um, you know, it's a it was kindof a clinical scientist full
time that worked there.
Craig Garrison, he was runningthe research lab at multiple
different clinics.
We had force plates in thefloor, motion capture cameras in
the clinic.
Um, so I was being a researchassistant, recording data, range
(04:00):
of motion strength, um, onparticipants that were also my
patients.
And so that kept kind of theresearch bug alive and then as,
as I mentioned, um, in thatenvironment, we're applying what
seems like the best evidencethat the stuff that's currently
coming out and I'm still fallingshort with my outcomes with what
I think my patient should beable to get back to.
(04:21):
So that's really the motivationis I have these lingering
questions surrounding, you know,what's going on in the nervous
system.
You have this, um, 50 percent ofyour census is patients with ACL
injury.
Um, they have this quadknockdown that you just can't
seem to address.
And, um, it's, it's not my, mystrength program, at least I
don't think it is.
Uh, and they're still fallingshort with that persistent
(04:42):
muscle inhibition.
So, um, that's the motivation togo back.
I love it.
And you know, you're helping allof us at such a higher level
with that, which I think isreally, really great, but.
Um, Arthrogenic muscleinhibition, you know, what
you've essentially said you're,you're focusing your career on,
at least at this point, untilyou figure it out and move on to
the next thing, I'm sure.
(05:03):
But, you know, this isn't,excuse me, this is an enormous
thing that we face in rehab,right?
You, like you said, evenyourself as a clinician, you're,
I don't know what the, you know,were you disappointed what it
was, but like, you know, you'redoing your best.
You're applying all theprinciples of basic science,
strength and conditioning stuff.
We're trying to get these peoplestronger and they're just not
getting stronger.
(05:23):
And we feel like we're failingthem, right?
Um, so, you know, it's tough.
And, you know, on a, on a pastpodcast episode with Terry
Grindstaff, we talked a littleabout some of these
neuromuscular consequences, but,you know, I'd be kind of curious
from, from your perspective,like, you know, why do you think
this is so prevalent?
Why do you think like, I knowyou've Put your head down and
try to figure this out.
Like, you know, why do you thinkthis, this muscle inhibition
(05:45):
after surgery is so common?
Um, the reason is it's a, it's areflex.
I mean, on the neurologicallevel, you have pain and
swelling in a joint.
Um, there's a change insensation in the periphery.
Uh, your nervous system is goingto integrate that change and,
and respond.
Um, I try to explain this asit's really no different than
(06:05):
touching a hot stove.
You have your agonist that'sreaching, uh, now inhibited and
your antagonist pulling backfacilitated.
Uh, similar phenomenon is what'sgoing on in the quadriceps.
That's why it shuts down.
I mean, you have, you can have apatient the day before a knee
surgery, they have a meniscustear in their knee, they can get
a nice quad activation.
It's the actual going in andhaving the meniscectomy that
(06:27):
creates inhibition.
Um, Entering into the joint,little pain, little swelling,
and the quad is now inhibitedfor the next few hours, days,
months, depends on thepathology.
Um, so, the thing to me is thata clinician cannot treat this
unless they can assess it.
And, um, it's really hard to seethe nervous system in clinical
(06:49):
practice.
I mean, there are some...
Some techniques like you coulduse EMG.
Uh, whether or not that's validfor measuring, uh, reduction in
activation is, is a, a broaderdiscussion.
Um, but that's, that's thereason why focus on, on AMI and
the, and the scientific lab asopposed to in the clinic is, is
hard to assess and know who hasit and who doesn't, and to what
(07:10):
extent.
Um, when you're out in the wildin the clinic, so.
Yeah, for sure, and you know,you recently just published a
really great paper, um, kind ofthat, that, you know, tried to
dig into this a little bit.
You're looking at neural drive,motor unit characteristics after
ACL reconstruction inparticular, which again,
hopefully we can extrapolate toother types of injuries and
(07:31):
stuff here, but.
None of us want to struggle withregaining strength, right?
None of us want to deal with thelong term issues that may come
from that, like maybe even, youknow, failure of the procedure
or, you know, not returning totheir activities or sport that
they want to get to or worse,like.
away down the road, right?
I, I'm starting to have friendsnow at my demographic that, hey,
(07:53):
ACL is 20 years ago that are nowgetting total knee replacements.
And I, I think we're young,right?
We're PTs.
We treat total knee patients.
I don't see a lot of people, youknow, 45, 50 years old getting
total knee replacements.
So, um, so let, so let's talk alittle bit about that article
and let's kind of shift gearsthere and, and, and kind of
explain that.
I, I think it was a really greatarticle.
It was.
(08:13):
It was in depth, dude.
I'll give you that.
It was, um, that was a detail.
That was a thick paper.
I loved it.
I read it.
I took notes.
I'm highlighting it.
Um, I love that stuff.
You did an amazing job kind oflike expanding on that.
So, um, I'm going to put a linkto that in the show notes for
the listeners that want to readit.
Like I didn't in detail.
It was awesome.
(08:34):
But tell us a little bit aboutwhy you wanted to conduct,
conduct that study and reallywhat you looked at in, in, in
that actual study.
Yeah.
So Thanks.
And, um, it's a very excitingstudy for me.
That was over three years ofwork now, now finally published
and out of the world to see it.
So appreciate you highlightingit here.
Um, the history and like themotivation behind the study is.
(08:59):
Arthrogenic muscle inhibitionfirst described, as far as I can
tell, almost a hundred years agocalled arthritic muscle
inhibition described in catswith osteoarthritis.
25 years ago, Chris Ingersolland Ty Hopkins are talking about
this as it relates to sportspathologies like ACL injury and
meniscus injury.
Um, and they're starting to dosome of the first neurophys
(09:20):
studies, uh, quantifying theamount of like quadriceps
knockdown and reallyhypothesizing like why that
happens on a neurological motoroutput level, like what's
happening to the motor neuronpool or the actual motor unit
firing behaviors, um, et cetera,right?
Our muscles are, areneurological effectors, right?
(09:40):
They only respond to the inputthat they get from the nervous
system.
We sought out in this study todo a kind, kind of a
comprehensive assessment ofneurophysiology in the face of
new technologies, um, in, in thelaboratory.
And so the, the primary one inthis study is what's called
decomposition, EMG.
So electromyography.
(10:00):
It records electrical activityof a muscle, uh, during a
contraction and by using like ahigher density array, multiple
different electrodes in a smallspace.
you can break down that signalinto individual motor units, uh,
and get a sense of how fastthey're firing, when they turned
on, when they turned off, andhow large their firing amplitude
(10:20):
was.
So that's kind of the outcomesthat we present in this study.
We also collect some of the moretraditional, um,
neurophysiological outcomesbeing Hoffman reflex, which is a
degree of Um, basically yourtendon tap reflex, how excitable
your muscle is in that, uh,rudimentary spinal level loop.
(10:41):
And then, uh, central activationratio, which is how much of your
muscle capacity as a percentageof your, of your capacity, can
you activate during a maximumvoluntary contraction?
And so, uh, we took, uh, thesample here is, uh, patients
with ACL reconstruction.
I think there are 14 in thisstudy, uh, and controls.
(11:02):
And, um, we we've put themthrough this array of tests.
We had them trace some force.
We decompose their their muscleactivity.
Um, and and then we cancharacterize in the sense of a
normal or abnormal spinalreflexive loop and with respect
to the amount of muscle capacitythat they can activate.
What are their motor unitbehaviors?
(11:23):
And how are they actually goingabout conducting a muscle
contraction on the neural level?
So that's the motivation for thestudy.
Yeah, and, and again, amazingclinicians like myself, and I
like to consider myself likewith a past, you know, history
of some clinical research andstuff.
Uh, it's this level of in depthresearch that really makes such
huge significant impacts on ourprofession and then eventually
(11:47):
our patients.
Right.
Um, so, you know, again, like,you know, people, you know,
obviously if Dave hasn't, hasn'tconvinced you yet that this,
this was a lot of hard work.
three years putting togethersuch an amazing project.
You should be ridiculously proudof getting this thing out there
so we can all learn from it.
So, you know, again, thank you.
Um, but you know, my nextquestion is going to be like,
(12:08):
okay, so what did you find?
Yeah.
So what, so, um, the, uh, thebig findings are that.
The individuals with ACLreconstruction in their involved
limb, the motor units fired moreslowly at any given recruitment
threshold.
So overall in the musclecontraction, their motor units
(12:30):
are firing, um, more slowly,which means that they're using
more of that like type oneendurant, um, muscle fiber,
right?
The less fatigable, uh, slowerfiring, um, fiber type.
This was in the context ofnormal activation, so they could
activate the same proportion oftheir muscle capacity, normal,
(12:51):
what's called central activationratio, and normal spinal reflex
excitability.
So we, um, we recorded those andall the participants and those
were no different between groupor limb.
And they also had muscleweakness.
So, um, that reduction in firingrate tends to explain the, the
weakness in, um, in thequadriceps because we also
(13:13):
quantified the compact musclecapacity, the percentage of
motor neuron pool.
Um, we also kind ofhypothesized, although it's
difficult to prove with thelimitations in technology, that
there are individuals with ACLreconstruction are also
activating fewer motor units, sothey're just not turning on as
much motor units, and thereforewe would conclude that there's
(13:35):
less available.
So, um, whether it's theinhibition process or the time
since injury, um, or muscleweakness, they've actually like
reduced or catabolized some oftheir, their muscle capacity
over the years.
Uh, which would not be a goodthing.
Correct.
I agree with that.
So, you know, when I was readingthe study, one of the questions
(13:55):
I had for you about this too, isthat I think you noted in your
subject pool that had ACLreconstruction, that they had
asymmetries, they had weakness,correct?
They did, yeah, so the involvedlimb was, um, was quite a bit
weaker than the contralaterallimb, uh, as well as the healthy
control limb.
(14:15):
I don't know the exact numbers,but the way I like to think of
this is...
I think it's easy clinicians torecord strength and normalize
the body mass.
Three, everyone throws out the2.
99 or three newton meters perkilogram.
The ACLR group was below thatthreshold in this study.
So I, what I wondered, right,was.
(14:35):
If we looked at people, becauseyou had a wide range of, you
know, how far out from surgerythey were, um, I wonder if we
looked at people that didn'thave that asymmetry and that
restored their strength to, youknow, would, would you assume
that these findings would beessentially reversed, right?
The fewer and slower motorunits, like, would, would be
different?
Is that, you know, and, and, youknow, I guess the million dollar
(14:58):
question is going to be, youknow, why are some people like
that and some people aren't,right?
But is, am I thinking about thatcorrectly?
Yeah, so, um, we did not, like,have the numbers, uh, quite
frankly, to look at, like, whowas driving that, that effect,
um, and we have a follow upstudy that I'm working on now
with similar methods, um,actually more neurophysiological
(15:22):
methods, uh, looking at similaroutcomes, and we do see a, a, a,
we will replicate thesefindings, fortunately, um, But
you're right to say that these,this sample was far away from
surgery, so these, uh, therecovery of the spinal reflex
has, has happened, as we knowhappens after about three
months, um, and their, theirkind of recovery of muscle
(15:46):
capacity has, has maybeplateaued and that they're not
going to get any stronger,they're out of rehab, they're
playing sports, um, and we seethis effect.
So I think the question is,like, yeah.
If somebody has recovered fullstrength, do they show the kind
of detriments in their motorneuron pool?
I can't answer that question,but to me, what's more
(16:08):
applicable to the clinician iswhen you still have the patient
in in your hands, and you canactually potentially impact
these.
Longer term consequences as werecorded in this study, um, with
interventions, that's kind ofwhat I would like to take away
from the study, at least in theshort term is something you need
to investigate for sure.
For sure.
Um, all right.
(16:29):
So help the clinician then.
So how do we take this research?
How do we apply it in practice?
Right?
And maybe we maybe we use Sure.
Two scenarios, right?
And I know this is a little bitbeyond the scope of your paper
too, but conceptually, like, howdo we deal with this?
Like, how do you work withsomebody, you know, acutely
following an ACL reconstruction?
We say that they have pain intheir swelling, they have muscle
inhibition.
(16:49):
What do you think's going on?
What's your goal here?
What would your suggestions forclinicians to do for
interventions for somebody likethat?
Yeah.
So I think, uh, about thenatural history of.
Of, um, arthrogenic muscleinhibition in this case.
So natural history being, um,why is it happening and how does
(17:10):
that change over time?
Um, early on pain and swellingare the catalyst for muscle
inhibition.
And so a clinician that's seeingsomebody immediately after
surgery or even before surgery,after their injury, getting
ready for surgery should look toreduce, uh, the catalyst.
So that's pain and swelling.
So, um, Interventions that dothat, uh, are, are, uh, focal
(17:34):
joint cooling or cryotherapythat's icing down the joint,
the, on the joint beforeexercise.
It's a little counterintuitive,but we know that that can
restore, uh, that spinal reflexexcitability and restore access
to muscle capacity.
Um, that's what we would call itare in open and exploit
strategy.
So you're basically.
allowing them this therapeuticwindow of access to their muscle
(17:58):
by numbing the pain or reducingthe swelling.
And then you can, you canexploit that in, in rehab.
So for the next 45 minutes,their joint is cold.
Um, do your quadricepsexercises, uh, work on, on open,
open chain, the extension, uh,use NMES use biofeedback.
Uh, throw everything you have atthem during that, uh, during
(18:20):
that therapeutic window.
Uh, so that's, that's oneintervention that kind of masks
the unmask the inhibition,allows them access.
And then I think of, uh, otherslike NMDS and biofeedback is
having different mechanisms,right?
You want to send all you can,all your neural power to the
motor neuron pool to preventatrophy and retrain the quad.
(18:41):
Um, so cryotherapy affects onething, and then NMES is forced
use, right?
You're, you're forcing themuscle to contract.
You're throwing an electricalstimulus, uh, through it.
Uh, it's non volitional, but youcan still, uh, use those motor
units.
And then biofeedback, uh, ismore of a top down approach.
That would be giving them asignal, uh, that they can, they
(19:03):
can try to amplify, by trying toincrease either EMG activity.
Um, or increased torque ifyou're, if you're using like a
10 deck or something moreclinically like dynamometer.
Um, that's a cognitive, likethrow more resources, try to
make the muscle contract harder.
So all three of those things,like take those three approaches
are really going to optimizeyour, your, uh, immediate post
(19:25):
op phase.
And then like more emergingstudy, which I, I, I do think,
uh, has a lot of evidence atthis point is, is the metabolic
cascade.
And Lindsay Lefley is doingreally exciting work here, and
whether eccentrics, earlyeccentrics, or, or tools like
blood flow restriction canaddress the metabolic cascade
of, um, of post operative muscleatrophy.
(19:49):
Which, which is great.
And, um, you know, the, theinternet, social media has, uh,
shamed anyone that has said theword ICE in the last eight
years.
So, um, you know, so it's, it'sgood to see, you know, and we
try to tell everybody, it'slike, this is a very simplistic
viewpoint that we're havinghere.
There's pros and cons toeverything, right?
So it's good to hear that thereis, uh, you know, some
(20:10):
beneficial use of ICE because,you know, we, we still use it
for some of its pros and, and,and, you know, I've taken it
away at other points as well,but I love that.
Um, you know, one, one thingI've always kind of educated and
I'm, I'm curious from yourperspective, you know, maybe if
you can tell me if I'm barkingup the right tree, if I'm doing
this right.
But, um, we've kind of shiftedto the same thing, some
cryotherapy beforehand for thesame reasons.
(20:31):
And then, um, um, we use NMESwhen a person is having a very
difficult time with volitionalcontrol.
But as soon as they tend to havevolitional control, we then
almost switch to biofeedback totry to get them to have better
control.
Um, am I doing that well?
Should I do anything differentor, or better?
What, what do you think aboutthat thought process?
(20:52):
If you're using EMG biofeedback,then you can't use them at the
same time, right?
The NMES would saturate thesignal.
So you don't have to discontinueNMES.
And some people would say thatyou shouldn't for, for many
months after surgery.
But you do want to apply bothinterventions.
So, um, NMES units at this pointare pretty affordable.
(21:15):
Send them home with a patient.
At our clinic, we send NMESunits home with people who are
post op.
We have them do it twice a day,uh, during their, during their
Therax home exercise program.
Um, and then bring it back forfor clinical sessions.
Um, and and biofeedback isharder to recreate in many cases
(21:37):
at home.
So, um, you can you can use yourtime in the clinic with the
patient to focus on that.
You really, I think, want tothrow everything you you can at
them.
So Makes sense.
I like, you know, in the sportsworld, I like that approach,
right?
Like, there's, you know, whynot, right?
We want, we want to get these,these people better as fast as
possible.
So, awesome.
Well, throw everything you canthat's evidence based, I should
(21:57):
say.
Yeah.
I like that.
Good answer.
I like that.
Alright, so tell me now, howwould your perspective change
here?
Now we have somebody, let's sayit's a few months out, or more
than a few months out I shouldsay, chronic persistent
weakness.
Maybe they don't have pain andswelling at this point, right?
Because I think if they do havepain and swelling, we'd probably
still use the same thoughtprocess to an extent.
(22:19):
But now this is the person thatcomes to your clinic.
Right there a few months out,maybe they did rehab elsewhere.
Maybe, maybe something happened,whatever, but they're still
super weak, have terriblevolitional control.
What do you think is going onhere now in this chronic setting
and how would your interventionschange for that person?
Yep.
So from, again, the naturalhistory.
(22:40):
You're now getting months out,the kind of catalyst of
inhibition being pain andeffusion are resolving.
Um, the nervous system isintegrating this change and, uh,
what we see in now systematicreviews is that people farther
out have cortical driveninhibitions.
So the muscle activationfailure, the muscle weakness.
(23:02):
is more associated with what'sgoing on in the brain than
what's going on in the spinalcord.
Um, and for that reason, you canprobably discontinue
interventions that target thespinal cord being cryotherapy or
TENS if you're using that andfocus more on interventions that
would address the cortex, um, orthe, or the top down control.
So for that, you're going toapply biofeedback, you're going
(23:23):
to apply NMES still if it'sappropriate.
Um, and you can do things like,like eccentrics, eccentric
overload, because that, uh, islike a throw everything you have
at this from a neural standpointto try to control that
eccentric, um, contraction.
Uh, so that's, that's reallythe, the big changes there, um,
when, when you're looking at,uh, longer, longer out is you
(23:46):
just say that the spinal levelcontrol or the spinal level
interventions are probably lessindicated now.
Um, that being said, we don'tknow when you look at a patient
in the clinic, what's going onin their nervous system.
That's one of the limitationsof.
of applying any of theseinterventions in the first
place.
You're kind of just looking atthem and where they're at in the
(24:06):
recovery and, and, and assumingkind of what their neurological
activation might be.
Um, and I've seen anecdotes andvideos on, on Twitter and
LinkedIn and stuff of peoplesaying, Hey Dave, this person's,
you know, six months out ofsurgery.
I iced them and their strengthwent up 20%.
So.
whether that single individualstill had spinal level
(24:27):
inhibition, it's, it's hard tosay.
We can't know.
So look at the patient in frontof you.
Um, a lot of times if you dothis like pre post intervention,
like just film their musclecontraction or get a, get a MVIC
before and after anintervention, you'll know
whether or not it's having aneffect.
Um, just that, that simple likeAB test pre post.
(24:48):
And if it doesn't, then youdon't have to do the
intervention.
If it does, then you should useit.
And to me, that's actuallyamazing advice for so much we do
in our profession right there.
That's the, you know, the assessreassess model that sometimes a
lot of people just forget about,right?
You know, they're so tied upwith, you know, what they want
to do and what's next that theydon't, they don't, they don't
look at basics like that.
(25:09):
So I think that's fantastic.
So, um, Dave, awesome stuff.
This is going to be superhelpful for clinicians that I
know that this has helped me,right?
You've, you've taught me somestuff on this and obviously
reading your, your article andyour past.
Stuff that you've published hasbeen great.
So I'm going to put some linksin the show notes to some of
Dave's work, especially this,this current article that we're
talking about, because I thinkit's a, it's a really important
(25:31):
one that hopefully will have animpact on our professions for
some time and hopefullystimulate people like Dave to do
more and more research in thisarea so we can get to the bottom
of this.
Right.
Um, but Dave, before I let yougo.
Quick high five at the end, fivequick questions, five quick
answers.
Just kind of want to hear alittle bit more about you teach
everybody a little bit aboutyour thoughts here.
But first question, what are youcurrently doing?
(25:52):
And like this question is neverfair, basically to the PhDs, by
the way, because you guys havevery finite topics you're
working on, but what are youcurrently working on for your
own professional developmentright now?
Um, yeah, that's a goodquestion.
So I, you know.
And changing in the midst ofchanging populations of
(26:12):
interest.
I worked my PhD at ACLreconstruction.
Now I study neo osteoarthritis.
I did a postdoc in between abouttechnology development for, for,
uh, patients with, with, uh,neurologically driven muscle
inhibition after stroke.
Um, so I'm just kind of learningand trying to, to find
consilience in the literatureand in the nervous system about
(26:34):
what's going on.
Um, one of the multipledifferent avenues for driving
muscle inhibition and whatapplies to which interventions
when, um, I'm also trying tolike, enjoy the postdoctoral
period and that I'm not afaculty member and just relax a
bit, which is, which is new forme.
So, um, you know, read, read afew books here and there and,
(26:55):
uh, and just enjoy time withfamily.
So.
I love it.
Yeah, you put your work in thelast 15 plus years.
Uh, it's, it's, it's time tospend a little, little time for
yourself.
I love it.
Thanks for recognizing that.
Yeah, absolutely.
You got my support.
But, um, what, what, what's onething you've recently changed
your mind about?
I think that, that no one iscoming to help me translate my,
(27:19):
my research, um, and that's likeruns counter to being on this
podcast.
So thanks for inviting me.
But what I mean is like in theacademic world and in physical
therapy research specifically,um, we call it like we have
researchers and we haveclinicians.
And what the way they wouldtreat this in industry is they
(27:39):
would have a research anddevelopment department, right?
Right, and there's nodevelopment in academic
research.
So when I publish something it'sup to me to market it and
disseminate it Um to teach andengage with clinicians, uh and
to innovate and like develop thetechnology that's going to make
the difference Or else we'restuck with that same like 17
(28:00):
year gap between us publishing astudy and clinicians Um, you
know, picking it up and applyingit, right?
I'm not, I'm not placing theblame on anyone.
I think it's just like this hugedisconnect between our worlds.
In industry, when you look attechnology and like, especially
artificial intelligence rightnow is a hot topic.
(28:20):
They have the development sideof things, like they're paying
people.
They have people.
And, uh, and I think that thatjob, as far as I can tell, falls
on me, if I'm, I'm in academia,so.
That's right.
That's, that's why research andacademia go so well together.
You do the research, then you,you put it into everybody's
mind.
So, you know, no pressure, butlike you've got to make sure you
(28:41):
have good methodology and, andyou're doing a good job.
You're not giving falsemisinformation out there to the
students.
Yeah, well, that's, and that'strue.
So the development part ofthings is if you have to, if I
have to take my research and putit into a technology that people
will adapt, adopt.
They need to actually see thatit works, right?
So if my research is flawed, thetechnology will never work.
(29:02):
It's a nice kind of litmus testto see, you know, is it, is it
worth it?
For sure.
Can, can my research interestsbe actually marketed and
translated to, um, to theindustry?
Yeah.
Awesome.
So that's one thing I'mrealizing.
Yeah.
What's your favorite piece ofadvice you love to give, uh,
students?
Um, I just talk to people,people want to talk to you, if
(29:24):
you have a question, read anarticle, reach out to them, um,
say hello, introduce yourself,uh, talk about a problem you're
working on, um, and yeah, andthis is a great profession,
it's, it's done a lot of greatthings for me, and, um, yeah,
network, connect, don't beafraid.
I love it.
I think Dave just gave you alla, uh, open invite to email him,
(29:44):
by the way, but I didn't, Ididn't want to say it, but yeah,
you can go on our website.
You can, you can, anyone canjust click a link and schedule a
video call with me to talk aboutany AMI interventions.
That's, that's, that's amazing.
That's pretty much what I didfor this podcast episode.
So yeah, it pretty much worked.
That's how Dave and I met, but,uh, awesome.
Uh, what's coming up next foryou, Dave, I know you've alluded
(30:06):
to some new research, but whatelse you got brewing?
Um, just focusing on familytime.
I think, like, I just had a son,uh, about four months ago.
So I have some, some jobapplications out for faculty
appointments.
Uh, it's kind of the season forthat.
So we'll see if anything,anything hits.
And in the meantime, just, uh,continue the postdoc grind.
(30:28):
That's amazing.
Uh, I'll put some info in theshow notes, but where can people
find out more about you and yourwork?
I'm on X and LinkedIn, and thenpeople can go to live4pt.
com to check out some of theblogs I have on these topics, or
as I said, find a link toschedule on my calendar to meet
up and just problem solveclinical cases or whatever.
(30:52):
That's great.
I think you're the first personI know to embrace calling it x
by the way.
So, um, yeah, you know, Ifigured I'd go for it.
It's been a few months now.
I mean, it's, it's accurate.
So everybody else is wrongstill.
So yeah, I love it.
That's, that's, that's what,that's what makes you, you Dave.
I like that.
Awesome.
But But Dave, thank you so much.
This was awesome.
Love sharing your stuff.
(31:12):
Love learning from, from some ofyour research.
So please check out Dave andsome of these, um, these great
topics that he's working on andtake them up on that offer.
He, he wants to talk to you and,and, and, and help.
So anything you can do.
So, um, thanks again, Dave.
Thanks for coming on the podcasttoday.
Cool.
Yeah.
Thanks Mike.
Thanks for having me.
On this episode of the sportsphysical therapy----podcast, I'm
joined by Dave Sherman.
After graduating PT school fromBoston university, Dave received
a PhD from the university ofToledo.
And is now doing postdoctoralresearch work in the area of
arthrogenic muscle inhibition.
In this podcast, we're going totalk about AMI and his recent
research publication on neuraldrive and motor unit
(00:21):
characteristics after ACLreconstruction.
But don't worry we're going todiscuss what the clinician can
do with this information as wellHey, Dave, welcome to the
podcast.
Really excited to have you.
(00:43):
Thanks, Mike.
I'm glad to be here.
Not everybody knows this.
Some people do know this aboutpodcasts, but Dave and I've been
talking for months and he's hada lot of exciting things going
on in his life that's beenkeeping him all busy.
But we've been really excited totry to get together and have
this podcast episode.
So it's, it's, it's great tofinally have you on.
Um, I, I've been following alittle bit of your research
lately and you've been producingsome really good stuff.
(01:04):
Um, why don't we start by, youknow, maybe filling the
listeners in a little bit ifthey're unfamiliar with.
Somebody to work, but when yougive them a brief information,
just like on your background,what you're currently up to,
where you're at.
Um, I think that'd be a greatstart.
Yeah, definitely.
So I'm a physical therapist andathletic trainer.
I trained at Boston University,uh, graduated now with my DPT
almost 10 years ago and then,uh, moved down to Fort Worth,
(01:28):
Texas.
We worked, uh, we worked, mywife and I, she is also a sports
PT.
She did a residency at TexasHealth Sports Medicine, Ben
Hogan at the time.
I was fortunate enough toconvince them to give me a job
so they could keep her around.
Uh, we stayed there for aboutfive years.
Um, you know, five years later,2018, we're looking around and,
(01:48):
um, I kind of had this, thisresearch bug.
I was frustrated with some ofmy, uh, clinical outcomes at the
time.
I thought, you know, we weredoing well applying the science
and, um, and still I was fallingshort of my patient's
expectations and decided, okay,there's something more to this
that I should go back and lookinto.
Did kind of a nationwide searchand ended up in Toledo with a
(02:10):
PhD program that was wellaligned with a mentor, um, and
like the questions, uh, lookingat the questions that I wanted
to answer.
So I just wrapped up that PhDafter five years, um, or five,
sorry, four years in Toledo andI've been in Boston, back in
Boston ever since.
So currently a postdoc at BostonUniversity in the division of
(02:33):
rheumatology that's in theschool of medicine and I study,
um, essentially arthrogenicmuscle inhibition in knee
osteoarthritis, which isamazing, which obviously has
tons of carry over to otherpathologies and stuff.
But I think that's, that's sucha great way to do it.
Um, you know.
There's a ton I want to talkabout, obviously, to your
expertise, um, but I do knowthat sometimes people have this
(02:56):
question, so I thought you'd bea great person to ask this too,
but like, what, what made you goback to get your PhD after you
were treating PT?
I know you kind of alluded to ita little bit there, but like,
like, I know a lot of PTs are,Maybe considering that, or maybe
they don't completely understandthat process, but that's like in
their, their thought process.
But why don't you tell us alittle bit about that and like
what went into trying to go, goback to school?
(03:16):
You know, did you really loveschool that much?
Like what was it that you wantedto go get your PhD?
Yeah, uh, well, that's funny.
So in PT school, I think I wasthe only one in my class that
actually liked the evidencebased practice course, you know,
just thought it was like moreinteresting than everyone else.
That's awesome.
So that was something.
And, uh, and so it was alwaysseemed like a possibility.
(03:37):
Oh, maybe there's something tothis research thing.
And then at Texas Health.
Um, you know, it's a it was kindof a clinical scientist full
time that worked there.
Craig Garrison, he was runningthe research lab at multiple
different clinics.
We had force plates in thefloor, motion capture cameras in
the clinic.
Um, so I was being a researchassistant, recording data, range
(04:00):
of motion strength, um, onparticipants that were also my
patients.
And so that kept kind of theresearch bug alive and then as,
as I mentioned, um, in thatenvironment, we're applying what
seems like the best evidencethat the stuff that's currently
coming out and I'm still fallingshort with my outcomes with what
I think my patient should beable to get back to.
(04:21):
So that's really the motivationis I have these lingering
questions surrounding, you know,what's going on in the nervous
system.
You have this, um, 50 percent ofyour census is patients with ACL
injury.
Um, they have this quadknockdown that you just can't
seem to address.
And, um, it's, it's not my, mystrength program, at least I
don't think it is.
Uh, and they're still fallingshort with that persistent
(04:42):
muscle inhibition.
So, um, that's the motivation togo back.
I love it.
And you know, you're helping allof us at such a higher level
with that, which I think isreally, really great, but.
Um, Arthrogenic muscleinhibition, you know, what
you've essentially said you're,you're focusing your career on,
at least at this point, untilyou figure it out and move on to
the next thing, I'm sure.
(05:03):
But, you know, this isn't,excuse me, this is an enormous
thing that we face in rehab,right?
You, like you said, evenyourself as a clinician, you're,
I don't know what the, you know,were you disappointed what it
was, but like, you know, you'redoing your best.
You're applying all theprinciples of basic science,
strength and conditioning stuff.
We're trying to get these peoplestronger and they're just not
getting stronger.
(05:23):
And we feel like we're failingthem, right?
Um, so, you know, it's tough.
And, you know, on a, on a pastpodcast episode with Terry
Grindstaff, we talked a littleabout some of these
neuromuscular consequences, but,you know, I'd be kind of curious
from, from your perspective,like, you know, why do you think
this is so prevalent?
Why do you think like, I knowyou've Put your head down and
try to figure this out.
Like, you know, why do you thinkthis, this muscle inhibition
(05:45):
after surgery is so common?
Um, the reason is it's a, it's areflex.
I mean, on the neurologicallevel, you have pain and
swelling in a joint.
Um, there's a change insensation in the periphery.
Uh, your nervous system is goingto integrate that change and,
and respond.
Um, I try to explain this asit's really no different than
(06:05):
touching a hot stove.
You have your agonist that'sreaching, uh, now inhibited and
your antagonist pulling backfacilitated.
Uh, similar phenomenon is what'sgoing on in the quadriceps.
That's why it shuts down.
I mean, you have, you can have apatient the day before a knee
surgery, they have a meniscustear in their knee, they can get
a nice quad activation.
It's the actual going in andhaving the meniscectomy that
(06:27):
creates inhibition.
Um, Entering into the joint,little pain, little swelling,
and the quad is now inhibitedfor the next few hours, days,
months, depends on thepathology.
Um, so, the thing to me is thata clinician cannot treat this
unless they can assess it.
And, um, it's really hard to seethe nervous system in clinical
(06:49):
practice.
I mean, there are some...
Some techniques like you coulduse EMG.
Uh, whether or not that's validfor measuring, uh, reduction in
activation is, is a, a broaderdiscussion.
Um, but that's, that's thereason why focus on, on AMI and
the, and the scientific lab asopposed to in the clinic is, is
hard to assess and know who hasit and who doesn't, and to what
(07:10):
extent.
Um, when you're out in the wildin the clinic, so.
Yeah, for sure, and you know,you recently just published a
really great paper, um, kind ofthat, that, you know, tried to
dig into this a little bit.
You're looking at neural drive,motor unit characteristics after
ACL reconstruction inparticular, which again,
hopefully we can extrapolate toother types of injuries and
(07:31):
stuff here, but.
None of us want to struggle withregaining strength, right?
None of us want to deal with thelong term issues that may come
from that, like maybe even, youknow, failure of the procedure
or, you know, not returning totheir activities or sport that
they want to get to or worse,like.
away down the road, right?
I, I'm starting to have friendsnow at my demographic that, hey,
(07:53):
ACL is 20 years ago that are nowgetting total knee replacements.
And I, I think we're young,right?
We're PTs.
We treat total knee patients.
I don't see a lot of people, youknow, 45, 50 years old getting
total knee replacements.
So, um, so let, so let's talk alittle bit about that article
and let's kind of shift gearsthere and, and, and kind of
explain that.
I, I think it was a really greatarticle.
It was.
(08:13):
It was in depth, dude.
I'll give you that.
It was, um, that was a detail.
That was a thick paper.
I loved it.
I read it.
I took notes.
I'm highlighting it.
Um, I love that stuff.
You did an amazing job kind oflike expanding on that.
So, um, I'm going to put a linkto that in the show notes for
the listeners that want to readit.
Like I didn't in detail.
It was awesome.
(08:34):
But tell us a little bit aboutwhy you wanted to conduct,
conduct that study and reallywhat you looked at in, in, in
that actual study.
Yeah.
So Thanks.
And, um, it's a very excitingstudy for me.
That was over three years ofwork now, now finally published
and out of the world to see it.
So appreciate you highlightingit here.
Um, the history and like themotivation behind the study is.
(08:59):
Arthrogenic muscle inhibitionfirst described, as far as I can
tell, almost a hundred years agocalled arthritic muscle
inhibition described in catswith osteoarthritis.
25 years ago, Chris Ingersolland Ty Hopkins are talking about
this as it relates to sportspathologies like ACL injury and
meniscus injury.
Um, and they're starting to dosome of the first neurophys
(09:20):
studies, uh, quantifying theamount of like quadriceps
knockdown and reallyhypothesizing like why that
happens on a neurological motoroutput level, like what's
happening to the motor neuronpool or the actual motor unit
firing behaviors, um, et cetera,right?
Our muscles are, areneurological effectors, right?
(09:40):
They only respond to the inputthat they get from the nervous
system.
We sought out in this study todo a kind, kind of a
comprehensive assessment ofneurophysiology in the face of
new technologies, um, in, in thelaboratory.
And so the, the primary one inthis study is what's called
decomposition, EMG.
So electromyography.
(10:00):
It records electrical activityof a muscle, uh, during a
contraction and by using like ahigher density array, multiple
different electrodes in a smallspace.
you can break down that signalinto individual motor units, uh,
and get a sense of how fastthey're firing, when they turned
on, when they turned off, andhow large their firing amplitude
(10:20):
was.
So that's kind of the outcomesthat we present in this study.
We also collect some of the moretraditional, um,
neurophysiological outcomesbeing Hoffman reflex, which is a
degree of Um, basically yourtendon tap reflex, how excitable
your muscle is in that, uh,rudimentary spinal level loop.
(10:41):
And then, uh, central activationratio, which is how much of your
muscle capacity as a percentageof your, of your capacity, can
you activate during a maximumvoluntary contraction?
And so, uh, we took, uh, thesample here is, uh, patients
with ACL reconstruction.
I think there are 14 in thisstudy, uh, and controls.
(11:02):
And, um, we we've put themthrough this array of tests.
We had them trace some force.
We decompose their their muscleactivity.
Um, and and then we cancharacterize in the sense of a
normal or abnormal spinalreflexive loop and with respect
to the amount of muscle capacitythat they can activate.
What are their motor unitbehaviors?
(11:23):
And how are they actually goingabout conducting a muscle
contraction on the neural level?
So that's the motivation for thestudy.
Yeah, and, and again, amazingclinicians like myself, and I
like to consider myself likewith a past, you know, history
of some clinical research andstuff.
Uh, it's this level of in depthresearch that really makes such
huge significant impacts on ourprofession and then eventually
(11:47):
our patients.
Right.
Um, so, you know, again, like,you know, people, you know,
obviously if Dave hasn't, hasn'tconvinced you yet that this,
this was a lot of hard work.
three years putting togethersuch an amazing project.
You should be ridiculously proudof getting this thing out there
so we can all learn from it.
So, you know, again, thank you.
Um, but you know, my nextquestion is going to be like,
(12:08):
okay, so what did you find?
Yeah.
So what, so, um, the, uh, thebig findings are that.
The individuals with ACLreconstruction in their involved
limb, the motor units fired moreslowly at any given recruitment
threshold.
So overall in the musclecontraction, their motor units
(12:30):
are firing, um, more slowly,which means that they're using
more of that like type oneendurant, um, muscle fiber,
right?
The less fatigable, uh, slowerfiring, um, fiber type.
This was in the context ofnormal activation, so they could
activate the same proportion oftheir muscle capacity, normal,
(12:51):
what's called central activationratio, and normal spinal reflex
excitability.
So we, um, we recorded those andall the participants and those
were no different between groupor limb.
And they also had muscleweakness.
So, um, that reduction in firingrate tends to explain the, the
weakness in, um, in thequadriceps because we also
(13:13):
quantified the compact musclecapacity, the percentage of
motor neuron pool.
Um, we also kind ofhypothesized, although it's
difficult to prove with thelimitations in technology, that
there are individuals with ACLreconstruction are also
activating fewer motor units, sothey're just not turning on as
much motor units, and thereforewe would conclude that there's
(13:35):
less available.
So, um, whether it's theinhibition process or the time
since injury, um, or muscleweakness, they've actually like
reduced or catabolized some oftheir, their muscle capacity
over the years.
Uh, which would not be a goodthing.
Correct.
I agree with that.
So, you know, when I was readingthe study, one of the questions
(13:55):
I had for you about this too, isthat I think you noted in your
subject pool that had ACLreconstruction, that they had
asymmetries, they had weakness,correct?
They did, yeah, so the involvedlimb was, um, was quite a bit
weaker than the contralaterallimb, uh, as well as the healthy
control limb.
(14:15):
I don't know the exact numbers,but the way I like to think of
this is...
I think it's easy clinicians torecord strength and normalize
the body mass.
Three, everyone throws out the2.
99 or three newton meters perkilogram.
The ACLR group was below thatthreshold in this study.
So I, what I wondered, right,was.
(14:35):
If we looked at people, becauseyou had a wide range of, you
know, how far out from surgerythey were, um, I wonder if we
looked at people that didn'thave that asymmetry and that
restored their strength to, youknow, would, would you assume
that these findings would beessentially reversed, right?
The fewer and slower motorunits, like, would, would be
different?
Is that, you know, and, and, youknow, I guess the million dollar
(14:58):
question is going to be, youknow, why are some people like
that and some people aren't,right?
But is, am I thinking about thatcorrectly?
Yeah, so, um, we did not, like,have the numbers, uh, quite
frankly, to look at, like, whowas driving that, that effect,
um, and we have a follow upstudy that I'm working on now
with similar methods, um,actually more neurophysiological
(15:22):
methods, uh, looking at similaroutcomes, and we do see a, a, a,
we will replicate thesefindings, fortunately, um, But
you're right to say that these,this sample was far away from
surgery, so these, uh, therecovery of the spinal reflex
has, has happened, as we knowhappens after about three
months, um, and their, theirkind of recovery of muscle
(15:46):
capacity has, has maybeplateaued and that they're not
going to get any stronger,they're out of rehab, they're
playing sports, um, and we seethis effect.
So I think the question is,like, yeah.
If somebody has recovered fullstrength, do they show the kind
of detriments in their motorneuron pool?
I can't answer that question,but to me, what's more
(16:08):
applicable to the clinician iswhen you still have the patient
in in your hands, and you canactually potentially impact
these.
Longer term consequences as werecorded in this study, um, with
interventions, that's kind ofwhat I would like to take away
from the study, at least in theshort term is something you need
to investigate for sure.
For sure.
Um, all right.
(16:29):
So help the clinician then.
So how do we take this research?
How do we apply it in practice?
Right?
And maybe we maybe we use Sure.
Two scenarios, right?
And I know this is a little bitbeyond the scope of your paper
too, but conceptually, like, howdo we deal with this?
Like, how do you work withsomebody, you know, acutely
following an ACL reconstruction?
We say that they have pain intheir swelling, they have muscle
inhibition.
(16:49):
What do you think's going on?
What's your goal here?
What would your suggestions forclinicians to do for
interventions for somebody likethat?
Yeah.
So I think, uh, about thenatural history of.
Of, um, arthrogenic muscleinhibition in this case.
So natural history being, um,why is it happening and how does
(17:10):
that change over time?
Um, early on pain and swellingare the catalyst for muscle
inhibition.
And so a clinician that's seeingsomebody immediately after
surgery or even before surgery,after their injury, getting
ready for surgery should look toreduce, uh, the catalyst.
So that's pain and swelling.
So, um, Interventions that dothat, uh, are, are, uh, focal
(17:34):
joint cooling or cryotherapythat's icing down the joint,
the, on the joint beforeexercise.
It's a little counterintuitive,but we know that that can
restore, uh, that spinal reflexexcitability and restore access
to muscle capacity.
Um, that's what we would call itare in open and exploit
strategy.
So you're basically.
allowing them this therapeuticwindow of access to their muscle
(17:58):
by numbing the pain or reducingthe swelling.
And then you can, you canexploit that in, in rehab.
So for the next 45 minutes,their joint is cold.
Um, do your quadricepsexercises, uh, work on, on open,
open chain, the extension, uh,use NMES use biofeedback.
Uh, throw everything you have atthem during that, uh, during
(18:20):
that therapeutic window.
Uh, so that's, that's oneintervention that kind of masks
the unmask the inhibition,allows them access.
And then I think of, uh, otherslike NMDS and biofeedback is
having different mechanisms,right?
You want to send all you can,all your neural power to the
motor neuron pool to preventatrophy and retrain the quad.
(18:41):
Um, so cryotherapy affects onething, and then NMES is forced
use, right?
You're, you're forcing themuscle to contract.
You're throwing an electricalstimulus, uh, through it.
Uh, it's non volitional, but youcan still, uh, use those motor
units.
And then biofeedback, uh, ismore of a top down approach.
That would be giving them asignal, uh, that they can, they
(19:03):
can try to amplify, by trying toincrease either EMG activity.
Um, or increased torque ifyou're, if you're using like a
10 deck or something moreclinically like dynamometer.
Um, that's a cognitive, likethrow more resources, try to
make the muscle contract harder.
So all three of those things,like take those three approaches
are really going to optimizeyour, your, uh, immediate post
(19:25):
op phase.
And then like more emergingstudy, which I, I, I do think,
uh, has a lot of evidence atthis point is, is the metabolic
cascade.
And Lindsay Lefley is doingreally exciting work here, and
whether eccentrics, earlyeccentrics, or, or tools like
blood flow restriction canaddress the metabolic cascade
of, um, of post operative muscleatrophy.
(19:49):
Which, which is great.
And, um, you know, the, theinternet, social media has, uh,
shamed anyone that has said theword ICE in the last eight
years.
So, um, you know, so it's, it'sgood to see, you know, and we
try to tell everybody, it'slike, this is a very simplistic
viewpoint that we're havinghere.
There's pros and cons toeverything, right?
So it's good to hear that thereis, uh, you know, some
(20:10):
beneficial use of ICE because,you know, we, we still use it
for some of its pros and, and,and, you know, I've taken it
away at other points as well,but I love that.
Um, you know, one, one thingI've always kind of educated and
I'm, I'm curious from yourperspective, you know, maybe if
you can tell me if I'm barkingup the right tree, if I'm doing
this right.
But, um, we've kind of shiftedto the same thing, some
cryotherapy beforehand for thesame reasons.
(20:31):
And then, um, um, we use NMESwhen a person is having a very
difficult time with volitionalcontrol.
But as soon as they tend to havevolitional control, we then
almost switch to biofeedback totry to get them to have better
control.
Um, am I doing that well?
Should I do anything differentor, or better?
What, what do you think aboutthat thought process?
(20:52):
If you're using EMG biofeedback,then you can't use them at the
same time, right?
The NMES would saturate thesignal.
So you don't have to discontinueNMES.
And some people would say thatyou shouldn't for, for many
months after surgery.
But you do want to apply bothinterventions.
So, um, NMES units at this pointare pretty affordable.
(21:15):
Send them home with a patient.
At our clinic, we send NMESunits home with people who are
post op.
We have them do it twice a day,uh, during their, during their
Therax home exercise program.
Um, and then bring it back forfor clinical sessions.
Um, and and biofeedback isharder to recreate in many cases
(21:37):
at home.
So, um, you can you can use yourtime in the clinic with the
patient to focus on that.
You really, I think, want tothrow everything you you can at
them.
So Makes sense.
I like, you know, in the sportsworld, I like that approach,
right?
Like, there's, you know, whynot, right?
We want, we want to get these,these people better as fast as
possible.
So, awesome.
Well, throw everything you canthat's evidence based, I should
(21:57):
say.
Yeah.
I like that.
Good answer.
I like that.
Alright, so tell me now, howwould your perspective change
here?
Now we have somebody, let's sayit's a few months out, or more
than a few months out I shouldsay, chronic persistent
weakness.
Maybe they don't have pain andswelling at this point, right?
Because I think if they do havepain and swelling, we'd probably
still use the same thoughtprocess to an extent.
(22:19):
But now this is the person thatcomes to your clinic.
Right there a few months out,maybe they did rehab elsewhere.
Maybe, maybe something happened,whatever, but they're still
super weak, have terriblevolitional control.
What do you think is going onhere now in this chronic setting
and how would your interventionschange for that person?
Yep.
So from, again, the naturalhistory.
(22:40):
You're now getting months out,the kind of catalyst of
inhibition being pain andeffusion are resolving.
Um, the nervous system isintegrating this change and, uh,
what we see in now systematicreviews is that people farther
out have cortical driveninhibitions.
So the muscle activationfailure, the muscle weakness.
(23:02):
is more associated with what'sgoing on in the brain than
what's going on in the spinalcord.
Um, and for that reason, you canprobably discontinue
interventions that target thespinal cord being cryotherapy or
TENS if you're using that andfocus more on interventions that
would address the cortex, um, orthe, or the top down control.
So for that, you're going toapply biofeedback, you're going
(23:23):
to apply NMES still if it'sappropriate.
Um, and you can do things like,like eccentrics, eccentric
overload, because that, uh, islike a throw everything you have
at this from a neural standpointto try to control that
eccentric, um, contraction.
Uh, so that's, that's reallythe, the big changes there, um,
when, when you're looking at,uh, longer, longer out is you
(23:46):
just say that the spinal levelcontrol or the spinal level
interventions are probably lessindicated now.
Um, that being said, we don'tknow when you look at a patient
in the clinic, what's going onin their nervous system.
That's one of the limitationsof.
of applying any of theseinterventions in the first
place.
You're kind of just looking atthem and where they're at in the
(24:06):
recovery and, and, and assumingkind of what their neurological
activation might be.
Um, and I've seen anecdotes andvideos on, on Twitter and
LinkedIn and stuff of peoplesaying, Hey Dave, this person's,
you know, six months out ofsurgery.
I iced them and their strengthwent up 20%.
So.
whether that single individualstill had spinal level
(24:27):
inhibition, it's, it's hard tosay.
We can't know.
So look at the patient in frontof you.
Um, a lot of times if you dothis like pre post intervention,
like just film their musclecontraction or get a, get a MVIC
before and after anintervention, you'll know
whether or not it's having aneffect.
Um, just that, that simple likeAB test pre post.
(24:48):
And if it doesn't, then youdon't have to do the
intervention.
If it does, then you should useit.
And to me, that's actuallyamazing advice for so much we do
in our profession right there.
That's the, you know, the assessreassess model that sometimes a
lot of people just forget about,right?
You know, they're so tied upwith, you know, what they want
to do and what's next that theydon't, they don't, they don't
look at basics like that.
(25:09):
So I think that's fantastic.
So, um, Dave, awesome stuff.
This is going to be superhelpful for clinicians that I
know that this has helped me,right?
You've, you've taught me somestuff on this and obviously
reading your, your article andyour past.
Stuff that you've published hasbeen great.
So I'm going to put some linksin the show notes to some of
Dave's work, especially this,this current article that we're
talking about, because I thinkit's a, it's a really important
(25:31):
one that hopefully will have animpact on our professions for
some time and hopefullystimulate people like Dave to do
more and more research in thisarea so we can get to the bottom
of this.
Right.
Um, but Dave, before I let yougo.
Quick high five at the end, fivequick questions, five quick
answers.
Just kind of want to hear alittle bit more about you teach
everybody a little bit aboutyour thoughts here.
But first question, what are youcurrently doing?
(25:52):
And like this question is neverfair, basically to the PhDs, by
the way, because you guys havevery finite topics you're
working on, but what are youcurrently working on for your
own professional developmentright now?
Um, yeah, that's a goodquestion.
So I, you know.
And changing in the midst ofchanging populations of
(26:12):
interest.
I worked my PhD at ACLreconstruction.
Now I study neo osteoarthritis.
I did a postdoc in between abouttechnology development for, for,
uh, patients with, with, uh,neurologically driven muscle
inhibition after stroke.
Um, so I'm just kind of learningand trying to, to find
consilience in the literatureand in the nervous system about
(26:34):
what's going on.
Um, one of the multipledifferent avenues for driving
muscle inhibition and whatapplies to which interventions
when, um, I'm also trying tolike, enjoy the postdoctoral
period and that I'm not afaculty member and just relax a
bit, which is, which is new forme.
So, um, you know, read, read afew books here and there and,
(26:55):
uh, and just enjoy time withfamily.
So.
I love it.
Yeah, you put your work in thelast 15 plus years.
Uh, it's, it's, it's time tospend a little, little time for
yourself.
I love it.
Thanks for recognizing that.
Yeah, absolutely.
You got my support.
But, um, what, what, what's onething you've recently changed
your mind about?
I think that, that no one iscoming to help me translate my,
(27:19):
my research, um, and that's likeruns counter to being on this
podcast.
So thanks for inviting me.
But what I mean is like in theacademic world and in physical
therapy research specifically,um, we call it like we have
researchers and we haveclinicians.
And what the way they wouldtreat this in industry is they
(27:39):
would have a research anddevelopment department, right?
Right, and there's nodevelopment in academic
research.
So when I publish something it'sup to me to market it and
disseminate it Um to teach andengage with clinicians, uh and
to innovate and like develop thetechnology that's going to make
the difference Or else we'restuck with that same like 17
(28:00):
year gap between us publishing astudy and clinicians Um, you
know, picking it up and applyingit, right?
I'm not, I'm not placing theblame on anyone.
I think it's just like this hugedisconnect between our worlds.
In industry, when you look attechnology and like, especially
artificial intelligence rightnow is a hot topic.
(28:20):
They have the development sideof things, like they're paying
people.
They have people.
And, uh, and I think that thatjob, as far as I can tell, falls
on me, if I'm, I'm in academia,so.
That's right.
That's, that's why research andacademia go so well together.
You do the research, then you,you put it into everybody's
mind.
So, you know, no pressure, butlike you've got to make sure you
(28:41):
have good methodology and, andyou're doing a good job.
You're not giving falsemisinformation out there to the
students.
Yeah, well, that's, and that'strue.
So the development part ofthings is if you have to, if I
have to take my research and putit into a technology that people
will adapt, adopt.
They need to actually see thatit works, right?
So if my research is flawed, thetechnology will never work.
(29:02):
It's a nice kind of litmus testto see, you know, is it, is it
worth it?
For sure.
Can, can my research interestsbe actually marketed and
translated to, um, to theindustry?
Yeah.
Awesome.
So that's one thing I'mrealizing.
Yeah.
What's your favorite piece ofadvice you love to give, uh,
students?
Um, I just talk to people,people want to talk to you, if
(29:24):
you have a question, read anarticle, reach out to them, um,
say hello, introduce yourself,uh, talk about a problem you're
working on, um, and yeah, andthis is a great profession,
it's, it's done a lot of greatthings for me, and, um, yeah,
network, connect, don't beafraid.
I love it.
I think Dave just gave you alla, uh, open invite to email him,
(29:44):
by the way, but I didn't, Ididn't want to say it, but yeah,
you can go on our website.
You can, you can, anyone canjust click a link and schedule a
video call with me to talk aboutany AMI interventions.
That's, that's, that's amazing.
That's pretty much what I didfor this podcast episode.
So yeah, it pretty much worked.
That's how Dave and I met, but,uh, awesome.
Uh, what's coming up next foryou, Dave, I know you've alluded
(30:06):
to some new research, but whatelse you got brewing?
Um, just focusing on familytime.
I think, like, I just had a son,uh, about four months ago.
So I have some, some jobapplications out for faculty
appointments.
Uh, it's kind of the season forthat.
So we'll see if anything,anything hits.
And in the meantime, just, uh,continue the postdoc grind.
(30:28):
That's amazing.
Uh, I'll put some info in theshow notes, but where can people
find out more about you and yourwork?
I'm on X and LinkedIn, and thenpeople can go to live4pt.
com to check out some of theblogs I have on these topics, or
as I said, find a link toschedule on my calendar to meet
up and just problem solveclinical cases or whatever.
(30:52):
That's great.
I think you're the first personI know to embrace calling it x
by the way.
So, um, yeah, you know, Ifigured I'd go for it.
It's been a few months now.
I mean, it's, it's accurate.
So everybody else is wrongstill.
So yeah, I love it.
That's, that's, that's what,that's what makes you, you Dave.
I like that.
Awesome.
But But Dave, thank you so much.
This was awesome.
Love sharing your stuff.
(31:12):
Love learning from, from some ofyour research.
So please check out Dave andsome of these, um, these great
topics that he's working on andtake them up on that offer.
He, he wants to talk to you and,and, and, and help.
So anything you can do.
So, um, thanks again, Dave.
Thanks for coming on the podcasttoday.
Cool.
Yeah.
Thanks Mike.
Thanks for having me.
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