February 6, 2025 • 36 mins
What does pre-stroke neurological health have to do with swallowing prognosis, post stroke?
In this episode, Dr. Janina Wilmskoetter, Assistant Professor at the Medical University of South Carolina, discusses her recent publication, Cerebral Small Vessel Disease is an Independent Determinant of Dysphagia After Acute Stroke. Join us for insights into clinical implications for patients with dysphagia!
For questions, reach out to Dr. Wilmskoetter at wilmskoe@musc.edu, and access the article via https://www.sciencedirect.com/science/article/pii/S2213158224001517
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Speaker 1 (00:00):
Today's episode is sponsored by Braco Diagnostics,
the manufacturer of Verabarbarium sulfate products, the
only FDA-approved bariumproducts for the modified barium
swallow study.
Learn more at Braco.
That's B-R-A-C-C-O dot com orVerabarMBScom.
Welcome everybody.
This is Dr Janina Vimskota.
She's an assistant professor atthe Medical University of South
(00:22):
Carolina and you can't see her,but she's laughing at me at my
production of her name becauseI'm trying so hard and
apparently it's not good enough.
Janina, is that right?
Speaker 2 (00:31):
Nor is it just too perfect.
It was fantastic.
Yeah, I love it, even betterthan the German pronunciation.
Speaker 1 (00:39):
Even better.
I'm trying so hard, Trying sohard, trying so hard.
But Janina, she works as aresearcher, an instructor and in
the clinic in an acute careclinic at the Medical University
of South Carolina.
We recently recorded an episodewith Julie Blair, who also is
at the Medical University ofSouth Carolina, so check that
one out too.
But that's not why we're heretoday, Janina.
(00:59):
Why are we here?
You published something.
Tell me about it.
Speaker 2 (01:03):
I did.
It just came out actually.
So it's an article that'stitled Cerebral Small Vessel
Disease is an IndependentDeterminant of Dysphagia After
Acute Stroke.
I had to read this right now.
It's not that I remember thatby heart.
Speaker 1 (01:17):
Yeah, so then there are a lot of words.
So Cerebral Small Vesseldisease is an independent
determinant of dysphagia afteracute stroke.
So I'm guessing that's what youfound.
Just a guess.
Speaker 2 (01:30):
I learned, like from a professor, like if the title
is a question and it's very,very likely that they didn't
find what they were looking for,and here we already give the
answer.
So you actually don't have toread the article.
If you don't have time, justread the title.
Nice, not even the abstract.
You don't have to read thearticle.
If you don't have time, justread the title.
Speaker 1 (01:46):
Nice, not even the abstract.
You don't have to dig that.
No, no.
Speaker 2 (01:49):
Just the title, yeah.
Speaker 1 (01:51):
We've got a lot of names of people on here who have
worked with you Bonnie MartinHarris I recognize that one.
Yeah, no, this is fantastic.
It looks like a collab betweenthe University of South Carolina
Northwestern and the MedicalUniversity of South Carolina.
Speaker 2 (02:06):
Yeah, I was lucky because when I did my PhD at the
Medical University of SouthCarolina years ago, dr Heather
Bonilla, leonardo Bonilla andBonnie Martin Harris were on my
committee.
So I was really, reallyfortunate, and this data that
(02:27):
I've analyzed was actually partof the patient data that I
collected at that time.
It's expanded out of it.
Speaker 1 (02:30):
So, yeah, very cool, very cool.
So it's a very an interestingsubject and, as I was looking
through it, I like the fact thatit not only looked at like new
stuff.
You know, someone has a stroke.
You're looking at these peoplewho had their first stroke, but
you're looking at all of thesepremorbid indicators.
So I'm very curious about whatprompted you to do this.
(02:52):
What was going through yourhead?
Speaker 2 (02:55):
Right, this is a really good question.
It's like oh, there are nicepictures in the article, but why
do we need this?
So I worked as a clinician manyyears in acute care and my
passion is like stroke, soneurological injuries.
And when I worked as aclinician and still do there can
(03:16):
be like two patients with thesame stroke lesion location.
So on paper they look prettythe same, but then you walk into
the room and they presentreally differently.
One patient has dysphagia, theother one doesn't really present
with dysphagia.
And my prior work in mydissertation looked at how much
can we understand from thelesion location, lesion size etc
(03:40):
.
To predict what swallowphysiological impairment is
there.
So my entire dissertation wason let's look at the lesion
location and see whatimpairments are correlated with
this.
But in clinic, to some degreewe can use that information.
But then we see these patients.
Well, they have the same lesionlocation but they present
(04:00):
differently.
So there must be something elsethat contributes to why some
patients present with moresevere or with no dysphagia.
And there are of course lotsand lots of different factors.
But one factor that weunderstand from our recent
literature overall in strokeseems to be the brain health
(04:22):
before the stroke.
So how healthy is the brain thatthen gets an injury and that
has been looked at in otherstroke functions like language,
so aphasia or motor recovery,and there seems to be really
good correlation that it is acontribution of like how healthy
(04:43):
you go into the stroke.
What kind of makes sensethinking also about analogies
like if you have pneumonia in apretty healthy lung, that's
probably not as damaging ordetrimental compared to someone
who already has COPD or otherdamage to the lung then gets
(05:05):
pneumonia on top of that, thisperson will probably struggle
more in terms of the severity orrecovery.
And that's what this brainhealth term tries to get at when
we think about like a brain canbe structurally more healthy or
more diseased, but also thiswill turn also into the function
that the brain can bestructurally more healthy or
(05:25):
more diseased, but also thiswill turn also into the function
that the brain can produce.
So that's kind of the idea Ifthings can explain, or help us
explain, how someone presentsafter a stroke that relates to
their brain health before thestroke.
Speaker 1 (05:42):
And you do a great job at explaining that.
Like I feel like I'm followingright along and so that brings
me to like if you're workingwith someone with pulmonary
issues and has dysphagia, thereare things like you mentioned
COPD that you look for.
So you look in their medicalhistory.
You'll look in the chest x-rayor chest CT reports to get a
(06:04):
better idea of some of thosechronic issues that may impact
their, their healing andrecovery.
What types of things did youspeculate or what types of
things did you look into thatwould be similar markers for
neurological health?
Speaker 2 (06:18):
oh yeah, so for, and of course, there's not like one
definition of like this is howwe should measure brain health.
Speaker 1 (06:27):
It's a healthy brain.
Looks like this Healthy brain.
Speaker 2 (06:29):
Like so what is a healthy brain?
And hey surprise, everybody hasa different definition for that
.
And then we took a definitionthat has been more recently used
, also in like standardradiology guidelines, and this
is small vessel brain disease.
This is just one marker how thebrain structure changes over
(06:51):
time with age.
Other functional definitionscould, for example, be, I don't
know, intelligence right.
Is that maybe a marker forhealthier brains, someone who is
more intelligent?
But how do we measureintelligence?
So we can like have thesediscussions.
We only looked at structure inthe brain, and cerebral small
(07:13):
vessel disease is one markerthat is like a standard measure,
and you will see that in yourMRI reports of any patient that
you have in the hospital who gota brain MRI and often it's
something worded like T2hyperintensities or unspecified
(07:35):
T2 hyperintensities, likelycerebral small vessel disease.
So this is like kind of theterminology that you will see.
But the big thing is that basedon that, you normally don't get
information on how severe isthat.
Is that just really mild?
Is that something I should careabout?
(07:55):
Sometimes you might seeexpressions like atrophy in the
MRI, but the interesting thingthat when I started with this
research is that there's a hugevariability, huge variance about
how a brain ages Kind of makessense, but I never like
translated that.
Yeah, the brain as well, andsome of the normal, normal
(08:19):
things that happen when we getolder, no matter if there's an
underlying disease or not, isthat?
Yep, our brain atrophies, sothe gray matter, white matter,
shrinks and that'scounterbalanced by an increase
in cerebrospinal fluid andthat's what we term atrophy.
So, yes, we all go through that, no matter how healthy or
(08:42):
unhealthy we are.
But the crux to that is thatit's very variable.
So two people who are 80 yearsold can have a very different
degree of atrophy.
So one person might have severeatrophy and the other person
doesn't.
And I think you can againtranslate that to someone who's
(09:05):
80 and really active.
I heard some people still run,like I don't know, half
marathons a minute.
It's probably not going to be me.
But there's, a huge variance oflike how people age, and that's
the same idea with a brain ageand that's the same idea with
(09:29):
the brain.
So cerebral small vesseldisease is a term that
encapsulates like many differentstructural pathologies in the
brain.
Atrophy is one, microhemorrhages, so like little tiny
bleeds in the brain, and thenanother marker of cerebral small
vessel disease is somethingthat's called white matter
hyperintensities, and it'sexactly what the name says.
When you look at a brain scan,a specific brain scan, that's T2
(09:51):
or flare, they look just reallybright because these are areas
that look white compared to theother tissue and we can go more
into what that might be.
And then also something likecalled perivascular spaces, and
these are just spaces around thearteries that perforate the
(10:11):
brain.
So, as you can imagine, sothese spaces around the arteries
, they are filled with fluid andthe larger they are, they take
up more space in the brain andit seems to be a marker that the
brain might not be as efficientto drain some of the dust or
the debris in the brain tissue.
(10:33):
So all these things are likedifferent markers that the brain
has several small vesseldisease.
So to the small vessels in thebrain, that they are not
functioning as well as theymight did when we were younger.
But the thing is really likehow much does a person have that
?
We're probably all going tohave it at some point, but some
(10:55):
people will have it more thanothers.
And these are findings that aretypical incidental, so you
don't know that you have thatuntil you get a brain scan.
Incidental, so you don't knowthat you have that until you get
a brain scan.
I was like, oh wow, there's alot of white matter, hyper
intensities, and so, while it'snot something that you feel from
one day to the other, it issomething that probably
(11:15):
contributes over time tospecific functions like
swallowing or memory, becauseit's one of the major
contributions to also peopledeveloping dementia.
Speaker 1 (11:26):
Yeah, so I know people who are listening to this
, probably in their car and in aplace where they can't really
like sit down and look at adiagram, but this article is
open access and I would highlyrecommend taking a look at some
of the images in here.
These are fantastic.
So the comparison so you weretalking earlier about the
increased volume ofcerebrospinal fluid, that kind
(11:48):
of compensates for the brainatrophy, like you get brain
atrophy, and so the parts ofyour brain let's I don't I want
to say that matter, but thatmaybe that makes us smart or
healthy?
Speaker 2 (11:58):
Gray matter and white matter.
Tim, Was that a pun?
Speaker 1 (12:08):
There you go, that matter.
No, it it yeah.
Yeah, sure it was.
I guess I'll pretend that itwas, but so you know, as you get
atrophy of those, then you getmore cerebrospinal fluid in
there.
So figure two is super cool.
There is patient one, 68 yearold female 0.25 liters of
cerebrospinal fluid.
And then patient two, also 68year-year-old female, was a
little over twice that.
You can tell the difference.
This is so interesting.
(12:30):
So if you get a chance, take alook at figure two.
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Speaker 2 (12:46):
And you know I've never learned as a
speech-language pathologist tolook at MRIs, right?
So I was fortunate to learnthat during my PhD and postdoc.
But it is also interesting thatthe people or the patients that
we included in the study, theyall were pretty clean cohort.
(13:07):
So, first ever ischemic stroke.
We excluded anyone with, like,prior diseases that could relate
to dysphagia.
So no neurodegenerativediseases, no head and neck
cancer, no other stroke beforethat, no TBI, right?
So all these these like typicalthings.
So these are supposedly peoplewho were healthy before they had
(13:30):
the stroke.
But again, all this, what wesee in these like examples, were
pathologies that were therebefore the stroke.
So it's not something that'srelated to the stroke because
these patients were acute strokepatients.
It was something that was therealready before the stroke, but
again, not something that wasapparent because it didn't cause
(13:52):
acute symptoms.
Speaker 1 (13:54):
Yeah, and maybe not even something that people would
recognize symptomatically overtime.
So like if you're interviewingsomeone's family, you'd be like,
well, did they have dementiabefore this?
They might not have anyindication of memory loss, so
you might not get it withoutthis imaging.
Speaker 2 (14:11):
Yeah, correct.
And I mean it's not somethingthat we would.
I think it's like human nature,right, If we don't feel
limitations, not functional loss, so why should we look into
that, right?
Sure yeah.
Speaker 1 (14:23):
Well, that's fascinating to see where that
kind of comes to bite you later.
For sure, yeah, so as aclinician, because you worked as
a clinician for a while beforegetting your PhD.
Is that right?
Speaker 2 (14:36):
Mm-hmm.
Yes.
Speaker 1 (14:37):
So I figured this was pretty clinically driven.
What are some of your takeaways, Like how do you think you're
going to use this from now on?
Speaker 2 (14:43):
Yeah, great question.
So what is always the bestquestion I got as a researcher
right?
Well, it's great research.
But so what?
I think it helps me as aclinician when you do a chart
review and we do that thoroughly.
I think we are used to lookingthrough like doctor's notes.
We look at chest imaging, weread the notes from the MRI or
(15:07):
CT, what we have.
I hope it helps to get a betterhypothesis of what you might
see when you walk into the room.
And I think it's also wehaven't proven that yet, knock
on wood that this research iscontinuing, but it will likely
be a marker for recovery as well.
Speaker 1 (15:27):
That's what I was going to.
Prognostic indicatorpotentially.
Oh wow, there you go.
Speaker 2 (15:32):
There we go.
So we showed that in aphasiaactually so language disorders
after stroke that patients withworse brain health, measured as
cerebral small vessel disease,had worse potential to recover
despite treatment.
So, and that's controlling fortheir chronological age.
(15:54):
What's really fascinating?
So it's not the chronologicalage, it's really the brain age.
So how healthy is the brain atthe time they receive treatment?
And so if you walk into a roomand patient presents with
dysphagia, then it's always thequestion of doctors hey, so do
(16:18):
you think this patient recoversor do we have to think about
putting a feeding tube inbecause we really want to
discharge this patient?
And then, as a SLP, I alwaysfeel like I wish I had an answer
, but why don't I have an answer?
And I think this is a factorthat comes into play that we can
say, yeah, okay, so the strokelocation.
We know this will lead towhatever severity of dysphagia.
(16:41):
That's what we're going to seeat bedside.
And if we have an idea of thepatient's status before their
stroke how healthy were they,how healthy was their brain
before the stroke this can helpus to say, oh, the chances are
actually really good for thispatient to recover because they
had a pretty good brainstructure before that.
(17:04):
So that's, I think, lends toour discussion, tim, about the
reserve that someone has torecover.
So how much capacity does apatient bring to, for example,
the brain for the brain toreorganize after a stroke?
So what we know from dysphagialiterature and Shaheen Hamdi I
(17:26):
love his research and his grouparound that brought us a lot of
knowledge that after dysphagia,after dysphagia in one
hemisphere, the other hemisphereis likely to help a lot in
recovery and also like areasaround the stroke.
But imagine if those areas thatwere not affected by the stroke
but are supposedly to help withrecovery if they are not
(17:49):
healthy, then the brain won'thave the same capacity to
reorganize or regain thatfunction compared to a brain
where these unaffected areaswere pretty healthy and had a
lot of white matter connections,had a really good volume of
gray matter.
So we're just like there aremore neurons that can change.
(18:11):
I hope that made sense.
Did this make sense?
Speaker 1 (18:15):
Somewhat.
No, no, you're making sense,but my brain's also going in
different directions withquestions and I'm like I'm
afraid to ask these questionsbecause I should probably know
some of these answers and likeit's probably already been
studied before.
Well, who knows, who knows, Iguess I got to put myself out
there some, but I mean I'mthinking of so as I understand,
kind of what you're saying, andI'm also I'm looking at another
one of these beautiful images.
It is figure four.
(18:36):
So this is cool.
Figure four has it highlightedthe corticobulbar tracts in the
right and left hemisphere, goingover from the motor cortex down
toward the brainstem, and itshows different lesion sizes and
different lesion locations andon this it's showing some of
them, basically, uh, the lesionscovering where the
(18:57):
corticobulbar tracts would be.
And so, as you're talking aboutthe recovery, like the, so say,
if the left side is affected,the health of the as I
understand what you're sayingthe health of the right side of
the brain and its ability tokind of take over some of these
functions.
Well, I mean, the premise beingis that it will help to
compensate, and the healthier itis, the better it's going to be
(19:19):
able to compensate, right,that's what I'm getting.
So I'm thinking about all thesepoor folks with spastic
dysarthria who they have likebilateral damage to the
corticobulbar tract.
I'm so sorry and so likethinking of that as a prognostic
indicator.
I'm sure there's probablyresearch out there that says
that, that I should know, that Idon't, don't know enough about
at least and tim.
Speaker 2 (19:37):
Let me plant a seed for the audience, because I saw
that you had the post aboutdysarthria, and dysarthria are
not my strengths, though I lovethe post that you included in
your instagram, I think oh,thank you.
Speaker 1 (19:51):
Yeah, no, I I've been .
Dysarthria has been veryinteresting to me, of the
various types of dysarthrias,and I was very fortunate to be
able to start teaching thiscourse at the University of
Hawaii.
But it's not.
Unfortunately I didn't get togo there, it's remote, but I
learned so much.
So Dr Kendrea Grand, as you canimagine, has a very robust
(20:15):
dysarthria course or motorspeech disorders course put
together and so she sent me hermaterials and I got to look
through them and get some otherthings.
But I learned so much goingthrough that and just like the
parallels with dysphagiatreatment, the upper motor
neuron or bilateral upper motorneuron lesions causing
spasticity, and how you mighttreat that differently than
(20:35):
somebody who has a lower motorneuron lesion and I.
The analogy I use is likeyou've got a cord coming from
your power outlet going to alamp and someone just cuts the
cord Like it's not getting poweranymore.
So just the flaccidity, theweakness, that type of thing.
But so you see, like I can seeso many parallels between this
and dysphagia.
So it's just like my world hasbeen blown up in that
(20:57):
perspective lately.
Speaker 2 (21:06):
So I think it's, I just think it's super cool, I
very much, and I because mybackground is also like in
aphasia.
So language disorders I oftencompared also like how is
recovery working in aphasia,compared to dysphagia,
dysarthria, and I think what isreally striking is like how much
in these functions do bothhemispheres contribute?
So we know that the typicallanguage organization in the
brain is heavily towards theleft side of the brain.
(21:28):
In those typical people, righthand, dominant etc.
The right hemisphere is alsoinvolved in language processing,
but not as much More like inthe ventral stream.
So semantic processing etcetera, with swallowing in
comparison and speaking.
We know it's a bilateral neuralnetwork and it's less
(21:50):
lateralized.
So language is a heavilylateralized function, swallowing
not so much.
So both hemispheres contribute.
And how I think about it isit's actually great when it's
really organized in bothhemispheres because that means
there's one hemisphere, theredundancy.
(22:11):
Exactly so.
If you have an injury, then theother hemisphere, because it
already contributes to thatfunction.
It will be easier for thehemisphere to okay.
I'm just going to do a littlebit more.
I already have theseconnections, I already kind of
know what I have to do.
In comparison to something likelanguage that's heavily
lateralized to the left, theright hemisphere does a little
(22:32):
bit, but not as much.
So that's why the oralhemisphere and language has a
more difficult time tocompensate.
So we don't see that as muchand the areas around the stroke
are more contributing inlanguage for recovery.
And that's why it's interestingwhen you pointed out the figure
four, I think long, long timeyou always think okay, brainstem
(22:55):
is swallowing rightCorticobulbar tract.
That's really, really important.
We know that and lots of thosestudies that look at recovery
also look at corticobulbar tract.
Makes sense.
Speaker 1 (23:05):
Oh, and real fast.
Just I don't want to assumeanyone knows anything.
Corticobulbar tract the motorneurons coming from the cortex
to the brainstem.
So I think corticobulbar iscortex to brainstem,
corticospinal is cortex to spine.
Speaker 2 (23:18):
So for motor neurons, yes, thanks, tim, that's right.
Speaker 1 (23:22):
I mean, you probably didn't know that either, but I'm
just showing off.
You just study it for a living,yeah.
Speaker 2 (23:30):
I was told, so I lost my train of thought.
Speaker 1 (23:32):
No, oh, dang on, I'm sorry.
Speaker 2 (23:34):
In this figure.
So corticobulbar tract, and inthe study that we did with a
cerebral small vessel braindisease, we controlled for the
stroke damage to these importanttracts, corticobulbar tract.
So we just wanted to make surethat we can like isolate the
contribution of the cerebralsmall vessel disease, no matter
(23:54):
how much or how little thecorticobulbar tracts were
lesioned, no matter how largethe stroke is, no matter how old
someone is, et cetera, etcetera.
And from some other literaturewe also know that, yeah,
corticobulbar tract is important, but that's not the only
connection the cortex has to thebrainstem.
(24:15):
What is also really reallyinteresting and I hope that some
neuroscientists who can do muchbetter work than I can do, will
tell us a little bit more aboutthat in their future research
so what other tracts than thecorticobulbar tract can we maybe
stimulate through electricalstimulation or whatever?
That could then even compensateif the corticobulbar tracts are
(24:37):
damaged.
Speaker 1 (24:38):
That's super cool.
It's like cracking open a wholeother pathway for dysphagia
rehabilitation.
That's super neat.
Speaker 2 (24:44):
Pathway Again.
Speaker 1 (24:46):
A pun Tim oh see, it's above my head over my head.
I'm going to have to listen tothat again and be like all right
, I got to learn from thoseaccidental puns.
So you were comparing the ideaof of language dominance, which
is typically more isolated toone hemisphere than the other,
at least relative to swallowing,and so that I guess the kind of
(25:10):
a question I'm going to throwback at you right, that is, if
we're also understanding thecranial nerves that are involved
in swallowing and the uppermotor neuron tracks that
eventually lead to these cranialnerves.
And the ones that I and thisoversimplification, I'm sure the
ones that I look at primarilytrigeminal, five, facial seven,
glossopharyngeal, nine, lessfrom a motor perspective, but
(25:32):
vagus 10 and then accessory yeah, hypoglossal, I was going to go
, I kind of accessory, yes, yes,of course, but I'm going more
like direct, but, yeah,hypoglossal, I was gonna go, I,
I kind of accessory, yes, yes,of course, but I'm going more
like direct, but, yeah,hypoglossal.
So, knowing so, I think so many,we learn that like, okay, brain
, right hemisphere controls theleft, left hemisphere controls
the right, but knowing theimportance of which one of those
(25:54):
, which of those cranial nervesare also bilaterally innervating
?
You like the face like thefacial nerve, especially the
upper face.
You get bilateral innervationfrom that.
So in looking at and trying tohypothesize imaging to function
and that sort of thing, just theimportance of knowing which of
those nerves provide bilateralinnervation.
Speaker 2 (26:14):
Yeah, that is so interesting, right.
And then the hypoglossal nerveagain hypoglossal nerve.
It's always so fascinating tome that some people naturally
have a really prominentbilateral representation and
some people have it moreunilateral.
So that's why, you see, in somecortical stroke patients some
(26:35):
have a tongue deviation andothers don't, because there's
like this mix, oh yeah.
Yeah, exact physiological mixLike I don't know's like this
mix.
Yeah, exact physiological mixlike I don't know.
Tim, do you have it bilateral?
I hope I do, but we don't knowyeah, I don't know.
Hopefully we won't ever find out, but yeah, we'll see and I
think for dysphagia, cranialnerves are so important and they
give us so much information atbedside to then come up with
(26:56):
hypotheses.
And again, a shout out to drgarland who has so much
knowledge about this and has somany great educational platforms
to help us understand that indysphagia, I think what we then,
taking it a step further, oftenalso need to consider is, of
course, the coordination piece.
(27:18):
Right, so cranial nerves tellus, like the information
directly to the muscles, can welike switch this on off?
But it doesn't tell us if themuscles work in synergy, because
that needs to be controlled byother areas in the brain that
are not, that are not thosecorticobulbar tracts that give
rise to the nerves, and I thinkthat's then, of course, always
(27:41):
the interesting piece.
It's like, okay, they don'thave cranial nerve damage, but
present with severe dysphagia,yeah, because there are other
areas in the brain that helpwith this coordination piece.
Speaker 1 (27:53):
Like the extrapyramidal system, the basal
ganglion cerebellar controlcircuits.
Speaker 2 (27:58):
Exactly.
Speaker 1 (28:00):
And those are so complicated.
Oh yeah, like I, oh yeah,there's just I'm just scratching
the surface with those there's.
To me they appear so much morecomplicated than just the direct
activation pathway or the, youknow, the corticobulbar and the
corticospinal.
Speaker 2 (28:16):
Right, yeah, I think that's why many researchers or
many studies, and we as well,look at the corticobulbar tract
because it's kind of like, okay,I get it, I get it, but yes,
there are many other areas inthe brain and circuits are
contributing to swallowing that.
Speaker 1 (28:32):
That's cool.
That's cool, I'm having fun.
I'm having fun.
This is why I do the podcast,like I learned so much, and just
have fun conversations.
I mean, this is one reason whyI do the podcast.
The post-production editing,that's a whole different story.
But this is this is I'm happyas a clam, happy as a clam,
right now.
Speaker 2 (28:50):
I am so thrilled that I can talk here today because
I'm kind of a fan girl of yourpodcast, so thanks for having me
.
Speaker 1 (29:00):
I appreciate it.
No, this is so.
Janina and I met at the hard toswallow catalyst for change in
dysphagia management conference.
It was two years ago.
That was a great year.
I think that was the biggestturnout that we had.
That was so much fun.
Don't know the date for thatyet and that's done through
Rocky Mountain University, notthrough, not through, gap
education, my company.
But oh, there is a plug though.
(29:21):
There is a plug real fast.
I got to take advantage of this, of this.
You're talking about dr kendriagarant and her marvelous work
on cranial nerve stuff.
So in march we are going tohave, or we're planning march
either early march or late marchto have a three-hour webinar
with her to really dive intothat stuff, hoping to record it
too.
So mark your calendars, keepthat open.
Speaker 2 (29:41):
No, you know I'll be there, yeah.
Speaker 1 (29:45):
Well, we'll all be there, right, where are you
going to be?
So, anyway, that's that, butnot to sidetrack us too much.
We talked about why you didthis study.
Why do we care?
Why should we care?
The clinical translationcerebral small vessel disease is
a standard measure of healthpotentially related to the brain
.
What do you think are some ofthe limitations of the study?
Speaker 2 (30:11):
Like what?
Should we not read the studyand be like all right, this
means this now?
Yeah, thanks for that question.
So this study was a preliminarystudy, right, and I feel like
every study can be titled apreliminary study, because
always we want to do more.
So we only had 40 participantsand of course, the goal is that
we increase the sample size by alot and then continue also the
(30:34):
measures in a more sophisticatedway.
So what the readers will see islike, for example, the
perivascular spaces and whitematter hypotensities.
We scored them on an ordinalscale and there are way better
ways to do this in a morequantitative way.
So so take this with a grain ofsalt.
But was that right video?
(30:55):
Great, okay.
And so while we did a lot ofanalyses, only very, very few
survived in the end to bestatistically significant, and
even fewer survived after verystringent corrections for
multiple comparisons.
So it's the way that we need todo is that we don't think some
(31:17):
of our results are true, eventhough they might just be an
accidental finding or anartifact.
So the limitation is definitelya small sample size, and it
doesn't mean that just becausewe didn't find something that
it's not there.
I think that's what's important.
For example, we didn't find asignificant correlation between
(31:39):
these measures and oral total.
That was something I wasexpecting, so I was thinking,
okay, these aging factors.
I think what we often see islike oral control difficulties.
We didn't find that.
However, it doesn't mean it'snot there, right.
Just because it wasn'tstatistical significant doesn't
mean that it's not there.
(31:59):
So we have to just keep that inmind, that maybe our sample
wasn't big enough, maybe ourmeasurements were not as
sensitive as they should be.
So I think this is reallyimportant when you read that
study, to keep that in mind.
And I feel like that we asclinicians are not trained to do
(32:20):
these measures that we used inthe study right.
I think I had no idea whatperivascular spaces are before I
did this and absolutely no ideahow they would look like.
So it's going to be difficultfor clinicians to really know in
the patient that they see ifthese things are present.
But just really look at the MRIreport and look for these words
(32:44):
like unspecified T2hyperintensities likely related
to cerebral small vessel disease.
So I think that's myrecommendation Look for these
things and start like thinkingabout oh, this might mean that
the brain health of this patientwasn't as great to begin with.
Speaker 1 (33:02):
Yeah, did.
Speaker 2 (33:02):
I answer your question, Tim.
Oh, and more.
Speaker 1 (33:04):
Yeah, okay, that's great.
Oh, with yeah, did I answeryour question, tim?
Oh and more.
Yeah, okay, that's great.
Oh, thank you so much.
Is it anything else that youwant to leave listeners with?
Speaker 2 (33:13):
No, I think I feel like the clinical driven
questions are what is reallyimportant to me.
So if anybody else has clinicalquestions, I think that's the
way to go, that we should thenresearch to get more answers for
when we practice clinically.
Speaker 1 (33:28):
Good deal.
Good deal, and it looks likeyour email address is also
listed within this article, soif I put it out there, I don't
feel quite so bad.
W-i-l-m-s-k-o-e at M-U-S-C likemedical university of South
Carolina, dot E-D-U.
All right, cool.
(33:50):
Well, thank you very much,really appreciate it.
It's great to see you.
This makes me want to have youdo a three hour course after
Kendra, I don't know sometime.
So we got to talk about that,talk about that Hang out, and
maybe we'll get something going.
We'll see, but thanks againeverybody.
Dr Janina Wilmskota Right, okay, okay, I'm very self-conscious
(34:10):
of my pronunciation.
Speaker 2 (34:14):
Yeah, thanks so much, tim.
Speaker 1 (34:16):
Awesome, thank you.
That was Dr Janina Wilmskotadiscussing cerebral small vessel
disease as a predictor ofrecovery and dysphagia after
acute stroke.
You can reach her at Wilmskoe,that is W-I-L-M-S-K-O-E, at
(34:37):
M-U-S-C.
Dot E-D-U, that's M-U-S-C likeMedical University of South
Carolina, and there's a link totoday's article in the episode
description.
Don't miss our upcoming eventon February 23rd, swallowing
Cinema.
It's an MBS case study eventthat has been a staple at ASHA
for years and this year it'sfound a home with us.
Visit SwallowTheGapcom orSwallowTheGapcom slash live
(34:58):
courses to learn more.
Thanks for listening today andif you think we're helping,
please spread the word, takecare.
Today's episode is sponsored by Braco Diagnostics,
the manufacturer of Verabarbarium sulfate products, the
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That's B-R-A-C-C-O dot com orVerabarMBScom.
Welcome everybody.
This is Dr Janina Vimskota.
She's an assistant professor atthe Medical University of South
(00:22):
Carolina and you can't see her,but she's laughing at me at my
production of her name becauseI'm trying so hard and
apparently it's not good enough.
Janina, is that right?
Speaker 2 (00:31):
Nor is it just too perfect.
It was fantastic.
Yeah, I love it, even betterthan the German pronunciation.
Speaker 1 (00:39):
Even better.
I'm trying so hard, Trying sohard, trying so hard.
But Janina, she works as aresearcher, an instructor and in
the clinic in an acute careclinic at the Medical University
of South Carolina.
We recently recorded an episodewith Julie Blair, who also is
at the Medical University ofSouth Carolina, so check that
one out too.
But that's not why we're heretoday, Janina.
(00:59):
Why are we here?
You published something.
Tell me about it.
Speaker 2 (01:03):
I did.
It just came out actually.
So it's an article that'stitled Cerebral Small Vessel
Disease is an IndependentDeterminant of Dysphagia After
Acute Stroke.
I had to read this right now.
It's not that I remember thatby heart.
Speaker 1 (01:17):
Yeah, so then there are a lot of words.
So Cerebral Small Vesseldisease is an independent
determinant of dysphagia afteracute stroke.
So I'm guessing that's what youfound.
Just a guess.
Speaker 2 (01:30):
I learned, like from a professor, like if the title
is a question and it's very,very likely that they didn't
find what they were looking for,and here we already give the
answer.
So you actually don't have toread the article.
If you don't have time, justread the title.
Nice, not even the abstract.
You don't have to read thearticle.
If you don't have time, justread the title.
Speaker 1 (01:46):
Nice, not even the abstract.
You don't have to dig that.
No, no.
Speaker 2 (01:49):
Just the title, yeah.
Speaker 1 (01:51):
We've got a lot of names of people on here who have
worked with you Bonnie MartinHarris I recognize that one.
Yeah, no, this is fantastic.
It looks like a collab betweenthe University of South Carolina
Northwestern and the MedicalUniversity of South Carolina.
Speaker 2 (02:06):
Yeah, I was lucky because when I did my PhD at the
Medical University of SouthCarolina years ago, dr Heather
Bonilla, leonardo Bonilla andBonnie Martin Harris were on my
committee.
So I was really, reallyfortunate, and this data that
(02:27):
I've analyzed was actually partof the patient data that I
collected at that time.
It's expanded out of it.
Speaker 1 (02:30):
So, yeah, very cool, very cool.
So it's a very an interestingsubject and, as I was looking
through it, I like the fact thatit not only looked at like new
stuff.
You know, someone has a stroke.
You're looking at these peoplewho had their first stroke, but
you're looking at all of thesepremorbid indicators.
So I'm very curious about whatprompted you to do this.
(02:52):
What was going through yourhead?
Speaker 2 (02:55):
Right, this is a really good question.
It's like oh, there are nicepictures in the article, but why
do we need this?
So I worked as a clinician manyyears in acute care and my
passion is like stroke, soneurological injuries.
And when I worked as aclinician and still do there can
(03:16):
be like two patients with thesame stroke lesion location.
So on paper they look prettythe same, but then you walk into
the room and they presentreally differently.
One patient has dysphagia, theother one doesn't really present
with dysphagia.
And my prior work in mydissertation looked at how much
can we understand from thelesion location, lesion size etc
(03:40):
.
To predict what swallowphysiological impairment is
there.
So my entire dissertation wason let's look at the lesion
location and see whatimpairments are correlated with
this.
But in clinic, to some degreewe can use that information.
But then we see these patients.
Well, they have the same lesionlocation but they present
(04:00):
differently.
So there must be something elsethat contributes to why some
patients present with moresevere or with no dysphagia.
And there are of course lotsand lots of different factors.
But one factor that weunderstand from our recent
literature overall in strokeseems to be the brain health
(04:22):
before the stroke.
So how healthy is the brain thatthen gets an injury and that
has been looked at in otherstroke functions like language,
so aphasia or motor recovery,and there seems to be really
good correlation that it is acontribution of like how healthy
(04:43):
you go into the stroke.
What kind of makes sensethinking also about analogies
like if you have pneumonia in apretty healthy lung, that's
probably not as damaging ordetrimental compared to someone
who already has COPD or otherdamage to the lung then gets
(05:05):
pneumonia on top of that, thisperson will probably struggle
more in terms of the severity orrecovery.
And that's what this brainhealth term tries to get at when
we think about like a brain canbe structurally more healthy or
more diseased, but also thiswill turn also into the function
that the brain can bestructurally more healthy or
(05:25):
more diseased, but also thiswill turn also into the function
that the brain can produce.
So that's kind of the idea Ifthings can explain, or help us
explain, how someone presentsafter a stroke that relates to
their brain health before thestroke.
Speaker 1 (05:42):
And you do a great job at explaining that.
Like I feel like I'm followingright along and so that brings
me to like if you're workingwith someone with pulmonary
issues and has dysphagia, thereare things like you mentioned
COPD that you look for.
So you look in their medicalhistory.
You'll look in the chest x-rayor chest CT reports to get a
(06:04):
better idea of some of thosechronic issues that may impact
their, their healing andrecovery.
What types of things did youspeculate or what types of
things did you look into thatwould be similar markers for
neurological health?
Speaker 2 (06:18):
oh yeah, so for, and of course, there's not like one
definition of like this is howwe should measure brain health.
Speaker 1 (06:27):
It's a healthy brain.
Looks like this Healthy brain.
Speaker 2 (06:29):
Like so what is a healthy brain?
And hey surprise, everybody hasa different definition for that
.
And then we took a definitionthat has been more recently used
, also in like standardradiology guidelines, and this
is small vessel brain disease.
This is just one marker how thebrain structure changes over
(06:51):
time with age.
Other functional definitionscould, for example, be, I don't
know, intelligence right.
Is that maybe a marker forhealthier brains, someone who is
more intelligent?
But how do we measureintelligence?
So we can like have thesediscussions.
We only looked at structure inthe brain, and cerebral small
(07:13):
vessel disease is one markerthat is like a standard measure,
and you will see that in yourMRI reports of any patient that
you have in the hospital who gota brain MRI and often it's
something worded like T2hyperintensities or unspecified
(07:35):
T2 hyperintensities, likelycerebral small vessel disease.
So this is like kind of theterminology that you will see.
But the big thing is that basedon that, you normally don't get
information on how severe isthat.
Is that just really mild?
Is that something I should careabout?
(07:55):
Sometimes you might seeexpressions like atrophy in the
MRI, but the interesting thingthat when I started with this
research is that there's a hugevariability, huge variance about
how a brain ages Kind of makessense, but I never like
translated that.
Yeah, the brain as well, andsome of the normal, normal
(08:19):
things that happen when we getolder, no matter if there's an
underlying disease or not, isthat?
Yep, our brain atrophies, sothe gray matter, white matter,
shrinks and that'scounterbalanced by an increase
in cerebrospinal fluid andthat's what we term atrophy.
So, yes, we all go through that, no matter how healthy or
(08:42):
unhealthy we are.
But the crux to that is thatit's very variable.
So two people who are 80 yearsold can have a very different
degree of atrophy.
So one person might have severeatrophy and the other person
doesn't.
And I think you can againtranslate that to someone who's
(09:05):
80 and really active.
I heard some people still run,like I don't know, half
marathons a minute.
It's probably not going to be me.
But there's, a huge variance oflike how people age, and that's
the same idea with a brain ageand that's the same idea with
(09:29):
the brain.
So cerebral small vesseldisease is a term that
encapsulates like many differentstructural pathologies in the
brain.
Atrophy is one, microhemorrhages, so like little tiny
bleeds in the brain, and thenanother marker of cerebral small
vessel disease is somethingthat's called white matter
hyperintensities, and it'sexactly what the name says.
When you look at a brain scan,a specific brain scan, that's T2
(09:51):
or flare, they look just reallybright because these are areas
that look white compared to theother tissue and we can go more
into what that might be.
And then also something likecalled perivascular spaces, and
these are just spaces around thearteries that perforate the
(10:11):
brain.
So, as you can imagine, sothese spaces around the arteries
, they are filled with fluid andthe larger they are, they take
up more space in the brain andit seems to be a marker that the
brain might not be as efficientto drain some of the dust or
the debris in the brain tissue.
(10:33):
So all these things are likedifferent markers that the brain
has several small vesseldisease.
So to the small vessels in thebrain, that they are not
functioning as well as theymight did when we were younger.
But the thing is really likehow much does a person have that
?
We're probably all going tohave it at some point, but some
(10:55):
people will have it more thanothers.
And these are findings that aretypical incidental, so you
don't know that you have thatuntil you get a brain scan.
Incidental, so you don't knowthat you have that until you get
a brain scan.
I was like, oh wow, there's alot of white matter, hyper
intensities, and so, while it'snot something that you feel from
one day to the other, it issomething that probably
(11:15):
contributes over time tospecific functions like
swallowing or memory, becauseit's one of the major
contributions to also peopledeveloping dementia.
Speaker 1 (11:26):
Yeah, so I know people who are listening to this
, probably in their car and in aplace where they can't really
like sit down and look at adiagram, but this article is
open access and I would highlyrecommend taking a look at some
of the images in here.
These are fantastic.
So the comparison so you weretalking earlier about the
increased volume ofcerebrospinal fluid, that kind
(11:48):
of compensates for the brainatrophy, like you get brain
atrophy, and so the parts ofyour brain let's I don't I want
to say that matter, but thatmaybe that makes us smart or
healthy?
Speaker 2 (11:58):
Gray matter and white matter.
Tim, Was that a pun?
Speaker 1 (12:08):
There you go, that matter.
No, it it yeah.
Yeah, sure it was.
I guess I'll pretend that itwas, but so you know, as you get
atrophy of those, then you getmore cerebrospinal fluid in
there.
So figure two is super cool.
There is patient one, 68 yearold female 0.25 liters of
cerebrospinal fluid.
And then patient two, also 68year-year-old female, was a
little over twice that.
You can tell the difference.
This is so interesting.
(12:30):
So if you get a chance, take alook at figure two.
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Speaker 2 (12:46):
And you know I've never learned as a
speech-language pathologist tolook at MRIs, right?
So I was fortunate to learnthat during my PhD and postdoc.
But it is also interesting thatthe people or the patients that
we included in the study, theyall were pretty clean cohort.
(13:07):
So, first ever ischemic stroke.
We excluded anyone with, like,prior diseases that could relate
to dysphagia.
So no neurodegenerativediseases, no head and neck
cancer, no other stroke beforethat, no TBI, right?
So all these these like typicalthings.
So these are supposedly peoplewho were healthy before they had
(13:30):
the stroke.
But again, all this, what wesee in these like examples, were
pathologies that were therebefore the stroke.
So it's not something that'srelated to the stroke because
these patients were acute strokepatients.
It was something that was therealready before the stroke, but
again, not something that wasapparent because it didn't cause
(13:52):
acute symptoms.
Speaker 1 (13:54):
Yeah, and maybe not even something that people would
recognize symptomatically overtime.
So like if you're interviewingsomeone's family, you'd be like,
well, did they have dementiabefore this?
They might not have anyindication of memory loss, so
you might not get it withoutthis imaging.
Speaker 2 (14:11):
Yeah, correct.
And I mean it's not somethingthat we would.
I think it's like human nature,right, If we don't feel
limitations, not functional loss, so why should we look into
that, right?
Sure yeah.
Speaker 1 (14:23):
Well, that's fascinating to see where that
kind of comes to bite you later.
For sure, yeah, so as aclinician, because you worked as
a clinician for a while beforegetting your PhD.
Is that right?
Speaker 2 (14:36):
Mm-hmm.
Yes.
Speaker 1 (14:37):
So I figured this was pretty clinically driven.
What are some of your takeaways, Like how do you think you're
going to use this from now on?
Speaker 2 (14:43):
Yeah, great question.
So what is always the bestquestion I got as a researcher
right?
Well, it's great research.
But so what?
I think it helps me as aclinician when you do a chart
review and we do that thoroughly.
I think we are used to lookingthrough like doctor's notes.
We look at chest imaging, weread the notes from the MRI or
(15:07):
CT, what we have.
I hope it helps to get a betterhypothesis of what you might
see when you walk into the room.
And I think it's also wehaven't proven that yet, knock
on wood that this research iscontinuing, but it will likely
be a marker for recovery as well.
Speaker 1 (15:27):
That's what I was going to.
Prognostic indicatorpotentially.
Oh wow, there you go.
Speaker 2 (15:32):
There we go.
So we showed that in aphasiaactually so language disorders
after stroke that patients withworse brain health, measured as
cerebral small vessel disease,had worse potential to recover
despite treatment.
So, and that's controlling fortheir chronological age.
(15:54):
What's really fascinating?
So it's not the chronologicalage, it's really the brain age.
So how healthy is the brain atthe time they receive treatment?
And so if you walk into a roomand patient presents with
dysphagia, then it's always thequestion of doctors hey, so do
(16:18):
you think this patient recoversor do we have to think about
putting a feeding tube inbecause we really want to
discharge this patient?
And then, as a SLP, I alwaysfeel like I wish I had an answer
, but why don't I have an answer?
And I think this is a factorthat comes into play that we can
say, yeah, okay, so the strokelocation.
We know this will lead towhatever severity of dysphagia.
(16:41):
That's what we're going to seeat bedside.
And if we have an idea of thepatient's status before their
stroke how healthy were they,how healthy was their brain
before the stroke this can helpus to say, oh, the chances are
actually really good for thispatient to recover because they
had a pretty good brainstructure before that.
(17:04):
So that's, I think, lends toour discussion, tim, about the
reserve that someone has torecover.
So how much capacity does apatient bring to, for example,
the brain for the brain toreorganize after a stroke?
So what we know from dysphagialiterature and Shaheen Hamdi I
(17:26):
love his research and his grouparound that brought us a lot of
knowledge that after dysphagia,after dysphagia in one
hemisphere, the other hemisphereis likely to help a lot in
recovery and also like areasaround the stroke.
But imagine if those areas thatwere not affected by the stroke
but are supposedly to help withrecovery if they are not
(17:49):
healthy, then the brain won'thave the same capacity to
reorganize or regain thatfunction compared to a brain
where these unaffected areaswere pretty healthy and had a
lot of white matter connections,had a really good volume of
gray matter.
So we're just like there aremore neurons that can change.
(18:11):
I hope that made sense.
Did this make sense?
Speaker 1 (18:15):
Somewhat.
No, no, you're making sense,but my brain's also going in
different directions withquestions and I'm like I'm
afraid to ask these questionsbecause I should probably know
some of these answers and likeit's probably already been
studied before.
Well, who knows, who knows, Iguess I got to put myself out
there some, but I mean I'mthinking of so as I understand,
kind of what you're saying, andI'm also I'm looking at another
one of these beautiful images.
It is figure four.
(18:36):
So this is cool.
Figure four has it highlightedthe corticobulbar tracts in the
right and left hemisphere, goingover from the motor cortex down
toward the brainstem, and itshows different lesion sizes and
different lesion locations andon this it's showing some of
them, basically, uh, the lesionscovering where the
(18:57):
corticobulbar tracts would be.
And so, as you're talking aboutthe recovery, like the, so say,
if the left side is affected,the health of the as I
understand what you're sayingthe health of the right side of
the brain and its ability tokind of take over some of these
functions.
Well, I mean, the premise beingis that it will help to
compensate, and the healthier itis, the better it's going to be
(19:19):
able to compensate, right,that's what I'm getting.
So I'm thinking about all thesepoor folks with spastic
dysarthria who they have likebilateral damage to the
corticobulbar tract.
I'm so sorry and so likethinking of that as a prognostic
indicator.
I'm sure there's probablyresearch out there that says
that, that I should know, that Idon't, don't know enough about
at least and tim.
Speaker 2 (19:37):
Let me plant a seed for the audience, because I saw
that you had the post aboutdysarthria, and dysarthria are
not my strengths, though I lovethe post that you included in
your instagram, I think oh,thank you.
Speaker 1 (19:51):
Yeah, no, I I've been .
Dysarthria has been veryinteresting to me, of the
various types of dysarthrias,and I was very fortunate to be
able to start teaching thiscourse at the University of
Hawaii.
But it's not.
Unfortunately I didn't get togo there, it's remote, but I
learned so much.
So Dr Kendrea Grand, as you canimagine, has a very robust
(20:15):
dysarthria course or motorspeech disorders course put
together and so she sent me hermaterials and I got to look
through them and get some otherthings.
But I learned so much goingthrough that and just like the
parallels with dysphagiatreatment, the upper motor
neuron or bilateral upper motorneuron lesions causing
spasticity, and how you mighttreat that differently than
(20:35):
somebody who has a lower motorneuron lesion and I.
The analogy I use is likeyou've got a cord coming from
your power outlet going to alamp and someone just cuts the
cord Like it's not getting poweranymore.
So just the flaccidity, theweakness, that type of thing.
But so you see, like I can seeso many parallels between this
and dysphagia.
So it's just like my world hasbeen blown up in that
(20:57):
perspective lately.
Speaker 2 (21:06):
So I think it's, I just think it's super cool, I
very much, and I because mybackground is also like in
aphasia.
So language disorders I oftencompared also like how is
recovery working in aphasia,compared to dysphagia,
dysarthria, and I think what isreally striking is like how much
in these functions do bothhemispheres contribute?
So we know that the typicallanguage organization in the
brain is heavily towards theleft side of the brain.
(21:28):
In those typical people, righthand, dominant etc.
The right hemisphere is alsoinvolved in language processing,
but not as much More like inthe ventral stream.
So semantic processing etcetera, with swallowing in
comparison and speaking.
We know it's a bilateral neuralnetwork and it's less
(21:50):
lateralized.
So language is a heavilylateralized function, swallowing
not so much.
So both hemispheres contribute.
And how I think about it isit's actually great when it's
really organized in bothhemispheres because that means
there's one hemisphere, theredundancy.
(22:11):
Exactly so.
If you have an injury, then theother hemisphere, because it
already contributes to thatfunction.
It will be easier for thehemisphere to okay.
I'm just going to do a littlebit more.
I already have theseconnections, I already kind of
know what I have to do.
In comparison to something likelanguage that's heavily
lateralized to the left, theright hemisphere does a little
(22:32):
bit, but not as much.
So that's why the oralhemisphere and language has a
more difficult time tocompensate.
So we don't see that as muchand the areas around the stroke
are more contributing inlanguage for recovery.
And that's why it's interestingwhen you pointed out the figure
four, I think long, long timeyou always think okay, brainstem
(22:55):
is swallowing rightCorticobulbar tract.
That's really, really important.
We know that and lots of thosestudies that look at recovery
also look at corticobulbar tract.
Makes sense.
Speaker 1 (23:05):
Oh, and real fast.
Just I don't want to assumeanyone knows anything.
Corticobulbar tract the motorneurons coming from the cortex
to the brainstem.
So I think corticobulbar iscortex to brainstem,
corticospinal is cortex to spine.
Speaker 2 (23:18):
So for motor neurons, yes, thanks, tim, that's right.
Speaker 1 (23:22):
I mean, you probably didn't know that either, but I'm
just showing off.
You just study it for a living,yeah.
Speaker 2 (23:30):
I was told, so I lost my train of thought.
Speaker 1 (23:32):
No, oh, dang on, I'm sorry.
Speaker 2 (23:34):
In this figure.
So corticobulbar tract, and inthe study that we did with a
cerebral small vessel braindisease, we controlled for the
stroke damage to these importanttracts, corticobulbar tract.
So we just wanted to make surethat we can like isolate the
contribution of the cerebralsmall vessel disease, no matter
(23:54):
how much or how little thecorticobulbar tracts were
lesioned, no matter how largethe stroke is, no matter how old
someone is, et cetera, etcetera.
And from some other literaturewe also know that, yeah,
corticobulbar tract is important, but that's not the only
connection the cortex has to thebrainstem.
(24:15):
What is also really reallyinteresting and I hope that some
neuroscientists who can do muchbetter work than I can do, will
tell us a little bit more aboutthat in their future research
so what other tracts than thecorticobulbar tract can we maybe
stimulate through electricalstimulation or whatever?
That could then even compensateif the corticobulbar tracts are
(24:37):
damaged.
Speaker 1 (24:38):
That's super cool.
It's like cracking open a wholeother pathway for dysphagia
rehabilitation.
That's super neat.
Speaker 2 (24:44):
Pathway Again.
Speaker 1 (24:46):
A pun Tim oh see, it's above my head over my head.
I'm going to have to listen tothat again and be like all right
, I got to learn from thoseaccidental puns.
So you were comparing the ideaof of language dominance, which
is typically more isolated toone hemisphere than the other,
at least relative to swallowing,and so that I guess the kind of
(25:10):
a question I'm going to throwback at you right, that is, if
we're also understanding thecranial nerves that are involved
in swallowing and the uppermotor neuron tracks that
eventually lead to these cranialnerves.
And the ones that I and thisoversimplification, I'm sure the
ones that I look at primarilytrigeminal, five, facial seven,
glossopharyngeal, nine, lessfrom a motor perspective, but
(25:32):
vagus 10 and then accessory yeah, hypoglossal, I was going to go
, I kind of accessory, yes, yes,of course, but I'm going more
like direct, but, yeah,hypoglossal, I was gonna go, I,
I kind of accessory, yes, yes,of course, but I'm going more
like direct, but, yeah,hypoglossal.
So, knowing so, I think so many,we learn that like, okay, brain
, right hemisphere controls theleft, left hemisphere controls
the right, but knowing theimportance of which one of those
(25:54):
, which of those cranial nervesare also bilaterally innervating
?
You like the face like thefacial nerve, especially the
upper face.
You get bilateral innervationfrom that.
So in looking at and trying tohypothesize imaging to function
and that sort of thing, just theimportance of knowing which of
those nerves provide bilateralinnervation.
Speaker 2 (26:14):
Yeah, that is so interesting, right.
And then the hypoglossal nerveagain hypoglossal nerve.
It's always so fascinating tome that some people naturally
have a really prominentbilateral representation and
some people have it moreunilateral.
So that's why, you see, in somecortical stroke patients some
(26:35):
have a tongue deviation andothers don't, because there's
like this mix, oh yeah.
Yeah, exact physiological mixLike I don't know's like this
mix.
Yeah, exact physiological mixlike I don't know.
Tim, do you have it bilateral?
I hope I do, but we don't knowyeah, I don't know.
Hopefully we won't ever find out, but yeah, we'll see and I
think for dysphagia, cranialnerves are so important and they
give us so much information atbedside to then come up with
(26:56):
hypotheses.
And again, a shout out to drgarland who has so much
knowledge about this and has somany great educational platforms
to help us understand that indysphagia, I think what we then,
taking it a step further, oftenalso need to consider is, of
course, the coordination piece.
(27:18):
Right, so cranial nerves tellus, like the information
directly to the muscles, can welike switch this on off?
But it doesn't tell us if themuscles work in synergy, because
that needs to be controlled byother areas in the brain that
are not, that are not thosecorticobulbar tracts that give
rise to the nerves, and I thinkthat's then, of course, always
(27:41):
the interesting piece.
It's like, okay, they don'thave cranial nerve damage, but
present with severe dysphagia,yeah, because there are other
areas in the brain that helpwith this coordination piece.
Speaker 1 (27:53):
Like the extrapyramidal system, the basal
ganglion cerebellar controlcircuits.
Speaker 2 (27:58):
Exactly.
Speaker 1 (28:00):
And those are so complicated.
Oh yeah, like I, oh yeah,there's just I'm just scratching
the surface with those there's.
To me they appear so much morecomplicated than just the direct
activation pathway or the, youknow, the corticobulbar and the
corticospinal.
Speaker 2 (28:16):
Right, yeah, I think that's why many researchers or
many studies, and we as well,look at the corticobulbar tract
because it's kind of like, okay,I get it, I get it, but yes,
there are many other areas inthe brain and circuits are
contributing to swallowing that.
Speaker 1 (28:32):
That's cool.
That's cool, I'm having fun.
I'm having fun.
This is why I do the podcast,like I learned so much, and just
have fun conversations.
I mean, this is one reason whyI do the podcast.
The post-production editing,that's a whole different story.
But this is this is I'm happyas a clam, happy as a clam,
right now.
Speaker 2 (28:50):
I am so thrilled that I can talk here today because
I'm kind of a fan girl of yourpodcast, so thanks for having me
.
Speaker 1 (29:00):
I appreciate it.
No, this is so.
Janina and I met at the hard toswallow catalyst for change in
dysphagia management conference.
It was two years ago.
That was a great year.
I think that was the biggestturnout that we had.
That was so much fun.
Don't know the date for thatyet and that's done through
Rocky Mountain University, notthrough, not through, gap
education, my company.
But oh, there is a plug though.
(29:21):
There is a plug real fast.
I got to take advantage of this, of this.
You're talking about dr kendriagarant and her marvelous work
on cranial nerve stuff.
So in march we are going tohave, or we're planning march
either early march or late marchto have a three-hour webinar
with her to really dive intothat stuff, hoping to record it
too.
So mark your calendars, keepthat open.
Speaker 2 (29:41):
No, you know I'll be there, yeah.
Speaker 1 (29:45):
Well, we'll all be there, right, where are you
going to be?
So, anyway, that's that, butnot to sidetrack us too much.
We talked about why you didthis study.
Why do we care?
Why should we care?
The clinical translationcerebral small vessel disease is
a standard measure of healthpotentially related to the brain
.
What do you think are some ofthe limitations of the study?
Speaker 2 (30:11):
Like what?
Should we not read the studyand be like all right, this
means this now?
Yeah, thanks for that question.
So this study was a preliminarystudy, right, and I feel like
every study can be titled apreliminary study, because
always we want to do more.
So we only had 40 participantsand of course, the goal is that
we increase the sample size by alot and then continue also the
(30:34):
measures in a more sophisticatedway.
So what the readers will see islike, for example, the
perivascular spaces and whitematter hypotensities.
We scored them on an ordinalscale and there are way better
ways to do this in a morequantitative way.
So so take this with a grain ofsalt.
But was that right video?
(30:55):
Great, okay.
And so while we did a lot ofanalyses, only very, very few
survived in the end to bestatistically significant, and
even fewer survived after verystringent corrections for
multiple comparisons.
So it's the way that we need todo is that we don't think some
(31:17):
of our results are true, eventhough they might just be an
accidental finding or anartifact.
So the limitation is definitelya small sample size, and it
doesn't mean that just becausewe didn't find something that
it's not there.
I think that's what's important.
For example, we didn't find asignificant correlation between
(31:39):
these measures and oral total.
That was something I wasexpecting, so I was thinking,
okay, these aging factors.
I think what we often see islike oral control difficulties.
We didn't find that.
However, it doesn't mean it'snot there, right.
Just because it wasn'tstatistical significant doesn't
mean that it's not there.
(31:59):
So we have to just keep that inmind, that maybe our sample
wasn't big enough, maybe ourmeasurements were not as
sensitive as they should be.
So I think this is reallyimportant when you read that
study, to keep that in mind.
And I feel like that we asclinicians are not trained to do
(32:20):
these measures that we used inthe study right.
I think I had no idea whatperivascular spaces are before I
did this and absolutely no ideahow they would look like.
So it's going to be difficultfor clinicians to really know in
the patient that they see ifthese things are present.
But just really look at the MRIreport and look for these words
(32:44):
like unspecified T2hyperintensities likely related
to cerebral small vessel disease.
So I think that's myrecommendation Look for these
things and start like thinkingabout oh, this might mean that
the brain health of this patientwasn't as great to begin with.
Speaker 1 (33:02):
Yeah, did.
Speaker 2 (33:02):
I answer your question, Tim.
Oh, and more.
Speaker 1 (33:04):
Yeah, okay, that's great.
Oh, with yeah, did I answeryour question, tim?
Oh and more.
Yeah, okay, that's great.
Oh, thank you so much.
Is it anything else that youwant to leave listeners with?
Speaker 2 (33:13):
No, I think I feel like the clinical driven
questions are what is reallyimportant to me.
So if anybody else has clinicalquestions, I think that's the
way to go, that we should thenresearch to get more answers for
when we practice clinically.
Speaker 1 (33:28):
Good deal.
Good deal, and it looks likeyour email address is also
listed within this article, soif I put it out there, I don't
feel quite so bad.
W-i-l-m-s-k-o-e at M-U-S-C likemedical university of South
Carolina, dot E-D-U.
All right, cool.
(33:50):
Well, thank you very much,really appreciate it.
It's great to see you.
This makes me want to have youdo a three hour course after
Kendra, I don't know sometime.
So we got to talk about that,talk about that Hang out, and
maybe we'll get something going.
We'll see, but thanks againeverybody.
Dr Janina Wilmskota Right, okay, okay, I'm very self-conscious
(34:10):
of my pronunciation.
Speaker 2 (34:14):
Yeah, thanks so much, tim.
Speaker 1 (34:16):
Awesome, thank you.
That was Dr Janina Wilmskotadiscussing cerebral small vessel
disease as a predictor ofrecovery and dysphagia after
acute stroke.
You can reach her at Wilmskoe,that is W-I-L-M-S-K-O-E, at
(34:37):
M-U-S-C.
Dot E-D-U, that's M-U-S-C likeMedical University of South
Carolina, and there's a link totoday's article in the episode
description.
Don't miss our upcoming eventon February 23rd, swallowing
Cinema.
It's an MBS case study eventthat has been a staple at ASHA
for years and this year it'sfound a home with us.
Visit SwallowTheGapcom orSwallowTheGapcom slash live
(34:58):
courses to learn more.
Thanks for listening today andif you think we're helping,
please spread the word, takecare.
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