June 3, 2024 • 14 mins
We continue our general survey of neurology with an overview of the spinal cord.
Things we cover in this podcast:
- Signs and Symptoms of Myelopathy
- Breakdown of some causes of compressive versus non-compressive myelopathies
- Infections
- Neoplasms
- Transverse Myelitis
- Metabolic Causes
- Vascular Myelopathies
- Genetic Disorders
- Check out our website at www.theneurotransmitters.com to sign up for emails, classes, and quizzes!
- Would you like to be a guest or suggest a topic? Email us at contact@theneurotransmitters.com
- Follow our podcast channel on 𝕏 @neuro_podcast for future news!
- Find me on 𝕏 @DrKentris
The views expressed do not necessarily represent those of any associated organizations. The information in this podcast is for educational and informational purposes only and does not represent specific medical/health advice. Please consult with an appropriate health care professional for any medical/health advice.
Mark as Played
Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Michael Kentris (00:00):
Hello and welcome back to the
Neurotransmitters, your sourcefor all things related to
clinical neurology.
I'm your host, dr MichaelKentris, and today we're going
to be talking about spinal corddisorders and it's going to be a
relatively short discussion,and that's not because there
aren't a lot of things that cango on in the spinal cord, but it
is because some of these issuesare covered in other recordings
(00:22):
and some of these disorders arepretty rare, which means they
don't get a lot of screen timein practice questions, nor do
they really show up on boardsvery, very often.
So, with all that being said,what are the signs and symptoms
that tend to make us think abouta myelopathy?
So I think we can group theseinto two main buckets that we're
able to observe either byhistory or on physical exam, and
(00:43):
I tend to lump these into motorand non-motor.
So if we have some sort ofdysfunction in the corticospinal
tract, we've got our uppermotor neuron signs, which is
spasticity, weakness,hyperreflexia and an extensor
plantar response or Babinskireflex.
Contrast that with our typicallower motor neuron signs, which
is more of a flaccid paralysis.
Now the tricky thing is thatflaccid paralysis can occur in a
(01:07):
very early hyperacute situation, say a spinal cord infarct, but
over time that should developinto a more hyperreflexic and
spastic type picture.
But the timing of when you'reencountering the patient does
matter.
Our other typical lower motorneuron signs are things like
fasciculations, atrophy,hyporeflexia or decreased
(01:28):
reflexes.
So you do need to pay attentionto what either the vignette is
telling you or what your actualphysical exam if you're using
this in real life is telling you.
On the non-motor side we've gota few other things as well.
One of the big buckets there issensory testing.
So we have proprioception andvibratory sense in the dorsal
columns and then we havetemperature and pain or pinprick
(01:48):
testing in the spinothalamicpathways.
And pinprick testing inparticular is very helpful if
we're concerned about myelopathy, as that can help us find a
sensory level which is usuallygoing to be at or a little bit
below the level of the lesion.
Other symptoms that may come toline, either in the history or
physical, are gait issues ordifficulties with bowel or
bladder control.
If you have involvement of thedistal spinal cord or the lower
(02:11):
roots that is, cauda equinasyndrome you may find decreased
tone, areflexia and loss ofperianal sensation described as
well.
Etiology-wise we can think intwo very broad categories
compressive and non-compressivecauses of myelopathy, starting
with compressive.
Very often people will describepain at the level of
(02:32):
compression and in some casesfocal percussion may help you
figure out which level that is.
There are several red flag signsthat may make you switch over
from just back pain intosomething more suspicious Fevers
, focal tenderness.
Someone with a recent historyof surgery, particularly spinal
surgery, or someone with ahistory of IV drug use.
(02:53):
This may make you think aboutthings like an epidural abscess,
dysgitis or other types ofinfection.
If someone has a history ofcancer, then you start to think
about things like bonymetastases.
If they're on anticoagulation,then you start worrying about
things like an epidural hematoma.
So the context, as always, doesmatter.
Timing also matters.
(03:13):
Is this more of a hyperacute,subacute or chronic process?
If we have someone who looksmyelopathic, chronic spinal
stenosis tends to affect thecervical and lumbar spine more
than the thoracic spine, butthere may be some common
symptoms that you can elicit inthe history.
Some things to ask aboutprogressive leg weakness or
trouble walking, which theyattribute to stiffness in their
(03:35):
legs, but on examination you mayfind evidence of spasticity.
They may also describe somenumbness or paresthesias,
distally more often in the legs,and they may also describe some
bladder control issues, whetherthis is incontinence or
retention.
You may also get some symptomssuggestive of claudication, in
particular spinal claudicationor quote-unquote
(03:57):
pseudo-claudication.
So they may have someexertional pain around the groin
, thighs or buttocks and againthere may be some associated
weakness and or numbness.
Our preferred test is going tobe MRI of the spine, aimed at
the level that we think isinvolved.
So you do need to base that offof the history and the
examination.
If someone is hyperreflexic inthe legs but not the arms,
(04:18):
you're thinking more thoracicspine.
If it's the arms and the legs,maybe you're thinking more
cervical spine.
So you do need to put your examtogether with your history so
that you know what test is mostlikely to get you a diagnosis.
For most causes of compressivemyelopathy, surgical
decompression is often going tobe required, but it does depend
(04:38):
on the underlying cause.
Now in most of these acuteonset emergent treatment is
going to be more important, assignificant symptoms, that is to
say significant neurologicdecline at the time of surgery,
can be associated with worsepost-op outcomes.
So mostly what we're doing withthis surgery is we're
preventing further neurologicdeterioration.
(04:59):
So if a neurologic deficit isconsidered-unquote, completed
surgery may be deferred as thesecan be quite high risk and if
there is low potential forbenefit, the risk may not be
worth the potential benefit.
Other adjunctive treatments toconsider.
If it is a bleeding diathesisand they have an epidural
hematoma, you're obviously goingto want to reverse that
anticoagulation If they have hadspinal cord trauma or an
(05:23):
abscess, steroids are consideredcontroversial and are not
routinely recommended.
However, they could beconsidered on a case-by-case
basis if the process is thoughtto be more neoplastic.
Moving on to the non-compressivemyelopathy camp and this is
where a lot of the quote weirdstuff might hang out let's start
off with transverse myelitis,and we're talking specifically
(05:44):
about quote idiopathic end quotetransverse myelitis.
Now I am throwing a lot ofquotes in here because
transverse myelitis is more of asyndrome and less of a
diagnosis.
There are a lot of things thatyou have to investigate before
settling on idiopathictransverse myelitis as a
diagnosis.
So historically this isconsidered a monophasic
(06:06):
inflammatory demyelinatingdisorder.
It can occur bothparainfectious and
post-infectious and the mostcommon symptoms typically
include subacute weakness,sensory changes and bowel or
bladder dysfunction.
People may also describe athoracic banding sensation and
on examination they will oftenhave a sensory level on
(06:27):
examination.
Now I want to take a moment andthis may be more detail than
what people need for their IMboards, but I think it's an
important point.
So, on MRI of the spine it's animportant point.
So, on MRI of the spine,typical MS lesions are usually
one to two vertebral segmentslong and there is an entity,
what we call longitudinallyextensive transverse myelitis,
(06:47):
which is usually three or morelevels long and that has a
different differential diagnosisand we'll talk about that in a
minute.
But those imagingcharacteristics should raise
some red flags that we're notdealing with.
Maybe just plain Jane MS or anidiopathic transverse myelitis,
and we definitely need to golooking for secondary causes.
So, as we had discussed inprevious recordings about MS,
(07:09):
specifically, if the MRI of thebrain doesn't show any lesions,
if on the spinal fluid testingthere is no evidence of
oligoclonal bands, ms is lesslikely and perhaps this will be
a monophasic event, as ishistorically recorded.
However, if we have lesions onthe brain, if we have O-bands,
(07:30):
then we might be leaning moreaway from just an idiopathic
transverse myelitis towards anactual diagnosis of multiple
sclerosis.
Similarly, if we havelongitudinally extensive
transverse myelitis, then weneed to go looking for other
entities such as neuromyelitisoptica or NMO with aquaporin-4
(07:50):
antibodies.
You may also go look for othercauses depending on the CSF
profile.
If it looks infectious, thereare a number of entities that we
have to keep in mind.
Fortunately, there aredifferent panels and PCR panels
that can check for a lot ofinfectious etiologies relatively
quickly these days.
So some viruses to keep in mindherpes simplex virus, varicella
(08:12):
, zoster virus, west Nile virus,which can look very similar to
polio, human T lymphotropicvirus or tropical spastic
paraparesis, lyme disease,neurosyphilis, hiv.
And HIV is a little unique.
It can happen at the time ofseroconversion or, in the more
long term you can get a vacuolarmyelopathy in people who have
(08:33):
chronic low CD4 counts.
Tuberculosis could alsopotentially present with similar
symptoms of myelopathy.
So you've ruled out infection.
It looks inflammatory, maybedemyelinating.
You're going to start sometreatment.
What are you going to start?
Well, like with so many thingsin neurology, we're going to
fall back on steroids.
Our first line is usually IVmethylprednisolone, one gram per
(08:54):
day for about five days.
If you can't use steroids forsome reason or they're not
working, you might considerplasma exchange for those
refractory cases.
Moving on to subacute combineddegeneration, this one's a
little bit unique.
Often due to B12 deficiency, ittypically presents with sensory
disturbances, often loss ofproprioception, vibratory sense,
(09:15):
paresthesias, weakness, ataxia,difficulty walking.
Obviously, one of our firststeps in suspected cases of
subacute combined degenerationis to check a vitamin B12 level.
You'll also be checking formethylmalonic acid and
homocysteine levels.
So in the typical subacutecombined degeneration picture,
b12 is low, methylmalonic acidand homocysteine are high.
(09:38):
In people with low normal B12,you may also get some mild cases
of subagute combineddegeneration.
So it is very common for peopleto use B12 as a screening test
and to only check themethylmalonic acid and
homocysteine if there is a highclinical suspicion.
So if you have that low normalB12, but your clinical suspicion
is high, do check thoseconfirmatory labs.
(10:01):
You may have a macrocyticanemia, you may not, so that is
not necessarily going to pointyou away from it if your
clinical suspicion is high.
Also.
Another reason this may happenis recreational nitrous oxide
use.
This can happen if you'rebreathing the nitrous oxide out
of a whipped cream can or peoplewho are buying what are called
whippets from gas stations orother kind of unreputable places
(10:24):
, and this can in turn lead to aB12 deficiency.
You can also see similarsymptoms from a copper
deficiency.
So this can be frommalabsorption, nutritional
deficiencies or excessive zincuse.
So sometimes you'll see this inpeople who are taking a lot of
supplements or take a lot ofzinc when they're not feeling
well and if their copper statusis a little borderline, this may
push them over into developingsome neurologic symptoms.
(10:47):
Both B12 and copperdeficiencies can be more common
in people who have had bariatricsurgery.
So definitely things to keep inmind in terms of prior surgical
history.
Let's move on to a couple ofvascular causes.
So a spinal cord infarct.
Most often this is going to bein the anterior spinal artery
distribution, and this isbecause there is one anterior
(11:10):
spinal artery as opposed to thetwo posterior spinal arteries.
So there's more redundancy inthe posterior spinal artery
territory than there isanteriorly.
Typically we're going to seesomeone presenting with acute
onset of flaccid paralysis.
Very often there will be somepain associated with this as
well, and over time they maydevelop the typical spasticity.
But in the hyperacute phasesyou may not see that on exam.
(11:33):
In fact you probably won't.
They will typically also havepreserved vibratory and
proprioceptive sense right thosedorsal columns, because it is
the anterior spinal arteryterritory that is infarcted.
Unfortunately, that meansthat's our motor pathways are
getting knocked out there prettyhard.
Some causes that may make youconsider this more in your
differential diagnosis.
If someone just recently wokeup from anesthesia after a
(11:57):
complicated cardiovascular oraortic surgery and they had a
lot of hypertension during theprocedure, that may raise a red
flag.
An area that's at particularrisk is the artery of
Adamkiewicz, which is a largeradicular artery, often in the
lower thoracic around TA to T12territory, although there is
some variability, and so that isvery susceptible to hypotension
(12:20):
, in particular in older adultswho may have some superimposed
stenosis or atherosclerosis ofthat vessel, and then you throw
that hypotension on top of itduring a prolonged surgery that
may lead to a spinal cordinfarct.
Another potential cause ofvascular myelopathy are dural
arteriovenous fistulas, or duralAVFs.
Now these are a little bit moresubacute to chronic in their
(12:43):
onset and it's thought thatthey're mostly causing these
symptoms due to venouscongestion, although they may
present as an infarct as well.
On imaging, typically MRI,we're going to be looking for
vascular flow voids,particularly on T2 sequences.
So if you see these little darkspots in the bright CSF, that
(13:03):
should raise your suspicion fora possible dural AVF.
However, it is a verychallenging diagnosis to make
and if the clinical suspicion ishigh.
Even with normal MRI, you mayneed to ask your
neurointerventionalist for aspinal angiogram.
So definitely a verychallenging diagnosis in these
patients.
Who is it going to happen to?
It's a little more common inmen over the age of 50 and those
(13:26):
with a history of prior spinalsurgery.
Last category I wanted to touchon during this recording genetic
disorders.
Most of these are fairly rareand in these cases family
history is going to be of theutmost importance.
Starting with that ishereditary spastic paraplegia.
So again, family history veryimportant, and the severity and
(13:49):
progression of these symptomscan vary significantly from
person to person.
Lastly, I'll mentionadrenomyeloneuropathy, which can
sometimes be seen in femalecarriers of X-linked
adrenoleukodystrophy.
So they'll have a lot of thesame symptoms that we mentioned
before in terms of spasticity,bowel bladder issues, difficulty
walking, etc.
But there will oftentimes besomething in the story to
(14:11):
suggest adrenal insufficiency.
So in these patients we mayalso be sending out very
long-chain fatty acid profilesor genetic testing, depending on
the presentation.
That is all I have for youtoday If you made it this far.
Thank you so much and if youenjoyed this podcast, please
leave us a five-star review onApple Spotify, wherever you get
your podcasts.
If you found the informationtoday helpful, please share it
(14:32):
with your friends, subscribe forfuture episodes, and you can
find me on X, formerly known asTwitter, at DrKentris
D-R-K-E-N-T-R-I-S.
And you can find the officialshow at Neuro underscore podcast
N-T-R-I-S.
And you can find the officialshow at neuro underscore podcast
.
You can also find more of ourresources on the website online
at theneurotransmitterscom.
Thank you again for listeningand we'll see you next time.
Hello and welcome back to the
Neurotransmitters, your sourcefor all things related to
clinical neurology.
I'm your host, dr MichaelKentris, and today we're going
to be talking about spinal corddisorders and it's going to be a
relatively short discussion,and that's not because there
aren't a lot of things that cango on in the spinal cord, but it
is because some of these issuesare covered in other recordings
(00:22):
and some of these disorders arepretty rare, which means they
don't get a lot of screen timein practice questions, nor do
they really show up on boardsvery, very often.
So, with all that being said,what are the signs and symptoms
that tend to make us think abouta myelopathy?
So I think we can group theseinto two main buckets that we're
able to observe either byhistory or on physical exam, and
(00:43):
I tend to lump these into motorand non-motor.
So if we have some sort ofdysfunction in the corticospinal
tract, we've got our uppermotor neuron signs, which is
spasticity, weakness,hyperreflexia and an extensor
plantar response or Babinskireflex.
Contrast that with our typicallower motor neuron signs, which
is more of a flaccid paralysis.
Now the tricky thing is thatflaccid paralysis can occur in a
(01:07):
very early hyperacute situation, say a spinal cord infarct, but
over time that should developinto a more hyperreflexic and
spastic type picture.
But the timing of when you'reencountering the patient does
matter.
Our other typical lower motorneuron signs are things like
fasciculations, atrophy,hyporeflexia or decreased
(01:28):
reflexes.
So you do need to pay attentionto what either the vignette is
telling you or what your actualphysical exam if you're using
this in real life is telling you.
On the non-motor side we've gota few other things as well.
One of the big buckets there issensory testing.
So we have proprioception andvibratory sense in the dorsal
columns and then we havetemperature and pain or pinprick
(01:48):
testing in the spinothalamicpathways.
And pinprick testing inparticular is very helpful if
we're concerned about myelopathy, as that can help us find a
sensory level which is usuallygoing to be at or a little bit
below the level of the lesion.
Other symptoms that may come toline, either in the history or
physical, are gait issues ordifficulties with bowel or
bladder control.
If you have involvement of thedistal spinal cord or the lower
(02:11):
roots that is, cauda equinasyndrome you may find decreased
tone, areflexia and loss ofperianal sensation described as
well.
Etiology-wise we can think intwo very broad categories
compressive and non-compressivecauses of myelopathy, starting
with compressive.
Very often people will describepain at the level of
(02:32):
compression and in some casesfocal percussion may help you
figure out which level that is.
There are several red flag signsthat may make you switch over
from just back pain intosomething more suspicious Fevers
, focal tenderness.
Someone with a recent historyof surgery, particularly spinal
surgery, or someone with ahistory of IV drug use.
(02:53):
This may make you think aboutthings like an epidural abscess,
dysgitis or other types ofinfection.
If someone has a history ofcancer, then you start to think
about things like bonymetastases.
If they're on anticoagulation,then you start worrying about
things like an epidural hematoma.
So the context, as always, doesmatter.
Timing also matters.
(03:13):
Is this more of a hyperacute,subacute or chronic process?
If we have someone who looksmyelopathic, chronic spinal
stenosis tends to affect thecervical and lumbar spine more
than the thoracic spine, butthere may be some common
symptoms that you can elicit inthe history.
Some things to ask aboutprogressive leg weakness or
trouble walking, which theyattribute to stiffness in their
(03:35):
legs, but on examination you mayfind evidence of spasticity.
They may also describe somenumbness or paresthesias,
distally more often in the legs,and they may also describe some
bladder control issues, whetherthis is incontinence or
retention.
You may also get some symptomssuggestive of claudication, in
particular spinal claudicationor quote-unquote
(03:57):
pseudo-claudication.
So they may have someexertional pain around the groin
, thighs or buttocks and againthere may be some associated
weakness and or numbness.
Our preferred test is going tobe MRI of the spine, aimed at
the level that we think isinvolved.
So you do need to base that offof the history and the
examination.
If someone is hyperreflexic inthe legs but not the arms,
(04:18):
you're thinking more thoracicspine.
If it's the arms and the legs,maybe you're thinking more
cervical spine.
So you do need to put your examtogether with your history so
that you know what test is mostlikely to get you a diagnosis.
For most causes of compressivemyelopathy, surgical
decompression is often going tobe required, but it does depend
(04:38):
on the underlying cause.
Now in most of these acuteonset emergent treatment is
going to be more important, assignificant symptoms, that is to
say significant neurologicdecline at the time of surgery,
can be associated with worsepost-op outcomes.
So mostly what we're doing withthis surgery is we're
preventing further neurologicdeterioration.
(04:59):
So if a neurologic deficit isconsidered-unquote, completed
surgery may be deferred as thesecan be quite high risk and if
there is low potential forbenefit, the risk may not be
worth the potential benefit.
Other adjunctive treatments toconsider.
If it is a bleeding diathesisand they have an epidural
hematoma, you're obviously goingto want to reverse that
anticoagulation If they have hadspinal cord trauma or an
(05:23):
abscess, steroids are consideredcontroversial and are not
routinely recommended.
However, they could beconsidered on a case-by-case
basis if the process is thoughtto be more neoplastic.
Moving on to the non-compressivemyelopathy camp and this is
where a lot of the quote weirdstuff might hang out let's start
off with transverse myelitis,and we're talking specifically
(05:44):
about quote idiopathic end quotetransverse myelitis.
Now I am throwing a lot ofquotes in here because
transverse myelitis is more of asyndrome and less of a
diagnosis.
There are a lot of things thatyou have to investigate before
settling on idiopathictransverse myelitis as a
diagnosis.
So historically this isconsidered a monophasic
(06:06):
inflammatory demyelinatingdisorder.
It can occur bothparainfectious and
post-infectious and the mostcommon symptoms typically
include subacute weakness,sensory changes and bowel or
bladder dysfunction.
People may also describe athoracic banding sensation and
on examination they will oftenhave a sensory level on
(06:27):
examination.
Now I want to take a moment andthis may be more detail than
what people need for their IMboards, but I think it's an
important point.
So, on MRI of the spine it's animportant point.
So, on MRI of the spine,typical MS lesions are usually
one to two vertebral segmentslong and there is an entity,
what we call longitudinallyextensive transverse myelitis,
(06:47):
which is usually three or morelevels long and that has a
different differential diagnosisand we'll talk about that in a
minute.
But those imagingcharacteristics should raise
some red flags that we're notdealing with.
Maybe just plain Jane MS or anidiopathic transverse myelitis,
and we definitely need to golooking for secondary causes.
So, as we had discussed inprevious recordings about MS,
(07:09):
specifically, if the MRI of thebrain doesn't show any lesions,
if on the spinal fluid testingthere is no evidence of
oligoclonal bands, ms is lesslikely and perhaps this will be
a monophasic event, as ishistorically recorded.
However, if we have lesions onthe brain, if we have O-bands,
(07:30):
then we might be leaning moreaway from just an idiopathic
transverse myelitis towards anactual diagnosis of multiple
sclerosis.
Similarly, if we havelongitudinally extensive
transverse myelitis, then weneed to go looking for other
entities such as neuromyelitisoptica or NMO with aquaporin-4
(07:50):
antibodies.
You may also go look for othercauses depending on the CSF
profile.
If it looks infectious, thereare a number of entities that we
have to keep in mind.
Fortunately, there aredifferent panels and PCR panels
that can check for a lot ofinfectious etiologies relatively
quickly these days.
So some viruses to keep in mindherpes simplex virus, varicella
(08:12):
, zoster virus, west Nile virus,which can look very similar to
polio, human T lymphotropicvirus or tropical spastic
paraparesis, lyme disease,neurosyphilis, hiv.
And HIV is a little unique.
It can happen at the time ofseroconversion or, in the more
long term you can get a vacuolarmyelopathy in people who have
(08:33):
chronic low CD4 counts.
Tuberculosis could alsopotentially present with similar
symptoms of myelopathy.
So you've ruled out infection.
It looks inflammatory, maybedemyelinating.
You're going to start sometreatment.
What are you going to start?
Well, like with so many thingsin neurology, we're going to
fall back on steroids.
Our first line is usually IVmethylprednisolone, one gram per
(08:54):
day for about five days.
If you can't use steroids forsome reason or they're not
working, you might considerplasma exchange for those
refractory cases.
Moving on to subacute combineddegeneration, this one's a
little bit unique.
Often due to B12 deficiency, ittypically presents with sensory
disturbances, often loss ofproprioception, vibratory sense,
(09:15):
paresthesias, weakness, ataxia,difficulty walking.
Obviously, one of our firststeps in suspected cases of
subacute combined degenerationis to check a vitamin B12 level.
You'll also be checking formethylmalonic acid and
homocysteine levels.
So in the typical subacutecombined degeneration picture,
b12 is low, methylmalonic acidand homocysteine are high.
(09:38):
In people with low normal B12,you may also get some mild cases
of subagute combineddegeneration.
So it is very common for peopleto use B12 as a screening test
and to only check themethylmalonic acid and
homocysteine if there is a highclinical suspicion.
So if you have that low normalB12, but your clinical suspicion
is high, do check thoseconfirmatory labs.
(10:01):
You may have a macrocyticanemia, you may not, so that is
not necessarily going to pointyou away from it if your
clinical suspicion is high.
Also.
Another reason this may happenis recreational nitrous oxide
use.
This can happen if you'rebreathing the nitrous oxide out
of a whipped cream can or peoplewho are buying what are called
whippets from gas stations orother kind of unreputable places
(10:24):
, and this can in turn lead to aB12 deficiency.
You can also see similarsymptoms from a copper
deficiency.
So this can be frommalabsorption, nutritional
deficiencies or excessive zincuse.
So sometimes you'll see this inpeople who are taking a lot of
supplements or take a lot ofzinc when they're not feeling
well and if their copper statusis a little borderline, this may
push them over into developingsome neurologic symptoms.
(10:47):
Both B12 and copperdeficiencies can be more common
in people who have had bariatricsurgery.
So definitely things to keep inmind in terms of prior surgical
history.
Let's move on to a couple ofvascular causes.
So a spinal cord infarct.
Most often this is going to bein the anterior spinal artery
distribution, and this isbecause there is one anterior
(11:10):
spinal artery as opposed to thetwo posterior spinal arteries.
So there's more redundancy inthe posterior spinal artery
territory than there isanteriorly.
Typically we're going to seesomeone presenting with acute
onset of flaccid paralysis.
Very often there will be somepain associated with this as
well, and over time they maydevelop the typical spasticity.
But in the hyperacute phasesyou may not see that on exam.
(11:33):
In fact you probably won't.
They will typically also havepreserved vibratory and
proprioceptive sense right thosedorsal columns, because it is
the anterior spinal arteryterritory that is infarcted.
Unfortunately, that meansthat's our motor pathways are
getting knocked out there prettyhard.
Some causes that may make youconsider this more in your
differential diagnosis.
If someone just recently wokeup from anesthesia after a
(11:57):
complicated cardiovascular oraortic surgery and they had a
lot of hypertension during theprocedure, that may raise a red
flag.
An area that's at particularrisk is the artery of
Adamkiewicz, which is a largeradicular artery, often in the
lower thoracic around TA to T12territory, although there is
some variability, and so that isvery susceptible to hypotension
(12:20):
, in particular in older adultswho may have some superimposed
stenosis or atherosclerosis ofthat vessel, and then you throw
that hypotension on top of itduring a prolonged surgery that
may lead to a spinal cordinfarct.
Another potential cause ofvascular myelopathy are dural
arteriovenous fistulas, or duralAVFs.
Now these are a little bit moresubacute to chronic in their
(12:43):
onset and it's thought thatthey're mostly causing these
symptoms due to venouscongestion, although they may
present as an infarct as well.
On imaging, typically MRI,we're going to be looking for
vascular flow voids,particularly on T2 sequences.
So if you see these little darkspots in the bright CSF, that
(13:03):
should raise your suspicion fora possible dural AVF.
However, it is a verychallenging diagnosis to make
and if the clinical suspicion ishigh.
Even with normal MRI, you mayneed to ask your
neurointerventionalist for aspinal angiogram.
So definitely a verychallenging diagnosis in these
patients.
Who is it going to happen to?
It's a little more common inmen over the age of 50 and those
(13:26):
with a history of prior spinalsurgery.
Last category I wanted to touchon during this recording genetic
disorders.
Most of these are fairly rareand in these cases family
history is going to be of theutmost importance.
Starting with that ishereditary spastic paraplegia.
So again, family history veryimportant, and the severity and
(13:49):
progression of these symptomscan vary significantly from
person to person.
Lastly, I'll mentionadrenomyeloneuropathy, which can
sometimes be seen in femalecarriers of X-linked
adrenoleukodystrophy.
So they'll have a lot of thesame symptoms that we mentioned
before in terms of spasticity,bowel bladder issues, difficulty
walking, etc.
But there will oftentimes besomething in the story to
(14:11):
suggest adrenal insufficiency.
So in these patients we mayalso be sending out very
long-chain fatty acid profilesor genetic testing, depending on
the presentation.
That is all I have for youtoday If you made it this far.
Thank you so much and if youenjoyed this podcast, please
leave us a five-star review onApple Spotify, wherever you get
your podcasts.
If you found the informationtoday helpful, please share it
(14:32):
with your friends, subscribe forfuture episodes, and you can
find me on X, formerly known asTwitter, at DrKentris
D-R-K-E-N-T-R-I-S.
And you can find the officialshow at Neuro underscore podcast
N-T-R-I-S.
And you can find the officialshow at neuro underscore podcast
.
You can also find more of ourresources on the website online
at theneurotransmitterscom.
Thank you again for listeningand we'll see you next time.
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