August 12, 2025 • 43 mins
Dr. Divij Sharma presents a challenging case of altered mental status.
Dr. Karlos Acurio-Ortiz tackles this mysterious presentation.
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Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:01):
Hello everyone and welcome back to another
recording of theNeurotransmitters.
I'm your host, dr MichaelKentris, and today I'm very
fortunate to have two guests onand we are going to be doing a
case presentation.
So first off, let me have ourcase presenter go ahead and
introduce himself.
Speaker 2 (00:22):
Hi, michael, pleasure to be on this podcast.
I'm Tevij.
My name is Tevij Sharma.
I am one of the doctors who'sright now working in Mumbai,
india.
I have tremendous experience ofworking in neurology and
subspecialization of neurologyover the last two years in India
and in Australia as well, andI'm just very delighted to just
here, very delighted to presentabout the cases which I
(00:43):
encountered in Australia and upfor a very good-paced discussion
.
Speaker 1 (00:47):
Awesome.
Thank you so much, and ourdiscussant, who has bravely
stepped into the arena.
Speaker 3 (00:56):
Hello everyone.
I'm Carlos.
I'm a physician from Peru, Ilove neurology and, if I can
apply into neurology residencythis year, hopefully I will make
the cut.
Happy to start this challengeAwesome.
Speaker 1 (01:14):
So Divyaj has some excellent cases for us, and he's
going to be hitting us with onetoday, so go ahead and start us
off.
Speaker 2 (01:22):
Yeah, sure, thanks, michael.
So the case hasn't changed inchat.
So it was a bit of a dramaticpresentation, fine of a puzzle
than we first encountered thisdays.
So she's a 54 year old lady,the past history of mycobacteria
and dysmenitis.
Representative of october.
The confusional state the twodays she was first admitted to a
(01:44):
local hospital with complaintsof carcass, fatigue, tiredness,
breathlessness and male jointpains for about 8-9 months, for
which she was given steroids andGCR and then discharged.
No other history was given.
When she came to our hospitalshe was caught when she started
experiencing multiple episodesof anxiety and effects in psych
pieces.
This was in addition to theconfusional state that she was
(02:05):
having for the last daughter andshe started experiencing
multiple episodes of anxiety andattacks in psychosis.
This was in addition to theaccusation she was having for
the last two days.
In one further questioning thefamily stated that she has been
experiencing visualhallucinations for the past two
days.
Family had also noticed mildcognitive decline and
intermittent behavioral changesfor the past eight to nine
months.
The family family as well gotsome information from the
(02:26):
patient gave history of pain inthe lower extremities for the
several patients for the past 1year, including joint pains and
also neuropathy.
Her personal history and familyhistory was on the map.
Now, on the examination front,we did a manual status
examination.
It was less than 24 by 30.
We were true of the diffusionthat she was in already.
(02:48):
Cardiovascular, respiratory andcapillary intrasomal
examination was long.
All the respiratory examinationhad some mild repetitions and
high glossing.
How about the neurological andphysical examination?
We did a whole upper extremityand lower extremity and I load
the positive findings here.
Muscle bulk and tone was moving, the power was grade 4 upon 5
(03:13):
or either the MRC or MRC gradingin both lower limbs.
The sensory examination waslong.
We peeped in with jerks ornormal, or the flexes were
normal and most like there wasno flexes.
Or the disability examinationthere was no rash, no next
preference or no back edema onfront disc repeat.
There was no such sweating orfingers or written names loose
(03:34):
down.
Don't know about persons.
Now I'm clinical examination.
Now, panos, what do you think?
Where does the wholesymptomology mobilize you?
Speaker 3 (03:50):
Okay, that's very interesting.
So for me, the first thing Iwill do is try to define this
pattern of presentation in time.
So this looks like it was a fewdays right.
Speaker 2 (04:08):
Yes, the confusion falls for a few days, but the
panic attacks, the anxietyattacks and visual
hallucinations were out of thepast one or two weeks.
Speaker 3 (04:17):
One or two.
So I will define this as asub-acute presentation of a
multi-symptom disease.
So we have altered mentalstatus, we have visual
hallucinations, we have thepanic attacks and anxiety.
(04:38):
So if I think in my mind aboutpossible causes, probably more
metabolic or autoimmune diseaseswill come into my mind.
Speaker 2 (04:57):
I will not think so much in something vascular, for
example, but mainly somemetabolic or other or autoimmune
encephalopathies but in termsof if you were to say, if you
were to point it out as acomplete, where would the
symptom occur?
Is you can know?
(05:18):
Is it looking at the pain?
Is it something?
Are you looking at the pain?
Is it something when you'remeddling something in the
cerebellum, something in thespinal cord, something in the
nose?
Where do you think the problemis?
Speaker 3 (05:32):
That's a very good question.
Is she only confused, or she'salso somnolent or lethargic?
Speaker 2 (05:41):
Yes, so there's confusion and visual
hallucinations exactly inpanoplycics, which are the
sub-proposal.
This was the background ofhaving fatigue, lethargy and
joint pains in the last 19months.
Speaker 3 (05:56):
Okay, okay, so, because I'm thinking fatigues
and joint pains that make methink you know out immune.
But regarding localization,she's having visual
hallucinations and confusion andaltered mental status.
Speaker 2 (06:20):
spread involvement of the cortex, perhaps, or more
localized involvement of somepart of the brain stream so it
does localize your cerebralcortex because it's more of an
encephalopathy right where yousee behavior changes, visual
(06:41):
hallucinations and all that.
So let's ignore the you knowmarket fatigue and the joint
pain, behavioral changes, visualexhibitions and all that.
So let's ignore the you knowmarket stream fatigue and the
joint pain spots right now andlet's just focus on neurologics.
That's likely said.
It does look nice to asettlement for vaccine day and
so, based on the history andexamination findings, what all
etiologies would you considerhere?
(07:02):
What are etiology causes?
Or maybe in a what alletiologies would you consider
here?
What are etiology causes?
Or maybe in a differentialseptum scene?
Just based on the history ofthese examinations, Okay.
Speaker 3 (07:11):
so if we define this as encephalopathy, then our
differential probably wouldinclude something infectious
like herpes, encephalopathy orother viruses.
Our differential will alsoinclude some other autoimmune
(07:35):
causes like autoimmuneencephalitis.
If we are thinking aboutmetabolic causes, then we can
think in hepatic encephalopathyand let me think other causes of
(08:09):
infection can also causedelirium which can give you
confusion and dyssymptomatology.
That's what I will think fornow.
Speaker 2 (08:20):
Perfect.
So great list of differentionsthere, carlos, and I really
agree with you that how you werenot in favor of a vascular
cause.
Yes, it doesn't seem likesomething which is frasque
considering.
It's very simple, if you canpass it quite.
So it has varied psychiatricsymptoms, which is basically how
the solution came out, whenother than infusion has been in
the back, and some of thesesymptoms.
(08:41):
So, with all the differentialsthat you mentioned, infectious,
systemic, autoimmune metaboliccauses like hepatic or endemic
anti-epiphany, how would youlike to start the investigation
plan?
What would you like to send inthe next or emerging, how would
you like to start theinvestigation?
Speaker 3 (09:01):
So, I will definitely start with some basic metabolic
panel See her glucose BUN.
I will take out perhaps a CBC,looking at the other
(09:30):
differentials.
Maybe I will ask for someautoimmune biomarkers ANA.
I haven't mentioned this, butother autoimmune diseases with
systemic involvement can giveyou this.
Lupus, for example, can giveyou this.
(09:51):
If I'm thinking about systemicinfection, perhaps I will also
ask a URI analysis.
I would like oh yeah, go ahead.
Speaker 2 (10:12):
Yeah, go ahead.
Speaker 3 (10:14):
Yeah, I would like an MRI, but I'm not sure if I can
ask it at this point In Peru.
It's something we definitelywouldn't have access to
immediately.
Speaker 2 (10:25):
So let's take next, taking two components.
Let's do mild chemicals first,that you ordered, okay, and
imaging modalities next.
So let's first discuss aboutthe biochemical which you
already ordered, and second isthe aging modality.
So one thing you probablymissed out would we would like
to do a CSF here as well.
Right, it's not that it's acube, but we would like to know
defilitis and infections.
(10:47):
So that's one thing we wouldlike to know.
So this patient had all of it.
She initially.
Now I'll read out the findingswhich she had in presentation.
So hemoglobin was 8.1, fairlylow.
Total leukocyte count onhemogram on platin was 8800,
(11:09):
which is within normal limits.
Platelet count was about 98000.
Blood urea was 37, which iswithin normal limits.
Creatinine was 3, again, sodiumwas 153.
Potassium was normal.
Erythrocyte sedimentation ratewas 100.
Crp C-reactive protein was 90.
(11:31):
Again the Bacchus, boba Bium.
The urine analysis, urineculture was negative.
Urine protein had plus 4proteins, so the urine had 2 red
blood cells.
Otherwise there were no puscells.
No plus 4 proteins, so theurine urine had 2 red blood
cells, otherwise they were lowblood cells, no crystals, no
bacteria.
And in terms of the workup forautoimmune serology, so for ANE
(11:55):
cause, ane type, are stronglypositive.
So anti-DSD is also positiveand the anti-RNP, which is the
ribonucleotide, is also positive.
C-anca, p-anca was negative.
The C3 levels, which is thecomplement levels, were 60,
which was mean, and the C4levels were the low levels.
(12:17):
The CSF planin was completelynormal.
The proteins and glucose werenormal.
The serum glucose was alsonormal was completely normal.
The proteins and glucose werenormal.
The serum glucose was alsonormal and CSF planning was
negative for any bacteria orbacteria and viruses, as you
know.
So biofying and CSF culture wasnot so bad, which was negative.
One notable thing which wementioned about the other which
(12:41):
we are exploring, autoimmuneentomitis.
At this juncture she was veryearly on in her admission and
investigation phase.
No autoimmune bio was sent offat this point, so we didn't do
that investigation right now.
The investigations, the otherinvestigations, the bio can be.
Really you had the answer now,carlos, just what imaging
(13:03):
modalities let's say you passedon these results and what
imaging modalities would youlike to volunteer?
Speaker 3 (13:18):
Also just thinking in the differential.
Now that we have some lapse, Iwill think my possibility of
something being infectious likeherpes encephalitis is less now.
Encephalitis is less now justbecause the CBC is normal and
(13:45):
the CSF does not show a patternof HSV with blood or low glucose
.
Considering metabolic causes,it seems like the basic
metabolic panel is also normal,but we have found some elevated
(14:06):
biomarkers regardingautoimmunity, so my suspicion of
autoimmune disease,particularly considering other
symptomatology I know you don'twant that, but it's higher.
So if I want to see an adhesioncaused by autoimmune
(14:28):
involvement, probably I will askfor a brain MRI.
Speaker 2 (14:35):
So that's it.
You summarized them well.
Obviously, in the context ofpositive autoimmune markers and
slightly high inflammatorymarkers and also high reactants,
they're thinking somethingalong which is multi-system
declines where the autoimmunefalls through.
So the MRI brain was completelynormal, literally on two
occasions actually, and my brainwas normally in both the
(14:59):
occasions.
Oh, that's so.
We actually started off withthe CT scan.
I was considering Q10 to be.
We started off with the CT scanand soon was the MRI, and the
MRI and the GPT was also savingbeyond the risk and the positive
, especially some sub-approvedclassical items which stands in
(15:23):
acute and different.
We had that in the thing whichwas also, which was also the MRI
, and geography was also good oh, that's, that's very
interesting.
Speaker 3 (15:36):
Yeah, so so you are was also.
Oh, that's very interesting.
So you ordered also a CTbesides the MRI.
Speaker 2 (15:44):
Yes, we ordered a CT before the MRI just to exclude
any major mass damage andsomething that we may list early
on.
So, as a protocol, we did itwith a CT scan, which was
normally done in patients withan MRI, and geography in a
unanimating list early on.
So, as a protocol, we did a CPSgame, which was normally done
in Indian patients with an MRIangiography, which was also done
.
So let's say what are yourthoughts, whether you are there
(16:12):
as a clinician, as an intern,where do you think you're stuck
right now?
Who's helpful?
You see?
Speaker 3 (16:22):
So I think it's kind of harder now.
From my perspective, I wouldsay clinical symptomatology
comes always first.
Of course the MRI may be normal, but regarding the
symptomatology again, that ismultisystemic and just the
(16:49):
positive autoimmune by Markovs,I would still think something
autoimmune.
My guess will be to considersomething like steroids just to
see if the patient gets anybetter.
I am a little worried about thecreatinine.
(17:10):
Maybe if I am thinking of that,she has an elevated creatinine
due to an autoimmunepresentation of the disease, or
maybe she's having a pre-renalAKI.
I will have to consider thatand perhaps give some fluids,
(17:32):
probably.
But I think that I can't startsteroids because, uh, my, my
suspicion for infection is low,so I don't think I will be
hurting the patient.
Speaker 2 (17:44):
Hopefully well, I do agree with you, before starting
steroids you've got to becareful and judicial right.
What if you actually suppressan immune system and something
else goes onward?
Right?
Especially if you're dealingwith an autoimmune disease and
only plays out in certain ways.
So before we actually speakabout in the past, about what
(18:05):
management, managementbeforehand, just want to
summarize the cases for you.
So this patient's tongue,behaving symptoms, psychiatric
symptoms, confusion, visualhallucination, attacks we did a
blood work.
We did find no hematitis, noPHS.
We did find positive autoimmunemarkers, that is, a BSDNA.
(18:26):
She had elevated P apne, whichwas very, which was very bad in
her team.
And she also had a positiveurine protein Now in the gym and
she also had a positive urineprotein.
Now, urine protein was in therange of the nephrotic range
broken lid which is more than3.5 grams per hit.
And you have all these, youhave all these case history with
you right now.
So before you actually decideto go ahead and use steroids or
(18:49):
something else, do you thinkthis patient will be able to
have a patient will need areferral, other specialities, so
he can stop seeking and haveboth to reach you out.
What speciality would you liketo embody?
Speaker 3 (18:59):
and you can seek a legless NPC oh, that's a very
good question and yes,definitely I will ask perhaps
rheumatology to give me a handhand.
I don't know if I can askinfectious diseases to rule out
infection in here, or they willbe super mad if I do that, but
(19:22):
if I can yeah I can I will askalso.
Speaker 2 (19:31):
So we will talk about rheumatology and infectious
diseases.
So well, in spreadsheetdiseases I'm writing off saying
that urine masses is normal.
Blood birth has been generatedin BC.
Csf is normal.
The urine masses is normal.
She doesn't have a female,she's not in sepsis.
Why does it complete the normal?
(19:51):
So why it was?
You're like it's something likean autoimmune technology and
the same thing and in the lightof this years, I'm probably
different in ecology and greenand white, you know great.
Speaker 3 (20:10):
What does chromatology says?
Speaker 2 (20:14):
so lumbar, as chromatology says.
So look how Z has come to youand you know they're really
interested, I'm saying, in theDNA is possible and the DNA is
possible.
So the thinking along the mindof you is very specific for me
personally.
They're concerned about thehydrogens of repressor.
(20:35):
They are concerned about beinghigh proteins in the urine and
very high creatinine.
So who do you think they aregoing to be next?
Speaker 3 (20:42):
yes, nephrology will be of a lot of help.
Yes, definitely yeah excellent?
Speaker 2 (20:47):
yeah, of course.
So nephrology is a newphenomenon and they are also
interested in the case,considering.
Now we are dealing with veryhigh creatinine, very high
protein protein in your genes,which is very annoying, and they
are actually aware of howluteus 10 was very debilitating
for the team.
So, yeah, they now.
(21:08):
Now they turn to you, the team.
Okay, your main team is goingto do the case, he is going to
make up this patient and theywant to advise management.
How would you propose with thepatient, considering now that
you have a definition, you havea blood definition in our
diagnosis, you have all thepains of being deflated in view
(21:32):
of these acute confusion and weneed, in view of this acute
confusion and being in amatchmaking.
It wasn't well psyched, right?
Yep, it's even more psyched.
Back to your screen.
Speaker 3 (21:42):
That's a good question.
I would say, if I'm dealingwith something that is, you know
, in some ways calledorganically cause, at least not
at the beginning, I will thinkin psychiatry.
I will hope to treat first thecause of this probable
(22:08):
symptomatology and then see ifshe persists, perhaps thinking
additional causes.
But at the beginning, beginning, I will not consider psychiatry
okay, that's wonderful.
Speaker 2 (22:24):
So psychiatry has signed up.
Now you have this team and youare basically proposed with this
decision of starting equipment.
What people do you make thismove?
Speaker 3 (22:39):
So yeah, if I'm thinking of a medication to
start, steroids definitely willbe at the top of my list.
I think that if she already hasthe positive autoimmune markers
DNA, double stranded weight,yeah, dna then if she also
(23:07):
fulfills several certainclinical criteria also we can
consider this lupus and thentreat accordingly to a lupus
flare.
So, yeah, I think she fits thepattern, at least to my mind,
and I will start definitelysteroids.
(23:28):
The dosing of that steroids, Iwill say high, but I don't know
the number exactly.
And yeah, that's my thought sofar good.
Speaker 2 (23:42):
So you want to create health for new person who wants
to start with very highsteroids and there won't be any
minimal suppression control,it's just steroids won't do the
trick for you yeah, so high doseIB and MP is the best way to
start.
Yeah, so material presence aloneyes, high dose IV and MP is the
best way to start, you know soyou as a team you decide to get
(24:07):
IV and ethyl and it was athousand grams given in five
days and the real thing was veryactively and very closely
involved.
They wanted to go ahead and doa renal biopsy to stage the so
that they can take a form of thetreatment.
But the patient and patientfamily quickly refused the renal
(24:27):
biopsy so they went toRosenpum's and they did not want
any medicine Now.
Nevertheless, we had to getsome systematic in that person's
immunotherapy.
So she was also started onOrin-Y-Koshimong Morphidine.
It's a remunerative suppressantwhich is very, very protective
in lupus patients who need tosuffer from weak injuries, and
(24:50):
also anti-coagulation andanti-pregnancy therapy was
started in the patient whostopped to prevent thrombosis.
Newer patients had increasedpregnancy to 11th level versus
deep brain thrombosis and somebrain surgery strokes.
So that was the.
Speaker 1 (25:06):
So there's a couple of things Really really
challenging case so far.
You know, when we think aboutlike a neuropsychiatric onset of
lupus and this is a patient whohad no history of autoimmune
diseases that we know of Is thatcorrect?
Unusual characteristics here,right when the CSF panel
(25:34):
sometimes with systemicautoimmune encephalitis you can
have a relatively unremarkablelooking CSF profile, like you
maybe can have like a mildincrease in the white blood
cells, sometimes very low, likestill like 10 to 15, you know,
enough to be abnormal but notenough to point you in the
direction of an infection.
It's very unusual for theprotein to be normal also.
(25:56):
So I thought that was the thingthat was the most surprising to
me, because usually with mostencephalitis you're going to at
least see some abnormalities inthe CSF profile and a new onset,
neuropsychiatric lupus kind of,as the presenting symptoms is
very in and of itself veryremarkable, especially in
(26:20):
someone in her age group Usuallywe're going to be looking at
more young adults as opposed tosomeone squarely in the middle
age, in their 50s.
So some, some atypicalpresentations in this
presentation of an atypicalentity so this was the case.
Speaker 2 (26:36):
This was the interesting part because I
remember carlos.
In the initial history I toldyou that she had initially
presented to all of hospitalwith fatigue, joint pains and
fatigue, joint pains and moretiredness, and she was just
given steroids, analgesics anddischarged.
So I think that was the onsetwhere she actually developed
these mucosal symptoms.
That was about 9-10 months ago.
(26:58):
And now she developed thesefull-blown neuropsychiatric
manifestations which you want towatch.
Yes, exactly.
And if you see her blood work,if you see in her blood work her
hemoglobin is 91, I believe,which is low, which is low for
any age group.
So she always had that typicallupus-like symptoms history.
(27:20):
Her blood work was not knownfrom there, but if you see, her
hemoglobin is all all the lowand so so her platelets.
So she, for all you know, shemay happen to have dyspnea,
thrombocytopenia in addition tothese lupus classic syndromes
she was having the last 10, 11months.
We just saw it right nowbecause she's blown into this
(27:41):
neuropsychiatric component.
Speaker 1 (27:44):
Chris, you did a single import yeah, yeah, it is
one of those things we do seefairly often in neurology where
someone may have an underlyingneurologic autoimmune condition
like myasthenia gravis orsomething, and they got this
little short course of steroidsand they got better for a period
of time.
It is right, this kind ofnonspecific fatigue can
(28:04):
definitely be a red herringsometimes, but sometimes it's
also the missing link in thestory.
I also thought the spinal fluidbeing normal was very
surprising as well.
With a lot of autoimmuneencephalitis presentations,
you'll at least have maybe amild increase in the white blood
cells or at the very least,some elevated protein.
(28:25):
So I thought that was also veryunusual.
Protein, so I thought that wasalso very unusual.
The mri being normalunfortunately not as uncommon in
these cases.
Um, so very challenging whenyou don't have anything
specifically in the neuro realmthat tests positive per se.
But uh, good point going backto kind of like the serum
(28:46):
biomarkers and a good example ofhow you know you need those
follow-up tests when you have apositive ana.
Speaker 3 (28:52):
Yeah, definitely, and I will just add that that is a
common what you described like apatient just giving steroids
and then going back a year laterto a hospital at least, at
least that is common in myexperience in Peru and I think
in other low and middle incomecountries.
We don't have an electronicrecord history, so, yeah, going
(29:17):
back and asking the patientabout possible diagnosis, this
is a very important thing to do.
Speaker 1 (29:32):
And you know, I'll say, even here in the US, where
we do have electronic recordseverywhere, a lot of them don't
talk to each other, so it's notnecessarily as good in practice
as it is on paper per se.
So it is one of those thingswhere you know you may not have
the records.
Also, even from just within myown state, we'll sometimes have
people who went to a hospital 40miles from here.
You would think we'd be able toget those records without too
(29:53):
much hassle.
Not always the case.
So unfortunately I don't thinkit's it's restricted to any
particular global region.
It's pretty a universalexperience, I think, for anyone
taking care of patients who gettheir health during different
areas, sadly, but um, but yeah,uh, divvish.
What other uh teaching points doyou have for us?
(30:14):
Or how did this patient do with,or actually before we get to
that, uh, the treatment I knowyou said you know obviously high
dose steroids withmethylprednisolone, pretty
common for a lot of neurologicautoimmune conditions like
multiple sclerosis, flares andthings like that.
Um, the the mycophenolate.
So I think that's that's a goodpoint uh, to bring up as well,
(30:37):
right, because we can't keeppeople on steroids necessarily
forever without some long-termside effects, but I think for
people who aren't as familiarwith mycophenolate, uh, it's
important to know that the timeto where you're going to be
getting a therapeutic effect canbe very prolonged.
Sometimes we're talking 6 to 12months of being on the
medication before it will reallyhit its stride in terms of its
(31:01):
immunosuppressive effect.
So a lot of times you'rekeeping them on some dose of
steroids or otherimmune-modulating medication
while you're waiting for theseother longer-term medications,
like mycophenolate orazathioprine or what have you,
to kind of be more effective.
And I assume that was kind ofthe long-term plan with this
patient.
Is that correct?
Speaker 2 (31:22):
Oh yeah, no.
So in addition to themycophenolamide pill and before
this patient strictly and thepatient's families were strictly
fused brain biopsy, we couldn'texplore more treatment options.
So additionally high dosesteroids that we had prepared,
we did for her the microserolate and we also started
some benzodiazepines for heranxiety, panic attacks, stuff
she was having.
A good part of this case washer.
(31:45):
Her mental status improveddramatically after we started
the screening, including thebenzodiazepines.
Her creatinine was stillblacklining, it was still the
same 3.1.
It went down to more than thisonce.
Her urine wasn't routinelywater but we were happy that in
terms of her weight and statusshe was much better than before
and this was a very dramaticimprovement.
(32:05):
Let's say four or five days onB1B.
So the neuropsychiatric part isdefinitely taken care of here
and we're happy with that.
In terms of the reunion part,obviously it was a mom film plan
and she was destined for afollow-up three-monthly
follow-up, six-monthly follow-uphow 28% had decommunications
(32:27):
then and we were hoping down to9.
If she ever comes back to us in3-6 months time and she's
fitter, but I'm seeing right nowshe may consent for biopsy and
we may be able to get a pictureof her with her 40 days, but
sadly so.
There's one part which I did.
What mentioned in the casewhich I sent to you was that
this patient actually got COVIDin the hospital.
(32:49):
She did get COVID-19.
She actually succumbed toCOVID-19.
She went to the ICU.
She was really sick.
This patient succumbed toCOVID-19.
Speaker 1 (33:01):
Was this during kind of the height of the pandemic
when this case occurred?
Speaker 2 (33:07):
This was actually so.
This was in 2020.
Was perhaps sitting blocktoward behaving?
Speaker 1 (33:17):
and that's.
That's always a consideration.
You know we have these peoplein the hospital and we're
immunosuppressing them.
Um, yeah, was that thought toplay a factor in in this
patient's uh immune course?
Uh, with a, did she have worselung injury than normal for this
particular variant?
Speaker 2 (33:36):
Yeah, we don't show it.
This was the time in the thirdday was third day.
We had people in there, so itwas obvious it was tough for us
to actually decide for middle,for immunity got so bad because
he put in on high-dose steroidsand used essence, or by virtue
of her age which was not thatbad, which was okay she
succumbed to COVID, or was itnaturally?
(33:57):
The COVID-19 just made her mad.
Each way was exceedingly badand she got so sick that she was
unlucky.
She had a certain.
So these were some importantconsiderations.
It was a lot of backing fromthe family In some cases.
That's how it goes, and so Imean if you're not seeing the
patient, who's finding this isable to mean something.
Speaker 1 (34:20):
Yeah, a challenging situation in a lot of fronts,
both the diagnostic and thetreatment side, unfortunately.
Any final thoughts or teachingpoints about this particular
case that you think that youreally took away taking care of
this patient Divij.
Speaker 2 (34:37):
Yes, sure.
So there are a few criticalpoints in the history of the
Jhavnagra this time.
First of all, neosychiatrichunkus, or widely known as NTSLE
in literature, is a CVcomplication or a very
documented way complicationcharacterized by these
revanchakuru and psychiatricmanifestations on the CV.
Interestingly, thesemanifestations can also occur.
(34:59):
They can precede diagnosis ofSLE, they can proceed
simultaneously as SLE diagnosisor even months and years after
SLE was diagnosed.
The second interesting pointwas that the diagnosis of
leucocytic lupus is indeedchallenging even for skilled
physicians, even from neurology,phleology, rubicology.
First, there is no diagnosticcriteria for NPSAE and you may
(35:23):
have this diagnosis even in thesetting of normally serum, open
CSR biomarkers, normallymuonogen imaging and others in
the middle.
So it most likely comes in thatlimb of a diagnosis of
excretion.
Apple is ruined by themetabolic, autumnal and pymeic
infectious and radioactiveprocedures.
The third interesting part wasthere were some mimics, actually
(35:46):
some mimics, when you actuallyconsidering all of these
extremely rare and probablyworking chemo-neuropsychiatric
rooters.
One was CNS.
Some mimics actually somemimics, when you're actually
considering all of theseextremely rare could be working
on neuropsychiatric disorders.
One was CNS vasculitis.
Second was Jordanian syndrome.
Basically it was you know adifferent moment the
jaw-pinching boy.
You're thinking of Wippel'sdisease, especially CNS Wippel.
You're thinking ofneurobedships disease, as Karan
(36:11):
and she won Orgelium.
So in Shinkansen group Batcheloralso comes with these many
psychiatric manifestationsAvothygmo flashing report,
encephalopathy B, botanicalencephalitis, anti-inflammatory
opium encephalitis, whichincludes the NMDA encephalitis.
Cns lymphoma is simulated toreproduce this only good name.
These were interesting dynamicswhich we thought of when Nebo
kind of working up this case.
(36:32):
And last but not the least, thepatent model of the Peking
Minority News is verymerit-making.
So these were some interestingpoints which I'm chaining them
for these days.
Speaker 1 (36:46):
That sums it up really well and that was a great
rundown of the differentialdiagnosis in these types of
cases with this kind of subacuteonset of neuropsychiatric
symptoms.
It's definitely one of thosethings where you're definitely
looking after all of the strangethings that are on the
neurologic differentialdiagnosis.
Speaker 2 (37:07):
I yes, a little bit of these three.
Speaker 1 (37:10):
I've worked up a number of these cases over the
years myself and it is always achallenge.
They didn't necessarily end upbeing I think only one of them
was neuropsychiatric lupus, butsometimes you end up with the
CNS vasculitis or theneurobechets or, on and on right
CNS lymphoma flunctial,unfortunately.
I've come across that severaltimes as well, and it's it's one
(37:32):
of those things if you, as oneof my attendings, would say to
me right, if you don't know it,you can't diagnose it.
So I think that's a great listof things to consider in these
uh types of situations.
And there's right with thosefolks cranking out new
antibodies.
You know you can always throwperineoplastic syndromes on
there as well, but yeah, itbecomes a real laundry list
(37:55):
sometimes.
So it's great to have aframework to pare these down
somewhat.
Carlos, I'll throw it over toyou Any points of this case that
really struck you or thatyou're going to be taking
forward with you in your futurepractice.
Speaker 3 (38:11):
Yeah, definitely.
So the first thing, alwaysgetting a good history is very
helpful.
So definitely, going over thepast medical history regarding
past diagnosis is very helpful.
Past diagnosis is very helpful.
(38:31):
I will say that, even though wehad somewhat confusing findings
in this patient regarding theMRI and the CSF, thinking about
the most clinically logicalexplanation for this is also
(38:57):
important, particularly to notruling out a disease or ruling
out lupus.
That, in this case, was thediagnosis right.
Speaker 1 (39:08):
Yeah, and this even if we right, because the other
thing is that and I think youpointed this out earlier divvage
is that we're fortunate in thiscase that we got those serum
biomarkers positive.
It is not, unfortunately,uncommon to have those come back
normal or kind of in theintermediate zone.
And right, there's this, thisold adage on the neurology
(39:29):
service, somewhattongue-in-cheek, that no one
dies on the neurology servicewithout a course of steroids.
So that's why I was like, couldit be autoimmune?
That's always the question markthere.
So it's if we don't know whatit is, we ruled out infection.
We think it could be autoimmune, just based on the timeline,
the presentation, things likethat.
Sometimes you do kind of adiagnostic slash, therapeutic
(39:51):
trial of steroids or plasmaexchange or IVIG, kind of these
first-line autoimmune types oftreatments, and do we feel great
when we're kind of treatingblindly and we have a suspicion?
No, but sometimes you have tosay like, well, the patient's
getting worse and this is apotential diagnosis that has a
(40:14):
potential treatment.
So it can be very challengingbecause like, for instance,
let's say it was likeneuropechets, right, and the
person doesn't have any aphthousulcers in their mouth or their
genitals.
Well, you may not have anything, any markers at all, to go off
of, and so you wind up with someof these challenging situations
where you're like I think it'sthis, maybe you don't have that
(40:36):
neuro immunologist to call in toback you up, or things like
that, and so you do have to kindof make a decision, and they're
very challenging cases almostuniversally, as as demonstrated
in this case.
So so thank you both for yourparticipation today and any
final things that you want toplug or resources that you found
(40:58):
useful either in presentingthis case or what have you.
Speaker 2 (41:05):
No, the thing about keep the code in has always been
the American Academy ofNeurology journey.
There are a few interestingpresentations over there and
it's just this one resourcewhich I found.
Second is the practicalneurology podcast, which is the
British podcast which I doactively follow and I did a blog
(41:26):
follow and I did a blog becauseI'm not a neuropsychiatrist but
was in consideration of thediagnosis with the open human
mouth.
I think it's like I can do thisalso.
That's fit in this whole likelost chip when it's not actually
the symptoms.
So for me, for neurology andfor when am I at night?
(41:47):
When do I go off?
And this is what, when you arespeaking about any cases, or at
night or any cases, these twoother or two resources will lead
you back in June and eventuallyyou can meet each other in June
excellent.
Speaker 1 (42:02):
I love the.
The Primal Neurology podcast isa favorite of mine also oh yes.
Speaker 3 (42:08):
I will add, looking at Continuum is also one of the
things that do help me a lot.
Speaker 1 (42:15):
I think they have also an ultimate neurology
edition that is as someone whoworks with Continuum as part of
one of my other hats, I am, ofcourse, an advocate for everyone
to read continuum and for folkswho are in middle or lower
(42:36):
income countries, there usuallyis some plans out there that can
help you get an issue in yourhands as well If you reach out
through, sometimes, the nationalmedical societies depends on
which country you're in and soforth but there are different
ways and you can always reachout to the continuum directly,
uh, depending on where you arelocated geographically, because
(42:57):
it can be a little costlydepending on where you're living
.
All right, gentlemen, thank youboth very much and, uh, you
know, hopefully we'll get togetting together and do another
one of these really soon.
If you want to uh findobviously, subscribe to the
podcast, give us five stars.
Uh, you can find more of ourinformation at the
(43:20):
neurotransmitterscom and you canfind our twitter slash x feed
at neuro underscore podcast.
All right, thanks again,everybody.
Appreciate y'all listening.
Hello everyone and welcome back to another
recording of theNeurotransmitters.
I'm your host, dr MichaelKentris, and today I'm very
fortunate to have two guests onand we are going to be doing a
case presentation.
So first off, let me have ourcase presenter go ahead and
introduce himself.
Speaker 2 (00:22):
Hi, michael, pleasure to be on this podcast.
I'm Tevij.
My name is Tevij Sharma.
I am one of the doctors who'sright now working in Mumbai,
india.
I have tremendous experience ofworking in neurology and
subspecialization of neurologyover the last two years in India
and in Australia as well, andI'm just very delighted to just
here, very delighted to presentabout the cases which I
(00:43):
encountered in Australia and upfor a very good-paced discussion
.
Speaker 1 (00:47):
Awesome.
Thank you so much, and ourdiscussant, who has bravely
stepped into the arena.
Speaker 3 (00:56):
Hello everyone.
I'm Carlos.
I'm a physician from Peru, Ilove neurology and, if I can
apply into neurology residencythis year, hopefully I will make
the cut.
Happy to start this challengeAwesome.
Speaker 1 (01:14):
So Divyaj has some excellent cases for us, and he's
going to be hitting us with onetoday, so go ahead and start us
off.
Speaker 2 (01:22):
Yeah, sure, thanks, michael.
So the case hasn't changed inchat.
So it was a bit of a dramaticpresentation, fine of a puzzle
than we first encountered thisdays.
So she's a 54 year old lady,the past history of mycobacteria
and dysmenitis.
Representative of october.
The confusional state the twodays she was first admitted to a
(01:44):
local hospital with complaintsof carcass, fatigue, tiredness,
breathlessness and male jointpains for about 8-9 months, for
which she was given steroids andGCR and then discharged.
No other history was given.
When she came to our hospitalshe was caught when she started
experiencing multiple episodesof anxiety and effects in psych
pieces.
This was in addition to theconfusional state that she was
(02:05):
having for the last daughter andshe started experiencing
multiple episodes of anxiety andattacks in psychosis.
This was in addition to theaccusation she was having for
the last two days.
In one further questioning thefamily stated that she has been
experiencing visualhallucinations for the past two
days.
Family had also noticed mildcognitive decline and
intermittent behavioral changesfor the past eight to nine
months.
The family family as well gotsome information from the
(02:26):
patient gave history of pain inthe lower extremities for the
several patients for the past 1year, including joint pains and
also neuropathy.
Her personal history and familyhistory was on the map.
Now, on the examination front,we did a manual status
examination.
It was less than 24 by 30.
We were true of the diffusionthat she was in already.
(02:48):
Cardiovascular, respiratory andcapillary intrasomal
examination was long.
All the respiratory examinationhad some mild repetitions and
high glossing.
How about the neurological andphysical examination?
We did a whole upper extremityand lower extremity and I load
the positive findings here.
Muscle bulk and tone was moving, the power was grade 4 upon 5
(03:13):
or either the MRC or MRC gradingin both lower limbs.
The sensory examination waslong.
We peeped in with jerks ornormal, or the flexes were
normal and most like there wasno flexes.
Or the disability examinationthere was no rash, no next
preference or no back edema onfront disc repeat.
There was no such sweating orfingers or written names loose
(03:34):
down.
Don't know about persons.
Now I'm clinical examination.
Now, panos, what do you think?
Where does the wholesymptomology mobilize you?
Speaker 3 (03:50):
Okay, that's very interesting.
So for me, the first thing Iwill do is try to define this
pattern of presentation in time.
So this looks like it was a fewdays right.
Speaker 2 (04:08):
Yes, the confusion falls for a few days, but the
panic attacks, the anxietyattacks and visual
hallucinations were out of thepast one or two weeks.
Speaker 3 (04:17):
One or two.
So I will define this as asub-acute presentation of a
multi-symptom disease.
So we have altered mentalstatus, we have visual
hallucinations, we have thepanic attacks and anxiety.
(04:38):
So if I think in my mind aboutpossible causes, probably more
metabolic or autoimmune diseaseswill come into my mind.
Speaker 2 (04:57):
I will not think so much in something vascular, for
example, but mainly somemetabolic or other or autoimmune
encephalopathies but in termsof if you were to say, if you
were to point it out as acomplete, where would the
symptom occur?
Is you can know?
(05:18):
Is it looking at the pain?
Is it something?
Are you looking at the pain?
Is it something when you'remeddling something in the
cerebellum, something in thespinal cord, something in the
nose?
Where do you think the problemis?
Speaker 3 (05:32):
That's a very good question.
Is she only confused, or she'salso somnolent or lethargic?
Speaker 2 (05:41):
Yes, so there's confusion and visual
hallucinations exactly inpanoplycics, which are the
sub-proposal.
This was the background ofhaving fatigue, lethargy and
joint pains in the last 19months.
Speaker 3 (05:56):
Okay, okay, so, because I'm thinking fatigues
and joint pains that make methink you know out immune.
But regarding localization,she's having visual
hallucinations and confusion andaltered mental status.
Speaker 2 (06:20):
spread involvement of the cortex, perhaps, or more
localized involvement of somepart of the brain stream so it
does localize your cerebralcortex because it's more of an
encephalopathy right where yousee behavior changes, visual
(06:41):
hallucinations and all that.
So let's ignore the you knowmarket fatigue and the joint
pain, behavioral changes, visualexhibitions and all that.
So let's ignore the you knowmarket stream fatigue and the
joint pain spots right now andlet's just focus on neurologics.
That's likely said.
It does look nice to asettlement for vaccine day and
so, based on the history andexamination findings, what all
etiologies would you considerhere?
(07:02):
What are etiology causes?
Or maybe in a what alletiologies would you consider
here?
What are etiology causes?
Or maybe in a differentialseptum scene?
Just based on the history ofthese examinations, Okay.
Speaker 3 (07:11):
so if we define this as encephalopathy, then our
differential probably wouldinclude something infectious
like herpes, encephalopathy orother viruses.
Our differential will alsoinclude some other autoimmune
(07:35):
causes like autoimmuneencephalitis.
If we are thinking aboutmetabolic causes, then we can
think in hepatic encephalopathyand let me think other causes of
(08:09):
infection can also causedelirium which can give you
confusion and dyssymptomatology.
That's what I will think fornow.
Speaker 2 (08:20):
Perfect.
So great list of differentionsthere, carlos, and I really
agree with you that how you werenot in favor of a vascular
cause.
Yes, it doesn't seem likesomething which is frasque
considering.
It's very simple, if you canpass it quite.
So it has varied psychiatricsymptoms, which is basically how
the solution came out, whenother than infusion has been in
the back, and some of thesesymptoms.
(08:41):
So, with all the differentialsthat you mentioned, infectious,
systemic, autoimmune metaboliccauses like hepatic or endemic
anti-epiphany, how would youlike to start the investigation
plan?
What would you like to send inthe next or emerging, how would
you like to start theinvestigation?
Speaker 3 (09:01):
So, I will definitely start with some basic metabolic
panel See her glucose BUN.
I will take out perhaps a CBC,looking at the other
(09:30):
differentials.
Maybe I will ask for someautoimmune biomarkers ANA.
I haven't mentioned this, butother autoimmune diseases with
systemic involvement can giveyou this.
Lupus, for example, can giveyou this.
(09:51):
If I'm thinking about systemicinfection, perhaps I will also
ask a URI analysis.
I would like oh yeah, go ahead.
Speaker 2 (10:12):
Yeah, go ahead.
Speaker 3 (10:14):
Yeah, I would like an MRI, but I'm not sure if I can
ask it at this point In Peru.
It's something we definitelywouldn't have access to
immediately.
Speaker 2 (10:25):
So let's take next, taking two components.
Let's do mild chemicals first,that you ordered, okay, and
imaging modalities next.
So let's first discuss aboutthe biochemical which you
already ordered, and second isthe aging modality.
So one thing you probablymissed out would we would like
to do a CSF here as well.
Right, it's not that it's acube, but we would like to know
defilitis and infections.
(10:47):
So that's one thing we wouldlike to know.
So this patient had all of it.
She initially.
Now I'll read out the findingswhich she had in presentation.
So hemoglobin was 8.1, fairlylow.
Total leukocyte count onhemogram on platin was 8800,
(11:09):
which is within normal limits.
Platelet count was about 98000.
Blood urea was 37, which iswithin normal limits.
Creatinine was 3, again, sodiumwas 153.
Potassium was normal.
Erythrocyte sedimentation ratewas 100.
Crp C-reactive protein was 90.
(11:31):
Again the Bacchus, boba Bium.
The urine analysis, urineculture was negative.
Urine protein had plus 4proteins, so the urine had 2 red
blood cells.
Otherwise there were no puscells.
No plus 4 proteins, so theurine urine had 2 red blood
cells, otherwise they were lowblood cells, no crystals, no
bacteria.
And in terms of the workup forautoimmune serology, so for ANE
(11:55):
cause, ane type, are stronglypositive.
So anti-DSD is also positiveand the anti-RNP, which is the
ribonucleotide, is also positive.
C-anca, p-anca was negative.
The C3 levels, which is thecomplement levels, were 60,
which was mean, and the C4levels were the low levels.
(12:17):
The CSF planin was completelynormal.
The proteins and glucose werenormal.
The serum glucose was alsonormal was completely normal.
The proteins and glucose werenormal.
The serum glucose was alsonormal and CSF planning was
negative for any bacteria orbacteria and viruses, as you
know.
So biofying and CSF culture wasnot so bad, which was negative.
One notable thing which wementioned about the other which
(12:41):
we are exploring, autoimmuneentomitis.
At this juncture she was veryearly on in her admission and
investigation phase.
No autoimmune bio was sent offat this point, so we didn't do
that investigation right now.
The investigations, the otherinvestigations, the bio can be.
Really you had the answer now,carlos, just what imaging
(13:03):
modalities let's say you passedon these results and what
imaging modalities would youlike to volunteer?
Speaker 3 (13:18):
Also just thinking in the differential.
Now that we have some lapse, Iwill think my possibility of
something being infectious likeherpes encephalitis is less now.
Encephalitis is less now justbecause the CBC is normal and
(13:45):
the CSF does not show a patternof HSV with blood or low glucose
.
Considering metabolic causes,it seems like the basic
metabolic panel is also normal,but we have found some elevated
(14:06):
biomarkers regardingautoimmunity, so my suspicion of
autoimmune disease,particularly considering other
symptomatology I know you don'twant that, but it's higher.
So if I want to see an adhesioncaused by autoimmune
(14:28):
involvement, probably I will askfor a brain MRI.
Speaker 2 (14:35):
So that's it.
You summarized them well.
Obviously, in the context ofpositive autoimmune markers and
slightly high inflammatorymarkers and also high reactants,
they're thinking somethingalong which is multi-system
declines where the autoimmunefalls through.
So the MRI brain was completelynormal, literally on two
occasions actually, and my brainwas normally in both the
(14:59):
occasions.
Oh, that's so.
We actually started off withthe CT scan.
I was considering Q10 to be.
We started off with the CT scanand soon was the MRI, and the
MRI and the GPT was also savingbeyond the risk and the positive
, especially some sub-approvedclassical items which stands in
(15:23):
acute and different.
We had that in the thing whichwas also, which was also the MRI
, and geography was also good oh, that's, that's very
interesting.
Speaker 3 (15:36):
Yeah, so so you are was also.
Oh, that's very interesting.
So you ordered also a CTbesides the MRI.
Speaker 2 (15:44):
Yes, we ordered a CT before the MRI just to exclude
any major mass damage andsomething that we may list early
on.
So, as a protocol, we did itwith a CT scan, which was
normally done in patients withan MRI, and geography in a
unanimating list early on.
So, as a protocol, we did a CPSgame, which was normally done
in Indian patients with an MRIangiography, which was also done
.
So let's say what are yourthoughts, whether you are there
(16:12):
as a clinician, as an intern,where do you think you're stuck
right now?
Who's helpful?
You see?
Speaker 3 (16:22):
So I think it's kind of harder now.
From my perspective, I wouldsay clinical symptomatology
comes always first.
Of course the MRI may be normal, but regarding the
symptomatology again, that ismultisystemic and just the
(16:49):
positive autoimmune by Markovs,I would still think something
autoimmune.
My guess will be to considersomething like steroids just to
see if the patient gets anybetter.
I am a little worried about thecreatinine.
(17:10):
Maybe if I am thinking of that,she has an elevated creatinine
due to an autoimmunepresentation of the disease, or
maybe she's having a pre-renalAKI.
I will have to consider thatand perhaps give some fluids,
(17:32):
probably.
But I think that I can't startsteroids because, uh, my, my
suspicion for infection is low,so I don't think I will be
hurting the patient.
Speaker 2 (17:44):
Hopefully well, I do agree with you, before starting
steroids you've got to becareful and judicial right.
What if you actually suppressan immune system and something
else goes onward?
Right?
Especially if you're dealingwith an autoimmune disease and
only plays out in certain ways.
So before we actually speakabout in the past, about what
(18:05):
management, managementbeforehand, just want to
summarize the cases for you.
So this patient's tongue,behaving symptoms, psychiatric
symptoms, confusion, visualhallucination, attacks we did a
blood work.
We did find no hematitis, noPHS.
We did find positive autoimmunemarkers, that is, a BSDNA.
(18:26):
She had elevated P apne, whichwas very, which was very bad in
her team.
And she also had a positiveurine protein Now in the gym and
she also had a positive urineprotein.
Now, urine protein was in therange of the nephrotic range
broken lid which is more than3.5 grams per hit.
And you have all these, youhave all these case history with
you right now.
So before you actually decideto go ahead and use steroids or
(18:49):
something else, do you thinkthis patient will be able to
have a patient will need areferral, other specialities, so
he can stop seeking and haveboth to reach you out.
What speciality would you liketo embody?
Speaker 3 (18:59):
and you can seek a legless NPC oh, that's a very
good question and yes,definitely I will ask perhaps
rheumatology to give me a handhand.
I don't know if I can askinfectious diseases to rule out
infection in here, or they willbe super mad if I do that, but
(19:22):
if I can yeah I can I will askalso.
Speaker 2 (19:31):
So we will talk about rheumatology and infectious
diseases.
So well, in spreadsheetdiseases I'm writing off saying
that urine masses is normal.
Blood birth has been generatedin BC.
Csf is normal.
The urine masses is normal.
She doesn't have a female,she's not in sepsis.
Why does it complete the normal?
(19:51):
So why it was?
You're like it's something likean autoimmune technology and
the same thing and in the lightof this years, I'm probably
different in ecology and greenand white, you know great.
Speaker 3 (20:10):
What does chromatology says?
Speaker 2 (20:14):
so lumbar, as chromatology says.
So look how Z has come to youand you know they're really
interested, I'm saying, in theDNA is possible and the DNA is
possible.
So the thinking along the mindof you is very specific for me
personally.
They're concerned about thehydrogens of repressor.
(20:35):
They are concerned about beinghigh proteins in the urine and
very high creatinine.
So who do you think they aregoing to be next?
Speaker 3 (20:42):
yes, nephrology will be of a lot of help.
Yes, definitely yeah excellent?
Speaker 2 (20:47):
yeah, of course.
So nephrology is a newphenomenon and they are also
interested in the case,considering.
Now we are dealing with veryhigh creatinine, very high
protein protein in your genes,which is very annoying, and they
are actually aware of howluteus 10 was very debilitating
for the team.
So, yeah, they now.
(21:08):
Now they turn to you, the team.
Okay, your main team is goingto do the case, he is going to
make up this patient and theywant to advise management.
How would you propose with thepatient, considering now that
you have a definition, you havea blood definition in our
diagnosis, you have all thepains of being deflated in view
(21:32):
of these acute confusion and weneed, in view of this acute
confusion and being in amatchmaking.
It wasn't well psyched, right?
Yep, it's even more psyched.
Back to your screen.
Speaker 3 (21:42):
That's a good question.
I would say, if I'm dealingwith something that is, you know
, in some ways calledorganically cause, at least not
at the beginning, I will thinkin psychiatry.
I will hope to treat first thecause of this probable
(22:08):
symptomatology and then see ifshe persists, perhaps thinking
additional causes.
But at the beginning, beginning, I will not consider psychiatry
okay, that's wonderful.
Speaker 2 (22:24):
So psychiatry has signed up.
Now you have this team and youare basically proposed with this
decision of starting equipment.
What people do you make thismove?
Speaker 3 (22:39):
So yeah, if I'm thinking of a medication to
start, steroids definitely willbe at the top of my list.
I think that if she already hasthe positive autoimmune markers
DNA, double stranded weight,yeah, dna then if she also
(23:07):
fulfills several certainclinical criteria also we can
consider this lupus and thentreat accordingly to a lupus
flare.
So, yeah, I think she fits thepattern, at least to my mind,
and I will start definitelysteroids.
(23:28):
The dosing of that steroids, Iwill say high, but I don't know
the number exactly.
And yeah, that's my thought sofar good.
Speaker 2 (23:42):
So you want to create health for new person who wants
to start with very highsteroids and there won't be any
minimal suppression control,it's just steroids won't do the
trick for you yeah, so high doseIB and MP is the best way to
start.
Yeah, so material presence aloneyes, high dose IV and MP is the
best way to start, you know soyou as a team you decide to get
(24:07):
IV and ethyl and it was athousand grams given in five
days and the real thing was veryactively and very closely
involved.
They wanted to go ahead and doa renal biopsy to stage the so
that they can take a form of thetreatment.
But the patient and patientfamily quickly refused the renal
(24:27):
biopsy so they went toRosenpum's and they did not want
any medicine Now.
Nevertheless, we had to getsome systematic in that person's
immunotherapy.
So she was also started onOrin-Y-Koshimong Morphidine.
It's a remunerative suppressantwhich is very, very protective
in lupus patients who need tosuffer from weak injuries, and
(24:50):
also anti-coagulation andanti-pregnancy therapy was
started in the patient whostopped to prevent thrombosis.
Newer patients had increasedpregnancy to 11th level versus
deep brain thrombosis and somebrain surgery strokes.
So that was the.
Speaker 1 (25:06):
So there's a couple of things Really really
challenging case so far.
You know, when we think aboutlike a neuropsychiatric onset of
lupus and this is a patient whohad no history of autoimmune
diseases that we know of Is thatcorrect?
Unusual characteristics here,right when the CSF panel
(25:34):
sometimes with systemicautoimmune encephalitis you can
have a relatively unremarkablelooking CSF profile, like you
maybe can have like a mildincrease in the white blood
cells, sometimes very low, likestill like 10 to 15, you know,
enough to be abnormal but notenough to point you in the
direction of an infection.
It's very unusual for theprotein to be normal also.
(25:56):
So I thought that was the thingthat was the most surprising to
me, because usually with mostencephalitis you're going to at
least see some abnormalities inthe CSF profile and a new onset,
neuropsychiatric lupus kind of,as the presenting symptoms is
very in and of itself veryremarkable, especially in
(26:20):
someone in her age group Usuallywe're going to be looking at
more young adults as opposed tosomeone squarely in the middle
age, in their 50s.
So some, some atypicalpresentations in this
presentation of an atypicalentity so this was the case.
Speaker 2 (26:36):
This was the interesting part because I
remember carlos.
In the initial history I toldyou that she had initially
presented to all of hospitalwith fatigue, joint pains and
fatigue, joint pains and moretiredness, and she was just
given steroids, analgesics anddischarged.
So I think that was the onsetwhere she actually developed
these mucosal symptoms.
That was about 9-10 months ago.
(26:58):
And now she developed thesefull-blown neuropsychiatric
manifestations which you want towatch.
Yes, exactly.
And if you see her blood work,if you see in her blood work her
hemoglobin is 91, I believe,which is low, which is low for
any age group.
So she always had that typicallupus-like symptoms history.
(27:20):
Her blood work was not knownfrom there, but if you see, her
hemoglobin is all all the lowand so so her platelets.
So she, for all you know, shemay happen to have dyspnea,
thrombocytopenia in addition tothese lupus classic syndromes
she was having the last 10, 11months.
We just saw it right nowbecause she's blown into this
(27:41):
neuropsychiatric component.
Speaker 1 (27:44):
Chris, you did a single import yeah, yeah, it is
one of those things we do seefairly often in neurology where
someone may have an underlyingneurologic autoimmune condition
like myasthenia gravis orsomething, and they got this
little short course of steroidsand they got better for a period
of time.
It is right, this kind ofnonspecific fatigue can
(28:04):
definitely be a red herringsometimes, but sometimes it's
also the missing link in thestory.
I also thought the spinal fluidbeing normal was very
surprising as well.
With a lot of autoimmuneencephalitis presentations,
you'll at least have maybe amild increase in the white blood
cells or at the very least,some elevated protein.
(28:25):
So I thought that was also veryunusual.
Protein, so I thought that wasalso very unusual.
The mri being normalunfortunately not as uncommon in
these cases.
Um, so very challenging whenyou don't have anything
specifically in the neuro realmthat tests positive per se.
But uh, good point going backto kind of like the serum
(28:46):
biomarkers and a good example ofhow you know you need those
follow-up tests when you have apositive ana.
Speaker 3 (28:52):
Yeah, definitely, and I will just add that that is a
common what you described like apatient just giving steroids
and then going back a year laterto a hospital at least, at
least that is common in myexperience in Peru and I think
in other low and middle incomecountries.
We don't have an electronicrecord history, so, yeah, going
(29:17):
back and asking the patientabout possible diagnosis, this
is a very important thing to do.
Speaker 1 (29:32):
And you know, I'll say, even here in the US, where
we do have electronic recordseverywhere, a lot of them don't
talk to each other, so it's notnecessarily as good in practice
as it is on paper per se.
So it is one of those thingswhere you know you may not have
the records.
Also, even from just within myown state, we'll sometimes have
people who went to a hospital 40miles from here.
You would think we'd be able toget those records without too
(29:53):
much hassle.
Not always the case.
So unfortunately I don't thinkit's it's restricted to any
particular global region.
It's pretty a universalexperience, I think, for anyone
taking care of patients who gettheir health during different
areas, sadly, but um, but yeah,uh, divvish.
What other uh teaching points doyou have for us?
(30:14):
Or how did this patient do with,or actually before we get to
that, uh, the treatment I knowyou said you know obviously high
dose steroids withmethylprednisolone, pretty
common for a lot of neurologicautoimmune conditions like
multiple sclerosis, flares andthings like that.
Um, the the mycophenolate.
So I think that's that's a goodpoint uh, to bring up as well,
(30:37):
right, because we can't keeppeople on steroids necessarily
forever without some long-termside effects, but I think for
people who aren't as familiarwith mycophenolate, uh, it's
important to know that the timeto where you're going to be
getting a therapeutic effect canbe very prolonged.
Sometimes we're talking 6 to 12months of being on the
medication before it will reallyhit its stride in terms of its
(31:01):
immunosuppressive effect.
So a lot of times you'rekeeping them on some dose of
steroids or otherimmune-modulating medication
while you're waiting for theseother longer-term medications,
like mycophenolate orazathioprine or what have you,
to kind of be more effective.
And I assume that was kind ofthe long-term plan with this
patient.
Is that correct?
Speaker 2 (31:22):
Oh yeah, no.
So in addition to themycophenolamide pill and before
this patient strictly and thepatient's families were strictly
fused brain biopsy, we couldn'texplore more treatment options.
So additionally high dosesteroids that we had prepared,
we did for her the microserolate and we also started
some benzodiazepines for heranxiety, panic attacks, stuff
she was having.
A good part of this case washer.
(31:45):
Her mental status improveddramatically after we started
the screening, including thebenzodiazepines.
Her creatinine was stillblacklining, it was still the
same 3.1.
It went down to more than thisonce.
Her urine wasn't routinelywater but we were happy that in
terms of her weight and statusshe was much better than before
and this was a very dramaticimprovement.
(32:05):
Let's say four or five days onB1B.
So the neuropsychiatric part isdefinitely taken care of here
and we're happy with that.
In terms of the reunion part,obviously it was a mom film plan
and she was destined for afollow-up three-monthly
follow-up, six-monthly follow-uphow 28% had decommunications
(32:27):
then and we were hoping down to9.
If she ever comes back to us in3-6 months time and she's
fitter, but I'm seeing right nowshe may consent for biopsy and
we may be able to get a pictureof her with her 40 days, but
sadly so.
There's one part which I did.
What mentioned in the casewhich I sent to you was that
this patient actually got COVIDin the hospital.
(32:49):
She did get COVID-19.
She actually succumbed toCOVID-19.
She went to the ICU.
She was really sick.
This patient succumbed toCOVID-19.
Speaker 1 (33:01):
Was this during kind of the height of the pandemic
when this case occurred?
Speaker 2 (33:07):
This was actually so.
This was in 2020.
Was perhaps sitting blocktoward behaving?
Speaker 1 (33:17):
and that's.
That's always a consideration.
You know we have these peoplein the hospital and we're
immunosuppressing them.
Um, yeah, was that thought toplay a factor in in this
patient's uh immune course?
Uh, with a, did she have worselung injury than normal for this
particular variant?
Speaker 2 (33:36):
Yeah, we don't show it.
This was the time in the thirdday was third day.
We had people in there, so itwas obvious it was tough for us
to actually decide for middle,for immunity got so bad because
he put in on high-dose steroidsand used essence, or by virtue
of her age which was not thatbad, which was okay she
succumbed to COVID, or was itnaturally?
(33:57):
The COVID-19 just made her mad.
Each way was exceedingly badand she got so sick that she was
unlucky.
She had a certain.
So these were some importantconsiderations.
It was a lot of backing fromthe family In some cases.
That's how it goes, and so Imean if you're not seeing the
patient, who's finding this isable to mean something.
Speaker 1 (34:20):
Yeah, a challenging situation in a lot of fronts,
both the diagnostic and thetreatment side, unfortunately.
Any final thoughts or teachingpoints about this particular
case that you think that youreally took away taking care of
this patient Divij.
Speaker 2 (34:37):
Yes, sure.
So there are a few criticalpoints in the history of the
Jhavnagra this time.
First of all, neosychiatrichunkus, or widely known as NTSLE
in literature, is a CVcomplication or a very
documented way complicationcharacterized by these
revanchakuru and psychiatricmanifestations on the CV.
Interestingly, thesemanifestations can also occur.
(34:59):
They can precede diagnosis ofSLE, they can proceed
simultaneously as SLE diagnosisor even months and years after
SLE was diagnosed.
The second interesting pointwas that the diagnosis of
leucocytic lupus is indeedchallenging even for skilled
physicians, even from neurology,phleology, rubicology.
First, there is no diagnosticcriteria for NPSAE and you may
(35:23):
have this diagnosis even in thesetting of normally serum, open
CSR biomarkers, normallymuonogen imaging and others in
the middle.
So it most likely comes in thatlimb of a diagnosis of
excretion.
Apple is ruined by themetabolic, autumnal and pymeic
infectious and radioactiveprocedures.
The third interesting part wasthere were some mimics, actually
(35:46):
some mimics, when you actuallyconsidering all of these
extremely rare and probablyworking chemo-neuropsychiatric
rooters.
One was CNS.
Some mimics actually somemimics, when you're actually
considering all of theseextremely rare could be working
on neuropsychiatric disorders.
One was CNS vasculitis.
Second was Jordanian syndrome.
Basically it was you know adifferent moment the
jaw-pinching boy.
You're thinking of Wippel'sdisease, especially CNS Wippel.
You're thinking ofneurobedships disease, as Karan
(36:11):
and she won Orgelium.
So in Shinkansen group Batcheloralso comes with these many
psychiatric manifestationsAvothygmo flashing report,
encephalopathy B, botanicalencephalitis, anti-inflammatory
opium encephalitis, whichincludes the NMDA encephalitis.
Cns lymphoma is simulated toreproduce this only good name.
These were interesting dynamicswhich we thought of when Nebo
kind of working up this case.
(36:32):
And last but not the least, thepatent model of the Peking
Minority News is verymerit-making.
So these were some interestingpoints which I'm chaining them
for these days.
Speaker 1 (36:46):
That sums it up really well and that was a great
rundown of the differentialdiagnosis in these types of
cases with this kind of subacuteonset of neuropsychiatric
symptoms.
It's definitely one of thosethings where you're definitely
looking after all of the strangethings that are on the
neurologic differentialdiagnosis.
Speaker 2 (37:07):
I yes, a little bit of these three.
Speaker 1 (37:10):
I've worked up a number of these cases over the
years myself and it is always achallenge.
They didn't necessarily end upbeing I think only one of them
was neuropsychiatric lupus, butsometimes you end up with the
CNS vasculitis or theneurobechets or, on and on right
CNS lymphoma flunctial,unfortunately.
I've come across that severaltimes as well, and it's it's one
(37:32):
of those things if you, as oneof my attendings, would say to
me right, if you don't know it,you can't diagnose it.
So I think that's a great listof things to consider in these
uh types of situations.
And there's right with thosefolks cranking out new
antibodies.
You know you can always throwperineoplastic syndromes on
there as well, but yeah, itbecomes a real laundry list
(37:55):
sometimes.
So it's great to have aframework to pare these down
somewhat.
Carlos, I'll throw it over toyou Any points of this case that
really struck you or thatyou're going to be taking
forward with you in your futurepractice.
Speaker 3 (38:11):
Yeah, definitely.
So the first thing, alwaysgetting a good history is very
helpful.
So definitely, going over thepast medical history regarding
past diagnosis is very helpful.
Past diagnosis is very helpful.
(38:31):
I will say that, even though wehad somewhat confusing findings
in this patient regarding theMRI and the CSF, thinking about
the most clinically logicalexplanation for this is also
(38:57):
important, particularly to notruling out a disease or ruling
out lupus.
That, in this case, was thediagnosis right.
Speaker 1 (39:08):
Yeah, and this even if we right, because the other
thing is that and I think youpointed this out earlier divvage
is that we're fortunate in thiscase that we got those serum
biomarkers positive.
It is not, unfortunately,uncommon to have those come back
normal or kind of in theintermediate zone.
And right, there's this, thisold adage on the neurology
(39:29):
service, somewhattongue-in-cheek, that no one
dies on the neurology servicewithout a course of steroids.
So that's why I was like, couldit be autoimmune?
That's always the question markthere.
So it's if we don't know whatit is, we ruled out infection.
We think it could be autoimmune, just based on the timeline,
the presentation, things likethat.
Sometimes you do kind of adiagnostic slash, therapeutic
(39:51):
trial of steroids or plasmaexchange or IVIG, kind of these
first-line autoimmune types oftreatments, and do we feel great
when we're kind of treatingblindly and we have a suspicion?
No, but sometimes you have tosay like, well, the patient's
getting worse and this is apotential diagnosis that has a
(40:14):
potential treatment.
So it can be very challengingbecause like, for instance,
let's say it was likeneuropechets, right, and the
person doesn't have any aphthousulcers in their mouth or their
genitals.
Well, you may not have anything, any markers at all, to go off
of, and so you wind up with someof these challenging situations
where you're like I think it'sthis, maybe you don't have that
(40:36):
neuro immunologist to call in toback you up, or things like
that, and so you do have to kindof make a decision, and they're
very challenging cases almostuniversally, as as demonstrated
in this case.
So so thank you both for yourparticipation today and any
final things that you want toplug or resources that you found
(40:58):
useful either in presentingthis case or what have you.
Speaker 2 (41:05):
No, the thing about keep the code in has always been
the American Academy ofNeurology journey.
There are a few interestingpresentations over there and
it's just this one resourcewhich I found.
Second is the practicalneurology podcast, which is the
British podcast which I doactively follow and I did a blog
(41:26):
follow and I did a blog becauseI'm not a neuropsychiatrist but
was in consideration of thediagnosis with the open human
mouth.
I think it's like I can do thisalso.
That's fit in this whole likelost chip when it's not actually
the symptoms.
So for me, for neurology andfor when am I at night?
(41:47):
When do I go off?
And this is what, when you arespeaking about any cases, or at
night or any cases, these twoother or two resources will lead
you back in June and eventuallyyou can meet each other in June
excellent.
Speaker 1 (42:02):
I love the.
The Primal Neurology podcast isa favorite of mine also oh yes.
Speaker 3 (42:08):
I will add, looking at Continuum is also one of the
things that do help me a lot.
Speaker 1 (42:15):
I think they have also an ultimate neurology
edition that is as someone whoworks with Continuum as part of
one of my other hats, I am, ofcourse, an advocate for everyone
to read continuum and for folkswho are in middle or lower
(42:36):
income countries, there usuallyis some plans out there that can
help you get an issue in yourhands as well If you reach out
through, sometimes, the nationalmedical societies depends on
which country you're in and soforth but there are different
ways and you can always reachout to the continuum directly,
uh, depending on where you arelocated geographically, because
(42:57):
it can be a little costlydepending on where you're living
.
All right, gentlemen, thank youboth very much and, uh, you
know, hopefully we'll get togetting together and do another
one of these really soon.
If you want to uh findobviously, subscribe to the
podcast, give us five stars.
Uh, you can find more of ourinformation at the
(43:20):
neurotransmitterscom and you canfind our twitter slash x feed
at neuro underscore podcast.
All right, thanks again,everybody.
Appreciate y'all listening.
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