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The Neurotransmitters: Clinical Neurology Education
Case Report: Altered mental status with Dr. Divij Sharma
Dr. Divij Sharma presents a challenging case of altered mental status.
Dr. Karlos Acurio-Ortiz tackles this mysterious presentation.
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Hello everyone and welcome back to another recording of the Neurotransmitters. I'm your host, dr Michael Kentris, and today I'm very fortunate to have two guests on and we are going to be doing a case presentation. So first off, let me have our case presenter go ahead and introduce himself.
Speaker 2:Hi, michael, pleasure to be on this podcast. I'm Tevij. My name is Tevij Sharma. I am one of the doctors who's right now working in Mumbai, india. I have tremendous experience of working in neurology and subspecialization of neurology over the last two years in India and in Australia as well, and I'm just very delighted to just here, very delighted to present about the cases which I encountered in Australia and up for a very good-paced discussion.
Speaker 1:Awesome. Thank you so much, and our discussant, who has bravely stepped into the arena.
Speaker 3:Hello everyone. I'm Carlos. I'm a physician from Peru, I love neurology and, if I can apply into neurology residency this year, hopefully I will make the cut. Happy to start this challenge Awesome.
Speaker 1:So Divyaj has some excellent cases for us, and he's going to be hitting us with one today, so go ahead and start us off.
Speaker 2:Yeah, sure, thanks, michael. So the case hasn't changed in chat. So it was a bit of a dramatic presentation, fine of a puzzle than we first encountered this days. So she's a 54 year old lady, the past history of mycobacteria and dysmenitis. Representative of october.
Speaker 2:The confusional state the two days she was first admitted to a local hospital with complaints of carcass, fatigue, tiredness, breathlessness and male joint pains for about 8-9 months, for which she was given steroids and GCR and then discharged. No other history was given. When she came to our hospital she was caught when she started experiencing multiple episodes of anxiety and effects in psych pieces. This was in addition to the confusional state that she was having for the last daughter and she started experiencing multiple episodes of anxiety and attacks in psychosis. This was in addition to the accusation she was having for the last two days. In one further questioning the family stated that she has been experiencing visual hallucinations for the past two days. Family had also noticed mild cognitive decline and intermittent behavioral changes for the past eight to nine months. The family family as well got some information from the patient gave history of pain in the lower extremities for the several patients for the past 1 year, including joint pains and also neuropathy. Her personal history and family history was on the map.
Speaker 2:Now, on the examination front, we did a manual status examination. It was less than 24 by 30. We were true of the diffusion that she was in already. Cardiovascular, respiratory and capillary intrasomal examination was long. All the respiratory examination had some mild repetitions and high glossing. How about the neurological and physical examination? We did a whole upper extremity and lower extremity and I load the positive findings here. Muscle bulk and tone was moving, the power was grade 4 upon 5 or either the MRC or MRC grading in both lower limbs. The sensory examination was long. We peeped in with jerks or normal, or the flexes were normal and most like there was no flexes. Or the disability examination there was no rash, no next preference or no back edema on front disc repeat. There was no such sweating or fingers or written names loose down. Don't know about persons. Now I'm clinical examination. Now, panos, what do you think? Where does the whole symptomology mobilize you?
Speaker 3:Okay, that's very interesting. So for me, the first thing I will do is try to define this pattern of presentation in time. So this looks like it was a few days right.
Speaker 2:Yes, the confusion falls for a few days, but the panic attacks, the anxiety attacks and visual hallucinations were out of the past one or two weeks.
Speaker 3:One or two. So I will define this as a sub-acute presentation of a multi-symptom disease. So we have altered mental status, we have visual hallucinations, we have the panic attacks and anxiety. So if I think in my mind about possible causes, probably more metabolic or autoimmune diseases will come into my mind.
Speaker 2:I will not think so much in something vascular, for example, but mainly some metabolic or other or autoimmune encephalopathies but in terms of if you were to say, if you were to point it out as a complete, where would the symptom occur? Is you can know? Is it looking at the pain? Is it something? Are you looking at the pain? Is it something when you're meddling something in the cerebellum, something in the spinal cord, something in the nose? Where do you think the problem is?
Speaker 3:That's a very good question. Is she only confused, or she's also somnolent or lethargic?
Speaker 2:Yes, so there's confusion and visual hallucinations exactly in panoplycics, which are the sub-proposal. This was the background of having fatigue, lethargy and joint pains in the last 19 months.
Speaker 3:Okay, okay, so, because I'm thinking fatigues and joint pains that make me think you know out immune. But regarding localization, she's having visual hallucinations and confusion and altered mental status.
Speaker 2:spread involvement of the cortex, perhaps, or more localized involvement of some part of the brain stream so it does localize your cerebral cortex because it's more of an encephalopathy right where you see behavior changes, visual hallucinations and all that. So let's ignore the you know market fatigue and the joint pain, behavioral changes, visual exhibitions and all that. So let's ignore the you know market stream fatigue and the joint pain spots right now and let's just focus on neurologics. That's likely said. It does look nice to a settlement for vaccine day and so, based on the history and examination findings, what all etiologies would you consider here? What are etiology causes? Or maybe in a what all etiologies would you consider here? What are etiology causes? Or maybe in a differential septum scene? Just based on the history of these examinations, Okay.
Speaker 3:so if we define this as encephalopathy, then our differential probably would include something infectious like herpes, encephalopathy or other viruses. Our differential will also include some other autoimmune causes like autoimmune encephalitis. If we are thinking about metabolic causes, then we can think in hepatic encephalopathy and let me think other causes of infection can also cause delirium which can give you confusion and dyssymptomatology. That's what I will think for now.
Speaker 2:Perfect. So great list of differentions there, carlos, and I really agree with you that how you were not in favor of a vascular cause. Yes, it doesn't seem like something which is frasque considering. It's very simple, if you can pass it quite. So it has varied psychiatric symptoms, which is basically how the solution came out, when other than infusion has been in the back, and some of these symptoms. So, with all the differentials that you mentioned, infectious, systemic, autoimmune metabolic causes like hepatic or endemic anti-epiphany, how would you like to start the investigation plan? What would you like to send in the next or emerging, how would you like to start the investigation?
Speaker 3: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 differentials. Maybe I will ask for some autoimmune biomarkers ANA. I haven't mentioned this, but other autoimmune diseases with systemic involvement can give you this. Lupus, for example, can give you this. If I'm thinking about systemic infection, perhaps I will also ask a URI analysis. I would like oh yeah, go ahead.
Speaker 2:Yeah, go ahead.
Speaker 3: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 definitely wouldn't have access to immediately.
Speaker 2: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 about the biochemical which you already ordered, and second is the aging modality. So one thing you probably missed out would we would like to do a CSF here as well. Right, it's not that it's a cube, but we would like to know defilitis and infections. So that's one thing we would like to know. So this patient had all of it. She initially. Now I'll read out the findings which she had in presentation.
Speaker 2:So hemoglobin was 8.1, fairly low. Total leukocyte count on hemogram on platin was 8800, which is within normal limits. Platelet count was about 98000. Blood urea was 37, which is within normal limits. Creatinine was 3, again, sodium was 153. Potassium was normal. Erythrocyte sedimentation rate was 100. Crp C-reactive protein was 90. Again the Bacchus, boba Bium.
Speaker 2:The urine analysis, urine culture was negative. Urine protein had plus 4 proteins, so the urine had 2 red blood cells. Otherwise there were no pus cells. No plus 4 proteins, so the urine urine had 2 red blood cells, otherwise they were low blood cells, no crystals, no bacteria. And in terms of the workup for autoimmune serology, so for ANE cause, ane type, are strongly positive. So anti-DSD is also positive and the anti-RNP, which is the ribonucleotide, is also positive.
Speaker 2:C-anca, p-anca was negative. The C3 levels, which is the complement levels, were 60, which was mean, and the C4 levels were the low levels. The CSF planin was completely normal. The proteins and glucose were normal. The serum glucose was also normal was completely normal. The proteins and glucose were normal. The serum glucose was also normal and CSF planning was negative for any bacteria or bacteria and viruses, as you know. So biofying and CSF culture was not so bad, which was negative. One notable thing which we mentioned about the other which we are exploring, autoimmune entomitis. At this juncture she was very early on in her admission and investigation phase. No autoimmune bio was sent off at this point, so we didn't do that investigation right now. The investigations, the other investigations, the bio can be. Really you had the answer now, carlos, just what imaging modalities let's say you passed on these results and what imaging modalities would you like to volunteer?
Speaker 3:Also just thinking in the differential. Now that we have some lapse, I will think my possibility of something being infectious like herpes encephalitis is less now. Encephalitis is less now just because the CBC is normal and the CSF does not show a pattern of 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 biomarkers regarding autoimmunity, so my suspicion of autoimmune disease, particularly considering other symptomatology I know you don't want that, but it's higher. So if I want to see an adhesion caused by autoimmune involvement, probably I will ask for a brain MRI.
Speaker 2:So that's it. You summarized them well. Obviously, in the context of positive autoimmune markers and slightly high inflammatory markers and also high reactants, they're thinking something along which is multi-system declines where the autoimmune falls through. So the MRI brain was completely normal, literally on two occasions actually, and my brain was normally in both the occasions. Oh, that's so. We actually started off with the CT scan. I was considering Q10 to be. We started off with the CT scan and soon was the MRI, and the MRI and the GPT was also saving beyond the risk and the positive, especially some sub-approved classical items which stands in acute and different. We had that in the thing which was also, which was also the MRI, and geography was also good oh, that's, that's very interesting.
Speaker 3:Yeah, so so you are was also. Oh, that's very interesting. So you ordered also a CT besides the MRI.
Speaker 2:Yes, we ordered a CT before the MRI just to exclude any major mass damage and something that we may list early on. So, as a protocol, we did it with a CT scan, which was normally done in patients with an MRI, and geography in a unanimating list early on. So, as a protocol, we did a CPS game, which was normally done in Indian patients with an MRI angiography, which was also done. So let's say what are your thoughts, whether you are there as a clinician, as an intern, where do you think you're stuck right now? Who's helpful? You see?
Speaker 3:So I think it's kind of harder now. From my perspective, I would say clinical symptomatology comes always first. Of course the MRI may be normal, but regarding the symptomatology again, that is multisystemic and just the positive autoimmune by Markovs, I would still think something autoimmune. My guess will be to consider something like steroids just to see if the patient gets any better. I am a little worried about the creatinine. Maybe if I am thinking of that, she has an elevated creatinine due to an autoimmune presentation of the disease, or maybe she's having a pre-renal AKI. I will have to consider that and perhaps give some fluids, probably. But I think that I can't start steroids because, uh, my, my suspicion for infection is low, so I don't think I will be hurting the patient.
Speaker 2:Hopefully well, I do agree with you, before starting steroids you've got to be careful and judicial right. What if you actually suppress an immune system and something else goes onward? Right? Especially if you're dealing with an autoimmune disease and only plays out in certain ways. So before we actually speak about in the past, about what management, management beforehand, just want to summarize the cases for you.
Speaker 2:So this patient's tongue, behaving symptoms, psychiatric symptoms, confusion, visual hallucination, attacks we did a blood work. We did find no hematitis, no PHS. We did find positive autoimmune markers, that is, a BSDNA. She had elevated P apne, which was very, which was very bad in her team. And she also had a positive urine protein Now in the gym and she also had a positive urine protein. Now, urine protein was in the range of the nephrotic range broken lid which is more than 3.5 grams per hit. And you have all these, you have all these case history with you right now. So before you actually decide to go ahead and use steroids or something else, do you think this patient will be able to have a patient will need a referral, other specialities, so he can stop seeking and have both to reach you out. What speciality would you like to embody?
Speaker 3: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 hand hand. I don't know if I can ask infectious diseases to rule out infection in here, or they will be super mad if I do that, but if I can yeah I can I will ask also.
Speaker 2:So we will talk about rheumatology and infectious diseases. So well, in spreadsheet diseases I'm writing off saying that urine masses is normal. Blood birth has been generated in 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? So why it was? You're like it's something like an autoimmune technology and the same thing and in the light of this years, I'm probably different in ecology and green and white, you know great.
Speaker 3:What does chromatology says?
Speaker 2:so lumbar, as chromatology says. So look how Z has come to you and you know they're really interested, I'm saying, in the DNA is possible and the DNA is possible. So the thinking along the mind of you is very specific for me personally. They're concerned about the hydrogens of repressor. They are concerned about being high proteins in the urine and very high creatinine. So who do you think they are going to be next?
Speaker 3:yes, nephrology will be of a lot of help. Yes, definitely yeah excellent?
Speaker 2:yeah, of course. So nephrology is a new phenomenon and they are also interested in the case, considering. Now we are dealing with very high creatinine, very high protein protein in your genes, which is very annoying, and they are actually aware of how luteus 10 was very debilitating for the team. So, yeah, they now. Now they turn to you, the team. Okay, your main team is going to do the case, he is going to make up this patient and they want to advise management. How would you propose with the patient, considering now that you have a definition, you have a blood definition in our diagnosis, you have all the pains of being deflated in view of these acute confusion and we need, in view of this acute confusion and being in a matchmaking. It wasn't well psyched, right? Yep, it's even more psyched. Back to your screen.
Speaker 3:That's a good question. I would say, if I'm dealing with something that is, you know, in some ways called organically cause, at least not at the beginning, I will think in psychiatry. I will hope to treat first the cause of this probable symptomatology and then see if she persists, perhaps thinking additional causes. But at the beginning, beginning, I will not consider psychiatry okay, that's wonderful.
Speaker 2:So psychiatry has signed up. Now you have this team and you are basically proposed with this decision of starting equipment. What people do you make this move?
Speaker 3:So yeah, if I'm thinking of a medication to start, steroids definitely will be at the top of my list. I think that if she already has the positive autoimmune markers DNA, double stranded weight, yeah, dna then if she also fulfills several certain clinical criteria also we can consider this lupus and then treat accordingly to a lupus flare. So, yeah, I think she fits the pattern, at least to my mind, and I will start definitely steroids. The dosing of that steroids, I will say high, but I don't know the number exactly. And yeah, that's my thought so far good.
Speaker 2:So you want to create health for new person who wants to start with very high steroids and there won't be any minimal suppression control, it's just steroids won't do the trick for you yeah, so high dose IB and MP is the best way to start.
Speaker 2:Yeah, so material presence alone yes, high dose IV and MP is the best way to start, you know so you as a team you decide to get IV and ethyl and it was a thousand grams given in five days and the real thing was very actively and very closely involved. They wanted to go ahead and do a renal biopsy to stage the so that they can take a form of the treatment. But the patient and patient family quickly refused the renal biopsy so they went to Rosenpum's and they did not want any medicine Now. Nevertheless, we had to get some systematic in that person's immunotherapy. So she was also started on Orin-Y-Koshimong Morphidine. It's a remunerative suppressant which is very, very protective in lupus patients who need to suffer from weak injuries, and also anti-coagulation and anti-pregnancy therapy was started in the patient who stopped to prevent thrombosis. Newer patients had increased pregnancy to 11th level versus deep brain thrombosis and some brain surgery strokes. So that was the.
Speaker 1:So there's a couple of things Really really challenging case so far. You know, when we think about like a neuropsychiatric onset of lupus and this is a patient who had no history of autoimmune diseases that we know of Is that correct? Unusual characteristics here, right when the CSF panel sometimes with systemic autoimmune encephalitis you can have a relatively unremarkable looking CSF profile, like you maybe can have like a mild increase in the white blood cells, sometimes very low, like still like 10 to 15, you know, enough to be abnormal but not enough to point you in the direction of an infection.
Speaker 1:It's very unusual for the protein to be normal also. So I thought that was the thing that was the most surprising to me, because usually with most encephalitis you're going to at least see some abnormalities in the CSF profile and a new onset, neuropsychiatric lupus kind of, as the presenting symptoms is very in and of itself very remarkable, especially in someone in her age group Usually we're going to be looking at more young adults as opposed to someone squarely in the middle age, in their 50s. So some, some atypical presentations in this presentation of an atypical entity so this was the case.
Speaker 2:This was the interesting part because I remember carlos. In the initial history I told you that she had initially presented to all of hospital with fatigue, joint pains and fatigue, joint pains and more tiredness, and she was just given steroids, analgesics and discharged. So I think that was the onset where she actually developed these mucosal symptoms. That was about 9-10 months ago. And now she developed these full-blown neuropsychiatric manifestations which you want to watch. 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 typical lupus-like symptoms history. Her blood work was not known from there, but if you see, her hemoglobin is all all the low and so so her platelets. So she, for all you know, she may happen to have dyspnea, thrombocytopenia in addition to these lupus classic syndromes she was having the last 10, 11 months. We just saw it right now because she's blown into this neuropsychiatric component.
Speaker 1:Chris, you did a single import yeah, yeah, it is one of those things we do see fairly often in neurology where someone may have an underlying neurologic autoimmune condition like myasthenia gravis or something, and they got this little short course of steroids and they got better for a period of time. It is right, this kind of nonspecific fatigue can definitely be a red herring sometimes, but sometimes it's also the missing link in the story. I also thought the spinal fluid being normal was very surprising as well. With a lot of autoimmune encephalitis presentations, you'll at least have maybe a mild increase in the white blood cells or at the very least, some elevated protein. So I thought that was also very unusual. Protein, so I thought that was also very unusual. The mri being normal unfortunately not as uncommon in these cases. Um, so very challenging when you don't have anything specifically in the neuro realm that tests positive per se. But uh, good point going back to kind of like the serum biomarkers and a good example of how you know you need those follow-up tests when you have a positive ana.
Speaker 3:Yeah, definitely, and I will just add that that is a common what you described like a patient just giving steroids and then going back a year later to a hospital at least, at least that is common in my experience in Peru and I think in other low and middle income countries. We don't have an electronic record history, so, yeah, going back and asking the patient about possible diagnosis, this is a very important thing to do.
Speaker 1:And you know, I'll say, even here in the US, where we do have electronic records everywhere, a lot of them don't talk to each other, so it's not necessarily as good in practice as it is on paper per se. So it is one of those things where you know you may not have the records. Also, even from just within my own state, we'll sometimes have people who went to a hospital 40 miles from here. You would think we'd be able to get those records without too much hassle. Not always the case. So unfortunately I don't think it's it's restricted to any particular global region. It's pretty a universal experience, I think, for anyone taking care of patients who get their health during different areas, sadly, but um, but yeah, uh, divvish.
Speaker 1:What other uh teaching points do you have for us?
Speaker 1:Or how did this patient do with, or actually before we get to that, uh, the treatment I know you said you know obviously high dose steroids with methylprednisolone, pretty common for a lot of neurologic autoimmune conditions like multiple sclerosis, flares and things like that. Um, the the mycophenolate. So I think that's that's a good point uh, to bring up as well, right, because we can't keep people on steroids necessarily forever without some long-term side effects, but I think for people who aren't as familiar with mycophenolate, uh, it's important to know that the time to where you're going to be getting a therapeutic effect can be very prolonged. Sometimes we're talking 6 to 12 months of being on the medication before it will really hit its stride in terms of its immunosuppressive effect. So a lot of times you're keeping them on some dose of steroids or other immune-modulating medication while you're waiting for these other longer-term medications, like mycophenolate or azathioprine or what have you, to kind of be more effective. And I assume that was kind of the long-term plan with this patient. Is that correct?
Speaker 2:Oh yeah, no. So in addition to the mycophenolamide pill and before this patient strictly and the patient's families were strictly fused brain biopsy, we couldn't explore more treatment options. So additionally high dose steroids that we had prepared, we did for her the micro serolate and we also started some benzodiazepines for her anxiety, panic attacks, stuff she was having. A good part of this case was her. Her mental status improved dramatically after we started the screening, including the benzodiazepines. Her creatinine was still blacklining, it was still the same 3.1. It went down to more than this once. Her urine wasn't routinely water but we were happy that in terms of her weight and status she was much better than before and this was a very dramatic improvement. Let's say four or five days on B1B. So the neuropsychiatric part is definitely taken care of here and we're happy with that.
Speaker 2:In terms of the reunion part, obviously it was a mom film plan and she was destined for a follow-up three-monthly follow-up, six-monthly follow-up how 28% had decommunications then and we were hoping down to 9. If she ever comes back to us in 3-6 months time and she's fitter, but I'm seeing right now she may consent for biopsy and we may be able to get a picture of her with her 40 days, but sadly so. There's one part which I did. What mentioned in the case which I sent to you was that this patient actually got COVID in the hospital. She did get COVID-19. She actually succumbed to COVID-19. She went to the ICU. She was really sick. This patient succumbed to COVID-19.
Speaker 1:Was this during kind of the height of the pandemic when this case occurred?
Speaker 2:This was actually so. This was in 2020. Was perhaps sitting block toward behaving?
Speaker 1:and that's. That's always a consideration. You know we have these people in the hospital and we're immunosuppressing them. Um, yeah, was that thought to play a factor in in this patient's uh immune course? Uh, with a, did she have worse lung injury than normal for this particular variant?
Speaker 2:Yeah, we don't show it. This was the time in the third day was third day. We had people in there, so it was obvious it was tough for us to actually decide for middle, for immunity got so bad because he put in on high-dose steroids and used essence, or by virtue of her age which was not that bad, which was okay she succumbed to COVID, or was it naturally? The COVID-19 just made her mad. Each way was exceedingly bad and she got so sick that she was unlucky. She had a certain. So these were some important considerations. It was a lot of backing from the family In some cases. That's how it goes, and so I mean if you're not seeing the patient, who's finding this is able to mean something.
Speaker 1:Yeah, a challenging situation in a lot of fronts, both the diagnostic and the treatment side, unfortunately. Any final thoughts or teaching points about this particular case that you think that you really took away taking care of this patient Divij.
Speaker 2:Yes, sure. So there are a few critical points in the history of the Jhavnagra this time. First of all, neosychiatric hunkus, or widely known as NTSLE in literature, is a CV complication or a very documented way complication characterized by these revanchakuru and psychiatric manifestations on the CV. Interestingly, these manifestations can also occur. They can precede diagnosis of SLE, they can proceed simultaneously as SLE diagnosis or even months and years after SLE was diagnosed. The second interesting point was that the diagnosis of leucocytic lupus is indeed challenging even for skilled physicians, even from neurology, phleology, rubicology. First, there is no diagnostic criteria for NPSAE and you may have this diagnosis even in the setting of normally serum, open CSR biomarkers, normally muonogen imaging and others in the middle. So it most likely comes in that limb of a diagnosis of excretion. Apple is ruined by the metabolic, autumnal and pymeic infectious and radioactive procedures. The third interesting part was there were some mimics, actually some mimics, when you actually considering all of these extremely rare and probably working chemo-neuropsychiatric rooters. One was CNS. Some mimics actually some mimics, when you're actually considering all of these extremely rare could be working on neuropsychiatric disorders. One was CNS vasculitis. Second was Jordanian syndrome. Basically it was you know a different moment the jaw-pinching boy. You're thinking of Wippel's disease, especially CNS Wippel. You're thinking of neurobedships disease, as Karan and she won Orgelium.
Speaker 2:So in Shinkansen group Batchelor also comes with these many psychiatric manifestations Avothygmo flashing report, encephalopathy B, botanical encephalitis, anti-inflammatory opium encephalitis, which includes the NMDA encephalitis. Cns lymphoma is simulated to reproduce this only good name. These were interesting dynamics which we thought of when Nebo kind of working up this case. And last but not the least, the patent model of the Peking Minority News is very merit-making. So these were some interesting points which I'm chaining them for these days.
Speaker 1:That sums it up really well and that was a great rundown of the differential diagnosis in these types of cases with this kind of subacute onset of neuropsychiatric symptoms. It's definitely one of those things where you're definitely looking after all of the strange things that are on the neurologic differential diagnosis.
Speaker 2:I yes, a little bit of these three.
Speaker 1:I've worked up a number of these cases over the years myself and it is always a challenge. They didn't necessarily end up being I think only one of them was neuropsychiatric lupus, but sometimes you end up with the CNS vasculitis or the neurobechets or, on and on right CNS lymphoma flunctial, unfortunately. I've come across that several times as well, and it's it's one of those things if you, as one of 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 list of things to consider in these uh types of situations. And there's right with those folks cranking out new antibodies. You know you can always throw perineoplastic syndromes on there as well, but yeah, it becomes a real laundry list sometimes. So it's great to have a framework to pare these down somewhat. Carlos, I'll throw it over to you Any points of this case that really struck you or that you're going to be taking forward with you in your future practice.
Speaker 3:Yeah, definitely. So the first thing, always getting a good history is very helpful. So definitely, going over the past medical history regarding past diagnosis is very helpful. Past diagnosis is very helpful. I will say that, even though we had somewhat confusing findings in this patient regarding the MRI and the CSF, thinking about the most clinically logical explanation for this is also important, particularly to not ruling out a disease or ruling out lupus. That, in this case, was the diagnosis right.
Speaker 1:Yeah, and this even if we right, because the other thing is that and I think you pointed this out earlier divvage is that we're fortunate in this case that we got those serum biomarkers positive. It is not, unfortunately, uncommon to have those come back normal or kind of in the intermediate zone. And right, there's this, this old adage on the neurology service, somewhat tongue-in-cheek, that no one dies on the neurology service without a course of steroids. So that's why I was like, could it be autoimmune? That's always the question mark there. So it's if we don't know what it is, we ruled out infection. We think it could be autoimmune, just based on the timeline, the presentation, things like that.
Speaker 1:Sometimes you do kind of a diagnostic slash, therapeutic trial of steroids or plasma exchange or IVIG, kind of these first-line autoimmune types of treatments, and do we feel great when we're kind of treating blindly and we have a suspicion?
Speaker 1:No, but sometimes you have to say like, well, the patient's getting worse and this is a potential diagnosis that has a potential treatment. So it can be very challenging because like, for instance, let's say it was like neuropechets, right, and the person doesn't have any aphthous ulcers 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 some of these challenging situations where you're like I think it's this, maybe you don't have that neuro immunologist to call in to back you up, or things like that, and so you do have to kind of make a decision, and they're very challenging cases almost universally, as as demonstrated in this case. So so thank you both for your participation today and any final things that you want to plug or resources that you found useful either in presenting this case or what have you.
Speaker 2:No, the thing about keep the code in has always been the American Academy of Neurology journey. There are a few interesting presentations over there and it's just this one resource which I found. Second is the practical neurology podcast, which is the British podcast which I do actively follow and I did a blog follow and I did a blog because I'm not a neuropsychiatrist but was in consideration of the diagnosis with the open human mouth. I think it's like I can do this also. That's fit in this whole like lost chip when it's not actually the symptoms. So for me, for neurology and for when am I at night? When do I go off? And this is what, when you are speaking about any cases, or at night or any cases, these two other or two resources will lead you back in June and eventually you can meet each other in June excellent.
Speaker 1:I love the. The Primal Neurology podcast is a favorite of mine also oh yes.
Speaker 3:I will add, looking at Continuum is also one of the things that do help me a lot.
Speaker 1:I think they have also an ultimate neurology edition that is as someone who works with Continuum as part of one of my other hats, I am, of course, an advocate for everyone to read continuum and for folks who are in middle or lower income countries, there usually is some plans out there that can help you get an issue in your hands as well If you reach out through, sometimes, the national medical societies depends on which country you're in and so forth but there are different ways and you can always reach out to the continuum directly, uh, depending on where you are located geographically, because it can be a little costly depending on where you're living. All right, gentlemen, thank you both very much and, uh, you know, hopefully we'll get to getting together and do another one of these really soon. If you want to uh find obviously, subscribe to the podcast, give us five stars. Uh, you can find more of our information at the neurotransmitterscom and you can find our twitter slash x feed at neuro underscore podcast. All right, thanks again, everybody. Appreciate y'all listening.
