Nearly one in five patients in intensive care units (ICUs) requires neurologic consultation. The neurologic complications of critical illness can be unique to its underlying processes and can persist as independent disease states even after resolution of the inciting critical illness.
In this episode, Casey Albin, MD, speaks with Shivani Ghoshal, MD, author of the article "Neurologic Complications of Critical Illness" in the Continuum® February 2026 Neurology of Systemic Disease issue.
Dr. Albin is a Continuum® Audio interviewer, associate editor of media engagement, and an assistant professor of neurology and neurosurgery at Emory University School of Medicine in Atlanta, Georgia.
Dr. Ghoshal is an assistant professor of neurology for the Columbia University Vagelos College of Physicians and Surgeons in New York, New York.
Additional Resources
Read the article: Neurologic Complications of Critical Illness
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Social Media
Host: @caseyalbin
Guest: @ghoshal_shivani
Full episode transcript available here
Dr Albin: The ICU can be such an intimidating place. There's unresponsive patients, there's beeping equipment and a seemingly endless way in which the nervous system can be compromised. But fortunately, today I have the opportunity to speak with Dr Shivani Ghoshal about her paper, Neurologic Complications of Critical Illness, which is going to help us demystify the approach to these patients and provide some clinical pearls that you can take to your next consult in the ICU.
Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast.
Dr Albin: Hello, this is Dr Kasey Albin. Today I'm interviewing Dr Shivani Ghoshal about her article on neurologic complications of critical illness, which appears in the February 2026 Continuum issue on neurology of systemic disease. Welcome to the podcast, Dr Ghoshal. It's really such a treat for me to get to interview you, someone who I know and have worked with in the past. But for those who do not know you, please give us a little background about what brought you to this topic and what you do in your clinical life.
Dr Ghoshal: Thank you so much. It's a thrill to be interviewed by someone that I know well and get to work with. Outside of writing this article for Continuum, I am a neurointensivist. I'm an assistant professor of neurology at Columbia University and the program director for the Neurocritical Care Fellowship between Columbia Cornell and New York Presbyterian. So, a lot of what I do in my day-to-day is thinking about acute brain injury along with the neurology of systemic disease and how, really, the two interplay with each other, of how neurologic complications can arise from systemic illness and the other way around.
Dr Albin: Yeah, you are the absolute perfect person to kind of walk us through the complexity of the brain and body connection.
Dr Ghoshal: I don't know if I can deal with that kind of praise, but thank you.
Dr Albin: And you've really written a powerhouse article on just the myriad of complications that really arise in the ICU, and you've broken it down into what I think is a very thoughtful way of sort of bucketing these complications. So, tell us a little bit about the approach you took here.
Dr Ghoshal: I love this article because neurologic complications are just so common in so many types of acute critical illness. And I think we have to think for each organ system, how does this affect the brain, and then how does the brain then interplay, let's say, in kidney failure, in hepatic failure, in sepsis, right? Which is so common that I think we don't even think a lot about, like, what are types of septic encephalopathy for all the antibiotics we give; like, what are the implications of this? I really enjoy taking each system and thinking about, how does it specifically affect neurologic complications?
Dr Albin: Yeah. And then there was a really nice breakdown in terms of some of the procedures that will happen within the ICU in general. You know, the things that are happening to the patients at the bedside also put them at risk for neurologic complications. Then there are those neurologic changes that are happening because of some of the underlying problem that brought those patients to the ICU. And then the unfortunate number of problems that arise because the patient has been in the ICU for such a long period of time.
Dr Ghoshal: You know- and I think that that first part you mentioned, just about procedures in the neuro-ICU, right? Or in the ICU in general. I think that we don't think about that on a day-to-day level, right? Just like arterial lines are one of the most associated with any kind of peripheral nerve injury, especially axillary arterial lines. I learned quite a bit, even going through this article and then looking at other sources. So, thank you also for pointing that part out.
Dr Albin: Yeah. When I was thinking about how do we distill all of what was covered through this article, I actually really thought it would be sort of most interesting to have you model sort of your approach to these patient complications and how you approach the complexity of an ICU patient. And so, if it's okay with you, we'll just walk through a couple cases.
Dr Ghoshal: Oh my gosh, let's do it.
Dr Albin: All right. So, these are all, of course, composite cases. You know, there is no patient violation here. Let's say that this is a 64-year-old patient and they're admitted with influenza, and they develop ARDS. And they're in the MICU. And this patient, they were pretty sick on arrival and they were intubated for three days. But now the patient's been extubated, and the MICU team calls you because today she's having trouble swallowing and her voice, you know, the family says that this is not what she normally sounds like. And the team is really quite worried that she's had a stroke. And so they are calling for a neurology consult because they want to know what they should do. So, walk us through your approach to that patient.
Dr Ghoshal: Well, I think the primary team being concerned for a stroke is definitely reasonable, but I think, taking a bigger step back, what I would first want to think about, is this neurologic or non-neurologic? Neurology, you know, there's a parcel of things we can go through, but even just a non-neurologic, like, is this just primary injury to the vocal cords, right? I think about the cough were there, the ET tube, it wasn't overinflated which caused direct damage, right? And then after that, then I would think a little bit more about my approach for what is going on neurologically. Thinking about either, is this a brain process or is this a- more of like a spinal cord cervical cord injury process or more cranial nerve issue?
Dr Albin: Yeah. How would you approach the exam in that patient?
Dr Ghoshal: Yeah. You know, I- and just to, again, take a step back, right? To remember that when we do intubate someone, the physical maneuvers that we have are a chin lift and regular endoscopy, right? They have, like, significant movement for the cervical spine. So, I might want to know even before I examine the patient, right, or their history, right, do they have anything like, do they have known cervical stenosis? Do they have any, like, cervical spine pathology? Was it a difficult intubation? Right? So, these are the kind of the things I'd want to know even from the history, along with whatever vascular risk factors they may have. And then, to your question about the actual exam. Yes, you know, I may look for, like, crossed findings, right? If we're thinking about, let's say, a medullary lesion, etc. I think all listening to this podcast know about MRI testing there. But beyond what I would be looking for, let's say, in a medullary stroke, I'd also want to be looking at just, like, water paresis, right? I might want to be interested in, let's say, signs of neurogenic shock. You know, you mentioned they're in septic shock, ARDS. I might want to actually take a look to see, like, was this all septic, right? Or what are their other shock types present.
Dr Albin: So, what I hear you're saying is you're evaluating A, first of all, answering the consulting question, you know, is there a real risk for some sort of cerebrovascular phenomenon, but then actually going to the bedside to examine the patient, to say, does that make sense? Do we see hemibody involvement here? And it's a good thing that you're approaching it that way. Because actually, when you go to the bedside, she does have some difficulty speaking. And reading the notes, this was actually quite a difficult intubation. From just the cranial nerve, you know, where she has maybe some dysphonia and dysphagia. But you also, on exam, then find that she's got some pretty symmetric distal weakness in her arms bilaterally. And so, when you find that, what are some of the imaging that you're going to think through to try to pin down exactly what's going on here?
Dr Ghoshal: I love these cases because it's not so straightforward. Now, let's say if she has, like, an upper extremity weakness and lower cranial nerve deficits, you know, things I'd be looking for, like any injury to, like, hypoglossal nerve, vagus nerve. The vagus nerve is going to be hard to tell, right? Recurrent laryngeal nerve, you know, the lingual nerve. I might be thinking more about stretch injury, which we think of as tapia syndrome, right? So, just a textbook answer. The hypoglossal recurrent laryngeal nerve injury. And what we're going to be looking for is dysphonia, dysphagia, and unilateral tongue paralysis. Could be a bilateral as well. But I guess, then, the next question after I'm going through my physical exam findings is thinking about my imaging choice.
Dr Albin: So, for this patient, given that she's got this bilateral upper extremity, maybe some tepia syndrome where there may have been some stretch injury to some of those hypoglossal nerves. She may have also just had some trauma to the vocal cords. Like, as you said, these procedures can really put patients at risk for just mechanical injury to some of those structures. But knowing that upper extremity weakness, what kind of imaging, then, do you look at for the court?
Dr Ghoshal: I think it's not unreasonable to do an MRI brain, right; with that, it then cuts through the brain stem. And then doing an MRI of the cervical spine. I guess the point that you mentioned at the very beginning, that this is three days after she was intubated… you do run the risk beyond 72 hours of, let's say, a primary injury. Let's say if she had, you know, God forbid, an injury to the cervical spine, those hyperintensities, especially when associated with ligamentous injury, they can pseudonormalize beyond that time. I would say yes, absolutely. MRI of the brain, cervical spine, then cuts through the brain stem. But I would worry that if too much time elapses, you may miss some of those injuries that you would otherwise find.
Dr Albin: Yeah. I think those are some really important take-home pearls, and when we're thinking about the cord injury that could occur through the intubation process, that we really do need to be aware of student normalization of the T2 hyperintensities after that 72 hours. And so, I think that's a really important pearl for us to take home. So, kind of summarizing this case here, there was probably a multitude of things going on, which highlights to me the complexity of ICU patients. Less likely in this case, and they did not find a stroke. But that is, of course, something that we must keep on the differential for any critical care, critically injured, critically ill patient. But tapia syndrome where you have some stretch injury to the hypoglossal nerve and the recurrent laryngeal nerve, which can put people at risk for dysphasia or dystonia after intubation. And then that hyperextension injury that can happen for patients who are intubated, because people, especially for difficult intubations, are really having to manipulate the neck. And for an elderly patient who may have some cervical stenosis, that hyperextension can actually result in a central cord syndrome, which is what they discovered with the C-spine MRI in this case. So, cognizant of all of the cervical injuries that might accompany the procedure of intubation.
Dr Ghoshal: And you know what I would say, right. Because I think that our population is overall aging. I think with that, we're going to end up with, like, more cervical spine pathology for these patients that are ongoing intubation, just as you, you know, very astutely pointed out. Right? Trying to have at least, like, manual inline stabilization, right, or even like, considering fiber optic intubation in some of these patients is probably going to be a safer way to go to avoid these kind of injuries.
Dr Albin: Yeah, I think that that's so true and really emphasizes the importance of communication between the neurology team and the critical care team.
Dr Ghoshal: Totally.
Dr Albin: Neurology is probably not the person intubating the patient. Right? But it's really important for any of these consults to have a good appreciation and that robust communication with the critical care team about what has been going on systemically for this patient, even opening that intubation note and saying, was this an easy intubation? Was it a difficult intubation? I think sometimes we forget that key skill of just communicating across the teams to have a holistic picture of what's been happening in MICU.
Dr Ghoshal: Yeah, I totally agree. It's kind of why my first part of this case you mentioned is just like asking the team, like, what happened during the intubation, right?
Dr Albin: It's a really important takeaway. All right. We're going to shift gears from procedural complications, reminding our listeners there is a fantastic summary of all of the things that can happen to ICU patients, just because we're doing things to them, putting needles in places where needles aren't usually, such as for arterial lines, for central lines, intubating patients; all of these have complications that can affect neurologic function downstream. But let's shift gears and let's talk now about a 72-year-old man. And he's admitted to the ICU with pyelonephritis and bacteremia. He's got nephrolithiasis. And the team calls you because he, like many patients in the ICU, has some, quote, "shaking events." And he's altered, and they want to know what to do.
Dr Ghoshal: So, there's a lot to unpack there. Sepsis is so common, right? When you're saying this patient is altered, sepsis-associated encephalopathy occurs in 70% of patients. So, like, in sepsis or septic shock. And we know that, you know, they say it affects mortality, long-term cognitive outcomes. But because, I think, it's so common, we don't really take the time to think about what is going on in sepsis in the brain.
Dr Albin: The brain is an end organ perfusion. And the end organs are what we're sort of monitoring in sepsis, and the brain is such a key marker of that.
Dr Ghoshal: Absolutely. I think there are a lot of things that happen with sepsis in the brain. But if I were going to pick like 1 or 2 points that I really wanted to hone in on, it's thinking about that blood brain barrier disruption that happens in sepsis. And so, what that does when you disrupt the blood brain barrier is that you end up with this inflammatory milieu, for lack of a better term, that, like, comes into the brain. You have, like, a disordered sort of microglial activation, cytokine release. You know, all of these things are creating more oxidative stress, neuronal damage. And the other hand of this, right, along with that blood brain barrier disruption, is disordered cerebral auto regulation.
Dr Albin: And I think that those two things are probably underappreciated. The complications and why, maybe, they lead to this downstream difficulty in recovering and then probably are also setting the patient up to be at risk of downstream delirium that is so frequent in the ICU.
Dr Ghoshal: I couldn't agree more. And, you know, for this patient's case, right, where you're saying, like, they're altered, they're shaking, I bring up this idea of cerebral autoregulation. Right? Just because for normal patients---or normal people, rather, right?---normal cerebral autoregulation allows us to have, like, stable brain perfusion through whatever range of pressures we have. A lot of these patients are septic; whether they are hypertensive or not, they have significant changes in cerebral vasoconstriction, vasodilation, right? And this can create anything from, let's say, like, neuronal excitotoxicity, metabolic alterations. Right? Just in that setting of cerebral inflammation. So, these patients, yes, are at a very high risk of encephalopathy. And then from these changes, right, from blood brain barrier disruption, whether that's from a cerebral autoregulation or just from that inflammatory milieu, they're at a super high risk of stroke and seizure.
Dr Albin: Yeah. So, they… in calling you to the bedside, someone comes to meet you and they say, we sent a bunch of labs off and we just got one back, and it's his ammonia, and his ammonia is 92. So, do you think that's what's going on here? This is so common. Right? Hyperammonemia. Give us sort of your approach to kind of triaging, is the hyperammonemia really a problem or is it just some sort of bystander?
Dr Ghoshal: Oh, you know, ammonia is such a slippery lab, right? That… well, it's very hard not to have a strong opinion on it one way or the other. And so, I think what I would say is that ammonia can be elevated for, like, a parcel of reasons. Right? Like if someone has tonic colonic movements, you can have ammonia. That's just, like, part of like enteral metabolism, muscle breakdown, whatever it may be. And ammonia can go up for a lot of reasons. And it's true also that ammonia can contribute encephalopathy. And there are a few mechanisms that can go through in a little bit. I would first want to know… a part of understanding, I guess, any lab is understanding in this context of, like, what was the ammonia before? Right? What is their baseline ammonia? Is this a significant rise? Like, how much of a rise should you care about?
Dr Albin: Yeah, absolutely. So, you look back and they live sort of at the upper range of normal with 60 being their sort of baseline.
Dr Ghoshal: Yeah. You know, I don't know that I would be so concerned about this particular ammonia level. I may trend it. But, you know, just to talk a little bit about ammonia and why we care about encephalopathy, right? So, the reason why it's so concerning, I guess I should say, in any kind of acute illness is that ammonia will cross the blood brain barrier. And then it's converted into ammonium ions, and it will go into astrocytes and, like, they can increase interstellar osmolarity. Right? So, these cells swell. Right? And because water is drawn into the astrocytes, they cannot interfere with actual functioning of the astrocytes. Also worsen cerebral auto regulation and cause, I guess, sort of an excitotoxic environment. Right? So, ammonia can be concerning, I think when you send in a lab, right? I think it's important to remember that there's no direct relationship between ammonia level and encephalopathy severity.
Dr Albin: Right. I think that's a really key point to drive home that it's usually not until we're in the hyperammonemic ranges above the 120s-150s up into the high two, three, four hundreds that we really need to be concerned about that cerebral edema and potential, even herniation. But these low-level ammonias, just like you said, like we really need to understand the baseline, how much they've changed, the context of, you know, what the ammonia sent on ice? Was it laying out in the room for hours on end? That really contextualizes this lab that we otherwise have a very hard time interpreting.
Dr Ghoshal: You're absolutely right that an ammonia greater than 120, you know, from our guidelines, both in lymphatic disease along with kidney disease. So, let's say above 120, your patient may be more at risk for cerebral edema. I could also play the devil's advocate and just remind, you know, that because ammonia isn't converted into ammonium in the brain, a peripheral ammonia level really may not reflect central nervous system levels. Right? So, let's say your ammonia is a bit lower also. But let's say there's been a significant change in ammonia for the patient. That may cause some cerebral disturbance that, you know, let's say this ammonia is still below 120. I may still be worried about it just because of the trend. Right? And knowing that my serum level may not really reflect what's going on above.
Dr Albin: That's such a great point. So, lots of pearls around this lab, comes back abnormal all the time. In fact, I feel like it's more frequently abnormal than it is normal in our ICU patients. And so, I really wanted to give residents and listeners a way that we who work in the ICU contextualize that. So, in this case, you've been musing, hmm, this is probably not what's really going on here. He is still having these movements at the bedside. Let me ask you, when you hear shaking in the ICU, what's your big differential there?
Dr Ghoshal: I always want to know, is it something like a myoclonus? Right? Is it something like an actual coordinated movement? Is this also something like a chorea, right? There are so many movements. So, like, I think that Continuum actually in the past put out a great issue about, like, movement disorders in critical illness. But really what I want to know is, like, first of all, like, is this neurologic or not neurologic? Right? Is this a, you know, let's say a seizure? Is this something suppressible, nonsuppressible? I really want to know more about what that movement is before I could even create a differential.
Dr Albin: Totally. And so, when you're in the bedside, he's doing exactly that sort of classic myoclonus. He is having these short, jerky movements. They are not rhythmic. He is intermittently following some commands through this, but inattentive would be the best neurologic term for his mental status state. But then while you're there, he actually does have a GTC and you're in the room. It's generalized, it's convulsive, no longer responsive. His eyes are rolling up and you are well-convinced this truly is a seizure. As you start to approach, now, a seizure in the ICU, walk us through kind of some of the things that you think about in terms of labs you might want, what imaging you might want, what risk factors you're most concerned about.
Dr Ghoshal: It sounds like he's having two distinct types of movement, right? He's having some myoclonus, right, or multifocal myoclonus where he has an intact mental status, for better or worse, through it. On that sort of bucket, I'm thinking more of metabolic disturbances. So, I went through this whole thing about the ammonia. But I think what I'd really want to know is, like, what is happening with his uremia, right? What is happening to his kidney function? I think you mentioned you had nephrolithiasis on top of being, I think, critically ill. I think that's some of the things I'd be looking at. I also would like to know about his antibiotics, any medications he's taking. And then for the seizure, I may want to know some of the similar labs. Right? Even just whatever, like, what is his magnesium? What is his calcium? Like, simple things being simple. And then I can go down a little bit more of a list on what I would do for the actual seizure. Just knowing that sepsis, hepatic disease, renal disease, antibiotics themselves may all increase your risk of having a seizure.
Dr Albin: Yeah, absolutely. And I think what you said about sort of knowing the labs and knowing the medications plays such a crucial role in our workup for ICU changes in neurostatus. And so, in this case, because of that nephrolithiasis, you go scroll through his labs. And it looks like his creatinine has risen to 4 quite abruptly. So, he's got a pretty severe acute kidney injury. And his BUN has risen all the way to 80 over the course of three days. And then you're looking at the med list, and he is on a bunch of antibiotics, but one of them is cefepime. And so, walk us through, with just those couple of key words, what are some of the things that you are thinking about from the neurologic perspective?
Dr Ghoshal: I am, like, salivating. I love these cases. No, I'm serious, right? So, like, I'll take a few minutes at the beginning to talk about, like, uremia and uremic encephalopathy. You know, we see uremia often, and uremic encephalopathy, we think, maybe there's some part of cytotoxic edema, right? Because that urea accumulates in the brain; it accumulates similar to, like, almost ammonia, creates these toxic wanding compounds in the thalamus, like, in the cortex, wherever it may be. And that itself will cause, like, a, let's say, impaired cytokine clearance from the brain, neuronal apoptosis, also affects the blood brain barrier. So, all of these things itself, like, from urea, all right, like a worsening uremia, can cause a different sort of CNS changes that could affect both the seizure side along with the multifocal myoclonus.
Dr Albin: Yeah. Just putting him at risk of two very different types of neuropathology, right in the same case.
Dr Ghoshal: Totally. And you know what I'll say about like, uremia? I could talk about this for a very long time, but like, really what I want people to remember is that uremia really increases your risk of seizure. I talked a little bit about this accumulation of uremia, like a uremic exquisitely in the brain, but you have this metabolic acidosis that develops from urea and you increase the activation of your acid-sensing ion channels. Right? And these retaining creatine metabolite actually cause more inhibition of your GABA receptors and stimulation of your NMDA. Right? So, all of these things together, like I think uremia is so common that we don't really take the time to think about, like, all of these things that could be happening.
Dr Albin: Yeah. And then because of the poor kidney function, there's also accumulation of drugs. And there's this risk for toxic accumulation of some of the things that are sort of more renally metabolized.
Dr Ghoshal: Absolutely. And on top of that, if you include, you know, what we talked about before, let's say you have cortical edema or hypoperfusion or a disordered cerebral autoregulation just from sepsis itself. You know, all of these things do fit together, right? It's not just a one thing for every. I know that you mentioned also there, antibiotic. I loved writing the section on antibiotic-associated encephalopathy, in part because it's something we don't spend as much time thinking about. I will say just broadly, there are three subtypes of antibiotic-associated encephalopathy. The first one, I think, is the most common. That, like, I associate it with beta-lactam, cephalosporins, or penicillin. Right? And that is where we can often see, like, seizure and myoclonus, right? You're really between, like, in days from antibiotic use. We think some of that is just from competitive antagonism of GABA receptors. To quickly talk about, you know, we also have types that are associated with quinolones and macrolides. More of, like, an acute psychosis. And then absolutely metronidazole, which causes a subacute encephalopathy---takes a little bit longer, you know, and more associated with cerebellar dysfunction. But I think every time that I am looking at a patient like this, I am absolutely going through and looking at the antibiotics.
Dr Albin: I love that. And because it's not- cefepime is really the classic, and it's been the poster child for that type-one complication where you get mild blueness and seizure, usually within a day or two of starting the antibiotics---but it's all cephalosporins. It can be any beta-lactam. And so, cefepime is sort of our, like, poster child, but is not the only one. And so, with removing that antibiotic by getting him on a continual renal replacement therapy, this patient actually does quite well. And I think this is a take-home message for all of us, that helping the critical care team limit the risk to the patient from a medication perspective, us helping them say, you know, can we pull this off? Can we switch this to something that's going to be more neuro-friendly from their antibiotic perspective? really can make a huge amount of difference to that patient's long-term outcomes.
Dr Ghoshal: Totally.
Dr Albin: I think that you and I could talk about this all day long. I mean, this is just the, like, bread and butter of these complex patients that we see. But I think I'll summarize it for our listeners that really have to think about what procedures did the patient get, opening some of those notes to figure out where are their complications, and then taking a very holistic approach to the ICU patient and making sure that you're characterizing what kind of abnormal movements are they having? What are their labs? Being mindful about the context the lab was sent in and the patient's baseline, like we talked about with that hyperammonemia, really matters where the patient's been. And then that medication list is- can be culprit number one, two, and three for bad things that are happening to the patient. Again today. I've been interviewing Dr Shivani Ghoshal on her article on neurologic complications of critical illness, which appears in the February 2026 Continuum issue on neurology of systemic disease. Be sure to check out Continuum Audio episodes from this and all other issues. And thank you so much to our listeners and to Dr Ghoshal for joining today. It was a pleasure.
Dr Ghoshal: Thank you for having me.
Dr Monteith: This is Dr Teshamae Monteith, associate editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.
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