#98 Cerebellar syndrome

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With Quasmed and Paces ahead, they are all you need to smash your Paces exam and succeed in getting your MRCP sorted. But enough on that for now, let's get into this week's episode of the prepaces podcast. Welcome listeners, it's Sam here and welcome to this week's episode on a long requested topic, Sarah Bella Syndrome and I'm delighted to bring you another fantastic guest who has a real passion for medical education. Yezend Samurai is a founder of Quasmed, the new kid on the block when it comes to online revision resources. Yezend tells us all we need to know about Sarah Bella Syndrome including the differential diagnosis, investigations, management and what the difference is between a sensory and a Sarah Bella Ataxia. More on that later but now we pay homage to the Bimeo Coffee Heroes. Thank you to Priya, Parry, Mike, Soraya and Meg, all of whom. Thank you to Zoe, who left the most wonderful message after she listens on her daily commute and past first time despite being on a microbiology job. The sweetest bit was when she said she felt like I was her cheerleader throughout her revision and that's exactly how I want every listener to feel because I truly am your cheerleader if you're about to see your Paces and I want you all to pass. Enough on that for now, let's get into this week's show. Welcome to the Pre Paces Podcast with me, Dr Sam Williams. And this week we're covering another neurology station which is absolutely essential for your Paces preparation and that is Sarah Bella Syndrome. Joining me to discuss this topic, I've got a brilliant new guest for you wonderful listeners. I'm very pleased to welcome Dr Yezen Samurai, a neurology registrar in London who's currently taking a sabbatical to reaffirm his commitment to medical education as one of the joint founders of ChuesMed, the new kid on the block when it comes to medical education. So Yezen, thank you so much for joining me on the podcast. Thanks for having me. And Yezen, I guess the first thing to say is Sarah Bella Syndrome is one of the absolute essentials that our listeners will need to cover off in their Paces preparation. So the first thing is how often do you come across these types of patients in your clinical practice and I guess after that we can come onto how these patients will be presented in a sort of Paces style scenario. Yeah, absolutely. So I think Sarah Bella Syndrome is very common particularly on stroke and neurology awards, which I guess from a sort of Paces perspective you might expect to see them more often in your exam because they're quite easily transported to the Paces exam, especially if the hospital you work in has either a regional neurology award or probably more commonly a stroke ward. Yeah, fantastic. And because of that it means as you've said they're very easy to bring in short notice for Paces examinations because by and large providing they don't have any other sort of debilitating neurology they can be brought out without too many problems for the exam. I'm really excited to get into this episode. So without further ado let's get into Sarah Bella Syndrome's. So Yezen, we've already discussed how easy it is for the examiner to bring out these kinds of patients for a Paces station. Which station do you think these patients are most likely to appear in from a Paces scenario from a Paces style scenario perspective? So I think for Sarah Bella Syndrome the most common is always going to be the actual neurology examination station, probably similar to what you would get in a kind of peripheral nerve upper limb lower limb examination. There is a possibility that you might get it in the sort of consultation station because you could ask about, could take a brief history, but I think a lot of the history might give it away, especially if it's a stroke which is again most common, especially if it's a non-set. So yeah realistically the ones that you're going to find most challenging and most commonly definitely will be the neurology examination station. And I guess sort of going on to what you might get, you might have a very vague instruction. You might say please examine these patients upper limbs and then you kind of have to figure out that they're pushing you towards a Sarah Bella examination which is actually quite difficult because you kind of start in one way trying to examine the upper limb and then halfway through you realize this is a Sarah Bella exam and actually need to sort of switch. So that can be quite difficult and that's something I think you need to be more comfortable with to sort of switch modes as it were. But equally you might just get something a bit clearer, they'll say something like your patient has a tremor or they're having difficulty holding things or they have falls or they have a gate disturbance. So I think it's just very important to be flexible in terms of what might come up because it's such a wide variety of presentations. Yeah absolutely and I thought before we get into the examination itself because that's how we're going to approach this episode of the podcast. We're going to be talking about predominantly the examination stations rather than clinical consultations. I just wanted to outline for the listeners how they might structure their approach to their examination. Obviously, coordination is going to be one of the cornerstones of this presentation. But I wonder the listeners need to really be thinking about the possible causes if they have a vineyard as you've described, such as frequent falls, dropping things, something which hints to a possible Sarah Bella syndrome. So I wonder what approach would you recommend for our listeners in terms of thinking about the possible causes of a Sarah Bella syndrome? So I think the most important thing is to, especially for paces because in paces obviously in the vast majority of cases you won't really be examined by neurologists, you'll be examined by general medic or specialist, not a specialty. So it's really important that whatever does happen, you are sort of sticking to the same structure of tone, power, coordination, reflexes, sensory and then sort of having that confidence of flexibility to switch between things. What you really should be doing is once you see the initial instruction, you just have in your head thinking about, is this, if it's for example a tremor, the most common things tend to be either like a Sarah Bella disorder or if it's sort of part and sony and syndrome. Then you kind of, the way I do it in my head is I have the sort of points, the sort of tone, power, coordination, reflexes, sensory and I just sort of thinking in my head just for that sort of 30 seconds or so, what could it be? The tone be in Sarah Bella, what would the power be, what would the coordination and then therefore when you actually enter the station, you're kind of mentally ticking things off as you go along and you're just saying, okay, tone is, power is this, it's unilateral, bilateral and then you just sort of go into that mental model and that only really comes once you've actually examined enough people, which is why I always say, you need to really just try and find as many people as possible on the words. Yeah, absolutely. And so, I think probably, should we talk through the sort of different causes of a possible Sarah Bella syndrome? You already mentioned one at the top, which is infarction. So any type of stroke, which is affecting the Sarah Bella, is going to result in usually unilateral signs. So what other signs might cause a sort of unilateral Sarah Bella syndrome and then how does that contrast with the types of causes where you'd expect it to be affecting both sides? Yeah, so as I said, I mean, stroke is one of the most common neurological disorders and that is reflected within pace as well and it tends to be sort of very high up on the list. I think thinking about it from sort of unilateral versus bilateral perspective can be useful just as a sort of rule of thumb, heuristic, just to sort of think about what it could be, what it couldn't be, especially is it a stroke or not? That's kind of the first thing I would think about. But I guess, if we're to think about the most common things, there are different ways of categorizing things. Some people use the surgical sieve. That's what you all just like to do. But if we're thinking about it just in terms of a rule of thumb, unilateral versus bilateral, I think the first thing is stroke, as we said. Second thing I should think about is, especially in a younger patient, is if it's some sort of demyelination, like multiple sclerosis and then otherwise you can get a space of replying lesions. Again, less likely, I think in paces because they tend to be progressive. You may get a space of replying lesion that is non-progressive, but I guess that's less common. And that tends to be somewhere, for example, in the cerebellum. So that's kind of the unilateral causes. And I guess if we go to, if we narrow that down a bit, you think about stroke. Obviously 80% of strokes are a Scheme, like 20% are hemorrhagic, could be one or the other. But probably if you get a, you get a pure cerebellar stroke, which is common enough. And that would just have cerebellar findings, pure cerebellar findings, nothing else. That would localize there. But another one is less common from stroke perspective, but it's still possible. And they will have stable signs, is what is known as lateral medallary syndrome, which is a stroke usually of the picar artery, posterior cerebellar artery, which affects the medallar. And it leads to a very wide constellation of signs. And the idea really, the way I think about it, is that most of it is imsyllateral, but the thing that tends to be, control lateral, is going to be the motor fibers because they descend at the medallar. So you see a quite, again, a wide variety of findings you might see, sort of imsyllateral, cerebellar signs, and then you might see control lateral pain, temperature sensation, and power as well, as well as a wide variety of things like hornest syndrome. You get some swallowing dysfunction as well. So often these patients may have an NG2, for example, or a peg, which probably would be more difficult to find on examination, unless you're looking for it. There are other causes, we talked about sort of the bilateral causes. So calling back to my sort of revision for this topic. So the first thing, which I always thought of is the bilateral causes may well include bilateral events of all of the unilateral causes. So you can have demalination affecting both hemispheres of the cerebellum. It's not impossible to have bilateral cerebellar in parts. I'd say it's uncommon, but it's not impossible and not impossible, but uncommon to have bilateral posterior phosphatumus, which might well affect the cerebellum. So that's the first thing I would think. Would you say that's reasonable enough to say that all three of those could equally cause bilateral cerebellar signs? Yeah, I think so. I mean, it's sort of, you'd have to have a big syndrome or sort of have, you'd have to have a lot of demalination. You'd have to have sort of maybe multiple strokes, which, you know, it can happen, but yeah, it is less common. But I guess the one thing I'd say is, you know, the thing that you'd think is much lower down the list is going to be a stroke, which if it's unilateral, much, much higher up the list. So that helps you a bit to differentiate the two and a broader way, especially in the under-exampt stress. Yeah. And then what are the other sort of causes where you can find cerebellar signs bilaterally, which don't include sort of demalation, stroke and space occupying lesions? So that's sort of what we would call the systemic causes. Again, there's a wide variety, you know, that we think of, you know, as biologists, but again, the prevalence may be different. So the first one that we see often is alcoholic cerebellar degeneration is alcohol-related. Maybe less likely for those agropatients to come to paces, but still possible again, they can be fairly stable. The other sort of relatively common that we see possibly an atrushin neurology ward is a pernioplastic cerebellar syndrome, usually secondary to malignancy. Again, those tend to be fairly quickly progressive. So over like, you know, three, six months, nine months. So, and usually, you know, it can sometimes be the first presentation of a tumor. So, and which can be very severe. So therefore, I would say it's less likely to come up in paces, but you know, still so many to consider. The other thing, the atrogenic drug, so phenetone, caramazophenyl lithium can all cause cerebellar syndrome or lithium causes really a tremor that can look a bit like a cerebellar syndrome. It's not quite cerebellar, but it is a, it looks a bit like it. And again, these patients tend to be quite stable. So they're fair enough to come to paces. And then you get the sort of other degenerative conditions such as multiple systematrophy. Again, those tend to be relatively quickly progressive compared to Parkinson. So again, you may not see that group of patients in paces, but important to mention. And then obviously you have sort of, what, why, why, variety of hereditary causes, free deacetyl-speinocerebellateaxia, that's the rough, rough view of how I think about sort of cerebellar disorder. Yeah, I think that's really important, isn't it, to separate it into sort of systemic causes. So obviously the perineoplastic, the drugs, the alcohol, isn't going to cause any focal deficits. It's all going to be across both sides. So you mentioned one thing there, the spino-serebellateaxia is, and that's one thing which just always seem to crop up in the list of causes. I wonder if, can you just give us a bit more information about those, sort of, what are they, and how is it helpful for listeners to know about them? Yeah, absolutely. So one spino-serebellateaxia is, it's a progressive degenerative disorder that affects quite a wide variety of neurons, including the cerebellar system, also can affect the corticospinal tract, and also it can affect the sort of peripheral neurons as well. It tends to sort of present in the kind of 40s, 50s age group, and it just really progresses very, very slowly. Again, it's very rare, so the likelihood of you getting it is relatively low, but because they're relatively stable, it's still fair game. There are about, sort of, if I'm not mistaken, there's probably about seven different spino-serebellates axia, so it's probably even more now. And each one has its own phenotype. But the thing that should have shared between them is that they all have a cerebellarateaxia, it's a core feature, but the extra bits, as or would be things like peripheral neuropathy, and then in some people, if it affects the corticospinal tract, it can lead to spasticity and hyperreflexia. So there are some rare cause of the can lead to sort of Parkinsonism and cognitive disorder, but again, it's something I think we need to worry about too much. I think just generally, if you see someone sort of middle-aged-ish, it's got an ataxia, ataxic, or sort of cerebellarateaxia, with maybe some peripheral neuropathy, maybe some spasticity, I would say that it's very reasonable to consider that within your differential. Yeah, fascinating. And I guess because you mentioned it, let's talk about the cerebellar signs with spasticity, because that is sort of a syndrome in and of itself. And you've mentioned one of the spino-serebellateaxias as a possible cause, but I think the slight issue being is that coordination probably isn't going to be the first thing that the candidates are going to examine. A lot of people are taught to examine fatone and power first. And so as soon as you get a patient with spasticity, you automatically think, "Okay, well, this is an upper motor neuron sign," and actually finding two findings in coordination or ataxia in combination with an increase in tone or some spasticity, that's almost a syndrome in itself. So I wonder, are there any other causes where the list is might start the examination, some increased tone, maybe in the lower limbs, they've got a bilateral spasticity in the lower limbs, and then the candidates go on to find they have some ataxia. What are the sort of causes that would go through your head that helps, that would help our list of sort of narrow their differential down to a few sort of select causes? I mean, to be very honest with you, I think this is a very common issue, I think, because I want to point it out, particularly because I found it a lot when I was teaching people for paces. I think one of the problems that people seem to have is that they misconstrue weakness as ataxia, and the idea with that is because if you have someone who has very poor power, they aren't able to really coordinate their movements very much. The sort of classic thing that we see, especially on stroke boards, it looks like ataxia, but it's not, is like a lacuna stroke, and the reason for that is because if you have a very specific effect on your power, it leads to something called an ataxia chemi-preces, which basically just means that because they don't have enough power, it looks a bit wobbly, and I think some people, especially when you're examining, because you start off with power, you think, "Oh, power is not very good," and then they have their bit wobbly when you assess for tremor, people will think, "Oh, actually, this is a cerebellar disorder, but actually it's not, it's just that they don't have much power." If you follow that logic, then you could argue that a lot of things that affect your power will also lead to something that looks a bit similar to the differential. I guess any stroke with at least reduced power will cause this effect. You can also have things like free-dux ataxia or other things, but I think to me, that would be the thing I would think about most, is it a problem with power, or is it a problem with the cerebellum, and that's again why you have that initial thought process in your mind, and again, comes with examining more. There's one other thing which I wanted to get to before we jump into the examination itself, which is cerebellar ataxia versus sensory ataxia, which maybe speaks a little bit to what you're talking about, although talking about power. We're going to talk about cerebellar versus sensory ataxia. This is something again which I only really appreciated after I revised for my paces, but what are the differences between these two and how can Alice and accurately describe or differentiate between the two? The classic investigation that you would do on examination, especially when you're doing lower limb exam, is going to be something called a rhomburgs test, which helps you to differentiate between cerebellar ataxia and sensory ataxia. The idea really is that if you have someone who has sensory disorder like a peripheral neuropathy, it looks a bit cerebellar in the sense that they're a bit unsteady, so the rhomburgs test helps you to differentiate it. For example, if you start off, so the idea of rhomburgs test is, if you're not aware of it, is you bring your ice patients, bring their feet together, and then you test how steady they are with their eyes open and their eyes closed. If they have a cerebellar disorder, they tend to be fairly similar in terms of their steadiness if their eyes are open and eyes are closed. Whereas with a sensory ataxia, the idea is that you tend to rely more on your visual system. Once your eyes are closed, you become much more unsteady. The key point here is that in a sensory ataxia, you can't lose that sort of proprioception effect. So, therefore, when your eyes are closed, you can't really understand where you are in space and therefore you're a more unsteady. That's what's known as being rhomburg's positive. You do get this effect sometimes if you do have a sensory ataxia, something called a pseudo atatosis, which is just that you don't know where you are in space. But to be very honest with you, that sort of pseudo atatosis tends to be seen in the upper limb, which is unlikely, whereas if we go back to what we think about, perfectly orthodoxy, that most commonly tends to be in the lower limb. So, in the vast majority of cases, the rhomburg's test will help you differentiate between the two. So I think now let's get into the actual examination of our patient. This should always start following the vignette. You'll assess the patient from the end of the bed. So there's always things that we should look at first up from the end of the bed. So what would be the sort of things from the end of the bed that might tip you off that this person has a cerebellic syndrome? Yeah, so most commonly, I think, as in most examinations, you're really looking for any sign that they have problems with their mobility, which is most common. You can have mobility aids. I think most people with cerebellic disorder probably are okay with their mobility in the sense that they don't need any aids. Possibly if they do, they may have had a stroke, for example, especially if they have an end up in a frame or if they have a wheelchair, I guess the other thing is if they have, as I think we mentioned before, if they have an NG tube, if they have any problem with their swallowing, that probably is a much bigger indication that they have either a sort of, either a lot from the other syndrome or something affecting the brainstem or sort of a more systemic problem potentially. Again, if you look at them at the end of the bed, you should check if they have any tremor. If they have a cerebellic syndrome, you probably won't see a tremor. If you do, you may think, "Oh, could this be sort of Parkinsonism instead?" You could do a very brief speech assessment. It's not really part of the initial exam and you probably won't get them to say that much initially, so you could probably just park that to later once you have a bit more of a doubt about their cerebellar system. Yeah, absolutely. Important to note those things at the end of the bed as we discussed. As I've alluded to already, the slight difficulty is listeners will probably proceed through a bog standard neurological examination. As we've said, you'll examine the tone and power. I guess the importance of that, as yes and it's already alluded to, is whether or not this is a true cerebellic syndrome or whether or not it's simply an abnormality of their movement, which is contributed to by a level of weakness or spasticity. Just going back to the end of the bed. I guess the only other thing is if it's a particularly young patient, as you mentioned, the Spinosurbellate Axis. Often those with redrix ataxia, those patients present in the younger years of life, you know, the fourth and fifth decades, or maybe even younger. So that's just one thing to think about in terms of a hereditary condition. So tone and power assessment as normal, you're going to be noting if there's spasticity and you're going to be noting whether or not there's any degree of weakness contributing to their symptoms, which is obviously going to be pertinent to your differential diagnosis. I guess you as in reflexes would go along with that as well, but that would maybe just be indicative that there is sort of a true upper-motor-neural mythology if you find that they are hyper-reflexic. Yeah, I mean, classically cerebellic syndrome, a pure cerebellic syndrome should really lead to a hyporeflexia, sort of a low tone. So actually, if you do have signs of spasticity or sort of upper-motor-neural signs, then you're really thinking, you know, is this sort of broader issue? Is this a more generalized systemic cause, which I think is fair? I suppose in theory, if you've had a stroke, you will probably also have some signs of spasticity on that side as well. But again, you'd expect it to be unilateral compared to bilateral. So I think, yeah, if you have some with hyper-reflexia, then you should be thinking that this is a problem, probably not confined to the cerebellum, and you should be thinking maybe something like brainstem or, you know, if it's very wide, also affecting the subcortica spinal tract. So yeah, that definitely should really allow you to think more broadly about the differential. Yeah, excellent. And so, if we now go on to, if we talk about sort of assessing for a taxior specifically, listeners will be sort of quite familiar with the bog standard test of coordination for neurological examination. But what would you consider as the most important things to include in an assessment of coordination? So I think the classic thing that we always do, as you've alluded to, is, you know, things like distile cocaine easier and looking at dysmetry as well. I do something a bit different where actually I, because I want to get a better understanding of the coordination right from the outset, is I will ask patients to just, before I even start to sort of tone power everything, is I actually asked them to lift their arm up, and I check for drift and dysmetry at the same time. The reason I do this is because it gives me so much information to start off with, and actually helps me to figure things out. So I'll literally just say, come in, look, and then ask them to just put their arms out, for any drift, and at the same time check for dysmetry. And by dysmetry, I just mean that I ask them to put their arms out, and then I just ask them to keep the arm in the same position, and I tap the arm lightly and see if it goes back or if there's a bit of an overshoot. That's kind of what I mean by dysmetry. And then once I do that, I then know, okay, you know, is there a drift? Is there any weakness? Is there any sort of serabella disorder? Sometimes I even throw in the sort of a quick handshake as well. I'm looking for mitronic dystrophy as well. But that's the sort of something else if you wish, and that the sort of slow release. So even within about 10 seconds, I'll know if they have, you know, an instant dysmetria and mytonia, so that's very helpful. But then I kind of just do the sort of standard tone power, and then reflexes coordination. After that, really, it's a question of, as you know, you talked about, this diocochinese dysmetria, which hopefully should be familiar to the vast majority of people when you ask people to tap, alternate sort of the palm and the other side of the palm, it's axia. The finger nose, intention tremor, and really just trying to get the patients to extend, because sometimes if it's really subtle, it's very difficult to see the end of the movement. Even if you don't think it's a Parkinsonism, it's probably just worth getting them to leave the arms by the side and just assess for any of it as a diocomer, because it's just such a common differential of tremor, right? And it's important to mention when you're presenting later on. And then I think at that point, probably what I would do is probably two ways doing it. Either you just continue going on the same path, which is sort of reflexes and sensation, and then going back to doing more coordination stuff, or you can just crack on there and then, which I think I'd prefer to do just because it allows me to keep that trail of thought. So if I've done the styococaine, I've done my finger nose testing, I'll then do a quick look at checking for any stagmus, horizontal vertical stagmus, usually horizontal. I'm doing a quick speech assessment. I tell them to say something like baby hipopotsinus or British constitution or something like that. And then that kind of really is the vast majority of what I would do in a cerebellar font, the exam, at least in the upper limb. And then the other one last thing, as we mentioned, is hypotonia. So that would sort of hopefully be done earlier. So yeah, it's really just about how comfortable you are with either cracking on and going back or just sort of doing it as you go along, which comes with just more practice. Yeah, definitely. And obviously the equivalent for testing coordination in the lower limbs is the heel shithead test when you're asking patients to place their heel on their knees, slide it down to their ankle and then basically repeat the movement, place the heel back onto the knee. Are there any other tests for coordination that are commonly performed in the lower limbs? I suppose the one thing you can do is you can ask them to just tap their foot onto the edge of the bed, for example, and a sort of rhythmic manner. You can just sort of show them how fast you want them to tap. That's one thing I've done before. The main one, which you're looking, is sort of more for rather than looking for what we call a pindicular attack, or sort of, you know, attack of the limbs, you can check for trunkal attacks here, which is it mainly affects some, you know, it's mainly caused by things that affect the center of the cerebellum. If we're thinking about it sort of from a localization perspective, there's really no way of assessing it other than just gave them to walk. So, you know, if you've got someone even an upper limb exam, you might as well just get them to walk and just assess them and see how they go because that will also help you to do the rhomburg test at the end and then to see if they've got any, you know, surgery attack here, if they've got anything else that, you know, may reveal an unusual gate. And so, what type of gate would you expect, and how would the trunkal attacks just sort of manifest itself in their gate? So the classic example of cerebellar attacks here, sort of a trunkal attack here, is what we people call a broad base gate, which I think is very difficult to assess because it's not very broad. I think probably when I was a medical student, I used to think that broad base was just this sort of like, almost, you know, insanely wide, but actually it's very subtle. So it's really just a kind of a bit more than you might expect in someone who's normally walking. So if you look at someone walking normally, actually you'll realize that their legs are fairly close together or the feet rather, but actually in a broad base gate, it's just very slightly more. So it, you know, we get a lot of referrals. People think they have, you know, a broad base gate, but it's not. And then it can also be missed. Realistically, broad gate base gate is one of them, and the other thing is if you're getting them to heel toe walk, for example, or if you're getting them to sort of, what do you call a tandem walk, which is again, sort of heel toe walk, they just stumble. Yeah, apart from that, they just, they're just very unsteady, which is probably the most common thing that you would see. But if you miss a broad base gate, it's, you know, it's probably okay, but you really should try and sort of challenge them a bit and try and get them to do heel toe tests. And that should reveal some, some stumbling. And, but obviously make sure with the paces, as you know, you need to make sure that you're always right there next to them and making sure that they don't fall. So just a few steps should be fine with you next to them. Yeah, absolutely. And you mentioned about testing for nice stagmas as well. Now, one of the things that come across in my sort of reading, and I think I remember from my paces preparation myself is, is whether or not nest agmas is a more specific pointer towards cerebellate ataxia and whether or not the absence of nest agmas would point you maybe towards more of a sensory ataxia. Would that be accurate or what's your assessment of sort of the presence or absence of nest agmas in this type of patient? So I think the stagmas is, the problem with eye movements is that it's quite complex system there's a lot going on. So the way I think about it, I think most of you all just think about it, especially because we got to call the lot about it in stroke is this sort of, is it central or is it peripheral? And I think, you know, you wouldn't really expect nice stagmas in a sensory ataxia, but you may get any stagmas in a peripheral disorder. That's something we tend to do quite a lot on call, but to be honest, I wouldn't really expect a peripheral sort of a stimuler disorder to come up in paces. So I think it's fairly safe to say that if you've got some of my stagmas, it's probably, you know, probably a cerebellar to be honest, unless O.C. you know, it's not a sensory ataxia. So actually, you know, if you've seen this stagmas, you definitely really should be going down the cerebral roots for sure for the purposes of paces. Yeah, especially in the context of someone who's presented with ataxia that's, you know, clinically detectable on examination, it just adds that bit of specificity to your differential diagnosis, I guess. And then as we've discussed, sensation is something which you're going to be expected to perform as well. I have to say, as usual in paces, it can be very tight for time and sometimes you're not physically able to complete the whole of the examination. I guess for the most part, would it be sufficient to at least try and detect if there is a form of peripheral neuropathy and possibly the extent of it? But again, obviously if the listeners do run out of time, then just mentioning in the discussion with the examiner that given more time, they would want to sort of finish off the rest of their examination and complete any modalities that they weren't able to. Yeah, this is a real problem actually, the sensory assessment because especially if you sort of take some time to do some cerebellar stuff, you're really, you know, there really is no time. The way I actually do it and I found useful for paces was I did like a screening assessment which, so rather than go down the sort of dermatomal root, I kind of figured, you know, the most common is going to be glove and stalking distribution where sort of it's more the sensation. And by that, I mean the sensation is reduced more at the peripheries. So what I tend to do is I do a quick sort of screening assessment from the distal blow or limbs bilaterally compared to the sort of as we go more proximal and that takes about sort of 10 seconds and that I could do that with fine touch and I can do that with sort of pinpricks sensation. That doesn't take too long. But I think if you can do it like that and then if that's fine, then that may be, you know, instead of the sort of dermatomal distribution which actually takes quite a long time to be honest. So that's normal. You could argue that you don't necessarily need to do the dermatomal stuff. So that's one way I've, you know, went around it. But the only extra thing that I'd sort of make sure to do, especially if I'm thinking of sort of sensory tax here, I think you really should try and do a proper reception if you can just because it's such a wide, it's such a strong differential with cerebellular disorder. So yeah, I think yeah, screening tests and then maybe a proper reception probably enough if especially if you only have like 30 seconds left just on my iPad and then the rest you can kind of see the mention it. Yeah, absolutely. And that will probably bring you to the end of what is your conventional neurological examination. You'll have done tone power reflexes, coordination and sensation as I've discussed. There probably won't be time. But if there is time or maybe even when you're looking for nice stagmas and examining the eyes, other things such as a relative afferent pupillary defect or even an intonuclear ophthalm oplegia, an episode we've done recently, these are all things which might just add a bit of credibility to your differential diagnosis. Obviously, if you find them. So just important to think about those types of things, even if they are relatively small fry in the examination that you're performing. Absolutely, absolutely. It will probably come up as you say in your eye examination. So if you see a RAPD and if you see a I know that I think that it does really help you to point you towards sort of a deminalating disorder. We've discussed sort of the differential diagnosis at the top of the show. You're going to be talking about whether you're finding a unilateral, whether they're bilateral, is there evidence of loss of power or any spasticity that you've noticed? And whether or not this is more of a peripheral or a sensory attack, see a versus a cerebellar or more central cause. But I think it's important to then move on to the investigations. This is obviously going to depend on the presentation of the patients in front of you. But by and large, yes, and can you just talk us through what are sort of the main investigations which are going to help the listeners eventually get to the right diagnosis? Yeah, absolutely. So my way of doing it was always to, again, as a neurologist now, do a full examination. So I'd always say, even though it's obvious, but I'd say something like, it could be, I'd like to perform a full history and a full neural-trial examination of the cranial nerves and the other system which I didn't do, sort of upper limb or lower limb. So I'd always sort of preface with that. But realistically, I think, if you're looking at the main causes which we talked about, so it'll be stroke, demyelination, and then sort of perineoplastic, things like that. Or you really start off by saying, I do an MRI, brain, I do an MRI of the spinal cord, and that will help you look at, sort of, if it's a stroke, or if it's every sub-demyelination. For demyelination, you do it with contrast, so whole brain and cord with contrast. And then if stroke, then you can start talking about the cardiovascular examin. So you might say, I'd like to do a cardiovascular examination, you could even just check the pulse, actually, to be honest, because sometimes, if you have time and you really want to look slick, then you can check the pulse and then they have AF, and then you're like, ah, okay, preface, that's the cause of the stroke, that will make you look very good. But if you don't have time for that, that's also fine. You can just say that, you know, you'd want to do a full workout, so you do an echo, you do a 72-hour tape, you do a carotid Doppler, that sort of stuff. And then with blood, you do. You probably do it just in general screen, so, you know, you do full block count, you're in electrolyte, liver function, potentially might show you if there's any evidence to sort of alcohol-related damage, for example, but also sort of in Europe, in Europe, the screen, you know, which would include A&A, ANCA, ESR, you know, immunoglobulins, that sort of stuff. And again, if you're thinking down the sort of immunological stuff, sorry, peripheral neuropathy, you may also consider doing nerve conduction studies at EMG as well. So, and then, yeah, you could. Could an L-lumber puncture? Again, that probably would be more useful if you're thinking about demilation, so you can look for sort of oligoclonal bands in cases of multiple sclerosis, but in the sort of, again, broadly, if you're not sure of the diagnosis, especially for something like a pranic plastic, or if it's something sort of more autoimmune, then you may, you know, the lumped puncture will be helpful to see sort of protein and see if there's any antibodies in there as well. Yeah, absolutely. That's a really good wrap-up of everything that's going to be most important to say that you would do. And then, again, coming to the management, this is going to be slightly tricky as well, because it's going to, you know, equally depend on the cause. But there are some features which are going to be sort of universal among patients who have a cerebellic syndrome, if that's going to be involvement of sort of the MDT in managing any deficits that they have. So, I guess that's another thing, just to probably lead out with the management. And that almost goes across the board for any neurological condition, where they're going to have some sort of long-term deficits to their function. Yeah, as you say, I think it's fairly universal among neurological conditions. You can kind of say roughly the same thing as sort of the beginning. You're always going to be involving the MDT with a physiotherapist, you know, if you see an NG2, you might say on a speech therapist, dietician, etc. That's, you know, across the board, isn't it? Mobility aids, things like that. And then you can sort of be a bit more specific. So, you know, if they have a stroke, you can think about secondary prevention, you know, for, you know, anti-platelists, aspirin, clitorigial, or a direct or lanticoagulant, they have atrial fibrillation for multiple sclerosis, you're thinking about sort of disease-modifying drugs, you know, if it's alcohol-related, alcohol cessation, phthalmine, etc. And if it's drug-related, you can withdraw the offending drug. Sometimes, I think, you know, in the investigations, or before I would say, and I'd also like to have a look at the drug chart, that might be a good way to sort of go before talk about it, and then afterwards, saying, you might consider withdrawing the drug. And then depending really on the, very, really on the other causes, you understand we're getting a bit more niche. So, you know, if it's apparently a plastic, then we're thinking about treating the tumor, and then also maybe consider some immunological therapy, and then genetic testing, although in most, the vast majority of our energy causes, there isn't really much of a sort of cure treatment, it's mainly supportive. And then I guess, finally, if it's a tumor-space-wise combination, then you might consider involving the neurosurgeons. Yeah, if they're maybe a bit younger, I'd sort of try and lead with a bit more, you know, if it's still not clear at all what the cause is, and you may think more sort of, you know, multiple sclerosis first, or, you know, genetic testing from Spine Serbalate Axia, for example, or something else. But if they're a bit older, maybe probably lead with stroke, sort of stroke stuff, which you can, I'm sure, talk about a lot, but really think that probably will stop you and want to ask you a very specific question that they prepared to be honest, so you can keep going as long as you want, but yeah. Awesome. Well, yes, and I've been so grateful for you coming on the podcast to discuss cerebellicin dreams. This is an episode I've wanted to do for a long time, and it's been really good to get someone who's at the forefront of assessing patients, presenting acutely with these types of problems. So that only leads us to a huge thank you to Dr. Yezons Samarati. Yezons, thank you so much for getting involved with the podcast. Thank you very much for having me. It's a pleasure. And listeners, that is just about all the time we've got for this week's show. Please don't forget to like, follow, subscribe to the show wherever you get your podcast. We always love to hear from you, so give us a shout. You can get in touch via the website or via the email, [email protected]. If you want to go above and beyond and support the show, you can do that by meocoffb.com/prepacespodcast. But for now, we're just about out of time. I've been Dr. Sam Williams. Thanks for listening, and we'll see you next time on the pre-pacespodcast. [MUSIC]