ENT teaching session on LMN facial palsy!
ENT teaching session 3- Facial Palsy
Summary
This on-demand teaching session, third in the ENT teaching series at Prince Royal University Hospital, provides comprehensive knowledge on facial palsy. Presented by Dr. DEA Sharma Tibia, a senior clinical fellow in the Department of ENT, the session covers a wide range of topics including the facial nerve, upper and lower motor neuron palsies, how to assess a patient's facial palsy, the grading system, complications and management of facial palsy. The aim of this session is to equip medical professionals with the knowledge to confidently approach, diagnose, and manage a patient with facial palsy. The session will be of particular interest to those seeking to deepen their understanding of the complex structure and function of the facial nerve, and its role in facial expression.
Description
Learning objectives
- To understand and explain the anatomy and physiology of the facial nerve, including its origin, the course and its branches.
- To identify and discuss the clinical signs and symptoms of facial palsy, focusing on the differences between upper and lower motor neuron palsies.
- To gain competence in assessing and diagnosing a patient presenting with facial palsy, including essential elements of the patient's history and physical examination.
- To understand and interpret the grading system used to assess the severity of a facial palsy.
- To be able to discuss the potential complications of facial palsy and formulate an appropriate management plan, including therapeutic options for patients.
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Uh This is Nela. I'm one of the EN TSI work at Prince Royal University Hospital. This is our 3rd 3rd session of Ent teaching series. Um The session is about facial palsy and it will be uh taken by my lovely colleague, uh Doctor DEA Sharma Tibia. Do you wanna start? II, apologize for all the delays. There was just some technical glitches here and there. Sorry about that. Yeah, I take all the responsibilities for the delay because it was from my side. Anyway, thank you, Nala. Um So myself the best SOMA. I'm senior clinical fellow working in the Department of Ent at Princess So University Hospital. And uh today I'll be talking about facial palsy and I'm quite humbled to my colleague, Mahala and Hamza for providing me this opportunity to share my knowledge and I hope this will be beneficial to you all. So let's start. So the objective of the presentation today is I'll obviously be talking about the facial nerve. Then I'll talk about the facial palsy, both uh upper and lower motor neurone pulses. I will touch upon uh ep see how to ask the patient with a facial palsy. Then I'll talk about the grading and obviously about the complications and management uh of the facial palsy. So I hope at the end of this session, you should be able to approach a patient with facial palsy confidently to formulate initial diagnosis and management plan. So facial nerve uh as you can see here also is the nerve of facial expression. It's a mixed nerve because uh the fibers contain the facial nerve, contain motor as well as the other fiber. Most of the fibers are motor fibers. 70%. The other fibers comprises. As you can see here, sensory secretomotor and test fibers. The motor fibers supply all the muscles of facial expression as well as three other muscles. Those are stylohyoid, posterior bili of digastric and nerve tages. If you're wondering why this group of muscle because these are all the derivative of 2nd, 2nd branchial arches. And as we all know, facial nerve is also a derivative of second bronchial arch. The other uh innervation, sensory part of the external auditory meters, part of tympanic membrane and part of the pinna secretomotor fibers, they supply um uh uh tear gland, lacrimal gland, submandibular sublingual gland and some of the nasal and the palatine gland, the test fiber uh anterior two third of the tongue for test sensation via corda tymp nerve. Uh This is um the I think it's a good idea to refresh our knowledge. And would you be able to type me in the chat box. Um oh What is the not responsible for innovation of the parotid gland uh test for the posterior one third of the tongue and obviously the gentle sensation of the tongue. I'm sure you all know about it. Let's go to the next uh slide. So this is how the facial nerve looks from the start from the uh midbrain until it gives the final terminal uh muscle branches. I can see some of the answer in the uh yeah, that's right. Gloop four. And this is how uh the isolated facial nerve looks like. Uh let's see the other. So this facial nerve, as you can see is quite complex. I'll try to simplify this by explaining it um from this uh picture here. So the nucleus of the facial nerve lies within the midbrain. There are actually three nucleus of the facial nerve. Um One response, one is uh known as superior sal artery nucleus that is for uh giving the uh parasympathetic fiber for secretomotor uh innervation of um the lacrymal submandibular and sublingual gland. The another one is the solitary nucleus that's for sensory innervation. And the most important one is the motor nucleus. And please remember this is a mo uh lower motor nucleus. Yeah, because we will be talking about the upper motor nucleus as well. So the fibers of the lower motor nucleus and the fibers from the superior salivary nucleus and the um uh solitary nucleus, they combine together to form a facial nerve. However, while exiting from uh the sulcus, that is called pontomedullary junction, uh or pontomedullary sulcus. These two fibers uh the uh not the fibers, actually, the roots are not combined together. So they are, there are two different route. One is from the one is known as actually the proper facial nerve root from the motor fiber. And another one is combined from the parasympathetic and sensitive fiber known as the intermediate uh nerve. Why is this important? Clinically? It might be important because any lesion within the area can present with isolated motor palsy or can be isolated sympathetic or sensory paralysis. This is theoretically possible. However, in um most of the cases because they are, they lie close to each other because they are very close uh line with each other. That's why we see the combined picture. All right, once it exits through the prone to meu function, then it enters uh to the temporal um temporal pa uh uh I mean temporal bone. And um in the temporal bone, the facial nerve actually gets various uh name. So from pontomedullary junction when it enters to the internal acoustic meatus, because it is within that me part, it is called meal segment of the facial nerve. From the fundus of the internal acoustic meters somewhere here up to the geniculate ganglion. I'll talk about genital ganglion later on the segment is called labyrinthine segment from the geniculate ganglion. This part up to the pyramid, that's the part of the middle ear that's called the tympanic or the horizontal part. Why the tympanic? Because it lies within the tympanic cavity. And why horizontal is because uh the position you know how the nerve lies is it's horizontal in a horizontal uh plane within the facial canal of the mid cavity. Um Now next segment from the pyramid up to the stylomastoid for, I mean is the vertical or the mastoid segment. Again, the name mastoid because it lies very close proximity with the mastoid bone and because the facial nerve lies vertical. So it's called the vertical segment. And finally, when after it comes out from the stylomastoid for, I mean, that's when the facial nerve gets the name extratemporal and where it uh it gives it terminal branches. Uh Those are the motor branches and I'll in the next slide, I'll present I I'll talk about the motor branches. All right. One of the important um branch of the facial nerve here uh is uh nerve toed. Um Why I'm talking about this um motor branch speci specifically is because this is clinically important and, and I'll, I'll explain that later on. Uh So there are, you can see there are three ganglion associated with the facial nerve geniculate ganglion, uh spinal ganglion and submandible ganglion. Are these all the parasympathetic ganglion? The answer is no. Uh the spinal ganglion and submandibular ganglion are the parasympathetic ganglion. That means the preganglionic fibers, synapses here and give the postganglionic fiber to supply lacrimal uh sublingual as submandible gland, the geniculate ganglion. The name um gen uh genu means turn because uh why the name geniculate ganglion is because as you can see the facial nerve is taking a turn here and genu uh in Latin means the turn. So that's why this ganglion got the name geniculate ganglion and geniculate ganglion. Please remember um is for the sensory fibers. OK. Is this all clear so far? And if you have any questions, just a moment, um I am not able to see the live anymore, the slides. Um Do you want to press, you know, is the slide uh deck able to, are you able to press the again present again? Um I don't see where to present again, like uh initially where it showed the slide decks are already. Can you click on them? Yeah. Yeah, thank you. Can you see it now? Yes. Yes. OK. So from where is it from the genital ganglion? OK. So anyway, genital ganglion, like I said, um is responsible uh is not a parasympathetic ganglion but a a sensory uh ganglion. So the synapsis for the se uh sensitive fiber occur here. OK. So now what we need to know further is obviously um uh one of the um important function of the facial nerve, as I mentioned is uh uh chest sensation from two third of the tongue and that happens from the corda tympanal OK. So let's look at the next slide. So this slide shows all the motor branches of the facial nerve. Um And there are various ways uh to actually remember them. And I use the Pneumonic 10 zebras passed my car. Yeah. So you can use any Pneumonic uh which you can remember them. So, basically temporal branches, zygomatic branches as depicted by different color here, buccal branches, marginal mandibular and cervical branches. What do they do? Temporal branches um helps in obviously uh uh um uh I mean uh uh frowning. Um I mean contract all the muscle in the forehead and uh we can have frowning gma uh branches helps in open and closing of the um eye muscles, buckle branches um when we blow or uh p the cheek out and maslar mandible branches obviously helps in smiling and give that a good smile. Um Let's look at the next slide now. So this is so far, what we um what I explained is uh starting from the uh lower motor nu- um uh nucleus. Now, uh let's see at the upper motor nucleus of the facial. Now, where does it lie? It lies within the precentral guidance of the cerebral cortex. Yeah. And as we all know, um all the uh fibers from cerebral cortex, motor fibers uh they intersect, isn't it? So that means right side will uh innovate on the left side and left will innervate the right side. But the important thing here to remember is about the lower uh facial motor nucleus, lower uh motor nucleus of the facial nerve actually is divided into upper and lower half. That's because how it is innervated by this uh cortical bul fiber from the upper motor nucleus. Yeah. So the upper part of the lower motor nucleus gets innervation from both the sides. And one more thing, the upper uh part of the lower motor nucleus supply only the upper part of the face. This is very important clinically because this is why uh there is different in the clinical presentation where there is lesion in the upper motor neuron or upper uh motor tract, let's say, or um uh or if there is a lesion in the lower mo uh lower uh mo uh lower motor tract, let's say. Yeah. Is this all clear? I'm happy to repeat it again if it's not clear. Yeah. So there are a few points here. You can see upper part of the lower motor neuron gets bilateral cortical innervation. Like I've mentioned upper part of the lower motor neuron innervate forehead area, innervated by upper part of the lower motor neuron has bilateral innervation. OK. OK. This is the same thing which I explained already. And one thing I'd like to explain is not to stupidus muscle. This is quite important again, clinically, what does this staid muscle do? Is it uh stabilizes the foot plate of the stapes? And what does it do? It causes the damping effect. That means it um it the foot plate from loud noise and what happens if there is a damage of the stapedial nerve, the patient e even the normal sound will be perceived as a louse um uh sound by the patient. It is called a hyper uh aosis. And obviously, patient will have phonophobia. Yeah. So let's talk about the facial palsy. Now, now, I think we have a little bit of idea about the facial nerve uh about the lower motor neurone and the upper motor neurone. So we can talk about the facial palsy. Now, so what do you understand by facial palsy? Obviously, facial palsy means um in um I mean, uh for various reason, if there is um impairment in the function of the facial nerve that causes that is the facial palsy, isn't it? Yeah. So that means what happens when there is a facial palsy, there will be loss of facial expression, uh dry eyes, uh there will be a loss of test from the anterior two third of the tongue and patient will have hyos or homophobia. Now, I have a question again, is the facial palsy and Bell's palsy. The same thing, obviously, we'll discuss that in the coming slice later on. And again, when you see a patient with a facial palsy, let's say on the right side, which side is the lesion? Is it on the right side or the left side? Again, we will uh talk about that in the coming slides. OK. So now about the upper motor neuron uh lesion and the lower motor neuron lesion. The same thing like I explained earlier, upper motor neurone lesion, be it in the cerebral cortex or be it anywhere along the cortico uh tract? Here, this tract here it will cause contralateral on the opposite side. And that will c cause loss of function of only the lower part of the face. So there will be loss of nas will fold and drooping of the mouth. Whereas the patient still can wrinkle, the forehead still can lift the brows. There will be no dripping of the eyelid and the uh the patient can still close the eye. Is this clear? Yeah. Uh because I can't see any of you if you have any questions or, or if it's not clear, please uh type in the chat box so that I can address them uh same time or later on. All right. Um Here you can see the lower motor neurone lesion. So the lower motor neurone lesion will cause. So no lower motor neuron lesion means anywhere from the lower motor nucleus up to the terminal branches, motor motor branches. Yes. So that will cause loss of all the facial function. Yeah. So that means all these you can see there will be loss of nasal lo will fall, there will be drooping of the mouth. The patient will not be able to wrinkle the forehead can't lift the uh bruise. Uh there will be drooping of the eyelid and obviously can't close the eye. Is this all? No, this is only the motor function, right? But no lower motor neuro neurone will also cause disruption of the other function of the facial nerve. That is the patient will have alter se uh chest sensation from anterior two third of the song. The patient will have dry eyes and the patient will also have, what is that hyperechoic and photophobia? Yes. OK. So, you know, like I um briefly said in the earlier slide, also the clinical presentation of facial nerve palsy um will um be different from patient to patient. Yeah. Why is that? So it all depends upon where the lesion is. So upper motor neurone lesion presentation, clinical presentation is completely different from the one with the lower motor neurone. And I'm I'm sure you will understand that from the previous slide, isn't it? Yeah. So in this slide, um I have tried to um uh put all the causes for the facial palsy and where they can affect. Yeah, uh depending upon the cause. Yeah. So here uh this is where um if you see here any supranuclear palsy, obviously, uh palsy on the contralateral side, lower uh half of the face. And what are the causes stroke, tuber uh anywhere between any lesion from the lower motor nucleus up until the geniculate ganglion, any any lesion in that area be it because of the, you know, there are these are the causes which uh in the blue, you can see stroke, tumor, very syndrome, acoustic neuroma, meningioma. All these can will impair all the function of the facial nerve but on the contralateral side, uh sorry, ipsilateral side. Yeah. Now if the lesion lies below the um geniculate ganglion but above um above um uh before it gives branch, I mean, the before it gives the nerve to the stapedial muscle, what will happen, the patient will have all the symptoms but there will no dry eye because greater superficial um uh petrosal nerve is still intact, isn't it? Is this clear? Yeah. So if there is a lesion uh somewhere below uh after the facial nerve gives nerve toads, then what all symptoms, all the symptoms but patient will not have photophobia and um hyperechoic and patient will not experience the dry eye. However, rest of the function will be impaired. So it all depends upon where the lesion is. And here, as you can see, I have outlined the condition or the causes uh where um depending upon where the lesion can be. Yeah. So as you can see here, um mostly um upper motor neurone, lower motor neuron up until um yeah, lower motor motor neuron, they are basically the causes as you can see is basically, you know, stroke, tumor, all those kind of things. Whereas um after the CP angle, there are more of the ent causes. You can see. Yeah. And uh what is the cause after it um, exit the sta master foramen solely the parotid cause any lesion within the parotid causing the facial nerve palsy or surgery within the pid gland. Ok. Let's move on the next slide now. So these are the causes which I have mentioned uh in the previous slide, trauma, congenital, there is something called Mobi syndrome. That's the congenital facial palsy, which can happen along with the uh cranin of six palsy as well. Um uh Izic, any kind of both trauma, any surgery within the ear, mastoid palliative surgery, metabolic lyme, important to remember is also a Lyme disease because uh in the latest state of stage of the Lyme disease or as a complication, there can be a facial palsy and our favorite one, facial palsy is the idiopathic facial palsy, isn't it? Why is it favorite? That's because that's the most common. And I think all of us know our favorite Bell's Palsy. That's the idiopathic facial palsy. Yes. Uh As you can see from this and the previous slide, there are many causes for the facial palsy. But when someone uh talks about the lower motor neurone palsy, why we all think about the Bell's palsy? That's because most of as you can see 53 to 70% of the time lower motor neurone palsy is idiopathic uh facial palsy or the Bell's palsy and One more syndrome. I'd like you all to remember. This is, although uh it's a rare syndrome. Um but if the patient presents with, you know, recurrent facial palsy, a lower motor neuron, palsy with swelling of the face and lips. And you can see this kind of fold and fissure in the tongue. Then that is um uh Melkersson Rosenthal syndrome and this is something uh in the area of neurologist to treat. All right. So these are all the same thing I put in the uh slide so that you can see later on. So, grading of the future policy, is it important? Yes. Um this is important obviously for um to obviously to see how severely the facial nerve has um impairment in the function. And also it's also for the prognosis. If the patient is going to have a full recovery or not, there are actually various grading system we can use, but most commonly used. One is the House Brackman system. So the easiest way to remember how Backman is uh there is six grading system. The first one is totally normal. Sixth one is total paralysis in between. We just have to remember 2nd, 3rd, 4th and 5th. And how do you remember that for the second grading, you have to very closely monitor to see if there is a facial um asymmetry or not. Whereas in the fifth, severe dysfunction, you can see uh there is obvious asymmetry but there is no total paralysis. OK. Now, the remaining two is obviously, um, you possibly will have to um remember them so moderate dysfunction. What's the difference between the moderate dysfunction and moderately severe dysfunction is, it's almost similar. Um uh But um in the moderate, they say that it's not that disfiguring, whereas in the moderately severe dysfunction, it's quite disfiguring. All right now, um Like any other patient when a patient presents with a facial palsy, you have to take a history. I'm sure you all know how to take a history. These are some of the points which um I think is important. Uh and not to exclude while taking a history, obviously, onset of the facial paralysis is very important. If it's a uh if it's a, you know, sudden onset or a gradual onset, why is it important because sudden onset, facial palsy might be one of the presentation of the stroke. If it's a gradual presentation, gradual onset, it could be something chronic, ongoing. So, onset is very important. Duration is again, very important because if the patient presents in early hours of the uh facial palsy, um then the treatment uh also has a better prognosis site distribution. The associated symptoms, the associated symptoms are also again important. Why for differential diagnosis and also for the topo diagnosis. So what all associated symptoms, if the patient has solely the facial palsy or any other symptom like impairment in the chest, any ear problem, um any swelling in the parotid area. Um uh or um any headache, nausea or vomiting. Is this important? Yes, because one of the biggest differential diagnosis with the facial palsy is stroke. Yes. Past medical history, recent surgical history, very important, similar presentation in the past. Is it important? Yes. Again, important. And um if you remember from the previous slide, uh medical syndrome, dental syndrome will have a recurrent facial palsy along with the swelling after uh uh face and fissure in the tongue. Yeah. And another why is it important again, is it could be symptom of any slowly growing tumor as well? Ok. History of trauma. Is it important? Yes, and do not forget about the red flag sign because facial nerve we we can see in various facin palsy and I mean, we can see in various head and neck cancers. All right. Uh next slide. So examination. So what all to examine when a patient comes with the facial palsy? Obviously, you should uh be able to examine uh facial nerve. Um I don't think I'll be able to play this video here. Yeah, I can't play this. So what all thing uh you asked is obviously you are basically check um checking all the knob, I mean the motor knob route, right? So you'll ask the patient to frown, you'll ask the patient to close the eyes and try to open. So you basically are checking for the temporal branch, you're checking for the Zygomatic, you'll ask the patient to puff the cheek out and then uh press to see how well the uh buccal branches are working, ask the patient to smile to see if there is any drooping on one side. Um And other thing to ask is if the patient is experiencing loud noise. Yeah. And if the patient has any sensation in the tongue, this sensation in the tongue. Yeah, that's that completes the facial no examination. And along with that, you also ha will have to do a cranial nerve examination because sometimes facial nerve palsy can be associated with some other cranial nerve palsy, especially which one, the sixth one because they like very close, close proximity within the midbrain ear examination. You should do a thorough uh ear examination. Uh that, that includes infection. You will be looking for any rashes around the penis or ear canal. You should be able to do a autoscopy examination. Again. Sometimes uh patients especially with the ra hand syndrome, they will not have any rashes outside. But when you do the oscopy, you might be able to see some rashes in the ear canal. So, oscopy is very important. Um The importance of os oscopy is, you know, if the patient has um let's say otitis media, uh chronic otitis media, you can see the different findings. Yes, otoscopy is important. Um A tuning fork, you should always do um tuning fork of uh when a patient comes to the facial palsy just to see if the patient has any uh cochlear dysfunction as well and quickly do a vestibular examination as well. Ok. Thoropa gland examination is important to see if there is any lump within the gland. Um uh that could be one of the possible causes for the facial palsy neck examination. Obviously, that's because various head and neck cancer uh can uh uh can present with the facial palsy as well. And is it important to do a upper and lower limb examination? Yes, because like I already said, one of the important and not to miss uh differential diagnosis in facial palsy is stroke. I feel like I'm just talking, you know, I don't know if you all are able to hear. So maybe it's a good idea, you know, time to time just type in the chat box that you I'm audible. Yeah. Ok. So let's look at the next slide. So diagnosis for diagnosis um is the facial palsy purely a clinical diagnosis? The answer is yes and no. Uh yes and no. Thank you, Nala. Do we need any diagnostic tool again? Yes and no. Why I'm saying? Yes and no. Both. Most of the facial palsy is purely a clinical diagnosis, but we still do a diagnostic tool. I wouldn't say a diagnostic tool, but we do need other um investigation for, for a facial palsy. That's because those will add us in the management plan. So I can see a question. Do we have to do act scan if clinically Bell's palsy. Uh So the answer is how will, you know, it's a Bell's palsy without doing a CT scan because Bell's palsy is a idiopathic facial nerve palsy. Yes. So actually Bell's palsy is also a, you know, a diagnosis of exclusion. That means once we exclude everything, then only comes the diagnosis of Bell's palsy. So if you are very sure, you know, from your clinical uh from your history clinical examination, if you are very sure that there is no obvious cause, then you possibly will not need. But ideally speaking, Bill's palsy is once you exclude everything, then only you can say Bill's palsy is this clear GTA. So the investigation we do uh um are obviously we do the blood test in all of the patients, blood sugar monitoring is very important because you can see in the coming slide that one of the, you know, management medication we use very commonly is steroids. So we need to monitor the blood sugar either by doing random blood sugar or ba one C same. Um Varicella antibodies do we commonly do no, if it's you know, clinically very obvious that it's Ram Ilhan syndrome. But if diagnosis is not clear, then you can, we can do it. And again, we can do the antibodies for the Lyme disease. The other test I have mentioned here is topo diagnostic test, uh electrodiagnostic test, CT MRI and surgical explosion, surgical expression. That means you can only know which part of the facial nerve has injured when you surgically explore and find out. OK, topo diagnostic test, I've just mentioned the topo this is um here uh for your knowledge. However, to be honest with you, these tests are not used nowadays, it used to be used previously. Uh before the era of electrodiagnostic and amazing. Uh before the intervention I would say of electrodiagnostic test and CT MRI because now we have more advanced test, we usually don't do the topo diagnostics test here. But um I have included that in the slide uh for your knowledge. So this is the topo diagnostic test here, however, but I'm not going to explain them because we don't use them. Um Nowadays, like I said, OK, so electrodiagnostic testing, it is quite important. Uh although um depending upon institute, if it's uh uh well, uh you know, if uh if it's commonly used or not, but uh having said that the electrodiagnostic testing are very important. Why are they important? Um They are important as you can see for prognosis. Are these testing are used for um you know, stratifying the patient? So which patient qualify for the nurse surgical treatment and which one qualify for the surgical management. But this is not useful in diagnosis or making a differential diagnosis. Um Electrodiagnostic testing itself is actually a very uh huge topic and I think it requires a decent amount of time for me to explain everything But what I want you all to remember is the basic electrodiagnostic testing used are um eng and eg um So, electroneuronography and electromyography, electroneuronography is used first. Whereas electromyography is used uh in later, you know, uh usually after the six months of onset of the facial palsy. And the basic principle here is in electroneuronography, you are basically looking for degeneration of the nerve. How quickly the degeneration is happening. If the degeneration is happening very quickly, maybe we need to consider surgical um you know, management option for the patient. OK. Because uh if the this happens very quickly, possibly the conservative management might not work, make sense. And the electromyography, like I said, the principle is we are looking for the reinnervation. OK? If there is any, if, if there is any de innervation happening or not, if it's happening, how quickly it's happening? This is again, we add on the surgical management of the patient. All right. So now let's talk about the management of the facial palsy. Always remember management of the facial palsy is a multidisciplinary a team approach. OK. Um The options are um the conservative and the surgical, almost all the patient will require the eye care and the facial physiotherapy, which I have included here. Yeah. And as a junior doctor, you play a very vital role in the management of the facial palsy because you are usually the first contact. Yeah. And your role here is to take a proper history, do proper clinical examination. If there is any doubt in the diagnosis, please do not hesitate to discuss with your senior. Yeah, if you are very clear with your diagnosis, then start the initial management plan having said that do not hesitate to refer any patient with the facial palsy to other specialty because like I said, it's uh the facial palsy patients should always have a multidisciplinary team management. Yeah. Yeah. So I have included the eye in a special, I mean the separate light because like I said, eye care is very important to prevent the complication from the facial palsy. One of the complications uh from the facial palsy is um corneal ulcer and if that happens, uh we can't unfortunately treat it. So that's the reason why we want to prevent it. So all the patient, please do not forget to give them uh education about how important the eye care is. Yeah, please prescribe them artificial tear and lubricant and also please educate them to close their eye with the tape so that the eye will, the cornea will not be exposed uh for the dryness. And this patient will definitely need a ophthalmology referral. So please do not hesitate to refer them to the ophthalmologist, physiotherapy again on slide because all the patients with the facial palsy will require a physiotherapy at some point. Um And one of the recent advanced in fusio therapy uh is transcutaneous nerve stimulation. Um I was reading some literature before uh this presentation and it seems like this has a quite a promising role. So please all the patient with the facia uh further uh physiotherapy, the basic uh principle. I'm sure the phys uh if there is any physiotherapist here, uh um they might be able to explain it better. But my understanding is what you do uh with the tras Q 10 is not the stimulation is you stimulate the uh better side. Um At the meantime, um you try to s uh stimulate the other side as well. OK. With that, now, let's talk about the common um uh uh I mean um common um causes of uh the facial palsy. Yeah, the first one, Bell's palsy uh like I said from your um history clinical examination. Um and from the diagnostic tool you used, if you are very sure, this is a Bell's palsy, do not hesitate to start the treatment immediately because if you start the treatment within 72 hour, the prognosis is very good. Have you ever given a thought why this 72 hours? That's because the degeneration of the nerve starts after the 72 hours and we want to intervene before that. OK. So that's the reason why if you start any treatment before 72 hours, the prognosis is good. All right, the treatment for Bell's Palsy, obviously, the prednisoLONE, you will usually give 60 mg or the maximum dose of 1 mg per kilogram. Uh, in a tapering dose for two weeks. The role of, um, antiviral treatment with acyclovir or VR or Valacyclovir is controversial in Bell Palsy. Bell's palsy. Why? Um, because sometimes, you know, Bell's palsy could be the initial presentation, uh, of the Ramsay Hunt syndrome. In that case, the role of acyclovir is very much right. But if it's purely a Bell's palsy, I don't think, um, the acyclovir does anything. Is this clear? Invariably the Bell's palsy patient will need eye care and physiotherapy. Ok. Uh, next one Ramsay Hunt syndrome, we know this is the viral, um, herpes sister, uh, infection of the cranin of seven and eight. So the patient will have tried of the symptoms, right? Facial palsy is one of them. Apart from that, the patient will have a sensor, neural hearing loss and you can see lesion in the pinna or when you do the otoscopy, you can see lesion in the ear canal. The treatment again, steroid, uh, the same like, uh, in the Bell's Palsy. But, um, the antiviral treatment with Acyclovir or Valacyclovir has a great importance in Han Syndrome. And similarly, this patient will need, um, eye care and also the physical therapy. But, um, Bell's palsy carries a good prognosis, um, usual, um, in most of the cases, the recovery is within a few weeks time. Although, uh, there has been cases where, um, uh, there has been a delayed recovery and it can take up to six months to one year. Whereas in Ramsay Hunt syndrome, it's usually carries a poor prognosis due to residual hearing loss or the facial palsy. And I think it's important to educate the patient about it. Uh Now, um, uh the management of a facial palsy with any kind of ear problem, let's say I have said ear problem because it can be anything uh starting from acute otitis media to mastoiditis. And as a zia doctor, your role will be to start the initial treatment with the antibiotic. And obviously, this patient will need ent referral for surgical management. And what are the surgical management in a acute otitis media to release the pressure? Um We uh we do a myringotomy and grommet insertion. Whereas if there is uh uh chronic otitis media or masis is the cause of facial palsy, then basically, uh they will need uh extensive surgery um uh uh with mastoidectomy, facial nerve decompression and it will be um within the call of the ent referral, obviously, depending upon where the problem is. Yeah, for the Lyme disease. Uh it's uh as we all know, it's a tick. Uh I mean, uh i it is uh caused by the bacteria and tick, bone disease. The management depends upon the patient age and um disease severity. Uh and do not hesitate to, you know, discuss with the infectious disease specialist or the pharmacist about the treatment and the treatment are obviously the antibiotic treatment. Now, uh next one is an interesting one. the trazenin following autolog surgeries. Yeah. So let's say you are the on call and you are called uh by uh recovery nurse saying that. Ok, uh doctor, I have a patient who recently had the surgery and now the patient is um experiencing the facial palsy like he or she is developing the facial drooping and can't open the eyes. What will you do? You can write in the chat box if you want. So here a few things to remember. Is it early onset or is it a delayed onset, delayed onset palsy because the management is different? Yeah, the early onset uh facial palsy could be because of the effect of local anesthetic. So you always want to discuss with the operating surgeon or with the, with your senior who was assisting during the surgery to make the further management plan. If it's uh if it's because of the effect of the local anesthetic, you just want to wait, watch and see because there will be spontaneous recovery. Yeah, but if there is a early onset and there was no history of using any local anesthetic at the end of the procedure, but patient developed immediately after the surgery. Um the f uh um you know, the facial palsy, that means there is a possibility of nerve injury and we do not want to delay this and want to take this patient again to the theater for a decompression or the nerve repair. Sorry, I can see. Uh ok. So, oh, Aku, um uh in terms of timeframe, I do not think there is any specific time frame but because we all know that the local agent, I mean, local anesthetic agent can take up to 30 minutes to give the effect and we possibly would want to wait for another maybe 50 min uh 15 or 30 minutes before, you know, before um coming to the conclusion. So I think in terms of exact time frame, I'm not sure. Um but we just want to wait until the local anesthetic um uh you know, uh effect will wear off. So when I say delayed onset, uh it's um possibly is, but unfortunately, in terms of the um hours or days, I'm not entirely sure. Sorry about that. Uh So delayed onset could be because of edema, let's say uh the next day the patient developed uh um facial palsy the next day. Um So it possibly is because of the tight packing or because of the edema. In that case, you just want to remove the pack so that you release the pressure from the facial nerve or you just have to prescribe the steroid uh for the patient. Ok. Uh Next one, you might be called about a patient who has injury, who has a history of injury and presented with a patient of palsy. In those cases. Please remember in the trauma isolated, facial nopal is very rare and there there could be something um extra, I mean, not extra, something urgent, you know, uh there must be something um else which need urgent attention must be with the patient. Like um there there might be intra or extracranial hematoma, subdural hematoma which required urgent attention rather than attention to the facial nerve. However, having said that if you see a patient with the uh isolated facial palsy because of the trauma and if the palsy is immediate and complete, then the patient would require a nerve decompression. Yeah, if there is any delay in the onset, let's say uh when I say delay in the onset again. So today, patient had a trauma and you notice during the initial clinical examination, there wasn't any palsy. But the next day, you see the palsy, obviously, the palsy is either because of the hematoma or could be because of the edema. So you want to treat those patients with the steroid. Yeah. So delay in diagnosis, what does that mean? Let's say the patient um had a severe trauma history admitted under the neurosurgery because um uh the patient needed early attention as the patient has subdural hematoma, uh they evacuated hematoma and on the seventh day, they also noticed a facial palsy. So what do you do for those cases? Obviously, the uh electrodiagnostic testing will play important role. And if you see in uh electroneuronography, there is already uh more than 90% of the G generation. That means most of the fibers are already degenerated. So this patient will definitely be a candidate for immediate surgery. OK. So these are all the type of the surgery. I don't think I uh you need to know um all of this, but I've just uh put this on the slide uh for uh your knowledge. All right. Next one, the prognosis, uh there are certain prognostic factor um um uh for the facial palsy and the poor prognosis. Um is when there is a complete palsy, there is loss of stupid reflex. I would not only say the loss of stip reflex, but the higher the lesion is the poor, the diagno poor. The prognosis is uh if there is no sign of any recovery within the three weeks, that's also indication that's also one of the poor indicating um I mean poor uh uh um prognostic uh factor if the patient is elderly. Um uh any patient over the age of 50 with a facial palsy Ramsay hunt syndrome, as I already mentioned and poor response to electrophysiological testing. Are there any complications of facial palsy? Yes, like already mentioned of palmic complications. So that's the reason why educating a patient about a proper care, eye care from the first day is very important because ophthalmic complication can be prevented if the patient has a good knowledge about the eye care and do not. Um uh So, um do not forget to give them artificial tear lubricant and please educate them to tape the eye to prevent the complications of exposure, keratitis and ulceration. Ok. But if they develop this one, you obviously will have to refer to them ophthalmology. And the other complication is hyperkinetic uh complications. Uh Those are hemifacial spasm, facial asymmetry and synkinesis. What are they? So he uh facial uh spasm means there is involuntary muscle contraction. That's because of the axonal degeneration of the facial nerve from the para paralysis. Yeah, obviously, the facial asymmetry, we know if we compare from the uh you know, normal side to the other side, there will be dyin. That's the facial asymmetry. And obviously, it's one of the complications and syin is that's that is um when you do a voluntary um contraction of one muscle, there will be involuntary movement of the other one. And some of the examples are oculo oral syn kinases. That means when you are closing your eyes, you can also see movement in the uh muscle within the um lip lip area. Then another one is the Crocodile Clear Syndrome. Again, uh when you are eating something, uh you can have a tear. Yes. So Crocodile tear syndrome and what is the management for this one? Facial muscle therapy and the borderline toxin injection? So I have put this in separate uh slide with a very bold letter that the any patient with facial palsy. The patient education is very, very important. Mhm We must always um uh um um 10 to join various support groups. And obviously, it can be very debilitating uh for the patient and it can affect their um uh emotional and mental uh side as well. And this patient might also need a cognitive behavioral therapy. OK. So I think um this is what concludes uh our presentation and I have summarized all those points here. Let me quickly go through them. The facial nerve is a complex nerve and a mixed nerve. Uh, upper motor neuron lesion cause contralateral lower facial paralysis, lower motor neuron causes ipsilateral complete facial paralysis. Uh plus minus loss of taste and hyper ESIs and photophobia. Always remember while assessing a patient with facial palsy, always keep in mind. Could it be stroke in every step while taking a history while examining, while ordering any test? Always keep in mind stroke because we don't want to miss the stroke. Yeah. And for the stroke, time frame is very important for the management, isn't it? Could it be malignancy or could it be complications of surgery? Most common causes of lower motor neuro facial palsies are Bell's palsy Ramsay Hunt syndrome, complications of any ear infection or complications of palliative surgery. Although I said most common this is from the common to rare com uh, uh I mean rarely, uh common, uh, rare causes of lower motor neurone palsy Lyme disease, Merkel and a Rosenthal syndrome. Sometimes it could be because of the neurosyphilis as well. Ok. So uh during the examination, do not forget to do a facial nerve examination, ent examination, training folk testing um as well as uh uh sometimes even the vestibular testing as well. Topo diagnostic tests are not much used. CT MRI and electrodiagnostic testing are more commonly used and they are very important for diagnosis, prognosis and even for the surgical planning, conservative management, the drugs used are steroid antiviral antibiotic, eye care always and physiotherapy surgical treatment as facial nerve palsy requires proper planning? Ok. So before we conclude, so here you can see, actually, I meant to do it as a slide there. And then you were not meant to be seeing, you know, the uh the lower part. Uh But yeah, this is how we were struggling at the beginning of the presentation. So anyway, the you can see if, if you don't see, you know, just ignore the lower part where the diagnosis is. If you see the um the three pictures, 123, can you see the differences? And can you tell me which one is the normal, which one is upper and which one is lower? Motor neuron palsy you can, isn't it? First one, all the function uh preserved. Second one, the upper part is preserved. So that's why it's an upper motor neurone. Here on the third one, everything is impaired. So it's a lower motor neuron again, the same thing, you know, I II was we were not meant to see all this here. So there is one case here. So he uh 68 year old male patient suddenly had um uh a sharp ear ache and severe pain at the back of the head. Immediately, the wife noticed left side of the face is drooping and also patient is drooling from that side. Uh They were very um uh feared, uh it could be stroke, they called 999 and was uh taken to A&E. So how will you approach this patient and manage this patient? So, always start with fast. That's uh to rule out the stroke. Yeah, face um speech and time history taking. Uh you will take a detailed history including the risk factor because the age of the patient is 68 year old, he possibly will be a high risk for the stroke. And we do not want to miss that clinical examination. Again. All the cranial nerve examination, upper and lower limb neurological examination is important. And we also have to examine ear and palliative gland. And the finding for this patient was the patient had all um had only right sided facial palsy, altered test and tuning fork. Uh uh testing showed the uh sensor hearing loss. So, diagnosis um this obviously with the steroid and the antiviral. Why is it not a Bell's palsy? You can type me in the chat box. Are you able to hear me still? Yes, Tia we can hear you. Ok. Ok. So why is it not a uh bill's palsy if anyone can write? So let me explain because as you can see here, the patient has a sensor, neural hearing loss. As a finding does the patient with the Bell's Palsy has a sensor, neural hearing loss? No, right. Although here we have, I haven't mentioned in the finding that the patient has any rashes or anything, it could still be a early presentation of Ramsay he syndrome. If you pay attention in the question here, it mentioned that the patient had a severe pain at the back of the head or uh and the ear ache. So that means before even you can see the rashes, there could be a pain followed by in the few hours, you might see the rashes. OK. And the next case again, um of the same patient. Now, during the fast assessment, you saw the weakness of the right arm. So that means there is something else going on, isn't it? And when you take a history, there were some other associated symptoms like dizziness, nausea, blurry, vision, weakness in the right arm. Obviously, this is not a lower motor neuron pu pulse, isn't it? And the medical history positive for diabetes Meli melitis, uh He had a uh he was taking insulin, Losartan Bisoprolol clopidogrel, aspirin. He had a history of angioplasty. And when you do a clinical examination, there was a lower facial palsy with intact forehead and eye. That means it's an upper motoneuron lesion, isn't it? There was nystagmus and also weakness in the upper and the lower arms. Ok. So what is the diagnosis here? Stroke it. And I don't think we are uh specialized to manage these patients. Obviously, um the stroke specialist can manage. I think the next step would be uh because timeframe is very important. I think the next step would be to uh uh do the imaging as early as possible because we don't want to start any antiplatelet or anything unless we had the CT or MRI sent it. So I think that's all about the presentation. Sorry about delay start. And I think I took a little bit of longer time. So if you have any questions, anything, I'm happy to uh assist them. Thank you. Thank you so much DEA um even though we started slightly uh late, it was a very engaging session. Um I'm glad that we were able to sort everything in the end. Um But yeah, um I really liked your session and yeah, I am. Uh I saw only one attending answering about that question. You remember I asked about which nerve uh innervate parotid gland, someone. Yeah. Closer pharyngeal. Yes. Yes. I think it was uh Gian. Yes, yes. Uh But I did not get answer about the general sensation of the tongue, which nerve is responsible. Is it glossing again? How about if that's the case? How about posterior um One third of the tongue test sensation. I think you're right, isn't it? Ok. Yeah. Anyway, um, anyway, uh, uh, we have, uh, anyway exceeded our time limit. Yeah, sorry about all that. It's just because, uh, we have started a little bit late. But anyway, I'm glad that you managed it. It was a very detailed session and, uh, I really like the session. Thank you so much, Devia. Um I released the feedback form guys if you can kindly fill them and you will get your certificates. All right then. Thank you so much for attending. Thank you, Aku. Bye bye Devia.