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OK. Um And welcome to the Neuro Neuroanatomy Collaborative course. We're very excited for this year's set of talks. Uh We have a variety of eager coming to teach you on all the different aspects of neuroanatomy um and also linking it to clinical practice. Um So you should have all received a email with the Precose feedback form. Please fill this out before the start of the session if you haven't done so already. Um We'll also have a feedback form um post session at the end. Um And we'll be sharing the QR code and link at the end. Uh We'll also be distributing certificates at the end of the course for those who have attended over 75% of the sessions. Uh And we'll be using the feedback forms as a marker for attendance. So please be sure to fill these out and stay consistent with the name that you fill out throughout the course. If you have any questions, feel free to uh put a question in the chat and myself and Dany will be replying to the questions. Um And yes, so this is welcome to our first talk uh by Gary Sama Sama, an F three F three doctor working in trauma surgery at Imperial College Health Care. She'll be introducing the cranial nerves 3456 and seven, focusing on the surgically relevant anatomy. Thank you so much for coming and I hope you enjoy the talk. Thanks so much for having me, Laura. Um So I've decided to make this talk um relevant for you guys, both in terms of the surgical anatomy, but also the clinical relevance. I found that when I was um in medical school, um often it's quite difficult to understand which aspects can have you actually relevant to general clinical practice, particularly in your um sort of medical school finals. So try to make it useful for you guys in both settings. A quick set of learning aims. So we're going to start off by uh defining the cranial nerves that we've outlined and describing the functions that they have. Um We'll talk a bit more about the pathways and the connections of the different cranial nerves. We're then going to apply our knowledge of these cranial nerves to identify symptoms of dysfunction and causes. It will be more clinically relevant. We'll talk about some common conditions and disorders that can affect these cranial nerves and talk a bit more about their symptoms and other causes. And we'll also go, go through some sva case studies uh that will sort of help you guys identify the cranial nerves involved in specific disorders and their particular symptoms. So we're going to start off with, uh just having a few questions. So you, you're going to see five Sbas. Um I'll give you about 30 seconds to just jot down your answers for the Sbas and then we'll go through them at the end of the talk. So this is your first scenario. Um You have a 70 year old gentleman which presents to d reporting eye pain on examination. He is unable to abduct his eye past the MEDLINE and his diplopia. When he's looking superior immediately, he doesn't have any papi involvement and there are no contralateral signs. What's the most likely diagnosis? Diagnosis? Is it a surgical cranial nerve, three palsy B medical cranial level three palsy c, cranial level four, palsy D cranial level five palsy or E cranial nerve six palsy. So I'll give you guys about 30 seconds or so to jot down your answer. Then we'll move on to the next question. OK. The next SB is a 60 year old woman who presents to Ed on examination. She has a left sided facial droop with flattening of the nasolabial folds. And uh when smiling, uh the left corner of her mouth droops, she is unable to puff her cheeks during the cranial nerve exam. And you find that eye is weaker on the right compared to the left and the forehead wrinkles. What's the most likely diagnosis? Is it a right? Middle cerebral artery stroke? B, Caros Gland tumor. C, internal capsule stroke, D Bell's palsy or E cerebellar pontine angle tumor. Ok. Third SB A. So now you have a 38 year old man who presents to his GP with a headache. It's behind his left eye and forehead, who tells you that he has had sinusitis for one week prior and believes that the headache might be because of this. He's quite worried because his eye is bulging more on the left side and has restricted movement. What's the most likely diagnosis? Is it a sinusitis? B, cluster headache, C, subarachnoid hemorrhage, d, extradural hemorrhage or e cavernous sinus thrombosis. OK. Fourth SB A which of the following cranial nerves has the longest intracranial course. Is it a the oculomotor nerve? B, the trochlea nerve c the trigeminal nerve D the abdu nerve or e the facial nerve? Ok. And the final S va 59 year old woman presents to GP complaining of a intense stabbing pain across her left cheek and forehead. She reports that the pain lasted a few seconds and self resolved. She notes that she's got frequent pain on the left side, uh which is worse on touching the skin. She's tried simple analgesia and it does not help. What is the diagnosis? Is it? A trigeminal neuralgia? B, cluster headache, C, parotitis, D, temporal arthritis or E Bell's palsy? Ok. Excellent. So we're gonna try and make the first bit of the talk a little interactive. So um A key thing that you guys need to know. Uh Just to understand cranial nerve anatomy is uh the frin of the skull, essentially the holes through which the cranial nerves trans uh pass through going from sort of the intracranial skull to their uh exterior courses. So just either unmute yourself and shout out or you can write in the chat below. What is the foramen and the cranial nerve that accompanies it uh for number one, which is this purple section over here. So you can write it in the chat below. Um Or you can uh unmute yourself and shout out. So what's the answer to number one? Mhm Yup. So uh someone's correctly mentioned that it's the superior orbital fissure. That's correct. Uh And, and what is the cranial nerve that goes through the superior orbital fissure? Yep. So, uh correctly, that is the superior orbital fissure and this is one of the largest foramen of the skull base. And actually, you've got cranial nerve 34 V one and six going through it. So the correct answers were 34 V one, which is the first branch of, of the trigeminal nerve and uh cranial nerve six. OK. Uh Next up is the uh green uh foramen just underneath the superior orbital fissure. What is the, what's this foramen called? And which nerve or nerves go through this one? Yeah, just write in the chat below. What you think the answer is for number two. So it's a foramen that's below the superior orbital fissure rotund. Exactly. So it's the foramen rotund and the second branch of the trigeminal nerve goes through the foramen retin. Ok. Um Next one is the foramen. Below that, it's this yellow foramen over here which, which cranial nerves go through this yellow foramen. And what's it called? Yep, that's right. So it is indeed foramen ovale. And the third branch of the trigeminal nerve, the mandibular branch goes through the foramen ovale. Hold on. OK. Uh Next one underneath is number four. So number four is just uh lateral to the foramen ovale. And we know that the mandibular branch of the trigeminal nerve goes through the foramen ovale. So what is the answer to number four? What's the foramen and which cranial nerve passes through it? Yep. So it is the uh Foramen spinosa and you have the mandibular branch, the meningeal branch of the mandibular nerve going through the foramen spinosa. And then finally, the fifth foramen that we have underneath the foramen spinosa. What's the name of the foramen and which cranial nerve goes through it? Ok. Yeah, that's right. So that indeed is the internal acoustic meatus. And you have two cranial nerves going through the internal acoustic meatus, which is cranial nerve number seven and cranial nerve number eight. OK. So one easy way to remember some of the important foramen. So the superior orbital fissure, the foramen rotund and the foramen ovale through which you have branches to the trigeminal nerve passing through is a pneumonic called standing room only. So standing uh is for the superior orbital fissure and the first branch of the trigeminal nerve. Uh V one, the ophthalmic nerve room stands for the Foramen Und um which is the second uh branch of the trigeminal nerve. So, the maxillary nerve and only stands for the foramen ovale, which is V three, the mandibular branch of the uh trigeminal nerve. Ok. So we're going to briefly talk about the ocular motor nerve now. So the ocular motor nerve starts off in the cranial nerve, three, the ocular motor nucleus which is in the midbrain. And the ocular motor nucleus is subdivided into different sub nuclei. So every single muscle that the ocular motor nerve innervates, it also has the Edinger Reile nucleus which is close to the cranial nerve three nucleus and its nerve fibers run alongside underneath the uh cran nerve three sheath. And what's important to note is that the oculomotor nerve has parasympathetic fibers which are superficial within the nerve, which can be quite easily compressed because of pathology. So, with the oculomotor nucleus, um you have general sensory efferent fibers which uh travel from the craine of three nucleus through the inter pedunculated fossa through the posterior cranial fossa, exiting the skull base at the superior orbital fissure to then go to innervate the uh eye muscles. So the superior eye muscles and the inferior eye muscles you also have sympathetic fibers that come from the internal carotid artery which go to innervate the superior tarsals. And you also have uh the general visceral efferent fibers from the Edinger weal nucleus which innervate the ciliary ganglion, which then leads to further innovation of the ciliary body. The sphincter papillae and the uveal tract glands. A key thing to note is that uh the general uh visceral efferent fibers from the Edinger west bo nucleus uh travel to the sc ciliary ganglion following which they hitchhike onto the ophthalmic nerve fibers to innervate the ciliary body, the sphincter papillae and the UV I and the sympathetic fibers from the internal carotid artery, hitchhike from the internal carotid artery to innervate the superior tarsal muscles, the ciliary ganglion. But they don't sign up because they hitchhike onto uh the ophthalmic nerve fibers. Ok. Uh This is just a diagram to show you the close proximity of cranial nerve three to the posterior communicating artery. So it's important to note that as the oculomotor nerve leaves the midbrain and passes through the subarachnoid space. It's extremely close to the posterior communicating artery. Therefore, any pathology, the posterior communicating artery can directly lead to cranial nerve three pulses. Ok. So, in terms of the innervation of the oculomotor nerve, it only supplies four extraocular muscles. So it supplies the superior recti, it supplies the inferior reces, it supplies the inferior oblique and it supplies the medial rectus. It also supplies the levada palpebra superiors, which is the muscle of the eyelids. And in this case, it also carries preganglionic parasympathetic innervation that leads to papillary constriction. So, can you appreciate that as it supplies the superior recs and the inferior recs, this leads to elevation and depression of the eye from the midline. So essentially, it can move the eye up by contracting the superior rectus and it can move the eye down by contracting the uh inferior rectus. The inferior oblique allows for elevation of the eye when it's in the lateral position. And the medial rectus allows for abduction of the eye. So, moving the eye laterally from the midline. So therefore, it makes sense that if you have a cranial nerve, three palsy, um you're most likely to get signs that are eye signs. So the first thing that you get is horizontal diplopia. So patients report that they ha experience double vision when they are uh w when they're sort of gazing straight ahead. But the diplopia that they have uh involves images that are side by side that are horizontal, they also get ptosis. And that's because of leva uh levator PPE superiors, they have light insensitivity and they have a down and out gaze uh because essentially the innervation for the uh superior rectus and the inferior rectus is a is inadequate. And lastly, uh they can also get um autonomic lesions of cranial nerve three, which can lead to loss of the papillary reflex and a a positive rapd. So a key clinical point to note with cranial ne three is the differentiation between a surgical cranial level three palsy and a medical sur uh cranial three palsy. So in the surgical cranial le three palsy, you have impaired pupillary reaction but sparing of the motor function. And this is because of compressive lesions, for instance, a PCO aneurysm due to its close proximity to cranial E three. So in this case, the aneurysm itself compresses the pupillary fibers of cranial lev three leading to papillary dilatation. Whereas in a medical cranial nerve three palsy, you get predominantly auto sorry, not autonomic uh motor dysfunction and sparing of the people. And this is usually because of ischemic lesions. So for instance, patients that might have ischemic macroangiopathy or um destruction of the uh vaso uh nervosa that uh might be as a as a result of diabetes or syphilis or multiple sclerosis. So that is a medical pro in the three palsy that leads to a pupil sparing palsy. Ok. Any questions about um the oculomotor nerve? Ok. Bye. Moving on. Then the trochlea nerve. So the trochlea nerve has uh the trochlear nucleus in the brainstem. And from there, you have general uh sensory effector fibers that travel through the uh middle cranial fossa, the cavernous sinus, out of the superior orbital fissure to innervate the superior oblique. So what's important to note is that um with the cranial nerve four, it's it's only is innervates one muscle. So, therefore, often lesions of crane and therefore, might not present themselves as obvious eye signs because of compensation, because of the other eye muscles. And this is just a diagram to highlight to you the trochlea nerve craine, the four leading to innervation of the superior oblique and the superior oblique um leads to essentially in torsion, depression and abduction of the eye. So essentially it leads to a uh twisting motion of the eye. Which is why if you have a uh cranial nerve for palsy, if you have compensation and preservation of the other cranial nerves that also innervate the eye muscles. So for instance, the superior lateral rec and the inferior obliques, then you might not actually get a true cranial nerve for palsy because of this uh compensatory mechanism. Ok. So, key causes of a cranial four palsy include acquired causes. So, again, uh similar to the cranial of three palsy microvascular damage as a result of diabetes, infections, uh inflammation. So things like syphilis and multiple sclerosis can lead to a acquired trochlear nerve, palsy, cavernous sinus thrombosis as a result of the close proximity of the ran in their four to. So within the cavernous sinus can lead to a acquired cranial left four palsy and direct trauma to ran in their four can also lead to ac their four P and there are some congenital factors uh where uh patients might have a congenital cra and therefore full palsy. But this is obviously quite a small proportion and it's quite rare. So the most factors that you usually see are the acquired factors ie microvascular damage, cavernous sinus, thrombosis or trauma. And on clinical examination, you find that these patients have a vertical or a oblique diplopia, which essentially means that they have double vision where they're seeing uh images, one on top of each other or at a slight angle but superiorly. And this diplopia is worse on the down gaze because of the innervation of the superior oblique bi crane. And therefore, and they also have extortion of the eye where it looks like the eye is twisted outwards because they're unable to depress and abduct the eye because of inadequate innervation of the superior oblique. Ok. So, moving on to the sixth cranial nerve. So the sixth cranial nerve is the abdu nerve. It has its nucleus at the abdu nucleus. In the brainstem. You also have general sensory efferent fibers that lead to innervation of the lateral rectus. So the point to note about the craine ner six is that it's got the longest intracranial course. It starts off in the nucleus. It travels through the posterior cranial fossa, the medial cranial fossa, it passes in close proximity to the internal carotid artery within the cavernous side and it leaves the cranium through the superior orbital fissure to innervate the lateral rectus. So it's a very long intracranial course. Therefore, what this means is that most uh intracranial pathology, it this is the first nerve that will likely be affected because there is just a lot of it within the cranium compared to uh the other cranial nerves. Therefore, intracranial pathology like tumors or edema or raised IC P lead to palsies of cranial nerve six because it has the longest intracranial course and with innervation of the lateral rectus, as the name suggests, the lateral rectus is involved in the lateral movement of the eye. So, creatine of six palsies mean that patients are unable to abduct the affected eye with regards to the cranial left six palsy. Um Again, you've got your acquired and your congenital causes of cranial left six palsy. So, commonest causes include trauma, particularly at the superior orbital fissure pseudotumor, cerebri cavernous sinus thrombosis, as we said, because of its close proximity, uh in the cavernous sinus space occupying lesions like tumors, abscesses, infections, diabetic neuropathy and GC congenital causes uh include Douin syndrome, uh which is where patients have strabismus with impaired abduction and ptosis on abduction. And clinically, you find that in a cranial nerve, six palsy patients report a horizontal diplopia. So again, they report double vision where they're seeing objects side by side, which is worse on looking at distance objects. Uh They have a inability to abduct their affected eye because of the innovation of lateral Vexus and they have a immediately deviated, affected eye on primary gaze. Ok, um quickly run through some questions that people have asked uh regarding the three cranial nerves we've done so far. So the first question is, uh you mentioned a surgical cranial F three palsy causes relative sparing of motor function. What is this in relation to? So the reason why, because I'll just go back to cranial F three. OK. So when I, when I mean that they act that, that it has a relative sparing of the motor function. Um Essentially, it means that they are able like that most of the muscle groups um innervated by cranial E three in a surgical palsy are functioning. So they're able to perform the eye movements as you would expect through a cranial nerve three pulse that as you would expect through innervation of cranial E three. However, the, the key thing is that they have impaired pupillary reaction because of the fact that the parasympathetic fibers are on the outside of the cranial nerve. Therefore, compression of those uh fibers leads to a pupillary dilatation because they're unable to constrict, but the motor function is completely intact. OK. Um Someone has mentioned uh Belsky sign in the uh fourth cranial nerve. Yup, that is a patho pneumonic sign for the fourth cranial nerve, which cranial nerves are tested in the H test. So, in the H test, um essentially you test cranial nerves 34 and six. So when you're performing the H test, you are assessing all three cranial nerves and it's to ascertain to see um if, if sort of there are any pauses within those nerves and you can essentially find out which nerve is affected uh because you're doing opposing movements of the H test. Ok. Um Someone just mentioned how can you differentiate between the diplopia causing by third cranial nerve versus sixth cranial nerve? So you can't purely differentiate it based on diplopia. It would have to be based on the muscle groups that are innervated. And uh whether sort of the, the palsy that you're getting is a result of muscle dysfunction that would signify an ocular motor palsy or 1/6 nerve, palsy. What's primary gaze. So, primary gaze is just when a patient is looking um as you would normally, uh they are not um that they're not sort of doing anything else with their gaze. They're not, they're not, you're not testing an accommodation reflex or anything. It's, it's just their gaze as it is. How can we easily remember the cranial nerve pathways, how they come from the brain to the innovating site? So, um it's coming on to this actually. So with the three cran nerves that we've mentioned, creatine nerve, three, creatine nerve four and cranial nerve six. An easy way to remember. It is the uh pneumonic LR six. So four. So LR six S 04. So what this tells you is that the lateral ruptures is innervated by cranial nerve six, the superior oblique is innervated by cranial nerve four. And the rest of the eye muscles are all innervated by cranial nerve three. OK. So, LR six S A four, the rest of the eye muscles are all three. OK. Perfect. So, moving on then to the trigeminal nerve. So the trigeminal nerve uh has its origin uh within the mesencephalic nucleus and spinal nucleases which then converge into the trigeminal ganglion uh and the primary, the principal sensory nucleus as well. And then following the trigeminal ganglion, you then have decussation to the uh sort of V one branch, the V two branch and the V three branch. And so the sensory root of the trigeminal nerve leads to uh sort of the ophthalmic root, which is V one, the maxillary root, which is V two and the mandibular root, which is V three and all of these fibers are general sensory afferent fibers. Ok. So, with the trigeminal nerve, you have three main branches, ophthalmic, which is V one maxillary, which is V two and the mandibular branch, which is V three key branches that you need to know of. The ophthalmic branch include the frontal, the lacrimal and the nasociliary. For the maxillary branch, you need to know the infraorbital, the zygomatic and the palantine. And for the mandibular branch, you need to know the buccinator lingual, the inferior alveolar branch, which which leads to a nerve that innervates the mylohyoid. Ok. So essentially the trigeminal nerve provides sensory innervation and motor innervation. It provides sensory innervation to the skin, the mucous membranes and all of the facial sinuses. And it provides motor innervation to the muscles of mastication, the muscles that you use to chew. We'll talk a bit more about the sensory branch. So, with the ophthalmic nerve, um it essentially innervates the anterior temple, the middle of the face and the upper mouth of the teeth, gums and lips. And this is where the frontal, the, the lacrimal and the nall branch comes in. So the frontal branch innervates the forehead and the upper eyelids. The lacrimal branch innervates the conjunctiva, the sclera, the corneal epithelium and the inner eyelids. So, when you're testing for a patient's corneal reflex, you're testing the lacrimal branch of the ophthalmic nerve and the nasociliary branch innervates the nasal mucosa and the frontal sinuses. Ok, moving on to the maxillary nerve. So, there are three branches of the maxillary nerve, the infraorbital, the zygomatic and the palantine and the maxillary nerve innervates the anterior temple, the middle of the face and the upper mouth essentially. So this middle part as you can see here. And then lastly, you've got the mandibular branch of the trigeminal nerve. So, sensory innervation of the mandibular branch via the buccinator nerve is to the middle part of the temple, the cheeks and the floor of the mouth. The lingual nerve innervates the anterior two thirds of the tongue and the inferior areola nerve uh innervates the lower teeth, the gums and the lips. Just a quick point to note is that essentially the trigeminal nerve innervates everything forward of this line of the face. So it innervates the anterior face, the back of the head is innervated by the cervical nerves and the bottom. So below the jaw is innervated by the superficial cervical plexus. Ok. So, in terms of the motor function of, of the trigeminal nerve, the mandibular branch of the third branch of the trigeminal nerve innervates all four muscles of mastication. So it innervates the massacre, it innervates temporalis and innervates the medial and the lateral terras. OK. So we'll talk through them one at a time. So essentially, we've spoken about how the trigeminal nerve comes from the trigeminal nucleus through the foramen of valley. And then it has essentially three divisions. It's got the anterior division, the posterior division and the nerve to the medial pterygoid. The anterior division uh has two deep temporal branches, two lateral pterygoid branches, the masic branch of the buccal uh branch which leads to innervation of the temporalis, the mater and the lateral pterygoid. OK. The medial pterygoid is a separate component and it is innervated by the nerve to the medial pterygoid, which branches off separately to the anterior division. OK? And it also innervates four other muscles. So four muscles of mastication and four other muscles. The other four muscles include the tensor vili palan, the mylohyoid, the anterior belly of the digastric and the tensor tympany. OK. So, the mylohyoid down here is innervated by the mylohyoid nerve, which is a, which is sort of of the posterior division of the uh mandibular nerve. The tensor vili palan uh again is uh similar to the medial tero. It comes off the nerve to the medial tero, the anterior belly of the digastric is again, the mylohyoid nerve down here and the tens tympany is the uh it is is sort of the uh nerve, the medial tero which goes past the o a ganglion and innervates the Tensai of that. Ok. And so what makes it challenging with regards to creating the five palsies is that essentially the palsy depends on which aspect of the nerve is affected. So common etiology of a cranial left five palsy like all the other nerves that we discussed includes tumors. So compression of the cran of the cranial nerve as a result of a tumor, vascular compression or trauma, inflammation of the nerve and inflammatory demyelinating conditions like multiple sclerosis and cavernous sinus thrombosis because it also is a nerve that passes through the cavus sinus. So we'll talk through some common lesions. So, lesions of the ophthalmic nerve lead to an absent corneal reflex and loss of sensation of the ipsilateral forehead. Lesions of the maxillary nerve lead to loss of sensation of the IP S lateral midface. So if, if you remember that the maxillary nerve is innervating the middle of the face and lesions of the mandibular nerve leads to paresthesia of the IP slater lower face and the anterior two third of the tongue. You also get paresis of the ipsilateral muscles of mastication. And you get the jaw deviated towards the lesion because those muscles are essentially unable to contract. Therefore, uh the muscles on the other side are far stronger and you have an absent jaw jerk as well. And then finally, lesions of the tensor tympany branch leads to impaired hearing and lesion of the trigeminal nuclei. A nerve nuclei itself can lead to sort of gross weakness of uh mastication with a ipsilateral loss of sensation. Ok. So, moving on to the facial nerve. So the facial nerve again has its uh cranial nerve nuclei in the brain stem. It um crosses across the CP and runs through the parotid gland. What's key to note is that any surgery that involves the protid gland can therefore lead to lesions of the facial nerve. It's got motor sensory and parasympathetic outputs motor. It predominantly innervates muscles of facial expression and the stapedius muscle uh inside the inner ear, sensory, it has a taste sensation to the anterior two thirds of the tongue and parasympathetic, it innervates essentially the glands of the face. So that includes the salivary glands, the mucosal glands and the lacrimal gland. This is just to highlight the course of the facial nerve. So, can you appreciate how the facial nerve traverses of down the neck and the midline. Um and it is very close to the carotid gland. Therefore, pro pac parotid gland tumors or um surgeries involving the parotid gland can lead to facial nerve palsies at this level. Ok. So the facial nerve is relatively complicated. So I'm going to highlight some of its main uh sort of nerve branches and the main nerve functions of these branches. So, like we said, the facial nerve has multiple nuclei within the brainstem, the branches, then all travel through the geniculate uh ganglion and then you have 34 different nerves rather. So firstly, you've got the greater petrosal nerve. So the greater petrosal nerve uh is this branch up here, it travels through the p uh petrous bone uh to innervate the uh pterygopalatine ganglion, which leads to innervation of the uh palate, the nasopharynx and the lacrimal gland. You have the corda tympany branch here which travels through the uh terra tympanic fissure down here in the middle cranial fossa and the corda tympani uh synapses on the submandibular ganglion. And it leads to innervation of the anterior two thirds of the tongue and the salivary glands. And lastly, you've got the posterior auricular nerve uh which is down here. So, the posterior auricular nerve is responsible for innervation of the muscles of facial expression. And you have the nerve to the Stapedius here which innervates the middle ear and the stapedius. Ok. So, uh we've talked a bit about the main nerves that come off the facial nerve. You also need to remember and know the branches of the facial nerve. So that includes the facial branches of which there are five. So you have the temporal branches that leads to innervation of frontalis orbicularis oculi and the corrugator suli, which is the muscle group at the top. Over here, you have the Zygomatic branches which leads to innervation of the orbicularis oculi, which are the eye muscles, the buccal branches, which also leads to innervation of the orbicularis Oculus, uh the buccinator and the Zygomaticus. So, uh around the face, the marginal mandibular branches, which leads to innervation of mentalis, the depressor lais inferior ais and the depressor angulus aureus. And the cervical branch is the very bottom that leads to innervation of the plasma, which is the large uh muscle at the front of the neck in terms of uh facial nerve palsies. Um again, you have idiopathic causes of facial nerve palsies, of which the commonest is a peripheral uh facial nerve palsy, also known as Bell palsy. You have secondary uh causes of facial nerve palsy. So things like trauma, herpes zoster, of which the eponymous syndrome is Ramsay hunt syndrome, tumors and diabetes mellitus. And clinically what you find is that these patients will present with hyper cutis, uh impairment of uh taste in the anterior tongue and the dry mouth because the facial nerve supplies the uh lacrimal gland and salivary glands So, clinically, it's important to be able to differentiate between a central uh poor cause of a facial nerve palsy and a peripheral cause of a uh facial nerve palsy. So with the central lesion, you find that the uh area affected is contralateral to the lesion. So if the lesion is on the left side, in the left hemisphere, you find that the area affected is the right hemisphere. So in a central facial nerve palsy, patients are able to frown and lift their eyebrows, they are able to close their eyelids completely. However, they have a mouth droop with peripheral facial nerve palsy. So essentially bell palsy, you find that the muscles affected are ipsilateral. So on the same side as the lesion and you find that patients are unable to frown and lift their eyebrows, they are unable to close their eyelids completely and they have a mouth through present. And essentially this is because the muscles that are responsible for eyelid and forehead movements are innervated from nerve fibers from both sides. So you have innervation from this side and you have innervation from this side. So, therefore, in a central facial palsy, you get a unilateral upper motor neuron lesion between the cortex on and the pons. But the muscles of the eyelids and the forehead, which are still supplied with input from the other side. Therefore, you have preserved function in a peripheral facial nerve palsy. So in this case, over here, you get a unilateral lower motor neuron lesion between the nuclei and the muscles, which leads to paralysis of the ipsilateral eyelid and the forehead muscles because no other input reaches them. And lastly for the lower facial muscles, they're innervated from fibers from the opposite hemisphere. So they are paralyzed in both central and peripheral facial nerve pulses finally uh moving on to cavernous sinus SNRI. So what's important to note is that the cavernous sinus has the ocular motor nerve traveling through the trochlea nerve, the ophthalmic nerve, the abdu nerve and the maxillary nerve. And it has close proximity to the internal carotid artery. It has close proximity to the sphenoid sinus de pituitary gland and the optic chiasm. Therefore, in cavernous sinus syndrome, what we typically get is a unilateral ophthalmoplegia. As a result of dysfunction of cranial of 34 or six, you get autonomic dysfunction as a result of Horner Syndrome and you might get sensory uh loss in the um trigeminal one and trigeminal two distribution. And this can be as a result of any pathology that affects the cavernous sinus itself. So things like cavernous sinus thrombosis where you have clots forming within the uh venous sinuses can lead to compression of these nerves leading to the palsies. Tumors such as meningioma can lead to compression of the nerves, inflammatory disease like to lasso hunts syndrome and vascular causes like intracranial aneurysms of the IC A on either side can lead to cavernous sinus syndrome. OK. Um So that was a bit of a whistle stop tour covering the clinically relevant uh anatomy of the cranial nerves that we mentioned. We're now going to just quickly go through the ques the answers to the questions that you answered at the beginning. Um Hopefully, they make sense, but if not feel free to shout out or type below what the um what was the answers are? So, in the first instance, um, this patient has a medical Creon three palsy. The reason why he has a medical cran three palsy is because you are told specifically that there is no pupillary involvement. And so you can deduce that he has ac that three palsy based on the fact that he is not able to adopt his eye and he has diplopia. But because of the lack of pupillary involvement, it is a medical cran of that three palsy for the second S va um type down below which cranial nerve is affected in this instance. So it's a right MC A stroke that has led to this presentation, but which nerve is actually affected. Yeah, creatine of seven. So this is the, this is a central cran of, of seven palsy as a result of this right MC A stroke. Ok. Uh The third SB A uh So the answer to this was a cavernous sinus thrombosis and the significance with this is that, um, so clinically, you're told that the patient has had sinusitis for one week and he has bulging in his eye movement with restricted movement. Therefore, it's difficult to pinpoint whether it's just one cranial nerve or multiple cranial nerves. Therefore, if we're thinking that any of cranial nerves, 34 and six have been affected with a background of sinusitis, then in this instance, the most likely cause is probably a cama sinus, thrombosis sinusitis alone would not lead to impairment of the cranial nerve function. OK. So it's the fact that he has had a thrombosis within the verna sinus that has led to this particular presentation and uh which cranial nerve has the longest intracranial course. That is the absence nerve, cranial nerve six. And this lady, a 59 year old woman with stabbing pain across her left cheek and forehead, which is in the uh trigeminal distribution with pain lasting a few seconds that then self resolves. Uh she has pain that's worse on touching her skin. That is trigeminal neuralgia because as we discussed, the anterior of the face is purely innervated by the trigeminal nerve. OK. Um That's everything from me. Um Do you guys have any questions? Anything that you'd want uh clarification on? So the question is uh just wanted to double check. I thought the trochlea nerve as long as intracranial course. So I'm I'm pretty sure it is the abdu nerve. That's what sort of, most of the literature says. But please feel free to look that up if that is uh incorrect. It is a question that pops up a fair bit. So the next question is you mentioned S VA two, the patient has a central palsy. The Viet men mentioned that the patient has weakness and eye closing. Does that not indicate a peripheral lesion? So, not necessarily. No. So in a, in a central lesion, um you how one? So I I think that's probably a slightly poorly worded question. Um So it pro it, it is, it could be a peripheral lesion uh because of the eye closing, uh that should po possibly be, be taken out because like you said, in a peripheral lesion, um you would not have any difficulty, eye closing would GC A present similarly to trigeminal neuralgia. So GC A is giant cell arteritis, which is essentially inflammation of uh the arteries of the cranium, most typically the temporal artery. So a classic presentation of GC A is a patient that has a background of some form of rheumatological disorder um with uh eye signs that are that include a red watery eye, sudden onset with jaw claudication. So uh difficulty, uh they might sort of report difficulty chewing food, ie jaw claudication. And so the differentiator between this is that it's, it's, it's pain that had that sort of comes and goes and self resolves GC A is not likely to self resolve and um there's no mention of any eye signs. So with GC A typically in clinical vignettes. They specifically mention the fact that there's eye watering or uh visual disturbances or tenderness along the temporal artery or tenderness upon um uh sort of sort of uh touching the scalp. OK. Thanks very much. Thank you so much. That was such a helpful lecture. Um We just have there's one more question in the chat. Um I think so. Sorry. In my previous question, I meant the course of the nerve starting from the nuclei, they arise from all the way to the to innervation sites and the branches too. Uh Which question are they referring to you for that? That's the la um I think a bit higher. So I think they were asking about the pathway meant the whole course of the nerve from the nuclei they arise from to the site of innervation. Do you know which nerve they're referring to? Now? Um Sorry, could you clarify which nerve? Oh He's asking um how to remember them, how to remember those? So frustration. Uh Like I said, it depends on in, in general. So obviously, like you guys have sort of got to glance off. There is a, there, there's a lot of content even if, if this is just sort of four cranial nerves, I think the best way to remember the innovations and the muscle groups is to essentially think about the clinical picture that you get if you have a lesion of that nerve. So for instance, uh remembering, so I I'll just take the trigeminal nerve for instance. So for instance, remembering the effects of the trigeminal nerve, I found it easiest to remember what goes wrong if each branch is affected. So for instance, the fact that the trigeminal nerve is responsible for the corneal reflex implies that uh you know, if you have an absent corneal reflex, that's an ophthalmic lesion that there isn't really a easy way of remembering all of them. Um I think it's, it's one of those instances where you just have to sit down and match up the nerves to the functions and possibly find a way that works for you. Some people uh find it useful to have the diagrams like this. So actually, this is probably one of the simplest diagrams I could find for the, for creating an F seven in this case. Um So just having a having sort of a visual guide to allow you to draw out the roots of the nerves and to draw out which muscles they innervate and then the clinical functions as such. Some people find useful. But like I said, I find it most useful to essentially work backwards from the clinical picture to then remember what sort of the function of those nerves were and then you can work out the muscles based on that. Yes, thank you. Um So I think if no one has any other questions, um That's everything before you all leave, we have a post. Um talk feedback form. Um I'll just quickly share my screen. We also have a QR code if the so I'll just be taking over. Yeah, so this is the QR code uh for any of those who can't access the link. Uh Please fill this out. Um And thank you so much for joining. We hope to see you next week and thank you so much for the talk. It was really helpful. Amazing. Thanks very much. Have a good day guys. You too. Bye.