127: Cranial Nerve Palsies – Part 1

Hello and welcome to the Physician Assistant Exam Review Podcast. My name is Brian Wallace. I’m the host and creator here at Physician Assistant Exam Review, and today we’re going to be covering the cranial nerves.

Okay, so my plan for this section on the blueprint, it just says cranial nerve palsies, right? It doesn’t give a whole lot of detail. And I was talking with some students who are asking me about how deep to go into things that are like that, that don’t give you those more detailed bits of information as to what to cover. So for example, we’ll come to neoplasms, right? That’s a big topic, neoplasms under neurology. How do you cover that? What do you do?

And unfortunately, some of these things I just don’t have answers for, but I do have practices and principles and what I think I would do if I were in your situation and how I would handle them in my approach. And that’s how I bring this information to you. It’s just the best possible way that I would approach it with the information that I have. There’s no clear-cut answers, and I know everyone loves clear-cut answers, but we don’t always have them, right? We have what to do with what we have, right? We have, sometimes we’re stuck with two bad choices and we have to make the best of it. Just like, do I go to bed and get some sleep or do I stay up and study later, right?

Those are two not good choices if you’re not done studying for your test tomorrow. And you have to choose between those. I will always choose get some sleep because I think a well-functioning brain is worth more than the information I’m not going to retain after midnight as I’m studying. That’s just my opinion, how I would do it. It doesn’t mean it would work that way for you. You may be different. Maybe you work better at night than I do.

But my point is you sometimes you’re stuck with the situation that you’re in. And I find that a little bit with sections like cranial nerve palsies, right? So how deep do you go? What do you cover? What do you do? We’re going to dive into that today and hopefully get pretty close to an answer for you. And my goal, as always, is to get you to pass your PANCE, stay in school, pass your interpretation exams.

And with that in mind, the thing I’m always trying to balance is how little can I study? How little can I learn and still do well? That might not be the best way to phrase that, but I don’t want to overstudy. I don’t want to go too deep and waste time and not get any benefit from it. So it’s kind of, I’m always looking at it like, if I study this, do I think it’ll be on the test? If I study this, can it be a test question? Is there a way to approach this information that will better help me on the next exam?

Or am I just spinning my tires? Am I just feeling like I’m doing something good and working and working and working? But the reality is I’m not making any progress as far as my scores go. That’s always what I’m trying to keep in mind as I move through really any kind material, but material like this in particular. So where we’re going to go here is we’re going to start out with just an overview of the cranial nerves, just to walk through them one more time. You probably have already, hopefully you got some precursor to this. If not, go over to the website and you want to read through them because just listening to it probably won’t be good enough to impact your brain very much.

You’ll have to, you know, a lot of students will reach out to me and say, hey, I really like the notes on the website. I’ll read through them as you’re speaking. And I think that’s probably a really valuable way to go. So we’re going to start with an overview of the cranial nerves. Then in today’s show, we’re just going to cover cranial nerves one to five. I want to keep it shorter. I don’t want to overextend in this particular section because this particular section is a lot of memorization.

So if I’m attacking this, I’m attacking it with flashcards. I’m attacking by writing them out myself, not using pre-made ones, but writing them out myself and going through them and making sure that I’ve got the information that I think I need locked in. So before we get started, you can obviously hear my voice is a little different today. I have my tea in front of me and I’m definitely going to be coughing throughout this episode. I was just out and at Ashland, Ohio’s program and had a fantastic time working with the students there and the faculty there. I love traveling to schools and putting on workshop for students. It is a ton of fun.

But along with that, I had not only has my son and a couple of kids around here have been sick, but on the plane flight out, the person next to me coughed the entire, the entire flight. So maybe it was his fault. Maybe it was my kid’s fault. Hard to say, but I’ve definitely come down with something. Maybe it was just being run down as I was traveling and doing a lot for the past two weeks. But either way, I’m going to try to struggle through this and we’ll see how we do.

All right, let’s jump right in with the priming questions. Sorry, that was a little loud. We’re only going to cover cranial nerves one to four this week, so we’re just going to stick with priming questions for cranial nerves one to four. What does it mean when a patient tilts their head to the opposite side of a lesion? What does it mean when the patient tilts their head to the opposite side of a lesion? I don’t know if I phrased that perfectly, but you’ll get it when we get there. Why is a pupil involving cranial nerve three palsy a neurosurgical emergency?

Why is a pupil involving cranial nerve three palsy a neurosurgical emergency? How can you differentiate trigeminal neuralgia from other causes of facial pain? How can you differentiate trigeminal neuralgia from other causes of facial pain? Which cranial nerve palsy causes an eye drift down and out and why? Which cranial nerve palsy causes an eye drift down and out and why?

All right, we’re going to just run through the cranial nerves and do a very, very superficial pass by them. This is definitely something that you need to know. Unfortunately, this is something you need to memorize. I’ll often talk about recreating information during the exam based on information that you already know. Cranial nerves don’t really fall into that situation, at least not for me. It’s something I’ve just got to straight up memorize. So if you use mnemonics, if you use practice with flashcards, all kinds of different ways to do this.

But this is a, for me, this is a memory test, just the cranial nerves one to 12. There you go.

So let’s start with number one. Olfactory is for smell. Number two is optic is for vision. Number three is oculomotor. So we do eye movement, pupil constriction, and eyelid control. It moves the eye in most directions. So one is smell, two is vision, three is for most eye movements and pupil constriction.

So it moves up, down, inward toward the nose, and up and out diagonally, controls pupil constriction, and lifts the eyelid. So a lot of different motor functions going on with cranial nerve three. The palsies obviously get a whole lot easier if you remember what each of these nerves do, right? Four is the trochlear nerve. So this is eye movement downward and in. This is what you use when you’re doing something like reading a book, right? Down and in.

Trigeminal is five, so facial sensation and chewing. This feels touch, pain, and temperature from the face and moves the muscles for mastication. Abducens is number six. This is eye movement side to side. So away from the nose, eye movement side to side. Seven is the facial nerve. This is for movement, taste, tear, and saliva production.

Smiling, frowning, closing the eyes. Two-thirds of the tongue are innervated by this, where our sensation comes from there, controls the tear glands, and controls the salivary glands. Number eight is the vestibulocochlear nerve. This is for hearing and balance. Detects sound from the inner ear and helps you stay upright when you need when your head’s in space. So, it keeps you in a balanced position, the vestibulocochlear nerve or cranial nerve number eight. Number nine, the glossopharyngeal nerve.

This is for taste, swallowing, saliva, and blood pressure reflex. So, this is the back one third of the tongue. Swallowing. Controls the parotid gland for salivary saliva production. And also, senses blood pressure changes in the carotid arteries. The vagus nerve is number 10. This is autonomic control, swallowing, voice, and gag reflex.

So, it controls autonomic body functions like heart rate, breathing, and digestion. Helps with swallowing. Controls the vocal cord movement. So, it will affect the voice and also is part of the gag reflex. Accessory nerve, which is nerve number 11. This is for shoulder shrugs and head turns. Innervating the sternocleidomastoid and the trapezius.

And the hypoglossal nerve is number 12. So this is for tongue movement, for speaking, eating, and swallowing. This was a section I always struggled with in PA school. And I’m going to say that at every time there’s a straight memorization thing. So when it comes to something like cranial nerves or childhood vaccinations, this is an area that I struggled in because memorization was never really my thing. It still isn’t. I’ve developed and worked with some skills and some techniques to improve on that, but it just is what it is.

It takes the time and energy and focus to drill this stuff in. And you have to do practice and you have to do drills and you have to get it into your head, but knowing which of these nerves do which things, obviously super helpful as you move forward. Right. So that’ll be helpful.

All right. So that list you can find over on the website, physicianassistantexamreview.com/127 for this episode. I’ll have all those up here. And I’ll also have this next section, which I think is really important. And I’m really happy to include it here. And it’s the reason we’re only covering five of the 12 nerves today is because I wanted to have that list. And then I want to have this section, which is just an overview of what cranial nerve palsies are, what you should be thinking as you approach them, what they look like, what your tests are going to be, and what your treatments are going to be.

You can simplify all of this stuff right out of the gate and make life easier, right? I was actually talking with a friend yesterday, two days ago and their son had developed some wrist pain and maybe they’d fallen, maybe they hadn’t. This is a 13-year-old boy who’s very active and she was struggling with what to do and should she take him to urgent care? I think it was three or four o’clock on a Saturday. Should she take him to the ER? Should she wait because orthopedic offices were closed? And I kind of talked her through it a little bit and my recommendation in this case was to wait until Monday for a whole host of reasons.

One of, and really just to maybe immobilize him, maybe get some ice on it, maybe get some Advil into him. But the reality is waiting until Monday, even if it were a fracture, isn’t really going to change a whole lot if he has a fractured wrist. Now I saw pictures of the wrist. It wasn’t fractured, very unlikely. And he was, his complaints didn’t seem like it from the discussion I had with her and from the images that I saw that she took pictures of. But the reality is there’s only a handful of treatments he’s going to get, right? It’s going to be bracing and rest, maybe a cast, which would be an advanced bracing, or he’s going to need surgery because it’s broken and needs to be fixed, right?

There’s a pretty limited amount of things we’re going to do. So if I look at it from that perspective, waiting until Monday probably isn’t going to change a whole lot because most of the course is probably going to be a splint or a brace or a sling of some kind, getting it elevated, and then possibly he’s going to need surgery, but had a very low inclination for that. So my point in telling this story is that if you look at the bigger picture, it doesn’t need to get so panicky. It doesn’t have to get so worrisome when you realize that nothing changes, nothing’s going to happen. So same thing here. What I want you to think about as we go through nerve palsies is what does it overall look like? How do we treat them?

What are we doing? What’s the point? And although this is a little bigger than the example I just gave, it should help when we get down to generalized treatments for what we’re going to do, because there’s only a handful of things that we can do in the end. So if you understand what’s going on and you can understand those treatments, you can understand how we diagnose them, then everything can get a little bit easier, a little more simplified so we can think it through. And like I said before, it doesn’t have to be all pure memorization. If we understand what’s going on and we can walk through it.

Okay. So, with that long, drawn out introduction, let’s get started talking about our cranial nerve palsies and what does this overview for it.

All right. So, cranial nerve palsies is a dysfunction or a paralysis of one or more cranial nerves, leading to motor, sensory, or autonomic deficits. You can have one cranial nerve involved, or you could have multiple cranial nerves involved, right? Doesn’t mean there’s only going to be one thing. I was actually just out talking with the students at Ashland this week. And one of the things that came up is that, you know, could you have some two diagnoses on a patient? And I’m hoping you’re never going to see that in the test question.

In the clinic, 100%, yes. But on a test question, no, it seems very, very unlikely. But you can certainly have isolated or multiple nerves involved here. Causes of cranial nerve palsies, there’s a whole bunch of different causes, right? And this is important because it affects how we treat them. So you can have vascular issues, you can have traumatic problems, you can have an inflammatory response. You can have compressive, like something pressing on that nerve.

You can have an infectious issue. There can be a metabolic problem or degenerative diseases. And we’ll get to all of those. But I want you to just understand that overview. So there’s only so many things that will cause this, right? So you can either have a vascular problem, trauma, inflammation, something pushing on the nerve, an infection, metabolic problem, or degenerative problem. As far as classifications go, these are classified by their function, right?

So you have motor sensory or mixed. I think it probably makes sense to memorize which nerves are motor sensory or mixed. Now this requires a fair amount of work and you’re probably, I don’t know if you’ll see a question on it or not, it’s sort of up in the air, but I think it’s something right in front of you that you can learn. So this is the kind of thing that I would be putting on flashcards, putting on post-it notes and practicing over time. Looking at this once is useless, right? Looking at it once for a day, useless. Looking at it for two days, kind of useless for me.

It needs multiple touches over multiple days. So motor nerve palsies, these affect eye movement, swallowing or facial expression. So this is cranial nerves 3, 4, 6, 7, 9, 10, 11, and 12. Again, go back through the list of what those do, and it makes a whole lot more sense, right? There are those that are purely eye movement, right? So those are going to be your motor neurons. So understand your motor nerves.

So understanding them makes this part so much easier. Your sensory nerve palsies obviously affect vision, hearing, or sensation. This is cranial nerve one and two, right? That was our optic and olfactory. Then we have cranial nerve five and cranial nerve eight. Our mixed sensory palsies affect both motion and motor, excuse me, and sensation, right? So this would be five, nine, and 10.

Again, this is something I think that you really need to just spend some time on. One would be understanding what they do, and two would be just pure memorization.

Okay, so what do those things look like? Well, if you have a motor deficit, you have weakness, paralysis, or atrophy of muscles. Makes sense. If you have a sensory deficit, you get numbness, pain, loss of smell, loss of vision, or loss of hearing. Autonomic dysfunction, you get abnormal pupillary responses, dry eyes, excessive salivation, or lacrimation. Common causes of cranial nerve palsies. So, let’s just touch on these.

We talked about them a second ago, but let’s go just a smidge deeper. Vascular. So here we can have a stroke, either ischemic or hemorrhagic. You can have giant cell arteritis. Those are going to be two major common causes of vascular issues. Trauma, skull fractures, cribriform plate damage. So that would be cranial nerve one can be affected there or direct nerve injury.

Tumors, excuse me, an acoustic neuroma would be affecting cranial nerve eight. Meningiomas and skull base tumors can all create that mass effect. Infectious. So what can cause some infectious problems here? So stop and think for a second. I don’t want to just rattle these off and you just sit and listen and think you’re getting something out of this. I want your brain engaged.

So what infectious things might cause cranial nerve palsies? Well, meningitis, Lyme disease, herpes is another good one.

Next, we could have degenerative, so demyelinating, like multiple sclerosis. Neuromuscular disorders can cause a problem here, like myasthenia gravis. And then we have things like Bell’s palsy and Ramsay Hunt syndrome. Not going to go into deep detail on those, but we’ll talk about them when they we get to those nerves. Diagnosis. So, our diagnosis, again, pretty straightforward across the board, right? You’re going to do a clinical history and exam.

So, you’re going to look for weakness weakness or sensory deficits, right? Does that make sense? We’re going to be looking for weakness or sensory deficits. We’re going to do some imaging, so MRIs or CAT scans, rule out stroke, tumors or demyelination. We can do an EMG or nerve conduction study. And then we can do blood tests. So an ESR, CRP, Lyme test.

Glucose is a good one because we may have to be concerned about diabetes for some of these. B12 and an autoimmune panels make sense as well. This is going to be how we diagnose any of these though, right? So just going through that path. And then let’s talk about general treatments. We’ll wrap up this particular section with generalized ideas for treatment. So first and foremost, we’re going to address the underlying cause, whether it’s vascular, infectious, inflammatory, or neoplasm, we’re going to deal with the thing causing the problem.

Makes sense. So we may use steroids if we think it’s inflammation, like a Bell’s palsy or an optic neuritis. We may use antibiotics if it’s infectious, right? We may have to go in and surgically decompress the mass on the nerve. And finally, we may just have supportive care, physical therapy, eye protection, and symptomatic treatment, depending on what we’re working with. But our arsenal isn’t all that large. There’s only a handful of things we’re going to do.

And this is like what I was saying about the orthopedic issue, narrow down to what are the options, what are the things we could possibly do, and then what of those makes sense for this particular patient in this particular setting. Got it?

All right, sweet. Now let’s move on to cranial nerve one. And as we do that, I’m going to pause and take a sip of my tea, because I’m already starting to lose my voice, and we’re only starting cranial nerve one. I also have a meeting tonight with the 33 Days February cohort. Hopefully I’ll be able to get through that with some of my voice intact. Speaking of which, if you guys are interested in the April cohort, that is registration for that’s going to open in early March. We opened that a month beforehand because there’s a bunch of stuff to do.

And seats are going to be limited for the April cohort for different reasons that I’m not going to go into right now. Seats will be limited for that. If you want to get early notification of registration before the rest of the community. Just go to physicianassistantexamreview.com/33, and you’ll see where you can hop on the early notice list, and I’ll let you know two days before the registration goes out to the public. Like I said, it’s going to be a limited supply of seats for that particular class.

All right, cranial nerve one, the olfactory nerve. We’re going to talk about the cranial nerve one olfactory nerve palsy is what we’re going to talk about. This is a dysfunction of the olfactory nerve responsible for smell perception, right? So obviously our clinical presentation is going to be anosmia, which is loss of smell, unilateral or bilateral, interestingly enough. Altered taste perception, right? Because the smell can affect taste. Distorted smells like burnt or rotten odors, which is parosmia, and cacosmia, which is perceiving foul odors that are not present.

Man, that sounds terrible. My son is that constantly has a clogged nose. I think it’s allergies and he refuses to take any medication or try anything to make it better. So he actually thinks he has a superpower because he can’t smell anything and being around his brother and himself, he would rather not be able to smell the bad smells than be able to smell the good smells. So he’s very happy in his present condition. Physical exam. So how are we going to test this?

We’re going to look for the patient to identify non-irritating scents like coffee or vanilla. So strong scents that aren’t irritating. And then we can do a nasal exam I’m looking for obstructions, polyps, excuse me, or other sinus diseases. Lab studies and imaging. We’re going to get an MRI of the brain if we think there might be a tumor or a neurodegenerative disease or trauma. Get a scan of the sinuses if we have chronic disease and nasal polyps are suspected. And then the other one to look for now, right, would be COVID-19 testing because of the loss of smell.

So these are kind of weird. And I was trying to think about when I put the notes together, how to handle it, because it’s like, what would the patient come through the door complaining about with a cranial nerve one palsy? Well, they’d be complaining about lack of smell, right? So how, but I also, I don’t want to go too far down the path of working each of these up because the workups are kind of generalized and it depends on the other things. So I’m going to go through them step by step and then maybe wrap up with a little bit of how the workup would go. But I need you to think through a little bit, how would this look like as a patient came into the office? Well, they’d come in with lack of smell?

And I decided to say, okay, well, let’s just test it.

Let’s see. Can you smell coffee? Can you smell vanilla? Maybe we should look up your nose and see if we can find any polyps or any other diseases. If I’m really concerned, maybe I order an MRI to see if there’s a tumor or some sort of neurodegenerative disease going on. If there was some trauma, I might want to get a CAT scan or that MRI. If I think you might have had COVID and that might be the cause, then I’m going to do a COVID test, right?

And see if that comes back positive. Because our common causes here are just going to be head trauma, neurodegenerative disease like Parkinson’s or Alzheimer’s, viral infections like COVID. And so we’re going to look for those things in a patient who comes in with those symptoms. Does that make sense? So treatments address underlying causes. So in this case, sinus disease or neurodegeneration. You can do olfactory training, exposure to different scents, and then supportive care for post-viral anosmia, which means the smell often comes back.

So it’s really just reassuring people that wait it out and hopefully it gets better. I know some people who that’s not necessarily the case for, but they’re still holding out hope. Key takeaways. So lack of smell can be an early sign of neurodegenerative disease like Parkinson’s or Alzheimer’s. So let that be sort of on your radar. Head trauma can permanently damage cranial nerve one because of the way that it sits. And then post-viral loss of smell can last weeks to months.

Cranial nerve two, optic nerve palsy. This is a dysfunction of the optic nerve, which transmits visual signals from the retina to the brain. Hopefully that one we all have down and it’s pretty straightforward clinical presentation here. So again, I look for what can I not memorize? What can I just sort of understand and kind of know? And things like symptoms of cranial nerve one, I should just kind of know. Symptoms for cranial nerve two, I should probably just kind of know.

So unilateral bilateral vision loss kind of makes sense, right? Decreased visual acuity, blurry or dim vision. Loss of color vision is one you might not come up with just by thinking about it, but you can get a red desaturation, is an early sign of optic neuritis. And then the other one is a relative afferent pupillary defect. This is where you get a light reflex where the pupil doesn’t constrict normally when you compare one eye to the other. That’s the relative part. You’re comparing one eye to the other.

I will talk about that in just a second. So, if you’re looking for what you think might be an optic nerve palsy because the person has some vision issues, you may do a visual acuity test, right? Using that Snellen chart and see how their vision is. Mostly not how it is, but if there’s any changes in it. You’re going to want to do a fundoscopic exam. Optic disc swelling might be an indicator of increased intracranial pressure. A pale optic disc may be chronic optic neuropathy.

A blurred disc margins may be inflammatory causes like MS. And then you can do what’s known as a swinging flashlight test. And if this is going to be normal, so what you do is you take a flashlight and you shine it into one eye and you look at the pupils and you shine it in the other eye and you look at the pupils. Well, what should happen is when you shine a light into your eyes, your pupils should constrict, right? They should shut down. But what’s kind of cool is if I shine the light into one of your eyes, both pupils should constrict, right? It’s not just the one that is affected.

Both of them will constrict. So, what happens if you have a problem with the cranial nerve optic palsy, cranial nerve palsy of the optic nerve, you can get a situation that we just talked about, which was relative afferent pupillary defect, which is if you put light into the eye that’s not really working as well, into that nerve that’s not really working as well, both pupils will dilate instead of constricting, because the light’s not really moving into the brain. It’s not sending the signals back and forth. So the light’s going to cause both pupils to dilate instead of constricting in relative afferent pupillary defect. Hope that makes sense. Lab studies and imaging MRI brain with contrast if concerned about optic neuritis like an MS, tumor or stroke, a lumbar puncture with oligoclonal bands. If you’re concerned about MS-related optic neuritis, ESR, CRP, temporal artery biopsy, if you’re concerned about giant cell arteritis.

You can do fluorescein angiography if vascular optic neuropathy is suspected. Common causes. So optic neuritis would be MS or autoimmune disease, young female with painful vision loss. Ischemic optic neuropathy would be something like giant cell arteritis, diabetes, or hypertension. This would be a sudden painless vision loss. Papilledema, which is increased intracranial pressure, maybe from a tumor, or he had bilateral disc swelling. Glaucoma, optic nerve damage from high intraocular pressure, toxic optic neuropathy, so something like methanol poisoning, ethambutol, or amiodarone might cause toxic optic neuropathy.

You’ve learned about those in other settings, hopefully. Trauma, so direct optic nerve injury would be another cause. So, treatments. Like I said before, treatments are going to be dealing with the underlying causes, right? So, we’re going to go back up to our common causes. If we have optic neuritis, we might give steroids, methylprednisolone. If we have giant cell arteritis, we’re going to do high dose steroids immediately to prevent blindness.

If we have papilledema, we’re going to treat that increase in intracranial pressure and try to decrease that CSF production using something like acetazolamide. We might do a VP shunt or weight loss in obese patients so that we more not in the non-acute setting, but in the chronic setting. Glaucoma, we want to lower the pressure in that eyeball. So latanoprost, timolol, or acetazolamide. And then something like a toxic optic neuropathy. Remember, we got that from ethambutol or amiodarone, that sort of thing. So we remove the offending agent and provide supportive care.

Key takeaways. If you have painful vision loss, we’re thinking about optic neuritis. So MS until proven otherwise. If we have painless sudden vision loss, we’re considering ischemic optic neuropathy. So something like giant cell arteritis, a stroke, or diabetes, bilateral optic disc swelling would be your increased intracranial pressure and must rule out brain mass until proven otherwise. Cranial nerve three, oculomotor nerve palsy. So this is called the oculomotor nerve, right?

So it’s responsible for moving the eyeball around. A problem here would be a dysfunction of that nerve leading to eye movement impairment, ptosis and pupillary dysfunction. That’s a big key there is the pupillary dysfunction. That’s the part I would latch onto because I’m going to remember that I’m going to move the eyes in most directions. So I’m going to add the pupil part of it because that’s a little bit different than what I would think of. Excuse me. So palsies of this nerve can be pupil involving or emergent, usually a compressive or pupil sparing.

This is less concerning and often ischemic. So, if it has a pupillary factor, we need to do something about it. And it’s probably a compressive issue. And if it’s pupil sparing, it’s less concerning, but it’s probably ischemia. Clinical presentation. The eye deviates laterally and downward due to unopposed cranial nerves four and six So, the other nerves that innervate the eye, will those motor functions will take over if the muscles that are innervated by cranial nerve 3 aren’t functioning. So the eyes will turn down and out because those other muscles will still be functioning.

Does that make sense? The muscles from cranial nerve 4 and cranial nerve 6 will still be innervating the eye, so it will move down and out because it’s unopposed by the muscles that are innervated by cranial nerve 3.

All right, ptosis is a weakness of the levator palpebrae superioris. You can get diplopia, which hopefully you know by now is double vision. Mydriasis, which is a blown pupil. If pupil involving suggestive compression, cause like an aneurysm or a mass. You can get loss of accommodation, which is blurry near vision. So this is how they may present. Physical exam.

Well, it makes sense you’re going to test their eye movement, right? That’s probably a place to start. They have limited upward, downward, and medial movement. You can see they have a ptosis. If they have pupil involvement, if they’re dilated and non-reactive, this is an emergency situation. You’re thinking they have an aneurysm or a herniation or a mass, something pressing on that nerve. That’s a serious, serious problem.

If the pupil is normal, it’s likely an ischemic problem. So you’re thinking diabetes or hypertension. Labs, studies, and imaging, CT or MRI with contrast, rule out that aneurysm, especially if a posterior communicating artery. MRI or CTA for vascular causes if suspected. You’re going to want to do a blood glucose and an A1C if it’s pupil sparing because you’re thinking diabetes or microvascular disease, and an ESR, CRP if concerned for a giant cell arteritis, especially in the elderly. So, if we have what we think are our common causes, our treatments are going to be, if we have a compressive issue, so pupil involving, we’re thinking aneurysm, tumor, herniation, this is a neurosurgical emergency. This is get on the ball right now, make the phone call.

If we think it’s ischemic, because the pupils are not affected, again, we’re thinking diabetic here. I’ve said this two or three times. I know I repeat myself, but I know that that’s also part of learning is repetition, and it’s helpful for me to hear it. It’s helpful for you to hear it. If I have an ischemic, pupil sparing issue, I’m thinking ischemia, often diabetic, so I’m going to observe, and I’m going to get the sugars under control, and BP under control in order to hopefully reverse this. If they have strabismus, you’re going to correct that with the prism glasses. If for persistent diplopia, I don’t know if my sickness is getting me tongue-tied and I’m running out of gas already.

Steroids if inflammatory cause like giant cell arteritis. Key takeaways, this is important. Pupil involving cranial nerve 3 palsy is life-threatening until proven otherwise. Most common cause here is going to be ischemia from diabetes. The most common compressive cause is a posterior communicating artery. I’m not sure that that’s going to be super relevant to you, but I’m passing it along either way.

Okay, we got two more of these to get through. Cranial nerve 4 is the trochlear nerve. This is a dysfunction of the trochlear nerve, which innervates the superior oblique muscle. So this is just going to control one of the muscles for the eye, the superior oblique muscle. So what’s our presentation going to be here? Well, vertical diplopia. This worsens when looking down and toward the nose, common with reading or walking downstairs.

So, to me, the way that this question gets asked, and that’s again how I’m thinking about things, is a patient comes in complaining about diplopia as they’re walking downstairs, and they missed a stair, or they fell. And this is especially important in the office, right? If they, you have somebody who’s missing stairs and having issues, they may not even realize that their vision is the reason for it. Or if they complain of just when they’re reading, they’ve stopped reading because they get this weird double vision when they read. You’re looking at a cranial nerve 4 palsy. What these patients will do also as they come in through the door, their head will tilt to the opposite side of the lesion because it’s a compensatory reflex to realign their vision. So, if they get this vertical diplopia, by tilting their head toward the side of the lesion, they are now not needing that muscle to hold their eyes steady and straight.

So, that’s one of the ways, one of the key terms here for a cranial nerve four palsy is that head tilt. And that was one of our priming questions, if you remember. Physical exam, cover test. So, the diplopia worsens with a downward gaze. So, the cover test is where you just cover up one eye and see what happens, right, and see what happens to the direction of the other eye. For testing for the rest of the motor function, weakness in downward gaze while adducted. Do the Bielschowsky head tilt test, tilting head toward the affected side, worsens diplopia, tilting head toward the opposite side, improves symptoms.

Lab studies and imaging. You can do an MRI with contrast if you believe there’s, if there’s been trauma, if you believe there’s a tumor or vascular etiology suspected, excuse me, do a CT of the head. If acute trauma like an orbital fracture or something is present, ESR, CRP, if an inflammatory cause is suspected like giant cell arteritis. Our common causes here are going to be trauma. This is the most common cause. It is a, if you have to pick a nerve that’s going to be the most commonly injured, it’s going to be cranial nerve four because of the pathway it travels. I don’t want to go into detail here about the anatomy of it, but because of the way it travels, it tends to be one of the more commonly associated with traumatic issues.

It can be congenital, but the key here is that people often miss it until they’re adults, until they really realize it’s a problem. You can get microvascular disease causing every issue here, like diabetes and hypertension, just like we did earlier, increased intracranial pressure, like a hydrocephalus or mass effect, just like before, and stroke and demyelination issues like MS can cause a problem here. Treatments. Correct the underlying cause. So, trauma, vascular, inflammatory causes. And generally, we’re going to observe this otherwise, because most of the time, this is going to resolve, especially in a microvascular issue. Prism lenses help correct diplopia, and then surgery for this strabismus correction, if persistent and disabling.

Key takeaways. So, what you want to think about is if you have diplopia, especially when walking downstairs or reading a book, plus a head tilt, then you’re thinking cranial nerve four. This is the most commonly acquired cause is trauma. And this is the most common congenital palsy. Most common congenital palsy.

All right, last one for today, and then we’re going to wrap it up with our study tip and our answers to our priming questions. Cranial nerve five is the trigeminal nerve. This is a dysfunction of the trigeminal nerve, which provides sensory innervation to the face and motor control of mastication muscles. So this can affect one or more of its three divisions. That’s kind of important here. Again, I’m not sure how detailed your PANCE is going to be to ask you a question on the specific branches here, but I think you kind of need to know it and be prepared for it or choose, like I do on some topics, specifically not to know it and move on. But I think this is one that because it’s broken out this way, you should spend some time on it.

So of the branches, we have the ophthalmic branch, we have the maxillary branch, and we have the mandibular branch. So the ophthalmic branch is responsible for the forehead, the cornea, the upper eyelid sensation. The maxillary branch, V2, is for the cheek, upper lip, nasal mucosa sensation. And V3 is mandibular, so jaw movement and lower lip sensation. Clinical presentation. You can get facial numbness or paresthesia. Depends on the affected division.

Okay, so it makes sense, right? If I have a problem with the trigeminal nerve, and it’s responsible for forehead, cornea, and upper eyelid sensation, or cheek, upper lip, nasal mucosa sensation, or lower lip sensation, it makes sense that if I have a palsy in it, paresthesia or numbness in those areas is going to be one of my presenting signs. Jaw deviation toward the affected side if I lose motor function of V3, right, if I’m no longer controlling those muscles. The trigeminal trigeminal neuralgia is an neuralgia is another presenting symptom, which is nerve irritation rather than a true palsy. So you get shocking pain sort of through that nerve and some issues with it, but it’s not a true palsy. It can be triggered by light touch, chewing, or cold air. And it most commonly affects the maxillary or mandibular branches, V2 or V3.

The corneal reflex can be absent if it’s a V1 lesion and difficulty chewing if obviously the mandibular branch is affected. Physical exam.

All right, so sensory testing. We’re going to look for loss of sensation in V1, V2, or V3 distributions. It makes sense, like we just talked about. Jaw testing for weakness or if the jaw deviates towards lesion, like we talked about. Corneal reflex is either absent. Blink reflex, unaffected side. That would be if you have a ophthalmic branch involvement, V1.

And then the other part is just looking for those triggers if it’s trigeminal neuralgia, right? So if they’re affected by cold, that might be more in your history than in your physical exam. I’m not sure how you adjust for those. Maybe light touch and things in physical exam. It’s not really what I do in my practice, so it’s a little hard for me to come up with ideas there, but that’s sort of what I’m thinking. But you’re looking for triggers for that trigeminal neuralgia. So is it something that is affected by cold?

Is it something that’s affected by light touch? That sort of thing. Lab studies and imaging, MRI brain with contrast to rule out a mass, or multiple sclerosis, CT of the head if you have trauma. So again, you can see how these are repeating, right? Over and over and over. ESR, CRP, if a giant cell arteritis is suspected, especially in the elderly. You could do a lumbar puncture if you think there might be a herpes or meningitis causing this.

So the lab studies and imaging are going to repeat for most of these because again, if I’m looking for a cranial nerve palsy, I’m looking for the same things that might be causing it. Treatment, if I have a trigeminal neuralgia, I might try something like carbamazepine. If I have MS-related disease, I might do interferon beta or natalizumab, or post-herpetic neuralgia, I might use something like gabapentin or pregabalin. Tumor-related issues or mass effect would be a neurosurgical eval. I may have to do surgical decompression or microvascular decompression or things along those lines to free up those nerves. But I hope you get the point here. And the point is that you’re going to walk through these the same ways and then come to your conclusion and then treat them depending on what the underlying cause is in most of these cases.

Key takeaways. The trigeminal neuralgia is going to be like that shock-like feeling, unilateral, facial pain, that kind of thing along V2 or V3. MS should be suspected in young patients with bilateral symptoms. That’s a really good one that maybe I should include in other areas of this. The bilateral symptoms is should clue you into that. It’s an MS and not like a specific trauma thing, right? Absent corneal reflex suggests V1 involvement and jaw deviation occurs toward the side of the lesion.

Those are some good key takeaways. And that, my friends, will bring us to the end of today’s section on the cranial nerves. Again, something that I’ve always kind of struggled with, but something I think you can be able to handle with enough time and energy put into the right places and using the right practices. Some of the right practices would include things like the priming questions and being able to answer those. And we’ll go through those today. We’ll touch on some more next week when we do the companion episode for this show. And we’ll get into a little bit deeper into how, if you haven’t been listening to those, we go a little deeper into including the priming questions, but then going further with creating PANCE style questions from those and walking through those and giving you some ideas on how to memorize all of this stuff and have it ready for you even as you get moving.

So, but before I get to those answers, I want to go through today’s study tip with you. And today’s study tip was something I was thinking about a lot as I was working with those students out in Ashland this week. And it was the idea of exercise and how important exercise can be for your cognitive function. I do a whole section on exercise. And it’s one of the parts that I really hope gets through to the students because every study ever done on exercise shows an improvement. Every study ever done shows an improvement. There are new studies every day, but the reality is there hasn’t been one that’s like, you know what, you probably shouldn’t do that.

You know, it’s probably not good for your cognitive of function, it’s probably not good for your longevity. It’s probably not, it really doesn’t happen. Yes. Could you have overtraining and things of course, but come on, that’s not what we’re talking about. And one of the studies that I show them and I presented them, and I don’t have it in front of me. I probably should have, but I don’t talks about, where they took a group a and put them on stationary bikes for 10 minutes at a very mild to moderate pace. And then they had another group B sit and read magazines, right.

For 10 minutes. And they both had them do a cognitive test. And what they found minutes later after they ended this 10 minutes, and then what they found was that the group who had done the 10-minute bike ride had a 12% to 14% increase in their scores on this cognitive exam. I want that to sink in for just a second, because again, I wish I had it right in front of me so I could give you the details, but you can find literally probably hundreds of these. A 10… I’m sorry, 12 to 14% increase in cognitive function from a 10 minute moderate mild to moderate bike ride. That, to me, is phenomenal.

Meaning, why wouldn’t you get out for a walk before you sit down to study? Why wouldn’t you walk on your breaks? Why wouldn’t you do a couple squats or a couple lunges on your breaks? Why wouldn’t you, before your exam, rather than cycling yourself up and studying and trying to cram in as much as you could, why wouldn’t you go for a 10 minute walk and just move if it’s going to increase your… has the potential to increase your cognitive function by that significant amount, right? So to me, I could learn one thing in a five minutes before my test that I’m studying, and that one thing may or may not be on my test. But if I can improve cognitive function by 10% across the entire test in that same five minutes, well, that’s an easy choice, right?

Again, you have to make decisions. And like we talked about the very beginning of this episode, decisions are the key, you have to choose what you’re going to do. A lot of us just, and myself included in a lot of different places. Let things sort of happen. We use habits. We use what other people are doing. But if you stop and think and your choice is between cramming in one more piece of information or boosting your cognitive function by 10%, I don’t think it’s much of a choice at all, but we don’t usually frame it that way.

So whether you’re getting ready to study, whether you’re getting ready for a test, whether you’re talking about your breaks during your PANCE, I always, always, always push for exercise. And again, if you’re not someone who normally exercises, we’re not talking about going out and running five miles, right? I’m talking about a 10-minute moderate walk. So I’m pretty sure 90-95% of people can either do that or do something equivalent to that, right?

So let’s consider that moving forward.

All right, let’s jump into our answers to our priming questions. What does it mean when the patient tilts their head to the opposite side of a lesion?

Okay, so remember we talked about this. Here this was which nerve? With the patient tilting their head. It was cranial nerve four. This is to compensate for reduced vertical diplopia from a weak superior oblique, right? So we’re compensating for that muscle is what the patient’s doing. They’re turning their head in an effort to get their eyes to balance out because the muscle itself that controls the eye isn’t working.

Why is a pupil involving cranial nerve three palsy a neurosurgical emergency? Why is a pupil involving cranial nerve three palsy a neurosurgical emergency? Because it suggests a compressive aneurysm inside the patient’s skull. So there it becomes an emergency. So this is often a posterior communicating artery and we have a risk of brain herniation. So things to consider. How can you differentiate trigeminal neuralgia from other causes of facial pain?

Well, hopefully you at least now know what trigeminal neuralgia is, right? That’s that shooty pain that is in the face that comes from V2 or V3. And how do you differentiate that from other causes of facial pain? Well, you get that electric shocking pain and it’s usually triggered by either a light touch or change in temperature, but you get no sensory loss. That’s the key. And that’s something I didn’t quite mention earlier when we were talking about it. You don’t get sensory loss.

You just get that pain and that electric shock pain. Which cranial nerve palsy causes an eye to drift down and out and why? Well, cranial nerve three palsy causes that down and out deviation. And the reason is because then the cranial nerves, or the muscles that are innervated by the cranial nerves four and six are unopposed. There’s nothing working against them. So the eye will drift down and out because of those nerves innervations, because of those muscles innervations.

All right. I think we pretty much nailed it. This was a great start to cranial nerves. Really excited about where we’re heading, what we’re doing here. If you are getting a lot out of this show, if you’re finding that the notes are helpful, by the way, all of the notes will be over on the website, physicianassistantexamreview.com/127 for this particular episode. All the notes will be over there. If you find it helpful, please share it with someone in your class.

Please share it with a friend. Please share it with a colleague. Please share it with your faculty. Let them know that this information is available to them as an added resource they could be using. And it would help me, it would help them, and I would really, really appreciate it.

All right, so that’s going to take us out for today. I can’t wait to talk to you next week when we go over cranial nerves one to five, but we do it from this standpoint of how those questions are going to come, how you can memorize them better and so on in those companion episodes. I look forward to talking to you again next week. Take care.