all right hope everybody is doing well we're going to get started in just a couple minutes if you are just joining us go ahead and say hello in the chat box pull it up so that you can interact this whole hour and a half session well we're gonna get started in just a couple minutes if you are just joining us go ahead and all right so we have a international audience layla from the caribbean marie from new york laura is here kelly from new jersey is here we have hina from pakistan sarah from saudi arabia uzair from atlanta amy from northeast ohio we have chitra from new jersey this is absolutely epic if you haven't put into the chat a hello and where you're logging in from please do this really pumps me up for the session and we are going to really get started in a couple couple minutes we got ray coming in from nebraska that is awesome look at i i had to put a world map on because we have people from everywhere over 200 people have signed up for this uh webinar we're live streaming on facebook uh we have z ying from poland that's here sarah from new york roberto from houston uh nathaniel from ethiopia this is pretty epic i i am really grateful and pumped uh are you guys ready for a great webinar today go ahead and type in yes or no in the chat box you guys ready to review awesome all right great energy in the chat box now guys make sure that you are going to be engaged in this webinar today and most importantly i want you guys to keep your chat box open and type in the answers to the questions that i'm going to be flashing on the screen today honestly this is going to be a very active recall webinar and what i really will encourage you to do is type in the answers so that it really sticks in your mind some of these very high yield concepts all right excellent couple more minutes we're gonna let people log in and get settled make sure you're cutting out the distractions and i'll see you in just a little bit this is great all right it is 10 a.m eastern standard time let's go ahead and get started with our review today if you're just joining us open up the chat box make sure you are logging in saying hello today we are going to be covering a very challenging yet high-yield subject for the usmle and that is going to be top concepts in neurology if you're new to these series of webinars i humbly welcome you and if you have attended my prior webinars most importantly thank you so much for tuning back in i hope you're finding value in these webinars my name is rahul and i'm currently doing my fellowship in pediatric critical care i have been absolutely passionate over the past six years helping students just like you kick ass on the usmle exam if you have any questions regarding my resources or just want to get in touch with me there's my email i'm pretty responsive via email and i would totally encourage you to reach out for any questions which you may have now i know that there's already so much out there however i want to take one to two minutes while everybody's logging in putting away their distractions i want to take one to two minutes of letting you know why i think hi guru is just so unique when it comes to usmla preparation when i started this project about six years ago i really wanted to focus on evidence-based learning techniques most importantly i geared all of my lectures on active recall integrating material across domain and most importantly giving you the test taking strategies that you need for exam day when i prepare students for the usmle and you will see this sprinkled around this webinar today i want to focus on three major aspects i call this my triad for us mla and we're going to be going through a lot of triads today first thing i like to do is i like to give you the content the high-yield material which you are already getting from other resources but i really like to integrate it across domains i focus a lot on test-taking strategy yes the content is great but we got to know how they would ask it for example today we're going to be talking about multiple sclerosis the test taking strategy here is that any time you see a young female with focal neurological deficits you should always keep ms in your differential i like to focus also on productivity and scheduling at the end i'm going to highlight my dedicated study schedule on notion which is very customizable many students have really had great success with being organized with this plan and finally i like to type tap into test taking psychology i'm sure you all would agree with me that the usmle is not only a grind when it comes to hours of studying and focus but it is also important to stay emotionally balanced and make sure that you have a positive thinking throughout your dedicated and test day i think most importantly and we have over 200 people joining us today most importantly we are an absolute community i have been absolutely humbled over the past six years to teach live comprehensive review courses and you know this has really translated now to a global community of lifelong learners and my goal is to not only inspire you to do well on the usmle but to be a damn good resident a damn good clinician long term so i want to give you a little bit of a background as to what inspired me to create this webinar and that is this amazing post which i saw on reddit not too long ago that captured the most recurring concepts from the nbme practice exams and in essence highest yield concepts for the usmle i've synthesized them throughout all of the organ systems and today we're going to be covering neurology if you have not checked out my prior reviews they are on youtube and i have also placed each of these lectures under my free resources sign up for the golian style course and you will see all of the videos there chopped up into small bite-sized pieces so you all can interact with this concept content in a very micro learning type of way as you can see this is the kind of course curriculum from that golden style classroom course i did want to put some screenshots there so that you can easily find it and actually just last week i put in a whole section on cardiac physiology for the usmla again i think that this is a high-yield review and this course has just been growing and growing and growing and i hope that you all can really capitalize on this material and sign up for this course but without further ado i am so glad everybody is here and on time really thank you so much for being punctual and setting up early i do want to remind you to cut out distractions make sure that you're not multitasking this is an hour and 15 minutes of just questions questions questions and most importantly i want to start out with a question for all of you if you're ready to get started with neurology today go ahead and put in yes into the chat box are you guys ready awesome we have a lot of people that are putting yeah woohoo excellent well let's go ahead and get started with our top ndme concepts outline we will first cover brain hematomas followed by going into a review of uncle herniation and to transition this i'm going to be talking about increased intracranial pressure remember uncle herniations are going to affect cranial nerve 3 and then afterwards we're going to do a little bit of a cranial nerve brigade in which we're going to start with cranial nerve 1 and integrate all of the pathologies until cranial nerve 12. we're going to be doing a lot of compare and contrast between things like alzheimer's and frontotemporal dementia parkinson's dementia versus lewy body dementia we're then going to move into neurocutaneous disorders and even talk about the trinucleotide repeat disorders we're going to be talking about multiple sclerosis now this is going to be one of those pathologies on the usmle that incorporate many different organ systems they're under the heading of multi-system pathologies we're finally going to be going through brain tumors and stick around until the end because i'm going to take stroke questions and just make them very easy stroke questions on the us emily they have a little bit of a longer vignette the actual deficits can be very very confusing and remember that there's going to be anatomy integration as well and hey guys we're going to be covering that um throughout uh at towards the end of this session so let's go ahead and get started with brain hematomas let's start with our first question we have a 23 year old male who presents to the trauma bay after a motor vehicle collision which is an mvc he is noted to be awaken alert on primary survey and two hours later he is noted to have a loss of consciousness his vital signs are 140 over 80 so he's hypertensive his pulse is 60 a little bit on the lower end of normal and respirations are 10. his pupil is mildly dilated and bruising is noted in the temple what do you think is the most likely diagnosis and again pull up that chat a mca stroke b epidural c subdural d sub arachnoid and e rupture of a sharko bouchard aneurysm and we have many people who have put this into the chat and you're absolutely correct an epidural hematoma now an epidural hematoma is going to present on your usmle as a talk and dye phenomena and we're going to be integrating some of the imaging but remember that you are going to have this convex lens shaped lesion that will be found on your non-contrast head ct so when we're thinking about epidural hematomas we really want to integrate some of the key testable scenarios and when we think about the testable scenarios we always want to think about the head trauma so for example a skull fracture at the terion this talk and die phenomena in which they were alert and oriented and then the epidural hematoma started expanding now the usmle loves to go for what is the affected artery and the affected artery is actually going to be the middle meningeal artery now just to integrate a little bit more anatomy for you guys remember that the middle meningeal artery is actually going to be a branch off the maxillary artery and that's really high yield for you to know this is going to be one of the terminal branches of the external carotid so how do i tell the difference between internal and external carotid well remember guys that the internal carotid goes into the brain and that's going to make up your circle of willis whereas the external carotid has many branches the maxillary branch gives off that middle meningeal so one of the key test taking tips that i'm going to give you guys as you are preparing is that while you're studying any sort of pathology and there is a high-yield anatomical tie-in take that anatomical tie-in one step further and for example with the middle meningeal if there is an affected artery nerve lymphatic or or venous structure that is damaged track it back to a structure that you're familiar with like i did right now i said middle meningeal okay fine that can be one small fact but why don't you take that middle meningeal put it into google and then just look back and say middle meningeal comes from the maxillary which is going to be coming from the external carotid and then you're able to synthesize anatomical concepts much better one of the key things that the us emily likes to go for is the relationship of the middle meningeal artery to the foramina of the skull now do you guys know what is going to be the foramina of the skull in which the middle meningeal artery is going to exit from go ahead and type that in the chat as we're going through this and so that is going to be the foramen spinosum you're absolutely correct so remember that there are three major uh three major um openings in the base of the skull that i want you guys to recognize number one is going to be the foramen rotundum the second one is going to be the ovale and the third one is going to be the spinosum now when you're talking about the foramen rotundum foramen rotundum you're going to have the maxillary division of the trigeminal nerve for the foramen ovale you are going to have the mandibular division of the trigeminal nerve exit and then foramen spinosum that's going to be your middle meningeal artery and just to give you that space repetition remember we're talking about epidural hematomas related to damage the middle meningeal artery excellent job so now we will transition and go through some vignettes related to subdural hematomas and this is what i like to call thinking like the test maker so what would be possible scenarios in the test question and again guys put it in the chat we have things such as a baby who has bilateral retinal hemorrhages that's actually a very important one and this is classically unfortunately called non-accidental trauma or shaken baby syndrome the other vignette related to subdural hematoma are going to be nursing home patients in your exam questions or alcoholics and there's a key pathophysiologic mechanism in the sense that these patients are likely to have atrophy of the brain and that increases the risk of bleed leading to a subdural hematoma remember that when you're talking about subdural hematoma pathophysiologic mechanism is going to be the shearing of those bridging veins typically compared to subarachnoid hemorrhages which we'll get to the subdural hematomas in your exam questions have a very slow onset of symptoms and the affected not artery but most importantly the affected veins are going to be your bridging veins and these are going to end up shearing and breaking leading to that crescent-shaped lesion all right the next one we will be talking about is going to be subarachnoid when you're thinking about the subarachnoid hemorrhage let's go ahead and go through this vignette so here you have a patient with ultrasound confirmed cystic kidneys has a sudden onset of headache vomiting and photophobia where is the most likely lesion or location of this pathology and remember this is that sudden onset well when you're thinking about subarachnoid hemorrhages typically you're going to be thinking of rupture of aneurysms now there are many types of aneurysms but the one that are related to for example polycystic kidney disease are going to be your berry aneurysms now the classic pattern for subarachnoid hemorrhages on your usmle and ct imaging is going to be the blood following the sulci and the gyra it's going to be nice and lit up on your non-contrast ct because now you have blood within the csf and brain parenchyma you may see the xanthochromia which basically represents the breakdown products of heme within the actual csf the test makers love for you to recognize that the blood in the brain is actually going to be very irritating to the blood vessels and so patients can be at risk a few days later after a subarachnoid hemorrhage they can be at risk for developing ischemic strokes due to vasospasm and remember that pneumotipine is going to be a calcium channel blocker that is given to reduce the risk of vasospasm so if we just go ahead and just quickly integrate remember that you have calcium channel blockers and calcium channel blockers are going to come in two flavors you have your non-dihydropyridine which are going to affect the heart whereas the dihydropyridine are going to affect your blood vessels the non-dihydropyridine those are going to affect your heart and those are going to be diltiazem and varapamil and because they affect the heart i like to use the mnemonic take the v and turn it into a heart and then in the indian language the word dil means heart so now you know that diltiazem and varapamil are your non-dihydropyridine calcium channel blockers what are they going to do to the heart rate they are going to slow it down the dihydropyridine calcium channel blockers are primarily going to cause vasodilation and we saw this in the setting of nimotipine which is going to prevent that vasospasm and they typically the dihydropyridines are going to end in dipine so amlodipine nimotipine necardipi okay so there's a little bit of a farm tie-in for you as we integrate a lot of this material so one of the key things that we have to recognize is that the berry aneurysms can occur at this junction of the anterior cerebral and anterior communicating artery and at this 90 degree turn one of the histological components which actually ends up becoming a little bit weak and causing that aneurysmal dilatation is the lack of the media as you are making that turn into the anterior communicating artery so that is very high yield for us to recognize that in arteries you are going to have a tunica media that's actually going to be very very thick and that allows us to have that nice tone of a artery now as you are making that bend from the anterior cerebral artery into the anterior communicating you may lose a little bit of that media and thus you can get the aneurysmal dilatation now the pathophysiology is that if the aneurysmal dilatation is going to burst you are going to be getting that subarachnoid hemorrhage very high yield very important for us to recognize so at this junction there is no strong media so aneurysms are going to be prone to occur and rupture so let's go ahead and do a quick compare and contrast of the various brain aneurysms you're going to see on step one there are two major aneurysms one is going to be the charcoal bouchard and the other one is going to be the saccular berry which is what we talked about in our case vignette in the sharko bouchard aneurysms let's go ahead and look at the vignette it says that a patient who has long standing hypertension who presents with this gradual slurring of speech headache and weakness over a few hours as you note the charcoal bouchard aneurysms they are going to be yes very small but most importantly they are going to be located in the deep brain structures think about basal ganglia and thalamus now contrast this very slow indolent presentation with the saccular berry aneurysms so typically saccular berry aneurysms they are going to be present in patients who have connective tissue disorders such as marfan syndrome or who have cysts such as polycystic kidney disease remember polycystic kidney disease cysts in the kidney cysts in the brain these patients are going to have that thunderclap subarachnoid hemorrhage which we talked about these are a little bit of bigger aneurysms and they are primarily located in the circle of willis so as we summarize the brain uh pathologies right here we want to go through the most important u.s emily vignette so for example a patient who has a head trauma plus talk and die phenomena go ahead and put that in the chat which brain hemorrhage is that going to be that's going to be your epidural hematoma and that's that rupture of the middle meningeal artery excellent participation a patient with shear injury plus a crescent-shaped mass on imaging and as you can see it crosses the suture lines what do you guys think that is that's going to be your subdural and that's going to be a venous bleed tearing of the bridging veins and then finally you have a patient who has altered mental status a focal neurological deficit after a parenchymal bleed i.e they have vasospasm what are you going to be worried about here that is going to be your subarachnoid hemorrhage which is usually due to aneurysmal rupture excellent job guys so when we're talking about subarachnoid hemorrhages one of the major concerns that subarachnoid uh hemorrhages uh can cause is this concept of increased intracranial pressure and when you have increased intracranial pressure in your brain the brain starts to swell swell swells well swell and because the skull is kind of a confined space the brain can be prone to herniate and so one of the key herniations that the usmla goes for is this concept of uncle herniation before we get into this concept let's go into another multiple choice question you have a six-year-old male who presents to the intensive care unit after diagnosis of subarachnoid hemorrhage one hour after admission his vital signs are notable for blood pressure that is high heart rate that is 60 respirations of 12. he has a right pupil minimally reactive and 4 millimeters in diameter his left pupil is noted to be two millimeters and reactive so key thing in this question is that they're unequal pupils given normal cerebral autoregulation which of the following interventions may reduce elevated intracranial pressure in this patient remember we're talking about something that will reduce the high icp so a hypoventilation b no change in the respirations c increase blood pressure by stimulating alpha receptors or d hyperventilation and if you said hyperventilation you're absolutely correct and this gives us the opportunity to jump into a very important physiology tie-in and that is this relationship between cerebral blood flow as well as co2 levels in the blood one of the key areas that i'm going to highlight right now before we go on into cerebral autoregulation is how to recognize triads on the usmle it is not enough for you to recognize cushing's triad by just saying hypertension bradycardia irregular respirations that anki card though it is effective in getting that into your memory it's not going to be as effective as you taking that one step beyond and thinking like the test maker how can the usmle put in cushing's triad into your exam questions so for example they can put the vital signs that show the hypertension remember that 140 systolic blood pressure they can also give you in the vital signs a low heart rate and remember the mechanism there is that reflexive bradycardia and then finally because your high icp is starting to actually compress on the brainstem centers you are going to get irregular respirations so just as a little bit of a physiology tie-in here what is that mechanism behind the reflexive bradycardia and that is going to be this activation of the baroreceptors remember when you have high intracranial pressure you are going to have a reflexive increase in your mean arterial pressure your blood vessels that are perfusing the brain are going to vasoconstrict now if you vasoconstrict you're going to get increased carotid stretch and if you have increased carotid stretch you're going to activate the baroreceptor so cranial nerve 9 is going to send that signal to the central nervous system and then you have an efferent reflex of having increased parasympathetic activity and thus with high parasympathetic activity and the vagus nerve essentially putting down ach at the level of the saav node you're going to be getting bradycardia so it's very important for us to recognize that the hypertension with the reflexive bradycardia that all relates to the baroreceptor reflex now this is going to be a important figure for us to go through but i first want to give you a very important test taking strategy guys and that is that whenever you see graphs on the usmle for example you want to go through a systematic approach and i teach this in my test taking master class and that is that you first want to say all right i'm not going to panic second thing that i'm you need to say is let's define the x-axis and let's define the y-axis so on the x-axis you have millimeters of mercury so essentially some sort of pressure or concentration and then on the y-axis you have cerebral blood flow the third step after you define the axis the the third step is going to be established trends and if we look at this paco2 trend right here we want to really recognize that as the pa co2 is going to increase your cerebral blood flow is also going to increase and so that relates back to our question that if you have high amount of intracranial pressure you want to start reducing that cerebral blood flow otherwise your brain is going to be very prone to herniating so in fact we are going to be going the opposite way when it comes to hyperventilation because remember hyperventilation is going to decrease our co2 levels and when you decrease your co2 levels you are then going to reduce your cerebral blood flow what are the cerebral arteries going to do with hyperventilation i.e inducing a respiratory alkalosis again i'm trying to integrate many different components here you're going to get vasoconstriction and that's really important for us to know so let's look at this blue curve and the blue curve is the following where you have cerebral blood flow and then subsequently as you are going down or as you are uh going to be increasing decreasing excuse me the concentration of o2 for example you are going to have a reduced amount of cerebral blood flow what's really important for us to recognize guys is that when the brain senses hypoxemia i.e you have a very low p little ao2 when you have a very low p little ao2 the cerebral blood flow is going to go up and that's the best way to conceptualize it is that a low p little ao2 hypoxemia triggers the brain to actually vasodilate so what does high co2 do high co2 causes us to also vasodilate what does low o2 do low o2 causes us to vasodilate our cerebral vasculature and then finally we recognize this concept right here and that is this concept of blood pressure autoregulation and that is the fact that in between very tight wide range of mean arterial pressures your brain is going to have a constant cerebral blood flow and such that once you get to a very low blood pressure you can actually have reductions in your cerebral blood flow or the opposite can hold as well all right so that is this concept of cerebral autoregulation let's just quickly summarize some of the important concepts and that is that hypercapnia i.e a high co2 in your exam questions you can also have a respiratory acidosis all of those are going to cause a vasodilation and thus an increase in cerebral blood flow hypocapnia is going to be defined as low co2 that can be related to a respiratory alkalosis and that causes cerebral vasoconstriction and when you have cerebral vasoconstriction you're going to decrease cerebral blood flow when is this really important well when you have signs of herniation you want to hyperventilate in order for you to actually reduce that cerebral blood flow all right excellent so now we are going to be talking about the uncle herniation when we're thinking about the uncle herniation it is all about this temporal lobe the unkiss of the temporal lobe actually compressing a very important cranial nerve go ahead and put in the chat what do you think is the cranial nerve that is compressed in the uncle herniation and if you are saying cranial nerve three you're absolutely correct so we need to go through the mechanism here and that is the fact that when you compress cranial nerve number three as it exits the midbrain you will compress the preganglionic parasympathetic fibers if you disrupt parasympathetic fibers you're going to get pupillary dilatation let's take a step back what does normal parasympathetic do normal parasympathetic causes you to have pupillary constriction so if you compress the parasympathetics you are going to get pupillary dilation so if you damage parasympathetic what pupillary change you will get dilation of the pupils and so that's where you're going to see on your usmle questions pupillary exam is notable for four millimeters five millimeters minimally reactive pupils we saw that in our multiple choice question and that essentially is a telltale sign that the patient has a very dilated pupil when we're thinking about uncle herniation and this compression of the parasympathetics let's go ahead and do a high-yield neuroanatomy tie-in and that is looking at the anatomy of cranial nerve number three remember that the cranial nerve number three is actually very very interesting in the sense that the parasympathetics are going to be on the outside of cranial nerve number three whereas the motor fibers are going to be within the inside of cranial nerve number three such that if you have some sort of external compression initially the parasympathetics may get disrupted however if you end up having progressive compression not only are you going to get a dilated pupil but very high yield you will get unopposed lateral rectus and superior oblique contraction and that will give you that classic down and out pupil that we see with cranial nerve three palsy so this is that down and out and remember it is unopposed lateral rectus and superior oblique because remember that the lateral rectus is going to be innervated not by cranial nerve number three but cranial nerve number six and the superior oblique is gonna be cranial nerve four or the trochlear nerve so key points the outside parasympathetic inside is motor the next portion of this guys is going to be relating cranial nerve pathology very important when you're thinking about cranial nerve pathology let's go ahead and start with this important test question here you have a 16 year old female who presents with fever and throat pain she is noted to have increased fatigue for the past week vital signs are notable for a fever physical exam is notable for exudates on the tonsils and very important left-sided uvular deviation ct of the neck shows concern for injury to a cranial nerve which of the following nerves related to this patient's exam findings is most likely to be affected a vagus b glossopharyngeal c hypoglossal d trochlear e trigeminal go ahead and put in the chat what you think the answer is excellent i'm seeing a lot of a's and if you say a you're absolutely correct remember that palatal tone is primarily driven by your vagus nerve and how does a vagus nerve pathology manifest well many different ways however in the head and neck region you are going to be thinking of uvular deviation so let's go ahead and go into this as you can see in this image remember it's opposite that this is the patient's right side this is going to be the patient's left side when you're thinking about uvular deviation it is typically going to be away from the side of the lesion very high yield for us to recognize here that if you have a right cranial nerve 10 that is going to be shot i.e there is no good cranial nerve 10 on the right side you will get left-sided uvular deviation now the vignette that i was going for here is going to be a patient who has epstein-barr virus who has this exudative tonsillitis that could actually progress into getting a peritonsal or abscess and remember epstein-barr virus that's going to cause your infectious mononucleosis so this is a great way for us to springboard into the cranial nerve brigade and let's go ahead and just look at the table highlights here that is first we're going to look at the u.s emily vignette i'm going to go into key high yield presentation points and then we're going to be talking about the cranial nerve so here we start with a patient who presents with trauma plus a fracture to the ethmoid and cribriform plate and you have csf leaking from the nose that's really important that's csf rhinorrhea very bad sign you see that in for example basilar skull fracture the important thing when you have damage to this nerve is you're going to have a nosmia and what do you guys think is the cranial nerve that is going to be involved here that is going to be cranial nerve one exactly that's going to be the olfactory it'll be really helpful for you to not only type in the number but it will be important for you to also actively recall what is the name of that nerve so cranial nerve one that's the olfactory nerve let's go ahead and go through this vignette you have a patient with neurofibromatosis who presents with an optic nerve glioma and an abnormal pupillary reflex remember that cranial nerve this cranial nerve is going to be the afferent limb of your pupillary reflex such that if you don't have this cranial nerve you're going to have a loss of the direct pupillary reflex which cranial nerve is this this is going to be your cranial nerve number two and you guys are absolutely correct if you typed an optic nerve that is going to be cranial nerve number two and remember optic nerve glioma related to neurofibromatosis uncle herniation vignettes related to aneurysm of the posterior communicating artery or pca this one is really important we talked about this and that is going to be cranial nerve 3 which is going to be your oculomotor nerve and we already discussed the organization of the parasympathetics on the outside the motor on the inside so what's going to be very high yield for us to recognize is that we can get cranial nerve 3 palsies if we have a posterior communicating artery aneurysm because again that can actually compress this cranial nerve number three or if you have an aneurysm at the junction of the superior cerebellar artery and the posterior cerebral artery remember that the basilar artery comes on the back side of the pawns going into the midbrain and the terminal branch of the basilar artery is going to be your superior cerebellar as well as your posterior cerebral and the posterior cerebral artery makes up the back portion of your circle of willis moving on with their cranial nerve brigade a patient who has difficulty with walking downstairs and then has the head tilt that is away from the side of the lesion so away from the side of the lesion difficulty looking down key thing here is going to be the cranial nerve for palsy and that's going to be your trochlear nerve now this next nerve as you note i'm going in order but this next nerve is going to be the trigeminal nerve and remember that the trigeminal nerve really has three parts the ophthalmic division the maxillary division and the mandibular division the ophthalmic division of the trigeminal nerve remember exits the skull in which bony foramina and that is going to be the superior orbital fissure very high yield for us to recognize what's also very important for us to note is that the ophthalmic division of the trigeminal nerve is going to be damaged in patients who are is going to be affected in patients who have for example corneal scratches so any time on the us emily they put in a contact lens where they're going to be going to two things number one what is sensory to the cornea and that is the ophthalmic division of the trigeminal v1 the second thing is that contact wearers are going to be prone to what types of infection pseudomonal infections us emily loves to go for that let's go ahead and go through this cranial nerve palsy related to the trigeminal division or related to the trigeminal nerve a patient with the tumor who presents with difficulty chewing and jaw deviation very high yield guys towards the affected region so jaw deviation towards the affected region you're going to be thinking of the mandibular division v3 mandibular division of the trigeminal nerve now what i also did was i put in a little bit of a embryology tie in and remember arch number one is going to be related to the trigeminal nerve what's high yield for us to also recognize is that the reason why you get the jaw deviation towards the affected region towards the effective uh region is going to be due to unopposed opposite pterygoid contraction let's go ahead and go through this cranial nerve patient with the pimple in the danger triangle so right here with sudden proptosis and eye deviation medially this is going to be a very important uh uh cranial nerve palsy and that is going to be this inability to abduct because you have a abducens nerve palsy that's very high yield for us to recognize now when you're talking about the danger triangle you are going to be integrating the cavernous sinus and if infection or thrombi form in that cavernous sinus the most medial structure in the cavernous sinus is going to be the abducens nerve and you can get cranial nerve six palsies especially if there is going to be a clot that is going to be forming within the actual cavernous sinus what are going to be the other nerves in the cavernous sinus you're going to be thinking about your oculomotor your trochlear remember trochlear does what eye muscle that's going to be superior oblique you have v1 and v2 those are both going to be going through the superior orbital fissure let's go ahead and go through the next vignette and that is going to be looking at bell's palsy now everybody bell's palsy it is cranial nerve what which is affected go ahead and put it in the chat what cranial nerve is affected in bell's palsy you're absolutely correct it's going to be facial or cranial nerve 7. let's go through this u.s emily vignette avid hiker who presents with inability to raise her eyebrows she has dry eyes and is hypersensitive to sound what cranial nerve may be affected well we all know that this is going to be cranial nerve number seven but let's go through some important mechanisms here and that is what is the mechanism behind the hyperacusis ooh this is a good one and that is going to be the fact that cranial nerve seven innervates the stapedius muscle and when you have stapedius weakness in your bell's palsy you're gonna have more oscillations on the oval window again i'm going into autology tie-in and more conduction of the sound so you get hyper-accuses with bell's palsy what may happen to the patient's sense of taste is it going to be increased or decreased what do you guys think is going to be the sense of taste in this patient and that is going to be absolutely it is going to be decreased remember that the specific branch that is affected is the corta tympani and whenever you have a bell's palsy cranial nerve seven palsy you are going to have decreased taste why because at the anterior two-thirds of the tongue you are going to have cranial nerve seven that does taste and v3 that does sensation that's very important for us to know so right now i'm going to have this hot coffee the fact that the coffee is bitter that's going to be cranial nerve 7 because that's going to be taste whereas the fact that the coffee is very hot that's going to be hot or cold that's going to be sensation remember that the posterior 1 3 is going to be what cranial nerve everyone and that is going to be cranial nerve number nine yes you're absolutely correct that it's gonna be cranial nerve number nine both taste and sensation and hey just for fun what if i say what is going to be motor to the tongue go ahead and put that in the chat that's going to be cranial nerve 12. you're absolutely correct very good so let's go ahead and keep going in our review what pharyngeal arch is related to cranial nerve 7. go ahead and put that one in the chat pharyngeal arch that is related to cranial nerve seven and that is gonna be the second pharyngeal arch again guys what i like to do is i like to really integrate embryology anatomy pathophysiology pharmacology i like to put it all together so that you can have a different way of learning and as you can see this is very very engaging it's in an active recall way so it's kind of like a guided anki deck for you as you're going through the session all right so let's go ahead and integrate a little bit of microbiology here and we want to go into the organisms related to bell's palsy now when we saw the hiker we thought of a very important uh microbe which is borealis burdorferi however what's important for us to recognize is that hsv a double-stranded dna linear virus can also cause us to get bell's palsy and that's very high yield that if you have isolated bell's palsy without any history of hiking et cetera et cetera think about hsv causing it obviously when you're thinking about this obligate intracellular spiral key you're going to be thinking about borealis burdorfry this is another studying tip guys and that is that if you see a microbiological agent always just quickly integrate the morphology of that microbiological agent why that's important is because yes you may say oh bore yellow border fry however if the answer choices have different morphologies for you to uh recall then it can become very challenging on the exam so as soon as i see borealis bird or fry i just quickly look up okay this is an intracellular spirochete so borealis burdorfry what type of disease does it cause not only bell's palsy but that whole constellation of symptoms is known as lyme disease you're absolutely correct so remember that the first stage that you will see is the skin rash and that is known as erythema chronicum migraines this is that red ring with the central clearing it looks like kind of like a target sign what's important is that you don't get confused between erythema marginatum which is seen in rheumatic fever and erythema chronic migraines which is seen in the first stage of lyme disease the second stage you're going to have this migratory arthralgias you can get bell's palsy which is what brought us into this integration and then av blah how does av block present well the usmle can give you an ekg and that ekg has what we call atrial ventricular disassociation in which you have grouped beatings and the p waves are not going to be lined up with the qrs waves finally the third stage of lyme disease you're going to be thinking about aseptic meningitis chronic arthritis this is a very severe stage of lyme disease that affects the central nervous system moving on with our review we talked about cranial nerve number seven what is gonna be the next nerve yes you got it that's gonna be cranial nerve number eight i want to be very systematic but guys the key here is to focus on the vignettes very important so let's go through this vignette neurofibromatosis ii plus an abnormal mri in the auditory canal what are you worried about yes you're worried about that acoustic neuroma or schwannoma and that is going to be damage to the cranial nerve eat which is the vestibulo cochlear nerve now remember that they can also test this with abnormal weber and renee test those are going to be those tests that differentiate between conductive hearing loss as well as sensonurial hearing loss how about this one a patient with the loss of the carotid baroreceptor sinus reflex or taste in the posterior one-third of the tongue what is the nerve guys that is affected here you're absolutely correct if you put in nine into the chat box you're absolutely correct remember that when you're talking about the gag reflex or the baroreceptor reflex the glossopharyngeal nerve is going to actually uh be the afferent limb of both of these reflexes again synthesizing these things what's the embryology tie-in and that is going to be arch number three arch number three is going to give rise to the glossopharyngeal nerve and remember the pharyngeal muscle that is going to be innervated by the glossopharyngeal nerve is that stylopharynges that's very important for us to recognize all right next one a patient with a cervical lymph node surgery plus ipsilateral shoulder weakness and that is going to be the weakness of the sternocleidomastoid or the trapezius whenever you have the shoulder weakness you're going to be thinking about the trapezius and if you have issues with head tilting you are going to think about the sternocleidomastoid and that is going to be the spinal accessory nerve remember cranial nerve 9 10 and 11 go through the jugular foramen and that's another bony foramina high yield for your usmle finally we're going to be talking about ipsilateral tongue deviation along with atrophy and fasciculations of the tongue that is going to be the nerve that is motor to the tongue which is cranial nerve 12 and that is hypoglossal now guys i want you guys to really keep straight nine is called glossopharyngeal what is 12 12 is going to be hypoglossal i used to get that confused in medical school but remember nine glossopharyngeal palatal tone afferent limb of the baroreceptor whereas 12 that is going to be your hypoglossal motor to the tongue and if you have a damage to right cranial nerve 12 you're going to have tongue deviation toward the side of the lesion which is going to be towards the right all right speaking of cranial nerve palsies i'm going to be talking about multiple sclerosis now guys why are these two related well remember that when you have multiple sclerosis you get demyelination of what specific structure the medial longitudinal fasciculus and that mlf demyelination can lead you to intranuclear ophthalmoplesia but before we go into the nitty-gritty of ms let's go ahead and go through a important vignette 24 year old woman with multiple sclerosis has an mri that shows demyelination of the optic nerve on the left side on physical exam what will happen to both people when light hits not the left but the right pupil what do you think will happen to the pupils if you shine the light given this pathology in the right eye and that is going to be both of them will constrict and why this is a very high yield question is because it tests your knowledge on the consensual pupillary reflex remember that if you in this patient ended up shining the light in the left eye neither pupil will constrict and the reason why is because you have demyelination of the optic nerve and your afferent limb of the cranial nerve reflex is actually going to be affected so the u.s emily point that i want you guys to recognize is that any young female with this focal neurological deficit think multiple sclerosis the other differentials are going to be psychiatry related questions and those are going to be things like your munchausen syndrome or your malingering so what we'll do is talk a little bit about the pupillary reflex and as you can see this gif you see light being shined into the eye the afferent limb being cranial nerve number two building on your knowledge we're going to notice that cranial nerve two is going to synapse in the pre-tactile nuclei in the midbrain subsequently you're going to have the edding or westfall send projections via cranial nerve number three to the ciliary ganglion and that is then going to cause you to have sphincter i the iris sphincter muscle constrict and that's why when you shine a light in the eye you are going to get pupillary constriction key thing for us to kind of integrate here is the fact that cranial nerve number two is the afferent limb the efferent limb is going to be oculomotor very important all right so now what i did was i essentially took the various vignettes related to multiple sclerosis and i put it on one slide for you guys let's go ahead and go through this afferent pupillary light reflex defect that is going to be optic neuritis which we talked about in our vignette the high yield pathology here is the fact that you don't have good cranial nerve number two they sometimes cause call this proper noun the marcus gun pupil you can also get color blindness when you have optic neuritis a patient who has inability to look medially upon contralateral gaze and that is going to be intranuclear ophthalmoplegia very important for us to know that ino is failure of the affected eye to adduct upon contralateral gaze failure of the affected eye to adduct upon contralateral gaze and this is damage to the mlf typically comes up on usmle questions i have a video on my youtube channel going through the specifics of intranuclear abdominoplesia i will be sending it in an email after this session but we really need to understand the neural tie-in when it comes to ino patient just diagnosed with multiple sclerosis who now is going to have a csf that is going to have oligoclonal banding as well as periventricular plaques that oligoclonal banding essentially is going to represent elevated igg in the csf what is multiple sclerosis it's a hypersensitivity reaction it's gonna autoimmune reaction and that can cause you to have the autoimmune products which are going to be immunoglobulins periventricular plaques that's going to be demyelination of the oligodendrocytes let's integrate some neuroanatomy here oligodendrocytes are going to myelinate the central nervous system whereas your schwann cells which are neural crest derived pay attention guys schwann cells are going to be myelinating your peripheral nervous system remember that guillain-barre syndrome is going to be demyelination of the peripheral nervous system whereas your multiple sclerosis is primarily demyelination of your central nervous system flexion of the neck causes increased shooting down the back pain this is going to be the limit sign of multiple sclerosis speaking of cns pathologies we're going to be covering dementia in for uh our next section after dementia we're going to go through neurocutaneous disorders brain tumors stroke and then we're done are you guys learning a lot from this webinar go ahead and type in yes into the chat box if you're learning a lot in this webinar absolutely i really appreciate you guys staying active and engaged all right let's go through this question right here a 40 year old woman presents with a skin rash she is noted by her family members to have increased episodes of disorientation exam is notable for a skin rash on the arms along within the buttocks region further history notes increased loose stools and bmi of 18 a little low the patient has poor performance on mental status examination which of the following is the most likely pathophysiologic mechanism behind the diagnosis go ahead and type in the chat a nutritional deficiency b age related changes c degeneration of the frontal and temporal regions or e neurocutaneous syndrome and if you put in a you're absolutely correct guys this is that whole point that i was making about recognizing the triad this is going to be a niacin deficiency causing pellagra and so remember in pellagra you get dermatitis you get the diarrhea and you're going to get the dementia and again this brings me back to that triad component you have to think like the test maker loose stools that's the diarrhea when i talked a little bit about the skin rash that is going to be related to the dermatitis and the disorientation related to the dementia let's go ahead and integrate some biochemistry here what is the amino acid precursor to niacin which is vitamin b3 what is the amino acid precursor and if you typed in tryptophan you are absolutely correct very good so we're going to be in the next few slides comparing and contrasting different types of dementia and we're going to be doing it again in a vignette style manner i want to be very applicable for your usmle here so alzheimer's dementia typically presents with the male who forgets activities of daily living but has a relatively normal physical exam this decline in activities of daily living is an important trigger point or something for you to pick up in not only your psychiatry questions but in patients who have alzheimer's dementia they may not be able to balance their checkbook they may be lost when they're going to the grocery store leave the hot stove on etc from a microscopic pathology standpoint you see neurofibrillary tangles and a beta plaques in alzheimer's dementia the neurofibrillary tangles are going to represent a hyperphosphorylated tau protein alzheimer's patients are going to have this correlation with amyloid precursor protein and if you have increased amyloid precursor protein you may have an increased propensity especially if you have a ap apoe4 mutation you have an increased propensity to accumulate a beta plaques one high yield distinction here is that patients with trisomy 21 have three copies of app and thus they are going to be prone to earlier onset of alzheimer's now guys just for fun if i ask you what is going to be the heart lesion related to down syndrome you would say vsd asd and as well as endocardial cushion defects which essentially presents as bilateral regurgitation of your atrial ventricular vowels now frontotemporal dementia also presents with dementia however there is frontal lobe issues in the sense that you have executive function being compromised hypersexual patients aggressive behavior on brain brain imaging and gross pathology you have atrophy in the frontal and temporal lobe in fronto temporal dementia we also got pics dementia you're also going to see tau and this can be at times hereditary so why i put both of these on the same slide is they share that same relationship to the tao this one you gotta really recognize that they're going to be younger patients with that executive functioning being impaired let's now go ahead and compare and contrast lewy body dementia with parkinson's disease as you can see the similarity is that both of these have this alpha synuclein protein related to it in lewy body dementia you're going to have that younger patient who has parkinsonian-like features as you can see here however these visual hallucinations and these visual hallucinations on your usmle they can even put vivid dreams or sensitivity to neuroleptics or anesthesia these patients have issues with rem and sleeping so they have this waxing and waning consciousness patients with lewy body dementia are going to have subcortical inclusions of alpha-synuclein whereas patients with parkinson's disease are going to have those deep inclusions now how do parkinson's patients present very high yield slowing movements gait instability this rigidity they have this resting tremor and remember the pathophysiology here is the loss of dopamine in the substantia [ __ ] when you have loss of dopamine in the substantia [ __ ] you are going to have decreased nigrostriatal pathway activity as well as decreased basal ganglia transmission so your direct pathway of basal ganglia is not going to be as active and remember that in essence parkinson's disease is what we call a hypokinetic disorder lack of direct pathway you have relative hypokinesis let's go ahead and recognize that on the usmle there are various questions related to dopamine and i'm going to do my best right now to go through these three major neural anatomy pathways you have three pathways that the usmla likes to test about the mesolimbic pathway the nigrostriatal and the tubular infundibular why we went into this a little bit um in detail is the fact that the nigrostriatal is related to your parkinson's disease when you're talking about mesolimbic the mesolimbic pathway is going to regulate behavior so abnormalities in this pathway are going to be related to questions of schizophrenia as well as psychosis when you're thinking about the nigro striatal pathway you're going to be thinking about parkinson's but remember that you can have a copper buildup in the basal ganglia and that's known as your wilson's disease remember they have parkinsonian features as well as if it's a young patient with those visual hallucinations think about lewy body dementia finally you are going to be thinking about the tubulo-infundibular pathway of dopamine and that is this physiologic correlate that dopamine is going to actually inhibit prolactin such that if you have a loss of the tubular infundibular pathway you have less dopamine and thus you have increased amounts of prolactin where does the usmle like to go for this well patients who are on antipsychotics remember as a class effect antipsychotics mechanism of action d2 antagonism and that d2 antagonism say that these patients are for example respirator can cause you to inhibit dopamine thus increase prolactin what is another gi pharmacological agent that can cause d2 antagonism and that is going to be metaclopramide so this is what we call secondary causes of hyperprolactinemia in the sense that this is medication-induced hyperprolactinemia very good all right let's go ahead and go into this test question and guys stick with me we don't have that much uh many topics left please make sure you're staying active and engaged 48 year old male is found by law enforcement homeless on the street he has multiple domestic violence issues his family is contact and it says that he has been very threatening over the past few months and the patient during the interview is noted to be inappropriately smiling and moving his arms in an uncontrollable manner his paternal uncle had some neural issues and passed away in middle age what brain structure may be affected in this patient go ahead and type in the chat what do you think is going to be the brain structure affected and that is going to be atrophy of the caudate you're absolutely correct this is huntington's disease and as you note that caudate atrophy is going to be seen right at that ventricular region what is the genetic inheritance pattern of huntington's disease that is going to be a pattern related to the concept of anticipation in which you have this trinucleotide cag repeat and as you end up going from generation to generation to generation the disease shows up earlier earlier earlier and what i just defined was anticipation and that progression of the trinucleotide repeats what chromosome is going to be affected go ahead and put that in the chat box that is going to be you're absolutely correct if you put in cranial nerve number four you got it all right guys time to integrate the various amounts of trinucleotide repeats so go ahead and type in the chat what are going to be the various trinucleotide repeats huntington's disease we talked about the arm frailing flailing the writhing body movements that's going to be related to your cag repeats what about this one friedrich's ataxia in which you have a 15 year old male broad-based gait diabetes scoliosis and the patient has loss of sensation in his feet what is going to be that trinucleotide you're absolutely correct gaa and what's the cardiology tie-in guys hypertrophic cardiomyopathy you're absolutely correct myotonic dystrophy 30 year old male has been noted to be off balance has alopecia but also this failure to relax after shaking the doctor's hand myotonic high tone ctg with myotonic dystrophy and then fragile x syndrome in which you have a patient on your usmle with intellectual disability big years on the exam gonadal enlargement you're going to be thinking about your cgg repeats and the way that i like to think of it is take the g's make it into ears and then the c ends up being your large uh gonad all right excellent very good we're going to be talking about neurocutaneous disorders next a two-year-old patient presents with episodes concerning for seizure on exam her skin is noted to have small flesh-colored acne-like lesions wood lamps exam shows hypopigmented lesions on the trunk and extremities a murmur is heard which of the following echocardiographic findings would be most likely seen in this patient a regurgitation of the aortic valve b pulmonary valve stenosis c mitral regurgitation or d mitral valve prolapse go ahead and type into the chat what do you think this patient is likely going to have on echo and if you typed in the answer c you're absolutely correct what do you think is the diagnosis here this is going to be tuberous sclerosis and what i'm going for here is the cardiac rhabdomyomas so guys what i did here is i made it like an icu physician going through all of the systems again these multi-system pathologies for your us mla things like down syndrome cystic fibrosis tuberous sclerosis neurofibromatosis when they have many different systems involved you gotta recognize the word syndrome or a systemic condition many of you already know that test taking strategy for my strategies master class but what's important for us to do is integrate the various different organ systems that are affected in these syndromic pathologies so when you're talking about the cns manifestations these patients have these infantile spasms typically seen in children as well as the subopenable astrocytomas what about the heart manifestations well that's what i was going for the cardiac rhabdomyomas and this can present as a atrial mass that can cause a abrupt mid diastolic murmur what about the kidney manifestations of tuberous sclerosis that's going to be your renal angiomyolipomine why i put this picture in here guys is they can give you a histology slide that says okay recognize fat recognize the small blood vessels and recognize muscle as well angio blood vessel myo muscle lipoma fat and the skin lesions that i'm going for are the ash leaf spots those are hypo pigmented shag green patches which are going to be a leathery type consistency as well as hamartomas and so here is a classic example of your hypo pigmented ash leaf spots let's compare and contrast that with neurofibromatosis so with neurofibromatosis the cns lesion is going to be seizures as well as ninjaomas typically with nf2 you're going to get meningiomas these characteristic eye lesions that's going to be your lish nodules you can also get optic nerve glioma and we talked about that in the cranial nerve pathologies the other one is going to be in neurofibromatosis ii the acoustic neuromas and what cranial nerve is that going to affect cranial nerve eight and remember that cranial nerve eight not only is gonna have the cochlear uh component but the vestibular component if that is damaged you're going to get that vertigo which is that uh spinning of the room typically you see it in like questions related to meniere's disease and then finally the skin manifestations are a little bit different because these are going to be hyper pigmented patches and those are going to be your cafe olay spots all right so miscellaneous neurocutaneous syndromes think about sturge weber syndrome the characteristic rash here is that port wine stain which is called nevis flemis that's going to be in the trigeminal distribution in this case you see it in the v2 distribution the tram track calcifications you're going to see on skull x-ray these are buzz words related to sturge weber syndrome what about this one flank pain hematuria you're also going to have field chromocytomas angiomatosis of the cerebellum as well as even the retina which one is that going to be that's going to be your von hipalindao syndrome you're absolutely correct and then these small little vascular lesions on the face it could be in the cerebellum that's related to ataxia telangiectasia and ataxia telangiectasia is a neurocutaneous syndrome that watch has a immunodeficiency related to it and that is going to be the iga deficiency which presents on your usmle as multiple cyanopulmonary infections i think this is a very high yield pathophysiologic mechanism that they go for and that is that defective double-stranded dna break repair mutation that leads to ataxia telangiectasia all right guys two more topics we're going to be talking about brain tumors and then we're going to be finishing off with strokes let's go ahead and talk a little bit about brain tumors and the way that i break them up is adult and pediatric brain tumors and adult tumors are going to be supratentorial whereas pediatric tumors are going to be infra tentorium that is going to be in relationship to the tentorium cerebelli adult brain tumors you can think of the mnemonic mgm studios metastasis which is one of the most common oncological lesions to the brain glioblastoma meningioma and schwannoma mgm studios in childhood tumors you can think of astrocytoma medulloblastoma and ependymoma think about the mnemonic animal kingdom magic kingdom and epcot in the subsequent slides we are going to be going through a rapid review of these various brain tumors what's very important for us to recognize though is the test question in which a patient has a history of skin cancer and then they give you an imaging of multi-focal brain lesions and that is going to be very characteristic of metastatic melanoma to the brain very high yield all right let's go ahead and do a brain tumor rapid review stay engaged to your chat box here g fat positive cells plus rosenthal fibers plus a cystic solid component mass that is infratentorial so it's going to be a pediatric mass primarily you're going to be thinking of the pilocytic astrocytoma you're absolutely correct next one p-net positive cells a cystic mass at the cerebellar vermus drop metastases so it affects the spinal cord and the homer right rosettes that's going to be medulloblastoma the mnemonic that i use is think about homer simpson chugging a lot of meds so medulloblastoma but what's characteristic is that these can cause you to have spinal cord lesions and so patients can present with for example wobbly gait on your exam a rapidly progressive mass plus midline crossing on mri and pseudo-palliating tumor cells this is a very aggressive tumor and you're absolutely correct glioblastoma multi-form this is actually a high-grade astrocytoma middle-aged female plus new onset seizures and an er positive which is estrogen receptor positive brain mass and characteristics samoa bodies you're absolutely correct think about your meningiomas very good so what we're going to do is we're going to go ahead and integrate samoa bodies for the us emily and why i did that was because meningiomas have soma bodies now everybody take your finger and go ahead and recognize that this finger is also known as a papillary structure right papillary means finger and so what you'll do is start making the concentric world like mass which is known as that samoa body so i always think of papillary tumors such as papillary thyroid carcinoma which has the characteristic orphan antinuclei papillary cyst adenocarcinoma which is a surface epithelial tumor you can see that in females it presents with the abdominal fullness the omental caking it's an aggressive ovarian tumor and then take your fingers and start eating m m's finger papillary okay here we go meningioma and mesothelioma those are your m ms mesothelioma remember it's related to asbestos it's what we call a pneumoconiosis and you get these hemorrhagic pleural effusions very interesting enough also has some momo bodies but what i want you to recognize is that samoa bodies not only are these lamellar concentric lesions but they have central calcification and this is an example just to integrate some gen path of dystrophic calcification and what is dystrophic calcification guys well it's basically going to be calcification that is going to occur in the setting of normal calcium levels calcium that deposits in the tissues you see that also in various uh different pathologies such as aortic stenosis laid onset but you can also see it in the samoa bodies all right guys last concept of the day go ahead and type in yes into the chat box if you're ready let's go ahead and get pumped for this very high yield difficult but very very integrative concept and that is going to be strokes very good so here is my big picture test taking approach to stroke questions and that is understanding important principles number one you need to in your test question isolate a focal neurological deficit whenever you see focal neurological deficit you should think about stroke now strokes have ischemic and hemorrhagic subdivisions we talked about hemorrhagic subdivisions when we talked about for example subarachnoid hemorrhages when we talked about hematomas starting this session but when you're talking about ischemic strokes usmle likes for you to note that various vessels that can be involved so my general principle for stroke usmle questions is first off isolate the sensory and motor dysfunction if you have sensory and motor dysfunction you're going to be thinking of a large vessel stroke and that is going to be primarily your anterior cerebral your middle cerebral posterior cerebral remember they present with sensory and motor dysfunction the other thing for us to recognize is that innervation is contralateral so a right-sided brain lesion is going to cause us to have sensory motor deficits on the left side and vice versa and then finally we need to relate everything to the homunculus and remember the homunculus has a unique organization and that is that the lateral brain is going to be your mca distribution and that's going to be your arms and face and then the inside medial portion of your brain that's going to be your anterior cerebral artery and that's going to be the trunk and lower extremities so always watch for these three components sensory and motor deficits innervation is contralateral relate to the homunculus so let's put it to practice here 80-year-old male presents with left-sided numbness the patient also has weakness as well so as you can see sensory motor deficits the patient is noted to have prominent left arm weakness more than the leg so it's upper extremity patient has sensory deficits in the left arm visual fields are normal and mri is notable for an ischemic stroke which of the following vascular structures may be affected in this patient so we recognize that this is the left-sided lesion so likely the answer is going to be something right-sided we note that the patient has arm weakness and that's going to relate to what side of the homunculus well that's going to be your mca territory because it's the arms and their sensory and motor deficits so the answer is going to be b which is going to be the right mca again the three steps sensory motor relate to homunculus and contralateral innervation so strokes for the usmle let's just put it all together anterior cerebral artery you're going to get sensory motor deficits in this stroke and you are going to get sensory motor deficits in the lower limb anterior cerebral remember the homunculus the middle cerebral artery it's a little bit unique in the sense that yes we talked about it in the test question sensory and motor loss of the upper limb and face because that's going to be the outside homunculus however what's important is that if you have a non-dominant and typically that is going to be your right-sided mca your right mca that's in majority of patients your right mca then you can get this contralateral hemi neglect syndrome in which the patient only recognizes one side of the world if you have a dominant mca i.e usually a left mca stroke you're going to be thinking about either a broca's or a wernicke's aphasia so make sure that not only you recognize the sensory motor of the upper limb and face but you also integrate whether it's right or left based on your non uh your contralateral hemi neglect as well as your warranties or broca's and then finally pca aneurysm or pca stroke excuse me are going to have those visual defects and because it is post-optic chiasm it's going to be a homonymous hemianopsia with the macular sparing all right last question of the day let's go ahead and go through this which of the following arteries may be affected in this patient 40 year old male presents with vertebral trauma he is noted to have right-sided facial numbness exam is notable for hoarseness there is reduced sensation to pain and temperature on the right side of the face as well as the left side of the body so now do you see how confusing it can get just keep it straight contra face or sorry ipsy face excuse me and contra body loss of pain and temperature the patient is also noted to have ataxia which of the following arteries may be affected in this patient so if you are going to recognize this stroke is going to have that hoarseness that really gives away the answer and this is most likely going to be a posterior inferior cerebellar artery stroke pica so the mnemonic that i like to chant to myself is don't pike a horse pick a horse that can't swallow so you're going to have issues with swallowing and hoarseness going into this when you talk about ica and pica strokes pica which is a posterior inferior cerebellar artery that comes off of the vertebral there's an anatomy tie in and it supplies the lateral portions of the medulla you get the dysphagia the hoarseness the decreased gag so cranial nine and ten are infected whereas ica that's going to be related to lateral pons and ica strokes have the facial droop so when you see facial droop icah is pooped facial droop aika is poop but what's high yield for us to recognize guys is that usually ica and picostrokes on your u.s emily are going to have contra body ipsy face both of them look at this loss of pain and temperature whenever you see loss of pain and temperature in the face and then the contra side of the body you can think of a pica like a stroke watch for your horner syndrome as well as ataxia related to both of these strokes all right i want to close with an important study tip and that is a question which i always get asked by students and that is how do you how do you go through neuroanatomy and one of the key things that i will tell you is that in order for you to master neuroanatomy i would encourage you to use the pathologies to dive into the normal anatomy for example in ceringomyolia you can then go in and learn about the spinothalamic tract which does pain and temperature if you're talking about lou gehrig's disease or amylotrophic lateral sclerosis you can then go in and talk about upper motor neurons and corticospinal tract or b12 deficiency you're going to integrate dorsal column medial lumbnesses use that pathology and then go back into the regular neural anatomy all right guys well that is the end of our session today please stick around for some important important announcements that are coming up and that is the fact that i have my unique usmle courses number one that's my test taking strategies and rapid review course many students have already enrolled in this but i go through how do i go through a block how do i go through a question how do you attack different types of questions very innovative it also covers the highest yield concepts from first aid and this is a great great way for you to get that one-on-one private tutoring experience along with a quick review to get that nvme score up because it synthesizes many of the high-yield concepts just like this webinar i also want you all to recognize and make sure you mark down that in a few months i will be having a very unique rapid review pharmacology course that is going to be coming out i will send you all the details but i'm very excited to work on this and have you join that webinar if you are interested i also have a usmle study schedule and productivity system i have that on notion which is a very awesome scheduling platform many students already are using this for dedicated study and i offer one-on-one uh tutoring at a very limited availability but if you are interested feel free to uh email me i think most importantly for many of you there are two free resources that i want you guys to make sure you capitalize on that is number one my first aid outline which goes through the highest yield concepts related to each system so for example biochemistry you'll go into it in an organ system manner same thing with microbiology and you're going to have my golian style course which has my old nvme top concepts and my classroom lectures most importantly i want you all to connect with me email me tag me on instagram facebook i'm also on reddit i really enjoy helping students for step one step two ck so i'm very excited that you all join um today i do want to end before you leave if you can type in one thing that you learned in this webinar go ahead and type that into your chat box and most importantly finally if you have any questions i'm going to be doing a live q a both on youtube as well as on the zoom thank you guys so much we had so many people look at this excellent people who are doing uh the pica horsenet