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Neuro-Ophthalmology: Overview

Oct 09 | 1:30 PM

Here, we are with the very first session in 'Neurology Concepts' club. Dr. Sreenivas Sirugudi's goal with this session is to shed light on several interesting concepts in neuro-ophthalmology, as well as some common disorders associated with it and their management procedures. Let's get some wonderful facts!

[Music] uh i'm dr naveda from netflix and on behalf of team netflix i welcome you all to today's session we have with us dr srinivas who is a professor of medicine and consultant neurologist at gsl medical college andhra pradesh hey very good evening everyone i'm dr lalit it takes pleasure in inviting dr sheen wasser for this evening talk on neuro ophthalmology which happens to be a very important topic and very difficult topic for all the post graduates to understand this neuro ophthalmology topic is very fascinating to read and understand so today our guest speaker dr sirikura sinwasa who happens to be an author of the book focused neurology has his own youtube channel which is dr srinivas medical concepts which has more than 5 300 subscribers and more than 220 youtube videos uh which helps all the postgraduates to gain knowledge during this covered error he is very passionate teacher and always enthusiastic to help the students in making these difficult concepts easy and joy to understand so let's not waste our time and let's dive into the topic right away so i'll welcome dr sheen wasser to start the today's session yeah thanks a lot uh dr lalit for that wonderful introduction and i thank netflix especially dr nivedita for her kind words and a nice introduction it's always a pleasure to address students and i think this is one of the best platforms to address students across the country i'm dr srinivas i'm a neurologist consultant neurologist from rajmandri andhra pradesh india [Music] this is my email 3k lpm at gmail.com and as the resident has already introduced i have my own youtube channel a doctor's universe medical concepts with more than 35 300 plus subscribers and 200 plus neurologists almost all the topics of neurology i've covered and i i continue adding up the topics every week and this is i think one of the platforms because i can address a lot of students across the country and again from the bottom of my heart i thank netflix and dr niverita for giving me such an excellent opportunity yeah we started a neurology concepts club and i think this is the first episode of this neurology concepts club these have been my various illustrations and i'm very happy to see that i'm the medical author of the book focused neurology and when the netflix have asked me to give a talk on neuro of talonology i thought the best way to about such a vast exciting and challenging subspecialty of neurology the neuro of talmud is to go by a question and answer format so i've carefully selected some of the very fascinating but at the same time challenging concepts and i put it in a question and answer format so that it'll be very easy for the students to understand so it'll be a question and answer format i'll be asking questions and i'll give the explanations wherever necessary with diagrams yeah i think this is probably one of the most important questions a very practical question across all specialties medical nursing dental physiotherapy lab everybody who will be seeing patients and especially residents who are in the critical care medicine because they'll be dealing with comatose patients the question is why pupils are dilated after death why pupils are dilated after death we all know that the parasympathetic causes the constriction of the pupil and sympathetic causes the direction of the people so after death when both get affected people should be in the mid position but what we see in our clinical practice is that pupils are dilated fixed and not reacting to light how come they are not in the mid position and what is the mechanisms for they being dilated parasympathetic causes constriction of the pupil and sympathetic causes dilatation of the pupil but but parasympathetic has got more control over the people than sympathetic hence after death the predominant parasympathetic control over the pupil is lost and pupil therefore cannot constrict and starts getting directed so the explanation is that parasympathetic has got more control over the pupil though parasympathetic and sympathetic supply the pupil it is the parasympathetic which has got more control over the pupil and therefore after death it is a predominant action of the parasympathetic which gets affected so the action of parasympathetic is to cause constriction of the people and therefore when it gets affected the people will start dilating and therefore people is dilated fixed and not reacting to light the second question what is doll's eye movement and the mnemonic cows c-o-w-s called for opposite and warm for sale this is for nystagmus there have been any number of books lot of books talking about doll's eye movement but we read and then within few minutes we get confused and we are again beating around the bush trying to find out the exact answer it's a very interesting phenomenon very exciting challenging but unless you know the mechanism you will not appreciate the joy of clinical neurology especially doll's eye movement so this is the caloric reflex you put warm water cold opposite warm same so when you put warm water the moment is the nystagmus towards the same side when you put cold water the nystagmus is towards the opposite side yeah but to understand this to understand this we need to understand this psychotic pathway the horizontal eye movements and the vertical eye movements we can move eyes up and down these are known as vertical eye movements the center is in the midbrain we can move eyes horizontally towards right or towards left horizontally these are known as horizontal eye movements the center is in the pawns the horizontal eye movements again there are two types one is the psychotic pathway the quick moment second is the slow following moment pursuit moment so the center for horizontal moments is the pawns and horizontal eye movements there are two components one is the quick fast movement saccadic movement and second is the slow following moment which is known as pursuit moment i'll give you an example i am just addressing the crowd but someone knocks at the door i immediately turn to see who's knocking at the door this quick fast reflexive movement is known as success the second is that i see a nice shuttle match going between the badminton indian superstar sindhu and another world champion so i see the shuttle moving from one side of the court to the other side of code so it's a moving object and i try to look at that moving object so the moving object i keep trying to follow it so these slow following movements are known as pursuit time moments so horizontal line means we have two components the quick fast movement seconds and the second slow following moments which are known as pursuit movements whatever may be the component whether it is a saccadic moment or a perceived movement you can see in the diagram the center is the pprf para median pontain reticular formation the pprf is in the pons it is connected to the sixth now lateral rectus on one side the same side and it is connected to the medial rectus through mlf on the opposite side so what is the function of the pprf the pprf pulls the eyes towards its side the pprf paramedian content reticular formation will pull the eyes towards its side so you can see the sakatic pathway it's originating from the front line fields area number eight descending in the midbrain and at the level of the pawns it is crossing over and going to the opposite side going to the ppr for example my front line feels area number eight the psychotic pathway starts it comes down midbrain ponds at the level of the rostral part of the pawns it crosses over and goes to the pprf so pprf connects the sixth nerve lateral rectus on the same side and medial electrodes through mlf on the opposite side it pulls ice towards its side so when this front line feels area number eight is stimulated eyes will move towards the opposite side to the connections of ppr this is the psychedelic pathway the pursuit pathway comes from the parietal lobe ipsilaterally psychotic pathway contralateral whereas spirit loop ipsilaterally goes and connects to the pprf on the same side and pulls eyes towards its side slowly so these are the pursuit moments you can appreciate this in a phenomenon known as optokinetic nystagmus where you have a rotating drum and keep rotating it so persons follows it perceived moments quick corrective circuits pursue movements quick corrective seconds so horizontal line movements there are two types one the fast psychotic movement and second is the slow pursuit women's eye moments all right so the center for all horizontal moments is the pons the ppr paramedian content reticular formation the center for vertical eye movements is the midbrain we have up gaze we have downgas i look upwards i look downwards the upgas fibers cross over and then descend whereas downgrades fibers descend straight away so any lesion impinging on the top of the midbrain rostral part of the midbrain will affect the crossing of gaze fibers and therefore they cannot look upwards they'll be looking downwards classic example is hydrocephalus the sunset sign right now if you see in this diagram carefully we have two pathways one coming from the frontal line fields area number eight coming down going to the opposite side connecting to the pprf pprf connects the lateral rectus and the medial rectus to the opposite side and pulls the eyes towards inside so front line fields area number eight if it is stimulated eyes will go to the opposite side likewise we have the vestibular apparatus eighth now that is also connected to the pprf on the opposite side and this will also push the eyes to the opposite side very interesting very important the front line fields area number eight is connected to the pprf on the opposite side the vestibular nucleus is also connected to the pprf on the opposite side so both the frontline fields area number eight and the vestibular complex their primary function is to push the eyes to the opposite side by stimulating the pprf on the opposite side the only difference is that the front life is the second path will push the eyes in a fast manner whereas vestibular paths will push the eyes in this slow manner right this is the basic pathophysiology if you have understood this understanding oculocatholic reflex or doll's eye movement becomes very very easy but what is this doll's eye moment we as children would have played with the doll when we turn the head to the left side of the doll the ice goes to the right side when we turn the head to the right side the eyes goes to the left side and we when we turn the head upwards the eyes go down and when we turn when we put the head down the eyes goes up this is known as doll's eye movement or oculoplast which we've seen as children playing with the dot exactly same mechanism applies here when i turn my head to the one side this vestibular apparatus will get stimulated and vestibular apparatus is connected to the pprf on the opposite side so it will push the eyes to the opposite side that's the beauty of technical neurology so when you turn the head to one side you are stimulating the vestibular apparatus and you are pushing the eyes to the opposite side so when i turn the head to one side eyes go to the opposite side this is doll's eye movement the vestibular apparatus can be also stimulated by pouring warm water so the western law apparatus can be stimulated by two mechanisms one turning the head to the side of the vestibular apaches second by pouring warm water so when we pour warm water or when we turn the head to one side the vestibular apparatus will get stimulated and it will push the eyes to the opposite side this is this is the vestibular stimulation so oculopolic reference turning it one side eyes go to the opposite side by pouring warm water but body always tries to maintain homeostasis it tries to put everything back to normalcy so when i turn my head to one side or warm water and when i stimulate the vegetable apatos and eyes go to the opposite side body and the brain the nature tries to put ice back towards its normal position to drift it back so how does it drift back this frontal i feels area number eight will try to push it back to normalcy so you get nystagmus so when you turn your head to one side of your cataphalic reflex or doll's eye movement or poor warm water on one side eyes will go to the opposite side but front life is area number eight now will try to push the eyes to normal sales so you get the fast component mystagnus so when you put warm water the nystagmus is towards the same side ws cows this is the explanation for ws when you put warm water eyes go to the opposite side but nystagmus is towards the same side warm same side steps exactly opposite things occur when you put cold water when you put cold water you are inhibiting the vestibular practice when you put cold water you are inhibiting the vestibular apparatus so this vestibular apoptosis will over act and will push the eyes towards the opposite side but again body tries to compensate and tries to put it back to normalcy so this time this front line fields area number eight will try to push the eyes to the opposite side so you get unstackedness so when you put cold water this will override eyes will move towards the side of the lesion and the mistakens will be towards the opposite side so cold opposite warm same so this is the explanation when you put cold water the nystagmus is towards the opposite side when you put warm water the nystagmus is towards the same side why is this so important why is this so fascinating and how is it related to clinical neurology and clinical medicine many important points you can pick up and interpret one the eyes move to the opposite side by connecting the lateral rectus and through mlf medial vectors so when you put warm water and when you see the eye movement going to the opposite side that indicates the brain stem pathways are intact that indicates the brain stem pathways are intact the medial rectus mlf and the lateral vectors are intact so eyes are going to the opposite side so when a slow movement occurs in a good manner that means brain stem is intact and when you see that compensatory nystagmus coming that means frontal life is area number eight is intact so by just looking at this doll's eye moment or oculopolic reflex we get a wealth of information you see the nice horizontal slow moment brain stem is intact you see the nice compensatory nystagmus front line fields area number eight is intact so if the frontal cortex is affected it could be because of hypoxemia or any metabolic encephalopathy we don't see that compensatory nystagmus so if nystagmus is not found that means the frontal lobe is affected and if the slow eye movement is not seen that means brainstem is affected so we can see whether the brainstem is intact or the frontal lobe is intact or not by this moment this is known as the dolce moment or reflex so so what is this primarily when you turn the head to one side eyes goes to the opposite side [Music] then the residents may ask me a question when we turn the head to the opposite to one side you said the eyes go to the opposite side but here i am i turn my head to one side and i can push also my eyes also to the to the side where i have turned my head i can turn my head to one side and and my eyes also to the same side as i have turned my head but then the book says when you turn the head to one side ice goes to the opposite side what is this contradiction absolutely genuine doubt absolutely genuine joke when you turn the head to one side eyes have to go to the opposite side but but as long as you are conscious you're inhibiting this reflex and therefore it is up to you to look wherever you want you are conscious you can look to left side you can look to the right side up and down so as long as you are conscious you can look wherever you want this reflex becomes manifest as the conscious level comes down as the conscious level comes down this reflex manifests so this reflex is a normal reflex well seen in persons who are comatose in the comatose patient when you turn the head to one side eyes have to go to the opposite side it's a normal mechanism so in a comatose patient when you turn the head to one side eyes have to go to the opposite side it's a normal phenomenon when you turn the head to one side if the eyes do not go to the other side that means the brainstem is affected and if you turn the head to one side eyes go but there is no compensating nystagmus that means frontal lobe is affected so pprf connects to the sixth nerve nucleus which has got intra neurons connecting the lateral rectus and interneurons connecting the medial vectors through mlf another important point here to be noted is that you have pprf and the sixth node nucleate the pprf even if it is affected it can be overcome by stimulation where a sixth known nucleus cannot be overcome by stimulation so this is cause cold opposite warm shape when you put warm water eyes go eyes are drifted to the opposite side and nystagmus is to the same side so warm water same same when you put cold water you are inhibiting the rest of that pattern so this vestibular apparatus will over act eyes will move towards this side and the mistakens will be beating towards the opposite side so cold opposite warm same so with this reflex with this mechanism you get so much of information and one more important point is that by just looking at the gaze you can say whether the frontal lobe is involved or the pawns is involved i said frontal i feels area number eight will push the eyes to the opposite side known as saccadic pathway so the front line wheels area number eight is affected it cannot push the eyes to the opposite side eyes will move towards the same side and hemiplegia will be on the opposite side because corticospinal tract descends from the frontal lobe mid brain pawns at the level of the medulla crosses over to the opposite side so in a frontal lobe lesion since it cannot push the eyes to the opposite side the psychotic pathway is affected eyes will move towards the side of the lesion and hemiplegia is on the opposite side so i is looking to one side hemiplegia on the opposite side is a frontal location suppose if it is a pontine lesion it cannot pull the eyes towards each side so eyes will go to the opposite side and hemiplegia is also on the opposite side because corticospinal tract distance in the pond at the level of the medulla oblongate crosses over and goes to the opposite side so in a continuation eyes will look towards the side of hemiplegia whereas in a frontal location eyes will look to one side and it is on the opposite side so cows oculopolic reflex vestibulochlor reflex doll's eye movement very very important it gives you a wealth of information yeah the next question explain the maxim frontal lobe lesions causes eye to look to the same side and hemiparesis on the opposite side whereas quantile lesion causes the eyes to look to the same side of hemi parishes so these are the various eye signs but we'll now confine ourselves to the frontal lobe and the pawns this is the pathway i have really simplified it now you can see the frontal lobe on one side and the vestibular apparatus on the same side so frontal lobe also goes and connects the pprf the eighth note nucleus also goes and connects the pprf i request your kind attention to look at the diagram because if you have understood this diagram understanding this oculophilic reflex becomes very very easy interesting and exciting so the pprf is connected by both the front life fields area number eight as well as the vestibular apparatus but the connection from the frontal lobe to the pprf is very fast if you push the eyes in a fast manner to the opposite side known as saccadic pathway whereas the vestibular pattern is connected to the pprf though it pushes the eyes to the opposite side it's in a slow manner and you can see the corticosteroid coming from the frontal lobe descending in the midbrain pawns crossing at the level of the middle oblater going on the opposite side i have abbreviated it as cst corticospinal trauma so when the frontal lobe is affected it cannot push the eyes to the opposite side eyes will look to the same side of the lesion but corticospinal tract is affected and medullo oblongata crosses over to the opposite side so hemiplegia is on the opposite side so i is looking to one side hemiplegia on the opposite side is a frontal lobe lesion whereas you can see the ppr here para median pontine reticular formation it cannot pull the eyes towards its side so eyes will go to the opposite side hemiplegia is also on the opposite side so i is looking to the side of hemiplegia is a quantization eye is looking to one side and hemiplegia on the opposite side is a frontal location so the frontal lobe as well as vestibular factors both are connected to the pprf on the opposite side but frontal lobe acts in a fast manner pushes the eyes in a fast manner waste of blood apparatus pushes the eyes in a slow manner right very very interesting it is one of my favorite topic what is alexia without a graph here question number four what is alexia without a graphic alexia is difficulty in reading a graphic means difficulty in writing alexia means difficulty in reading a graphic means difficulty in writing so these are the persons who have difficulty in reading but they don't have any difficulty in writing this is what it means alexia without a graphic the best example is ask a person to write his name say mr x he writes his name mr rex and ask him to read he cannot read he has just written his name with his own hands the own handwriting with his own interpretation but what he has just written himself with his own handwriting he is not able to read so alexia without a graphic there is no difficulty in writing but there's difficulty in reading reading requires oxford look connections with the language area oxford low connections with the language area but for writing it does not need occipital lobe even blind persons can write so alexia without a graph here to understand this we need to understand one very very important principle the principle is the dominant cortex and language area so what is this dominant cortex and language area right-handed persons right-handed persons more than 90 percent of the right-handed persons the speech area is situated on the left side what we call this dominant cortex more than 90 percent of the people the speech centers are situated on the left side what we call this dominant cortex dominant cortex is that context where the speech centers are situated for left hand is also most of the time it is on the left but sometimes it is on the right so most of the time the speech centers are situated on the left side what we call this dominant cortex right okay now we have visual fields the right visual field and the left visual field suppose i look to one side right side this is the mirror image so it will appear in an opposite manner so when you look to the right side it goes to my left hospital cortex but my language areas are also on the left side so whatever i look on to the right side i can easily convert it into a language form say i would like to say your address is very good your attire is very good on a person who is standing on my right side i can see that and convert it into visual form easily because he is on the right side it goes to my left opposite cortex my language area is also on the left side so whatever i see i can convert it into a language form easily now imagine on the opposite side someone is standing on this side i want to say the same thing your dress is good but then this time it's on the left side so it goes to my right hospital cortex it goes to my right toxic cortex but where is my language areas my language areas is on the left side so it cannot access easily to go from the right occipital cortex to the language areas which are on the left side it needs a bridge to transfer information from the right side to the left side which is known as corpus callosum corpus callosum is the bridge inter hemispheric inter hemispheric connections which connect the right to the left side so whatever i see on the left side goes to my right hospital cortex unless the corpus callosum is intact i cannot convert it to a language form so if there's a lesion in the corpus callosum though i perceive well in the occipital cortex i cannot transfer it to my language areas on the left side so i will not be able to convert it to a language form so very easy on the right side it goes to my left top study cortex language area is also on the website i can easily convert it into a language form whatever i see but on the left side it goes to my right documentary context to assess the language areas which are on the left side it needs time it has to go to the corpus callosum and then access and if there's a lesion the corpus callosum it cannot access so in a person who has got left posterior cerebral artery lesion the left oxide cortex and the sphenium of the corpus callosum is affected since the left oxford cortex is affected he has no other growth and to use only the right oxygen cortex but then the information cannot be transferred to the language areas on the left side because the sphenium of the corpus callosum is also affected in the left posted several arterial part and therefore he cannot read so he has got difficulty in reading writing he has no problem because whatever i say it goes to my auditory practice to the wernicke's area parkway for cyclists and then it goes to the broca's area into the motor cortex corticospinal tract on the opposite side it does not need oxidative cortex for writing it goes straight away to the language areas and the motor cortex and then i can write so writing does not need oxygen but even blind people can write so these are the people who have alexia without a graphic they don't have problems with writing but they have problems with reading this is known as alexia without a graph here the lesion is left posterior cerebral artery lesion which affects both the left hospital cortex and the speeding of the corpus callosum which conveys information from the right hospital context to the language areas on the left side so with interruption of the left visual cortex and the splenium of the intervening white matter the words perceived in the right visual cortex they cannot access to the language areas which is present on the left side and therefore patients cannot read so this is alexia without a graph here right now question number five what is process pattern is again very fascinating concept inability to identify known faces they cannot identify no faces they cannot identify their own friends he must have been the best of friends with another person but the moment he gets prospect nausea he cannot identify his own friend's face leave alone his own friend's face even when he stands in front of the mirror he cannot identify his own face this is known as prosuppagnosia but by the way he walks by the way he talks he can identify but per se he cannot identify the face it appears blurred to understand this again we need to understand another concept occipital temporal connections occipital parietal connections occipital temporal connections is to do with what what of vision what is the space what does this face look like so that is ospito temporal connections occipital parietal connections is to do with the spatial orientation where is he situated where is his face where where of vision goes to the connections and what of vision goes to the occipital temporal connections so in persons who have process diagnosis inability to identify face he cannot identify the individual person's face the lesion being in the hospital temporal cortex inability to identify known case occipital temporal cortex what is affected so he cannot identify the known phase whereas if occipital parental connections are affected the spatial orientation is affected the spatial orientation is affected and therefore he cannot integrate the center of the vision with the periphery of the vision which is known as a simultaneous nausea inability to integrate the center with the periphery of the vision if he looks at a particular area his eyes get fixed to a center point he cannot integrate the center with the peripheral of the vision so how do we test it we give big a's and small a's and ask the person to encircle a's the small a's will fall into his vision and therefore he'll he'll encircle it but when he looks at the big a it is spaced apart so he cannot integrate the center of the periphery of the vision so when he looks at the big he either looks at the horizontal line or oblique line and thinks it's not a and therefore he'll not encircle it so very fascinating he'll be inserting the small ace in fact encircling the biggest is easier as compared to smaller areas normally but here it's paradox at the other end of the spectrum is encircling small is but not big he is not able to integrate the center of the machine with the peripheral with the peripheral division this is one of the most common diagrams used to explain simultaneously so in this picture you can see many things happening one this lady washing dishes second you can see the boy picking up some vessels and the girl trying to help and the guy is about to fall so when i look i am normal person my oxford of parallel connections are intense so when i look at the picture i can say all these things are happening but when you ask a person who's got a oxytocin lesion and a simultaneous nausea it gets fixed on a particular point he'll either look at the boy and say the boy is falling and he'll not look at the woman or he may be looking at the woman and say is she's washing the vessels he cannot integrate the center of the periphery of the vision and look at its entirety he will miss the forest for the tree so that is a simultaneous museum so oxytocin temporary connections what operation is loss oxytoc parietal conditions where of the vision is lost right next question why pontine lesions causes bilateral small pupils whereas medullary regions causes unilateral small pupils to understand this we need to understand an important concept we have both the sympathetic tracts running in the brainstem midbrain pawns medulla oblongata side by side medulla oblongata is supplied by two vertebral arteries pons is supported by a single artery basilar artery and midbrain is supplied by the two posterior central arteries so midbrain is supplied by two cerebral arteries forcible arteries middle oblong it is supplied by two vertical lattice but pons is supplied by a single artery the viscera tree so when the basilar artery ruptures the blood goes from one single vessel to both sides and affects both the sympathetic tract so it is known as bilateral hormone syndrome so in a pontine lesion because it's a supplement a single basilar atrophy when it ruptures blood diffuses and goes to both sides both the sympathetic gets affected so they get bilateral small pupils but in medulla oblongata is supplied by two vertebral arteries so generally either this vertebral artery is affected or the other vertebral artery gets affected and when it gets affected the sympathetic tracts on on the same side gets affected so it causes unilateral meiosis only one side quantile lesion causes bilateral small pupils whereas medulla oblongata causes a unilateral meiosis so pons is supplied by a single artery basilar artery therefore when a single basilar artery ruptures blood diffuses to both sides and affects both the sympathetic attacks and causes bilateral small pupils spontaneous whereas medulla oblongate is supplied by two vertebral arteries therefore affection of a single artery causes small people on the same type c lateral side example balance book syndrome in ballenberg syndrome you get a meiotic pupil or a small people on the same side whereas a quantilation you get bilateral small pupils right next question is how does one differentiates an extensive compression of the third node from an intrinsic pathology of the third node the third now if it gets affected it produces 4d dilatation of the pupil because the parasympathetic suffering the pupil is lost so there's direction of the pupil it causes drooping of the eyelid because levator palpably superior is affected so it causes drooping of the eyelid it causes divergent spin because media medial rectus is affected lateral rectus is over acting so it causes divergence and because of that there's double vision so double vision divergence quint drooping of the eyelid and dilatation of the people these are the classic 4d presentation of a third knob policy right now how does one differentiate between an extrinsic compression of the third now coming from outside and compressing and second an intrinsic intrinsic pathology they don't know where it affects the center of the third node the intrinsic pathology the classic example is diabetes it affects the vascular supply of the third node so it affects the center of the third node whereas extrinsic compression of the third node could be ankle herniation or posterior communicating arterialism where it affects comes from above and affects it so how do we differentiate between these two very easy and very interesting the parasympathetic fibers run superficially on the third node the parasympathetic fibers run superficially on the third node so when there's an extrinsic pathology of the third node like positive communicating artery aneurysm or an ankle herniation it will come and compress the superficially parasympathetic fibers and therefore the pupil will start dilating on one side because parasympathetic causes constriction of the people and therefore when the parasympathetic gets affected people start dilating especially a person say with head injury and ankle herniation it comes and compresses the parasympathetic fibers and thirdner so pupil on one side is dilated the other side cupil is normal so a symmetry of the pupils anisochoria pupil is affected first is a compressive lesion whereas if it's an intrinsic pathology of the third node the parasympathetic fibers which are faced superficially they they are spayed and therefore people does not get affected or even if people gets affected it is the last to get affected the classic example of a comprehensive revolution is a pre-communism positive communicating organism or uncle herniation where there is an early pupillary pupil being affected so pupillary dilatation whereas if it's an intrinsic pathology of the thermo like diatic third neuropathy the pupillary fibers are last to get affected that's why textbooks describe diabetic turnov as a pupillary sparing third no palsy or in case the pupil is affected it is lost to get affected so parasympathetic is run superficially on the third now and hence extrinsic temperature of the thermal affects the parasympathetic fibers and causes people to dilate the earliest sign example poster communicating artianism whereas an intrinsic pathology of the third one the parasympathetic fibers get affected the last because they are superficially placed so pupillary realitation is the last sign example diabetic therapy right very interesting clinically why in thalamic hemorrhage eyes look down and why pupils are small as i said in the beginning of my lecture all the horizontal eye movement the center is in the pons and for vertical line means the center is in the midbrain the vertical line means again there are two types up gaze and down gaze looking up looking down for looking up the fibers cross and then descend whereas when you look down the fibers go straight away so if there's any lesion example thalamic image which is very close to the top of the midbrain they come and press the top of the midbrain so the crossing up gaze fibers get affected so they cannot look upwards they'll be looking downwards so in thalamic hemorrhages which very close to the top of the membrane it affects the crossing of gaze fibers so they cannot look upwards they'll be looking downward thalamic image and why the pupils are small the sympathetic pathway causes the pupils to enlarge to dilate and the sympathetic path originates in the thalamus hypothalamus so when there's a thalamic hemorrhage the sympathetic path is get affected so p pupils cannot dilate they look they are very small and then the thalamic image affects the top of the midbrain so the crossing upgrades fibers get affected they look down so if you see this the up gaze fibers they pass through and cross to the opposite side and then they start descending whereas downgrades fibers descend straight away and therefore there is selective involvement and more frequent upgrades passes so thalamic hemorrhage affects the crossing upgrade levels so they cannot look upwards they'll be looking downwards the sympathetic pathway is affected because it starts from the thalamus hypothalamus tuples are small likewise even in hydrocapillaries hydrocarbons also affects the top of the midbrain so they cannot look upwards they'll be looking downwards what we call the sunset sign as the sun has said the eyes go down hydrocarbon sunsets and it is because of this mechanism parry knot syndrome the dorsal fondant pineal gland tumor it also affects the top of the midbrain so they cannot look upwards they'll be looking down so they'll have up gaze palsy so thalam is very close to the upper part of the midbrain where upgrades fibers cross and therefore when there is a thalamic hemorrhage upgase fibers are affected in eyes look downwards sympathetic fibers which originate from hypothalamus are very close to thalamus and gets affected with thalamic hemorrhage causing pupils to be small what is locked in syndrome very very interesting as i said the midbrain is centered for vertical gas pons is the center for horizontal gaze so when the pons gets affected the horizontal gaze gets affected the corticobulbar corticospinal fibers also get affected so they cannot move upper limbs and lower limbs but since mid brain is intact the vertical movements are spared so they can look up and down so this is locked in syndrome very interesting logged in syndrome they cannot move their eyes horizontally they cannot use upper limbs and lower limbs the only movement is possible is vertical eye movements up and down i mean this is locking syndrome they are completely locked so mid brain is the center for vertical case pawns is the center for horizontal gaze so in persons with locked in syndrome pawns is affected which damages horizontal case corticospine fibers are affected which causes weakness of all four limbs however however midbrain is paid and therefore vertical eye movements are preserved right another very interesting concept why only right hemispheric lesions cause hemi-neglect they completely neglect on the opposite side but not the left hemispheric lesion the right hemispheric lesion they have hemi neglect completely neglect on one side whereas left hemispherications they usually do not cause right any neglect what is the mechanism especially pareto low so much so that the heavy neglect is so much so that if you pinch their hand they'll ask whose hand you're pinching it in fact they deny the existence of illness on the opposite side a severe form of hemi neglect what is the mechanism right we have the extra person space or visual field the right pareto lobe controls both the right and the left visual field whereas the left pareto log controls only the right visual field so when my left parity loop gets affected the right visual field gets affected but this is compensated by the intact right pareto law which controls both the right and the left and therefore left parallel lesions usually do not produce a right enemy neglect but when right paradiddle gets affected both the right and the left extra personal space and the visual fields are affected when right gets affected both are affected this right field is compensated by the intact left parietal lobe but there is no compensation on the left side so hemi neglect is more commonly seen with right parity locations and usually the hemi neglect is not seen on the left parity lesions and how do we test this right parietal lobulations produces hemi neglect so how do we test it at the bedside we give the person a clock and ask them to put all the 12 numbers equally pleased when we ask a normal subject to draw a clock with numbers equally placed they put all the numbers equally spaced but in a person with hemi neglect he completely neglects one side so he will put all the 12 numbers on the same side not going to the other side at all this is hemi neglect seen in right pareto loop lesions yeah these are all the important concepts one has to know when a person when a clinician approaches a neuro-ophthalmologic case and with just clinical observation clinical acumen without even imaging we can pick up so much of information wealth of science so that is the joy and challenge of neuro of the moji one of the most interesting subspecialities and it's very close to my heart i thank netflix for giving me such an excellent opportunity to address a large crowd of students across the country yeah this is it from me i thank everyone for your patient listening and if you have any questions or clarifications or doubts i am willing to answer uh i'll be happy to answer your questions thank you matrix once again for giving me this excellent opportunity over to the uh organizers was a wonderful lecture sir uh we have one question from uh upper nasa uh which is uh why there is hyperthermia in patients with quantum lesions yeah very good question aparna i don't know where she's from but can can we know where she's from no but very interesting question the pons is supplied by a single artery in fact that produces bilateral small pupils unlike medulla oblongata or midbrain which are supplied by two arteries midbrain is supplied by two posterior cervical arteries medulla oblongata is supplied by two vertebral arteries but bones is supplied by a single basarate so we have the two sympathetic tracks coming on the either side of the brainstem so when the pawns rupture when the basilar art ruptures in the pawns the hemorrhage diffuses and goes to bilateral sympathetic tracts sympathetic track is one of the important tracks which play a role in the control of temperature it originates from the thalamus which is very close to the hypothalamus and therefore you get hyperpyrexia very interesting question thanks for asking such a good question thank you so much sir for this wonderful lecture uh we're looking forward for a few more lectures from youtube netflix yeah doctor please carry on yes thank you so much for not only mbbs and mdi but also for nursing dental and physiotherapy yeah so i it was quite a refresher course for me people who are doing bpt physiotherapy would now love to take up post graduation in neurology than in orthopedics yes the whole reason i didn't do it because i really found neurology confusing and the rehabilitation you take you need a lot of patience uh to get through the whole rehabilitation but yeah the concepts the way you explained it it was really amazing i mean i'm i'm really looking forward to your uh lectures that you conduct on our platform and um thank you so much for this session it was really great thank you dr nivedita and netflix for giving me such a great opportunity i thank you for all from the bottom of my heart thank you sir just a second please sir sorry to interrupt uh there is one question from one doctor called chatterjee he is asking can you please explain the intranuclear ophthalmoplegia sir and one of syndrome chatterjee i guess he's from west bengal calcutta kolkata jupiter [Music] again one of the fascinating concepts medial longitudinal fasciculus pprf as i said para median reticular formation say on this side it connects the lateral vectors on one side and medial vectors on the opposite side through mlf and it will pull the eyes towards each side pprf so as you have mlf connecting to the medial directors on the opposite side you have one more mlf on the same side coming from the opposite rf and connecting the medial vectors this side so if you have a combined deletion of pprf and mlf what happens if the pprf gets affected it cannot draw the eyes towards its side so this movement is affected half moment this half movement is affected and the pprf gets affected it cannot pull the eyes towards its side so this lateral vector and this half medial rectus is affected mlf is also affected it's a combined lesion of mlf and pprf if mlf gets affected again attraction is affected so how many movements are lost of the two movements one and half movements are lost this half moment this half moment and this half moon so one and half movements are lost only half movement is present on the opposite side and that too there is nystagmus on the opposite side we call that as abducting nystagmus and why do we have nystagmus on the opposite side because of a law known as herring's law equal and dual innervation according to the herring's law the yoke muscles get equal supply the yoke muscles are the pair of muscles which move eyes together for example if i want to look to this side my lateral rectus and medial vectors will combine and push the eyes towards this side if i want to look to the this side this lateral vectors and this medial rectus will have to act in concert to push the eyes to the opposite side these are known as yoke muscles they get equal innervation from the from the cortex and therefore when this when i want to look this side because mlf is affected i cannot attack so what happens is that herring's law now the brain comes to know that this is not able to move so these get same subjects so this gives an extra supply compensation mutant separate somehow try to move the eyes somehow try to move the eyes to the opposite side because his eye is not moving so this guy is not going to try to mightily move this eye like this because they get the same surprise so you get nystagmus so pprf and mlf lesion causes one and half syndrome when the pprf gets one moment is lost half moment half wins when mlf gets this half moment is lost and the other side is only half moment that is also nystagmus because of the yoked law because of the headings law of equal innervation dual and equal innovation it is mightily trying to push the eyes to the opposite side resulting in nystagmus known as abducting nystagmus uh i hope you have understood doctor chatterjee and nice that i'm able to connect with people from west bengal it is because of netflix thanks melissa again for uh connecting us to different people different students all over the country one from chennai down south one from west bengal the other area for probably a few from mumbai am i expecting questions yes sir that was the whole idea for netflix and thank you so much for this amazing session um i would actually like to run a quick poll with our um with the audience so that we get a good feedback uh and too that will help us plan our future sessions so this poll is it's a very general poll basically because um netflix is not only for clinical development of doctors it's also like overall development so this was just one thought that we came across uh for clinical communication a talk on clinical communication so if y'all could vote in it would really help us to navigate the app in the right direction [Music] oh good thank you so yeah clinical uh communication is really important um and here's a second uh question in on the same lines [Music] okay and one last so if you want to run any polls in your sessions uh we can run that for you as well yeah i just want a feedback how was my lecture was it good okay okay very good or boring not really good and how was it useful to them could you just post that question uh so it may not be possible in this session uh but we will definitely uh try to put those questions and get this feedback for you sir yeah if i can get some healthy criticism i will know a way to improve upon a way to concentrate that would be really great for me and not to improve myself sure so i will we will do that so actually the users can write to us at support dot netflix dot app support netflix netflix dot app and y'all can put in your feedback about this session about any other session that's taken place on netflix and anything related to this session so we'll get back to you with the feedback [Music] and whatever comments i read through the session they were really positive feedback so this session was really good so thank you i got one of the best feedback i think even more good yes they're just they're just coming up again and again yeah thank you everyone for attending this wonderful session

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