[Music] hello and welcome to insight of thermology this is dr amrit and today we are studying papilloedema what is papilloedema papilloedema is defined as the edema of the optic disc or the optic nerve head primarily due to the raised intracranial pressure we already know that the optic nerve head is closed up to the laminar cribrosa that is still here in the various meninges which are coming from the brain and the sub-arytenoid space and the subdural spaces are actually continuous around the nerve from the brain so any rise in the intracranial pressure will become evident around the nerve sometimes when this happens the subarachnoid space will swell so much and so be it'll be become so distended that it will become amply form just behind the globe moreover as a result of this raised ict that is raised pressure we can say that papillardima is purely a hydrostatic collection of fluid right there is no inflammatory component in papillaedema papillary mine is purely hydrostatic which is occurring because of the raised ict and why is it occurring is because the subarachnoid and the subdural space of the brain are in direct communication with the optic nerve as these spaces and the meninges are present around the optic nerve up to the laminar cribrosa there are several theories to as to what causes papillaedema however there are two basic theories the first one is the compression of the central retinal vein as we all know that the central retinal vein carries the blood from the retina and then enters the substance of the optic nerve and finally comes out through the optic nerve as it is coming out we can see that it is passing through the sub arytenoid space now in papilloedema there is actually swelling and uh increased pressure in the subarachnoid space because of the increased pressure and because of the thinner walls of the veins this central retinal vein will get compressed and there will be a back there will be blocked flow in the central retinal vein leading to edematous changes in the disc okay now however the arteries as we know they have much thicker uh thicker adventitia or thicker sheaths or thicker coats the central retinal artery however will not be compressed by the increased ict the increased interchangeable pressure will only affect the central retinal vein and cause compression of the weight the second theory is the blockage of the exoplasmic transport now as we all know that here we have our laminar cribrosa through which the the nerve fiber layer and its nerve is actually passing and making the optic nerve now whenever this increase in the ict it is transferred to the subarytenoid space and will also cause a pressure on these axons and because of the direct pressure there will be a blockage of the exoplasmic transport therefore it is basically the compression of the central retinal vein and along with that the blockage of the exoplasmic flow which occurs because of the raised intracranial pressure or the csf pressure which will cause stoppage of the axoplasmic exoplasmic flow which is called exoplasmic stasis and this exoplasm will build up behind the retina okay before the point where the veins are actually exiting and therefore it will cause the swelling of the optic disc because of the swelling there will be some mechanical changes and those are the changes that we seen see in the optic disc or the optic nerve so what are the causes of papillaedema let us consider this to be our skull okay so this is the skull and in the skull we have our meninges and the meninges are covering the brain right so what happens is that these these structures over here are our ventricles so these are the two lateral ventricles going into the third ventricle fourth ventricle and finally we have the spinal cord continuing now the green structure over here is nothing but the choroidal plexus right so these plexus will produce the csf after they are produced from the ventricle that is the second ventricle and the first ventricle they will go to the third ventricle fourth ventricle and from there they are going to actually circulate around the brain traveling in these subarachnoid and the subdural spaces right so in between the spaces of the meninges the csf is going to flow so our brain is actually floating in the csf so anything which causes increase in the intracranial pressure will lead to papillary this is what we know so what are the causes which will cause the race ict so number one cause is whenever the skull is too small okay so if we decrease the size of the skull what will happen there will be less space for the brain less space for the csf to flow and therefore the interchangeable pressure or the csf pressure will increase so where does this happen it happens in craniosynostosis that is early fusion of the sutures which will prevent the development of the skull and therefore we will have a smaller skull second thing is whenever the brain volume will increase so when will the brain volume increase whenever there is some space occupying lesion right so there could be a tumor in the brain which will lead to increase in the volume and that will cause pressing on the subarachnoid space causing increase in the csf pressure third is what if there is some obstruction over here in the passage of the csf from the ventricles right so either it could be a colloidal cyst over here which is pressing and you know compressing this canal okay so that could be the reason of uh raised ict or sometimes they could be hydrocephalus so this is nothing but hydrocephalus and it is also called obstructive hydrocephalus right now other reason is there could be a papilloma in this choroidal plexus itself so what will happen we will have more production of the csf so when we have more production in the csl what will happen the csf pressure will itself increase third thing is reduce absorption of the csf so what happens is when the csf reaches in the subalternate space part of which is it is going to get absorbed through the meninges right so whenever there is meningitis inflammation of the meninges or or there is any venous thrombosis cerebral venous thrombosis so what happens is the csf is getting absorbed by the meninges and then from the meninges it is being taken away by the cerebral veins right so when we have thrombosis of these veins or when we have defective meninges the absorption of the csf will be reduced so whenever production is increased but the absorption is reduced what will happen the amount of csf which is circulating in the brain will increase and therefore the pressure inside the head also will increase so any intracranial tumor can actually lead to raised ict right however the highest percentage is found in the tumors of the midbrain and in the parietal occipital region and in the cerebral tumors right so as i told you hydrocephalus is an important cause of papillaedema similarly an abscess in the brain right which can act as a space occupying lesion and can increase the volume of the brain then thrombosis of the cavernous sinus or thrombosis of any vein for that matter why because that will increase the backflow and the absorption of the csf will decrease and therefore the er raised interchangeable pressure will be there then again aneurysm aneurysm can again after the space occupying lesion subarachnoid hemorrhage subatomic space as i told you is the space from where the csf is flowing so if you have blood over there how will the csf flow therefore the csf pressure will rise pseudotumor cerebri which was previously called as the benign intracranial hypertension is actually a disorder associated with raised csf pressure but there will not be any intracranial space occupying lesion okay it tends to occur usually in obese females and they complain of headache photopsia and transient blurring of vision so pseudotumor cerebri is actually a diagnosis of exclusion after we have ruled out the other diagnosis and other causes of ict it only when we should consider pseudotumor cerebrine particularly in an obese woman malignant hypertension however can also cause raised ict in malignant hypertension it is usually uh considered that the raised blood pressure is associated with raised icd however this theory is not so well supported now let's see what are the common symptoms that patients complain of in a case of papillaedema actually to tell you that in the beginning stages symptoms are very weak okay and the vision is also normal for quite a long time okay and this particularly implies to the central vision which will most of the time be unaffected in patients with papillaedema however later on they can start developing transient attacks of blurred vision and usually they can be uh they are usually described as bilateral that means occurring in both the eyes or unilateral or monocular in one eye blackouts okay and these blackouts will last for very few seconds and they will be precipitated by changes in the posture and usually the patient tells that in the morning when they wake up from their sleep it is that time that they suffer from these blackouts in the early papilloedema the visual field of the patient might actually be normal however as the papillaedema progresses there will be enlargement of the blind spot and this enlargement is actually occurring because of the separation of the retina around the disc so this i will be telling you in the science as to why the enlargement of blind spot occurs so in the beginning patient will just have an enlargement of the blind spot on visual field and later on as the papadema spreads from around the disc and goes on to involve the macular also yes papillon can involve the macular and i will tell you that in the science so as it involves the macula then we can have even you know involvement of the central field of vision but to remember if you want to remember papillardima actually causes enlargement of the blind spot so along with the headache that occurs in the early morning after waking up from the sleep the patient can also have other signs of raised intracranial pressure so they can have nausea they can have vomiting they can have pulsatile tinnitus okay and along with that they can have double vision also and why does this double vision occurs in raised ict this double vision occurs because of non-specific viruses of the sixth nerve caused by the rays icd so why is the sixth nerve affected in race ict or in patients with papilloedema is because the sixth nerve in particular as it's coming out from the pons as you can see over here in yellow color it has a really long course number one second thing is that as it is passing through this petrous temporal bone over this petrous temporal bone it passes through a very tight canal and the canal is called the dorelo canal okay so whenever the ict is raised okay there will be compression of the abducen nerve along this petrous temporal bone in the canal of dorello and that will cause the paris that is weakness of the sixth nerve and that is the reason why there will be double vision because as the sixth nerve will be damaged in these patients with raised ict we will see esotropia that is inward deviation of the eye why because the lateral rectus muscle which causes outward deviation or abduction of the eye is supplied by the sixth cranial nerve and the sixth cranial nerve will be affected in raised ict and where is it affected it is affected near the petrous temporal bone why it is affected number one because it has a long course in the brain and number two it passes over the peter's temporal bone through the dorello so the abnormal ringing sensation that the patient experiences in the ear is called tinnitus and when this ringing sensation sounds like a whoosh bush is nothing but it's a sound of passage of fluid right so when it is like whooshing sounds and these are synchronizing with the blood flow okay or synchronizing with the pulse of the patient okay that is called pulsatile tinnitus and it is a sign of raised ict [Music] now let us see that what are the common signs that we find on the disk or in the retina when we examine a case of papilloedema right so the science can broadly be divided into the mechanical signs or the disc findings or we can say them we can call them as vascular findings right so let us start with the mechanical findings the disc findings the first one is blurring of the disk margins right and this blurring of the disk margin will start usually in the upper margin and the lower margin and in the nasal margin right the temporal margin of the optic disc will be affected in the end right so what i mean to say is in the early papilloedema it is the upper lower and the nasal margin of the disc which will get blurred and temporal margin of the disc will get blurred later the next sign is actually hyperemia and edema of the optic nerve head so why does the high premium occur hyperimage nothing but increased redness of the disc right so as i already told you that there will be actually compression of the central retinal vein because of the compression there will be reduced uh blood flow through that and because of the reduced blood flow there will be backflow instead increased congestion will be there and as there is increased congestion okay as the blood is not flowing back into the veins the optic disc will itself look hyperemic right or more red in color and because the similar reason because the blood is not draining into the vein the optic disc will look bigger in size and also it will look bigger in size why because of the exoplasmic stasis as i told you in the pathogenesis right so there will be hyperemia and edema of the disc now as the disc uh is increasingly becoming hyperemig and any matters what will happen to the cup this cup will get obliterated so we will no longer see the cup because the neural retinal rims are so swollen and they are encroaching onto the cup area so there will be obliteration of the cup which now as the disc is increasing in size so what i mean to say is as the edema is increasing and increasing in size what is happening to the vessels which are actually traveling into the cup traveling over the neural retinal rim those vessels also will look as if they are more torches okay and because of the backflow obviously they will be dilated so what we see is we see dilatation and tortuousness of the vessels moreover as the as the compression of the central retinal vein was occurring there is congestion of the veins right so all of the veins and the arteries will look more bigger in size they will look more reddish in color and they will look like this you know they will look tortuous in their appearance right and one more thing that we see is absence venus pulsations right so normally in the retina what we have what we see is central retinal vein will show pulsations and this pulsation is called spontaneous venous pulsation so these spontaneous spontaneous venous pulsations will become absent when the there is when there is raised ict so these venus pulsations or these spontaneous venous perception or the central venous pulsation of the central retinal vein will be absent in a case of papillaedema because of the rays ict next what we can see on the disc is this red streaks right so what is happening to the arteries i told you that the arteries are usually not affected so much because of the thick adventitia right however the arterioles can definitely get affected and they will be seen as red color streaks on the optic disc right now what happens is that the optic disc will keep on elevating from the surrounding retina as the edema keeps on developing right so at a point it starts mushrooming out uh mushrooming upwards or you can say outwards from the retina in such a way that when you do an indirect ophthalmoscopy there will be a parallax error between the retina and the optic disc so what i mean to say is the optic disc and the retina will now not be present at the same level initially when the disc was flat the retina and the optic disc they were all at the same level right so what i mean to say is if you were using your indirect ophthalmoscope to see a patient and you put on on the diet plus two diopters you were able to see both the disc and the retina clearly however once the papillardima develops because the disc is now at a higher level the two will not are not at the same level therefore when you put plus two either of them will be blurred right so you might have to put more power of plus power to focus on the disc right and at that time when you're focusing on the disc the retina will be blurred or when you try to focus on the retina the disc will be blurred right so there is an elevation of the disc which is quite apparent on the on the ophthalmoscopy right so when you do that examination often the disc will be about plus two to plus six diopter elevated right this is called elevation of the disc which is measured on the direct ophthalmoscopy and it is nothing but the amount of plus that you are dialing on your do or the direct ophthalmoscope to get the disc into focus what hap now what happens is that as the papilloedema is staying for some time that edema is going to start the edema is going to start spreading to the surrounding retina causing certain folds in the retina so initially it was located in the disc itself now this edema is going to spread all around with nerve fiber layer and spread like this to the retina and what happens when water enters within below a sheet okay there will be folds right so these retinal folds are called the patons lines right they also called the patents lines right now gradually however the disc realizes like okay fine it is a lot of time that i have stayed in papilla papillardima i have been hyperemic so now what happens is now the reddish hue will start decreasing right the normal pinkish disc will now not look that pinkish nor will it be hyperemic why what is uh why does it happen is because now what will start is opacification of the retina right so what happens in chronic papilloedema is that because of the constant mechanical pressure of that edema there will be ischemia right the vessels are now not going to supply the optic nerve head right in my blood in my video on blood supply of optic nerve head i told you how the optic nerve head gets it blood supply right so all that nutrition is affected there is ischemia and sometimes there might be total cut off of the blood supply which is called infa and moreover because of the direct pressure which is induced by uh induced okay there will be axonal damage right so these axons are going to die now when anything die in our body it is usually replaced either by the same tissue or it is replaced by the fibrous tissue right so that is what happens in uh our optic nerve also there will be axonal damage and that axonal damage will be replaced by the glial tissues right so these glial tissues are usually astrocytes okay so they are going to replace and when they replace they are usually whitish in color because they are whitish in color therefore the reddish hue is going to decrease and we are going to have opacification of the retina and this process is called gliosis okay this process is called gliosis and usually it is seen in the optic uh in the stage of optic atrophy so what i mean to say is after papilloedema becomes chronic at some point of time all the axon axons will start getting degenerated and will be replaced by the glial tissue this is called reactionary organization or gliosis or post papillaedema atrophy okay it is also called secondary optic atrophy because the optic atrophy is occurring secondary to the papillaedema right now similarly before this before this papilla optic atrophy sets in what happens is i told you that there was a lot of congestion of the veins right so as the congestion of the veins occurred the blood is staying there for a long time what happens is because of the increased pressure there will be hemorrhages around the disc right and to tell you that in acute papillaedema hemorrhages are constantly present right so whenever you see a case of papillaedema with hemorrhages you can actually tell that it is an acute papilloedema right however if you see a case in which there is gliosis and more whitish risk you can tell that it is a chronic papillaedema right other thing is as the vessels are staying over there as there is stasis of the blood this congestion what will happen is the lipids are also going to come out of the vessels and as the lipids come out of the vessel they form what is called as the exudates okay they will be yellowish in color yellowish deposits because of the extrusion of the lipids from the vessels so these are called the exudates right now what happens is as i told you from the disc the edema is going to spread to the surrounding retina and at some point of time if it is very massive it is going to reach even the macula and in the macula they will cause deposition of these exudates in the form of a star so in a picture i will tell you what is meant by macular star right so this is called macular star and however it is usually an incomplete macular star right which has a fanning towards the disc right now another thing which can happen is retinal micro in fact which is nothing but the infarcts in the axons and they will present as cotton wool spots which are whitish spots because of the infarcts so this is a picture over here which is showing you what is meant by the macular star so this is actually papillardima as you can see over here the disk margins are blurred we cannot see we cannot actually make out any disk margin right moreover the vessels you can see okay the vessels are also obscured and the vessels are quite congested torches and you can see that here there are hemorrhages which are present and these whitish lesions over here right these are nothing but a collection of the hard exudates and as you can see these hard weights are present more on the side towards the disc that indicates that the origin is coming from here from the disk part right so this is called an incomplete macular star right so if you have hard exudates radiating from the macula in 360 degrees that is called a complete macular scar right macular star and it is usually seen in case of neural retinitis however in case of papillaedema also we can get a macular star but this macular star will be incomplete and usually it will be projecting or complete towards the part which is towards the retina or nasally right now this is also one more case which is showing a severe or fluoride kind of papillaedema you can see almost a disc is not visible at all and we can see disc hemorrhages all around okay the disc which indicates how much acute this con this condition in this patient is then we can see these torticity dilatation of the vessels right and we can see some lipid exudates over here we can see some cotton wool spots also over here papilla edema can be graded using the fryson scale the it is graded into the stage 0 which is nothing but the normal optic disc okay so in the normal optic disc the disc is normal that means there is no blurring of the nasal superior inferior poles okay all of these are normal the retinal nerve fiber layer is also normal there is no torsity of the vessel that means there is no vessel vascular or mechanical or disc changes right that is our normal disc state zero in stage one we have very early papilloedema okay so i will tell you with pictures what is meant by stage one or very early papillardima then we have stage two which is early papilloedema then we have stage three which is moderate papilloedema stage 4 which is marked papilloedema and finally we have stage 5 which is severe papillaedema so over here is the image of the grade 1 papillaedema as you can see in grade 1 papilloedema only the superior nasal and the inferior part of the disc will be blurred right so as you can see over here there is a c shape halo okay so what i mean by c shape halo is nothing but a c shape area of blurring around the disc okay where we cannot make out the disc margin sharply right however you can see that the temporal disc margins are quite clear right so this is called grade one papilla edema in which there's a c shape hello usually on the nasal side of the disc and there is a temporal gap temporal gap means that the temporal margin of the disc is normal now in grade 2 papilloedema what happens is this halo will now become circumferential as you can see this is our disc but we cannot really make out where exactly is are the borders right so borders are not very sharp in this so in grey to papillardima the entire 360 degrees borders will be affected even the temporal gap will be filled up next is our grade 3 papillaedema as you can see that in grade 3 papilloedema it is characterized by loss of major vessels as they leave the disc so this is our disc okay we know that it is greater than grade 2 because all the disc margins are blurred after all the disc margins are blurred okay next thing what we have to see is the vessels right so here this vessel over here we can see that it is clearly seen till this point that is still the time it is on the disc once it goes away from the disc you can see here it is becoming blurred right so as the disc is leave as the vessel is leaving the disc it is becoming uh blurred right so grade three papillae edema is nothing but loss of the major vessel as they leave the disc right now great for papilloedema is loss of the major vessel as they are present on the disc now here you can see that if you trace this vessel over here onto the disc we don't know where it went right we cannot trace it further down similarly this vessel there is a gap over here right similarly this vessel there is a gap over here right so there is a gap or the blurring of these vessels as they are reaching on the disc right as they are present on the disc and this is great for papillaedema right so when the vessels are blurred as they are leaving the disc but they are clear on the disc that is grade three but when the vessels are lost on the disc itself it is grade four now coming to the grade five papillodima grade five is nothing but almost all the vessels are blurred in this picture almost none of the vessels can be made out on the disc right so this is great for papillary muscle it's nothing but grade 4 only but almost all the vessels are partially or totally blurred on the disc and then we have what is called as the chronic papilloma now i already told you that in acute papillaedema there will be a lot of hemorrhages the disc will be congested it will be hyperemic you know it looks angry right it looks red in color right but then as the edema settles down okay and as the papilloma becomes long-standing there will be certain adjustments okay in the architecture and we have what is called as chronic papillaedema appearance so the chronic papillartima actually the disc will be more pale in color right so this gives more pale in color the redness of the disc will subside so as you can see over here this is also papridema this but the disc is not as red as to what we have seen previously you know this is more hyperemic but this this is over here is pale second thing is those patent lines that we saw they are going to leave certain marks around the disc and these marks are now called the watermarks right you can see these marks radially sorry circumferentially present right so these are the watermarks apart from that slowly slowly anastomosis will start developing between the ciliary circulation and the retinal circulation and these anastomosis are nothing but the optocelery shunts right so what i told you that in papilloedema there is a pathology of ischemia and infarcts going on and because of that ischemia wherever ischemia goes on there might be some anastomosis because the natural tendency of the disc to restore its blood supply optocelery shunts might develop so these these cockscrew like vessels you know these ones turning here these are the optocelery shunts right they can be seen and the typical appearance of the uh disc of chronic papillaedema is a champion cork appearance right so over here is the champagne appearance now you can see we cannot make out where the cup is the cup is not very clear in the disc moreover this whitish appearance on the disc is nothing but the exudates because of the chronic isoplasmic stasis uh all the axoplasm is going to come out as uh stasis and they are going to come out as the exudates and also amyloid deposits will be there in chronic papillaedema which will look like this you know yellowish and whitish color deposit onto the disk surface so by now it would be very clear to you that papillardima starts as edema and gradually goes towards atrophy right so whenever we are seeing a disc which is showing secondary optic atrophy with water marks and all the features of chronic papillaedema we know that it is a papilla it is a disc which has passed through all stages of papilloedema right however in certain cases we might have we might actually be seeing bilateral papillaedema which is a symmetrical so a symmetrical means that a symmetrical in terms of the timing of the events in the disc that means one disc might be showing optic atrophy and the other disc might actually be showing acute papillaedema okay so one disc of one eye in chronic stage of papillaedema and the other disc in one eye is actually showing acute papillary right so whenever such a condition occurs we have to think about the foster kennedy syndrome right so foster kennedy syndrome is nothing but bilateral papillaedema which is a symmetrical okay and it has a localizing significance so what happens is there will be one eye papilla edema and the other eye is going to show optic atrophy and what does it suggest it suggests that there is a tumor present in the olfactory groove or the orbital surface of the frontal lobe or it could be in the piritory body now the question is to what side the tumor is present so the tumor is present on to the side of the eye where there is optic atrophy so let us consider this man and let us say that he is having optic atrophy or we can say chronic uh secondary optic atrophy because of papilloedema in one eye and in the other eye he has just the papillaedema right so this is nothing but foster kennedy syndrome papillary mind one eye and optic atrophy the other eye and what does it indicate it indicates that there is a tumor in the orbital surface of the frontal lobe or the olfactory group but to which side to the side where there is optic atrophy present that means to this side so the tumor is present onto the same side of the optic atrophy and this is the foster kennedy syndrome which has a localizing significance so what are the important diagnostic investigations that we need for the diagnosis of papilloedema often the diagnosis of papilloedema actually depends on the fundus examination so most of the time based on the fundus finding itself we can make out that papilloedema is present or not present now once the diagnosis of pablo edema is established the next thing what we do is we have to measure the blood pressure of the patient so after checking the blood pressure if the blood pressure is like really high and pointing towards the malignant hypertension the patient needs a immediate physician referral right so so first thing is diagnosing based on the fundus examination second is ruling out the malignant hypertension and after that we go for the individual investigations so the first thing we do is the ophthalmic investigations the ophthalmic investigations that could be used as an ancillary testing or an ancillary investigation just an ad just as an add-on investigations are the spectral domain oct that is we can do an rnfl scan or the macular scan of the patient a spectral domain oct act as an objective tool to detect very subtle disk uh swellings and also in cases where we want to monitor the improvement of the condition right so the retinal nerve fiber layer scan of the oct in case of papillae edema will detect the thickness of the papillaedema so whether if the swelling decreases the rnfl thickness around the disc also will decrease and therefore there will be improvement of the rnfl scan subsequently in spectral domain oct in a patient who who is having improvement in his papilloedema however sometimes what happen is that there might be atrophy which can set in and there will be actually thinning of the rnfl which might be seen so in certain in those cases we can actually go for the macular scan and find out the thickness of the or the amount of the ganglion cell layers which are remaining right so in cases where the optic atrophy has set in after the improvement of the papillaedema dis swelling we can go for the macular scan of the spectral domain oct instead of doing the rnfl testing protocol the second type of opthalmic investigation are the stereo disk images right so which can help us in the follow-up of the patient and as such we can use it for the documentation purposes the third thing what we do is automated uh automated perimetry in which we can see enlarged blind spots in these patients later on they can develop a nasal step or they can have architectural very similar to those patients with glaucoma and as the disease will spread towards the macula in certain conditions in certain patients where we can have a macular star development there can be the central vision involvement also which can be seen one more ophthalmic investigation that we can do is the fluorescent angiography right and this is particularly done to differentiate true disk edema that is true papilloedema from the pseudo papillaedema and pseudopapilloedema is seen in cases like the optic nerve hydroson which are nothing but the deposits present on the optic nerve head and because of the deposit the disc will look as if it is elevated however this is not true uh papilloedema in which there is leakage and there is edema so when we do a fluorescent angiography in case of papilloedema we will see leakage of the vessels however in a case of uh the in the case of the pseudo papillae that is optic nerve hydros there will be no leakage instead just there will be staining okay there will be staining in the ffa now one more way to differentiate these two is by doing an autofluorescence imaging so the optic nerve head drusens they have a property of autofluorescence and therefore they uh they will be seen as whitish autofluorescent area on the disc in the autofluorescent imaging now one more way of differentiating them is through the b scan ultrasonography right so it's very important to differentiate whether it is true papillaedema or it is pseudo papilloedema but going into the details of the topic is actually beyond the scope of this lecture so i'm not going to go into those details now the next diagnostic investigations for papilloedema are the neuro imaging right the immediate objective of an urgent ct scan that we do commonly is to rule out the space occupying lesion right along with the ct scan we can go for the ct venogram okay so that we can rule out a cerebral vein thrombosis now apart from that we can do an mri and mrv with contrast whenever we are suspecting the meningitis also one more important thing that we have to rule out on neuroimaging is something which is called tonsillar ectopia right here the tonsils is a term which is used for the cerebellum right a part of the cerebellum which is called tonsils so cerebellum isn't present in close association with the foramen magnum because from there the middle oblongata will pass and become the spinal cord right so in any condition if those cerebellum tonsils are present somewhere below to their normal location okay that is called ectopia right or tonsillar ectopia that means they are present in close relationship to the foramen magnum now such patients are very dangerous patients why because if we do a lumbar puncture in such patients those who have tonsillerictopia what will happen is the moment we are going to open this lumbar space these tonsil ectopia will lead to tonsillar herniation and cause the pressure over the middle oblongata where our vital center of breathing and our cardiac activities are located and it can lead to immediate death also right so the next diagnostic imaging investigation is the lumbar puncture but it should always be done after neuroimaging and after we have ruled out the tonsillar ectopia right so what do we actually check by lumbar puncture we will be checking the opening pressure of the patient and we will be checking the csf composition of the patient so how do we manage a case of papilloedema okay the first point to be managed is that we have to treat the underlying cause of papillaedema right so the first thing that we did was we were actually checking the pressure the blood pressure of the patient right so if the patient has high blood pressure or malignant hypertension what do we do we send the patient to the emergency department for the controlling of his blood pressure right if we find a mass the primary therapy of the patient should be directed towards the lesion right so mostly it will be surgery right the third thing is if we find that there is cerebral venous thrombosis which is present then what do we do we start the patient on anticoagulation if there are certain medications which can actually cause the pseudotumor cerebri like the tetracyclines and vitamin a analogues we will direct the patient towards uh stopping these medication if the if the patient is obese and that is the reason say he she is having intratraining hypertension leading to papilloedema we will we will actually motivate the patient to lose certain weight right so the first thing is to treat the underlying cause after treating the underlying cause we have to think about saving the vision so what i mean to say is only and only if there is severe problem uh severe visual loss then we have to go to the steps okay which are mostly the surgical steps to save the vision so the surgical decompression is considered in life threat in uh vision threatening conditions in papilloedema so what happens is suppose there is only a visual uh visual loss in a patient the first thing that we can do is an optic nerve fenestration right so what is meant by optic nerve fenestration if this is our optic nerve we know that the optic nerve is surrounded by the meninges and between in between the optic nerve and the meninges is the subarachnoid space and the subdural spaces which are carrying the csf along with them so whenever there's a raised icp the pressure is building around the optic nerve so in optic nerve head fenestration optic nerve fenestration what we do is we are going to create holes in these optic nerve head sheath okay or the optic nerve sheath so as we create holes in this optic nerve sheath what will happen the pressure will be actually relieved right so these holes are nothing but fenestration and therefore this process is called the optic nerve sheath fenestration now suppose the patient actually has headache also along with the visual field laws okay then we will do some csf diversion procedures also called the shunting procedures right they're called the dual venus shunting procedures now there are two types of shunting procedures the first one is the vp shunt and the second one is the lp shunt the vp shunt is nothing but it is the ventricular peritoneal shunt and the lp shunt is nothing but it is the lumbo peritoneal shunt ventricular peritoneal shunt means that we are causing an artificial diversion of the flow of csf normally from the ventricles as i told you how the csf flows into the third ventricle fourth ventricle subarachnoid space and then around the brain in ventricular peritoneal strength we create an artificial shunt between these ventricles lateral ventricles directly to the abdomen of the patient right so in the abdomen we have the abdominal peritoneum so directly the csf now will be draining into the peritoneum of the patient right relieving the pressure inside the head the second procedure is a lumbar peritoneal procedure or the lumbar peritoneal shunt in which the lumbar area of the spine where the csf is present from there we are going to create a shunt and put it into the abdomen or the peritoneum of the patient right so this is called the lumbo-peritoneal shunt now the recovery of the vision however may be faster than the substance of papilloma so sometimes we cannot exactly the edema will actually subside later and the recovery in the vision will be more faster right visual fields always should be carefully washed and decompression should be urged from the ophthalmological point of view before the peripheral constriction of the fields occur because once the peripheral constriction also occurs it means that the papilloma is quite advanced right and what i mean to say is even actually even before the central field gets involved it is better to go for the decompressive surgical options right so [Music] you