Transcript for:
Optic Neuritis

[Music] hello and welcome to insight of thermology this is dr amrit welcoming you to another lecture on the optic nerve today we are studying optic neuritis [Music] [Music] what is optic neuritis a demyelinating inflammation of the optic nerve is actually known as optic neuritis the word that we should actually be focusing over here is the demyelinating okay so it's not just any inflammation of the optic nerve specifically the term optic neuritis is used when demyelination is associated with inflammation of the optic nerve right now based on the part of the optic nerve which is affected by the inflammation there are different types of optic neuritis so if the optic nerve head or the disc is involved it is called the papillitis that is just the inflammation of the optic nerve head sometimes what happens is that the intraorbital part of the optic disc optic nerve will be involved right which is shown over here and that is called the retrobulbar neuritis so what i mean to say is only the intraorbital part of the optic nerve is involved and the disc is not involved as in papillitis the third thing is the neural retinitis in neuroretinitis as the name suggests the nerve is involved that is neuro and along with that the retina is also involved so there will be disc edema and along with that you will see certain changes in the macular area also and since the retina and the disc both are involved it is called neural retinitis so when i talk about the clinical signs of optic neuritis i would be touching papillitis new retinitis and retrobulbaneuritis in detail so what is the pathophysiology of optic neuritis the main word that we have to remember even in pathophysiology is the demyelination optic neuritis is caused mainly by the demyelination so over here we have a picture of an axon and we can see that this is the cell body and over here is the axon and we can see that the axon is actually enveloped by the myelin sheath okay and these myelin sheath is produced by the oligodendrocytes in case of the optic nerve the presence of myelin helps in the faster conduction of the impulse through an axon now let us try to understand this pathophysiology in more detail and specifically let us understand why does this demyelination of the optic nerve occurs the first thing is understanding the blood-brain barrier breakdown as we all know that the blood-brain barrier prevents the entrance of the t cells into the nervous system right so the blood print barrier is normally not permeable to these types of cells you know unless it is triggered by some infection or a virus so whenever there is an infection or there is a virus what happens is that the integrity of the tight junctions of the blood-brain barrier will be decreased and and later on as the infection heals the blood-brain barrier might recover however what happens is that these t cells will now be trapped inside the brain or inside the nervous tissue right so initially there was a blood brain barrier and this was preventing the entry of these t cells and the inflammatory cells but after an infection or after some virus infections specifically what happens is that this will become more permeable and then these cells will come inside later on as the infection will heal the blood-brain barrier will again form however these cells are now trapped inside the nervous tissue next what happens is the process of autoimmunology or autoimmunity now the immune system will now attack the nervous system leading to plaques and lesion formation so what happens is these t cells which were trapped inside the nervous tissue now they are going to go and attack our oligodendrocytes which were present around the axons and forming the myelin sheath right so as these t cells which are just trapped they're going to go attached to these oligodendrocytes they will cause demyelination and in the process of demyelination they will lead to plaques formation okay they will cause demyelinating plaques formation and this process of demyelination will particularly affect our white matter okay why because most of the axons are located in the white matter of the brain and therefore these t cells will go into the white matter and destroy the oligodendrocyte now the third step which occurs is the inflammation that means the t cells which have come and attacked the myelin sheath they're also they're not going to stop just by destroying the oligodendrocytes right so they are going to trigger some inflammatory processes also and stimulate other immune cells and soluble factors like cytokines to come to that place right so this will cause further swelling further leakage from the blood-brain barrier further activation of the macrophages and further damage of the nervous tissue right so these are the three processes in the pathophysiology of demyelination or optic neuritis that is the blood-brain barrier breakdown autoimmunology and inflammation so anything which can cause blood-brain barrier breakdown and cause finally autoimmunity leading to inflammation of the brain and finally demyelination can cause optic neuritis now this diagram explains the same thing so this is the blood blood brain barrier over here and usually it will not allow the monocytes to pass through it however some reason some systemic cause will cause the increased permeability of the blood-brain barrier or breakdown of the blood-brain barrier leading to coming up of the monocytes inside the neural tissue and then what will happen the monocytes will develop into macrophages these macrophages will get attracted to the myelin complex okay and then they are going to destroy the myelin sheath now the same macrophages again are going to come back and release some soluble factors these soluble factors will again come outside the blood brain barrier and they will call the other b cells and the t cells these are the b cells t cells will now produce antibodies and they will produce other inflammatory mediators and cause inflammation of the myelin sheath leading to further destruction and further demyelination so histopathologically we are going to see demyelination right so when we take a slide and see in that we are going to see perivascular coughing okay that means there will be blood vessels and around the blood vessels we are going to see cells okay and what cells are those t cells b cells and the plasma cells and i told you why these cells are coming right at the same time because the cells are causing inflammation inflammation will lead to edema of the myelinated nerve sheets right now as there is edema and this inflammation it will finally lead to myelin breakdown the smiling breakdown is occurring because of two reasons number one is inflammation and number two is auto immunity now the demyelination in the optic neuritis can actually occur alone or it can be associated with a lot of syndromes okay now if it is occurring alone without being associated with any kind of syndromes it is called clinical isolated optic neuritis or isolated optic neuritis okay now as it is associated with multiple sclerosis which is the most common association okay so multiple uh what i mean to say is whenever there is an episode of optic neuritis the first thing that most of the physicians will think is the presence and the probability or the risk of developing the multiple sclerosis in a patient right so this is the most common association with optic neuritis and that is multiple sclerosis now this association of multiple sclerosis with optic neuritis is so common that we usually label these patients who are isolated optic neuritis or with multiple sclerosis as the typical optic neuritis right these are called the typical optic neuritis cases now the third association or third type of demyelination which can occur is in the neuromyelitis optica also called device disease okay so i will go into details of these subsequently however neuromyelitis optica which is also called the nmo is nothing but it is the presence of optic neuritis along with transverse myelitis okay so there is not just inflammation of the optic nerve and demyelination of the optic nerve there is also the inflammation there is also inflammation present in the spinal cord and that is called the transverse myelitis now another association with optic neuritis is the acute disseminated encephalomyelitis which is also called aden okay in this also we have optic neuritis but what is typical with the acute disseminated enzyflo encephalomyelitis is that there will be a history of recent viral infection or recent vaccination and it is believed that this autoimmunity which is triggered with recent infection or recent viral infection to be more specific and specifically in certain kind of vaccinations okay which will lead to autoimmunity and cause demyelination and finally cause the optic neuritis now there are two important new antibodies in relation to the optic neuritis that we should be aware of okay and these are number one is the antibody which is present against the astrocyte aquaporin4 water channel okay and this is called the aqp4 igg antibody okay it is called aqp4 because it is aquaporin channel 4 right so this is seen in 2 of the cases with optic to writers okay now the second type of antibody which is important for us to know is the mog igg antibody that is the myelin oligodendrocyte antibody which is actually an antibody against the oligodendrocyte glycoproteins that will result finally in damage to the myelin insulation so as i told you if these are the axons and around that we have the myelin sheath this myelin sheath is actually formed by the oligodendrocytes and if you have antibodies which are directly going and attacking these oligodendrocytes then those are called the mog igg antibodies and the association is 15 percent right so this is the new antibodies that we must remember and they have a very important role in management of optic neuritis if patient is having these antibodies positive and that is the reason why i want you to know uh about them in brief in the pathophysiology one more thing what i want you to know is that the presence of aquaporin p4 antibodies and the emoji antibodies will actually make the patient fall to a category of optic neuritis which is not typical right so this is called a typical optic neuritis okay that is number one point number two concept which i want you to remember is that this aquaporin p4 igg antibodies is usually positive in patients with nmo that is neuromyelitis optica or the device disease now in a patient who has mog igg type of antibody that is also a typical optic neuritis and the optic neuritis is actually caused called mog optic neuritis now as i told you in the pathophysiology that anything which cause breakdown of the blood retinal the blood um brain barrier will actually cause the inflammation and cause demyelination so it is very obvious to think that optic neuritis can also be caused by certain infections and these infections can be both local infections and it could be the systemic infection so sometimes they could be endophthalmitis and orbital cellulitis sinusitis and sometimes spread from the brain and base of the skull so what happens is that this infections can either come to the optic nerve themselves or the inflammation which is associated with this infection can attack our optic nerve myelin sheath and cause demyelination leading to optic neuritis however this if it happens it will again be in a typical case of optic neuritis and not a typical one now there are a lot of systemic infection which can cause demyelination and can cause optic neuritis so it could be viral it could be bacterial fungal protozoan and parasites sort of these viral which are important are the influenza measles mums chickenpox herpes zoster cytomegalovirus and in bacteria in low developing countries we have in the developing countries we have tuberculosis and syphilis okay and then we have cat stress uh disease the lyme's disease okay fungal we think about cryptococcuses and histoplasmosis in protozoa we think about toxoplasmosis malaria toxocariosis and parasites we basically think about chisty sarcosis so if you have to think about few infections if you want to remember for you you can think about the measles mums influenza in viral with cytomegalovirus and infectious mononucleases and bacteria you can think about tuberculosis and syphilis particularly in fungal you can think about histoplasmosis and cryptococcuses protozoa think about toxoplasma and toxocara and parasitic is only one 60 circuses now as there was a role of autoimmunity as i explained you in the pathophysiology so any kind of autoimmune disease can also lead to demyelination so it could be systemic lupus erythematosus or polyarteritis no dosa what happens is that there will be ischemia in these vasculitis cases which will lead to demyelination right and then it can also cause necrosis or it can cause demyelination and axonal necrosis both right so the clinical profile will actually uh look very similar to optic neuritis okay or they can actually have acute ischemic optic neuropathy picture also because ultimately we are having vasculitis which is causing ischemia so if their ischemia component is more they will be ischemic optic neuropathy or and if there is an autoimmune component along with ischemia that might cause demyelination along with the axonal necrosis now there are a lot of metabolic causes and metabolic diseases which will lead to decreased nutrition and that decrease in nutrition can again trigger autoimmunity and can damage the normal pathophysiology and lead to demyelination okay however this is very rare okay so don't think it in the first if as first differential should always be in the it should always be thought in a typical optic neuritis and that too always in the end whether it is anemia b12 deficiency diabetes starvation okay and pregnancy some sometimes which can trigger autoimmunity now let us talk about the clinical features of optic neuritis the first thing that i want you to remember is that they will have loss of vision which could be subtle or which could be profound but it is going to typically deteriorate over hours to days and then it will reach the maximum trough in about one week after the onset right so very quickly it deteriorates and reaches its maximum deterioration number two the visual loss as i said could be subtle or could be profound okay and most of the patient can also have complete blindness then it is usually unilateral now this is what i want you to remember it is usually unilateral yeah now at this point i want to clarify that when i'm talking about the clinical features of optic neuritis i am talking about the typical optic neuritis okay so these are the clinical features of typical optic neuritis then one more important thing is the age of presentation 18 to 45 years of age and along with that there will be pain okay deep orbital or retro ocular or bro pain which is aggravated by the eye movement and it is increased by the pressure upon the glue now you might ask why is there pain with the eye movement so what happens is that the optic nerve is actually having the superior rectus the superior rectus and the medial rectus there are present in very close association with the optic nerve sheath so whenever there's a inflammation of the optic nerve sheath okay there will be inflammation of these muscle fibers also which are present in close association with the optic nerve at the optic orbital apex and therefore whenever the patient will have eyeball movement specifically when he tries to look up or when he tries to look medially there will be pain so other visual functions such as uh the loss of color vision typically the red desaturation okay that is present so i told you already that in optic neur neuropathy usually red desaturation is present and there's one more thing which happens is as is an altered perception of moving objects okay and this is called the pulstrix phenomena now what happens is that if we have two eyes and one eye is affected with optic neuritis okay so this axons will have damage to its myelin sheath so as the myelin sheath is damaged the conduction velocity will be decreased in this axon however this normal eye will have a normal speed of conduction okay or the normal conduction velocity so what can be seen is that there is a conduction velocity disparity between the two eyes right so there is a problem in velocity perception they cannot coordinate among there's no coordination among the two eyes because of which when an object which actually has a movement of its own its perception would become difficult for the patient and this is called the pulprex phenomena along with that some patients are going to complain of one more thing which is worsening of the symptoms with exercise or increase in the body temperature and this is called the utops sign okay so what is what is thought is that when this increase in the temperature the inflammatory mediators will increase and will lead to more signs in these patients so the patient will give history that usually after a hot bath or after doing exercise what happens is the body temperature will increase and he will have deterioration of his vision now what is the course of a typical optic neuritis so what happens is that what did i tell you that the coptic neuritis will progress within hour to days and will reach its peak it's trough sorry in about one week time right however what happens is that from the second week onwards it is going to start improving right so it starts improving from second to third week okay so improve second week improves third week and by about fourth week or fifth week the visual equity is going to return to normal or near normal that is about 6 18 to 6 12 right so it will progress very fast reaches the trough very fast and then starts improving by second to third week and then reaches fourth and fifth week the maximum visual equity right and this is going to happen irrespective of your treatment whether you give steroids or you don't give steroids the typical optic neuritis is going to follow this course now this is a very important point and you have to remember the timelines also for the course of typical optical writers because anything which does not follow this will fall to the category of a typical operanoritis and the treatment will be totally different so next what happens is that subsequently subsequently the vision is going to uh vision slowly and steadily improves over several months and ultimately will be restored to six by six so improvement starts from the second and third week however the improvement by fifth week is up to 6 12 and 6 18 however it will improve it will keep on improving right so improvement is also progressive in these patients over several months however there is something which does not improve or which takes longer to recover and that is the color vision okay the contrast sensitivity and the visual field effects these three things will not get recovered so soon and they are going to take longer period of time that is about 6 to 12 months and in some patient they might not improve or completely return to normal so based on the clinical features that i have discussed now i would tell you what do i mean by typical optic neuritis so in a case of typical optic neuritis the age range will always be 18 years to 45 years of age there will be pain and the pain is always mild and that pain will become worsened or it become more on eye movement the disc will usually be normal or there might be mild disc edema and the progression was very quick that is from hours to days and then the improvement will start from second to four weeks onward and the improvement will be there irrespective of the steroid treatment okay whether you give steroids or you don't give steroids and even after we stop steroids there will be no recurrence so these are the features of typical optic neuritis anything which is which is deviating from typical features is an atypical optic neuritis so if the age is present outside the typical range of 18 to 45 that means patient who is younger than 18 years or older than 45 years will fall to the category of a typical optimist then the pain will be absent on eye movements or the patient might have very severe pain so severe pain also should alarm you that it might be a case of a typical optic neuritis the poor vision will persist beyond two weeks from the onset so in the case of typical optic neuritis we saw that the vision was actually starting to improve beyond the second week there will be progressive diminishing of vision beyond the first week now what did i tell you in opting your writers a typical variety was that within hours to within days the vision is going to drop and within one week it will be the worst and then starts improving from the second week onwards now if there is a further drop after one week then you should think that okay fine maybe this isn't a typical optic neuritis and such patients if you give steroids and if you don't give steroids they are going to become worse and if you give steroids and when you stop stop giving steroids there might be recurrence right so such basic patients will also have bilateral involvement so what did i tell you a typical optic neuritis case usually will be unilateral so whenever there's bilateral optical writers you have to think in terms of a typical optic neuritis now this is all very important because whenever there is a case of a typical optimist you have to think in terms of certain specific further investigations because it might not be a simple multiple sclerosis it might be other demyelination uh disorders okay which will need a totally different approach and a different treatment now one more important difference is that in the typical optic neuritis there was a mild disc edema without any hemorrhages however in our typical optic neuritis you might actually see severe disc edema with the hemorrhages now what are the various signs that you see in the case of optic neuritis as i already told you that there will be a variable degree of visual equity loss decreased color vision specifically the red desaturation contra sensitivity will be decreased stereo equity will be decreased okay then the visual field effects might be present and there are a varied uh types of visual field effects that you can see in optic neuritis you can see central centros arcuate sectoral altitudinal or a generalized non-specific depression also there might be a presence of marcus gun pupil or the relative afferent pupillary defect which is very common in papillitis okay and uh there will be a on vep okay which will evoke potential the p uh hundred okay this will actually show prolonged latency right so what happens is that there will be increased latent period because the conduction velocity is going to decrease because of the loss of myelination the latent period is also going to increase right so on on vp we are going to see delayed p hundred now what are the ophthalmological signs that we see that is when we are actually going to see it using ophthalmoscope or during a fundus examination what are the signs that we see now the this could actually be totally normal in case of retro bulbaneuritis okay which is more common in case of adults and it's shown over here in this picture you can see that in this picture the disc almost looks normal and there are almost no signs that we see however the patient might be having rapd might be having red desaturation which should actually give alarm you that there is an optic nerve problem right so uh this is a retro bulbaneuritis and because the intraorbital part of the optic nerve is involved and not the disc we do not see any signs in the fundus okay it's more common in adults and also it is more common in multiple sclerosis now however sometimes only the disc will be involved which is called papillitis now in that case we will have a hyperemic disc with swollen disc margins the margins will not be clear and with or without flame shape hemorrhages right in which if there are no flame shaped hemorrhages and there's mild disc edema it goes more in favor of typical optic neuritis and if there are more hemorrhages which are present it goes in favor of the typical optic neuritis right and papillitis is more common in case of children and young adults now sometimes what we see is that we will see involvement of both the retina and also the optic disc right so in that case here we will have the stellate patterns of exudates okay present in the retina and this thing is called the neuro retinitis okay and probably the etiology over here is infectious etiology right and also this presence of neurotinitis also isn't a typical type of optic neuritis all right it is not seen in association with multiple sclerosis so in multiple sclerosis we can see papillitis we can see retro bulbaneritis however neurotonite is mostly seen in infectious etiol so you might have observed that from that time i'm mentioning after the multiple sclerosis with optic neuritis so there is a high risk of multiple sclerosis in patients who present with optic neuritis so let us see how much is that risk okay so the first thing that you should consider is the age of onset the patient who is younger the more is the risk of that patient having multiple sclerosis or developing multiple sclerosis in patients so younger patients should always raise an alarm number two is that women women are more prone to developing multiple sclerosis almost three times greater risk than men okay so if a woman come if a woman comes with autoineuritis you have to think about in terms of multiple sclerosis race the caucasians usually have more risk of developing multiple sclerosis and the northern latitudes have more risk of developing optic neuritis and associated with multiple sclerosis and clinical fixed features as i told you retro bulba involvement mild papyl ideas and sequential involvement of the other eye within two weeks is also a risk factor to developing the ms or multiple sclerosis so for such a patient for such patients it's very important to send the patient for investigations right and in optic neuritis according to the optic neuritis treatment trial they say that the investigation especially the mri orbit and mri brain to be input to be more specific it has a prognostic indication and it can also tell you about the risk of development of optic neura disc of development of multiple sclerosis right so we can go for mri orbit in brain to evaluate the optic nerve enhancement and cerebral demyelination now optic nerve enhancement is not something that we usually send the patients for in an mri orbit what we basically should use my the investigation or imaging is to rule out ms and to look for cerebral lesions and cerebral demyelination so a typical case of optic neuritis will be unilateral and will show optic nerve enhancement okay and this optic nerve enhancement will be seen on the t2 weighted images fat suppress images and usually what we see is a high t2 signal of the optic nerve right now there will be optic nerve enhancement the optic nerve enhancement could be parenchyma the parenchymal enhancement that is the substance of the optic nerve will look hyper intensive or just the perineuritis that is the the nerves which are present around it okay the vessels which are present around it they are going to take up the contrast and they will be just perineuritic enhancement so these two types of enhancements can be seen in optic neuritis in case of mri orbit however when we talk about mri brain it's a totally different thing now one more thing about mri orbit what i want you to tell uh here is that the involvement of the optic nerve will usually be short segment involvement in case of typical optic neuritis so what is meant by short segment involvement is that just less than three millimeter involvement of the optic nerve will be seen so along with that there will be demyelination plaques that we are going to see on the uh mri of the brain right and these demyelination plaques actually have a prognostic prognostic value and also in assessing the risk of developing the ms okay so just by having a demyelinating plaque on an mri does not mean that a patient has ms right however we can assess how much is the risk of developing ms now if there is no lesion present in the brain there is a 25 percent of risk of developing ms over 15 years if there is only one single lesion the risk will increase to 60 percent if the lesions are two the risk increase to 68 and if the lesions are three the reason the risk will increase to 78 percent now in the diagnosis uh criteria on diagnosing criteria of the ms the multiple sclerosis the criteria that we use is actually the mcdoubles criteria and this has been revised so according to the latest revised criteria for the ms diagnosis there are two terms which are used that is dissemination in space and dissemination in time now dissemination in space means that the patient should have at least one t2 hyper intense lesion in at least two of the four cns location so to assess the dissemination of space we are going to actually assess certain spaces inside our brain you can remember it like that and these certain spaces are four number what are the spaces number one periventricular space that is the space around the ventricle the cortical or the cortex or the juxta particle infra tintorial that is where the cerebellum is present and the spinal cord so these are the four locations now we are going to search for hyper intense lesion right so demyelination is going to look hyperintensive on t2 so such hyperintense solution at least one lesion should be present in at least two of these locations two of these four locations so one infrastructorial or one spinal cord or one cortical lesion or one periventricular lesion however when the patient is more than 50 years of age or has some ischemic disease what we take for periventricular is about three lesions more than three hyperintense lesion okay and for the other things we take usually one one lesion that is meant by that is what is dissemination in space so if there is a patient who has at least one hyperintensive lesion in an infratentorial or a spinal cord lesion for example then the patient is actually fulfilling the criteria of dissemination in space next what we are going to look at is the dissemination in time dissemination in time means that if there is a patient who comes for the first time and we get a baseline mri and in that we do not see any lesions and then again we check the patient and now we are seeing new lesion what does it mean it means that within this time period of baseline mri and the new mri the patient has actually developed a lesion that means within that time frame he has developed the lesion and this is called dissemination of the disease in time at the same time suppose we do a mri in a patient okay on one day and in that mri we see that certain lesions are gadolinium enhanced okay so usually we do an mri which is along with gadolinium so we see that certain lesions are showing enhancement and there are certain lesions which are not showing enhancement now what does it trigger in your mind what it should trigger in your mind is that the lesions which are getting enhanced on uh the mri are actually the active lesions and the non-enhancing lesions are the old lesions now since there are new and old lesions present on the mri and new or old are actually described in terms of time and that also indicates dissemination in time now over here it doesn't matter when you do the mri whether you're doing it two days after three days after 30 days after the time frame has been removed from the criteria of diagnosing the ms okay dissemination in time it is irrespective of the time frame and these lesions dissemination in space it is irrespective of whether they are gadolinium enhancing or not okay just the presence of these uh lesions is enough for dissemination of space and the presence of multiple lesions of different uh chronicity or uh detecting new lesion on the next mri is enough for diagnosing the dissemination in time so this was about the diagnosis of ms using the radiology so this is the image which is showing you the cortical lesions okay and over here we can see certain lesion here which is around the ventricle and the spinal cord lesions and this is the infertile part okay the cerebellum where you have to look and then again in the cortex also we have to look okay now this is a mri of the orbit and you can see the enhancement of the optic nerve in case of optic neuritis however this is not very commonly done now this picture over here shows certain white lesions around the ventricles so they're called the periventricular white lesions and since they're looking like fingers because of their organization along the medullary nerves which are oriented perpendicular to this ventricle these are also given a name which is called the dawson's finger right so they are nothing but the areas of demyelinating plaques now on the imaging what did i tell you the optic nerve lesions or the optic nerve enhancement is usually short segment now if you see a case in which on neural imaging or on the orbit uh cell scans or the orbital mri if you see the optic nerve lesion is actually more than 3 mm that means it's not short segment involving and if there's a bilateral enhancement that means both the optic nerves are involved and enhancement which is bilateral yeah and there's extension to the chiasm now where is the chiasm located the chiasm is actually located intracranially and our optic neuritis typical one is actually limited to the orbits right so anything which is enhancing beyond the the margin of the orbit or beyond the limits of the orbit and going to the intracranial region also should rise the suspicion about the typical optic neuritis so another thing that we do is a csf analysis so csf analysis is usually not necessary for the diagnosis of optic neuritis however presence of oligoclonal bands is actually correlated with the development of the ms now this was told to us by the optic neuritis treatment trial and other thing is the high igg index now the presence of oligoclonal bands actually does not give a stronger risk for ms as compared to those dissemination in time and dissemination of space and therefore csm analysis is not that important as a neuroimaging is then uh when we are suspecting in our typical neuritis optic neuritis then we have to think about these uh antibodies which are the aquaporin p4 igg and the mog igg antibodies [Music] now let us try to understand certain differences between the nmost and mog as i told you that the mson that is the multiple sclerosis associated optic neuritis is nothing but our typical optic neuritis and the nmost optic neuritis or the neuromyelitis optical spectrum disease associated optic neuritis and the mog optic neuritis that is a myelin oligodendrocyte glycoprotein antibody associated oligo sorry associated optic neuritis these two are falling under the atypical optic neuritis right however there are difference in all these three number one is that multiple sclerosis associated optic neuritis is usually unilateral right however these two are bilateral now the segment involvement the segment involvement in multiple sclerosis associated is always short segment right the short segment means less than three millimeters or focal involvement and which part it involves mostly it involves a retro bulba part the mog-o-n also involves irritable bow part however the nmo st will go and involve the intracranial chiasmal part or also it can go and involve up to the optic tract right now how do you differentiate this retro bulba and this retro bulba is that by the amount or the length of the lesion in multiple sclerosis it is a short segment involvement that is less than 3 mm however in mog optic neuritis it is a longitudinal extensive involvement similarly in nmo also it is longitudinally extensive that is more than 3 mm of involvement now based on the sign how can you differentiate in a case of multiple sclerosis optimists usually there will be a mild optic disc swelling right in nm also it can be mild because most of it is involving the intracranial part and the chiasmal part however in mog although it is retro bulb inflammation is very severe now what is the location of post contrast enhancement the optic nerve enhancement will be there at nmost similarly in ms or multiple sclerosis also it will be optic nerve parenchymal enhancement however what is specific over here is with respect to the mog in which we see this perineuritis or the perineural perineural enhancement now in which type do we have the mri lesions in multiple sclerosis definitely we know that it is very common to have those periventricular infractorial juxta cortical or cortical and spinal cord hyperintensive lesions however in emoji and nmosd it is not very common what we see in nmosd is these spinal lesions right and spinal lesion because what do we know about nmo is that it is devic disease in which there is transverse myelitis along with the optic neuritis and therefore we can have spinal lesions in nmo st right yeah so the type of lesions again in ms is periventricular ovoid subcortical juxta particle and in emoji that is uh the where there is damage to the myelin oligodendrocyte the lesions are really large and two effective okay they could be cortical or subcortical now in case of nmosd you can have hypothalamic lesions which are more common right along with that posterior fossa lesion and we will have the spinal lesion now spinal lesion can also occur in multiple sclerosis however usually they will not be contiguous okay and less than three segments of the spinal cords will be involved whereas in nmosd the more than three segments and that too there will be contiguous involvement of the spinal cord segment in neuromyelitis optica so why is this differentiation so important let us see now in case of the aquaporin p4 antibody that is nothing but neuromyelitis optical spectrum they have a very worse prognosis okay and they are not responsive to steroids also so what do we do for these patients we have to go for a plasma exchange in which we are going to remove these antibodies from the plasma and then push back the normal plasma and along with that we have to uh advise the patient regarding the long-term immune suppression using the antimetabolites or the immunosuppressive drugs similarly in moab mogav antibody associated optimuritis the response is very good to the steroids okay they're going to respond very nicely to steroids just like multiple sclerosis however when you stop the steroids what happens is that you will see more relapses so this also will give you a clue that you're dealing with a typical optic neuritis that means you start the steroids and the patient responds to steroids but when you stop steroids the patient is again having recurrence of opting uridis so in that case you have to think about the mog antibody and you can actually go for the serum labs and you will see that there is mog antibody present and such patients you should not give steroids and instead you should put them on lifelong immunosuppression right so that is the importance of aerotypical optic neuritis and that is the importance of knowing these antibodies because the treatment is totally different and the investigations are also totally different so in case of nmo or neuromyelitis optica as i've told you before that it is the antibodies or nmo igg antibodies which are going and attacking to these astrocytes footplates okay these astrocyte plates are having this aquaporin p4 channels on which these antibodies are going to come and sit and then that the complement is going to get activated and once the complement get activated a lot of mediators are going to come and they will cause demyelination and finally cause the necrosis right so for the diagnostic criteria of nmo there should be a history of optic neuritis number one there should be a history of acute myelitis okay that means the transverse myelitis that means the patient will have paraplegic symptoms paraparasites okay then along with that two of the following three should be present that is number one mri of the spinal cord will show involvement of more than three segments and an nmo igg antibody should be positive and the brain mri should not be consistent with ms that means you should not see those typical lesions with ms that is the periventricular injection cortical and infractionatorial instead in case of nmo the lesions that you see are the hypothalamic lesions or the posterior fossa lesions right so any two of the three will give you the diagnosis of nmo then what happens in any optimist is that finally there after damage as we know that the nerves of the uh our optic nerve they cannot regenerate so ultimately we are going to have optic atrophy and it is going to look very similar to that of the papilla papilla post papilloedema optic atrophy in which it will look like secondary optic atrophy which will have the dirty gray color of the optic nerve and however sometimes in patients who have retribulability because they are not much signs present in the disc what we are going to have is signs of primary optic atrophy which will look which will not be so dirty right and it will be actually described as white optic atrophy and sometimes the optic atrophy might be so mild that we might actually have just a temporal pallor right so this is a primary optic atrophy okay or it could be seen actually in patients with retro bulbar optic neuritis okay and you can see that the temporal pallor is more compared to the nasal pallor now so in case of our typical cases i told you already about the labs that you have to do and how do you differentiate it from the imaging and then there are other investigations also remember that i told you there can be infections which can lead to it and there can be autoimmune causes like sle which can lead to it so you might go and want to investigate if all these things are coming negative so you can go for a complete blood picture estimation of rapid plasma reagent for syphilis crp esr okay then we can go for fda abs test and nuclear antibody for the um connective tissue disorders right so these are the additional testing so in my next video i will go in details about the treatment of typical and typical optic neuritis so if you like this video kindly give it a thumbs up and share the knowledge and stay tuned for the next lecture on the treatment of optic neuritis thank you and have a 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