INI-SS December 2021 Recall- Neurology | Dr. Baishyak Renuji | Marrow Super Speciality

So, we have finished, right? Finished your exams. You all have finished your exams. And so, let us assess how was our planning and how was our program gone and how were the questions. I was able to get some, some questions from our students early, and there are on some 46 questions I was able to collect from some of the students, and I'm thankful to them for getting me the questions. And as these are questions which I got from the students, the options there, I didn't get all the options for some questions. I got only three options. I had recreated some options, but altogether, the theme of the question is what we are going to discuss. And this will be an aid to me as well as to you to have what all areas are important because this is the first INAS exam conducted in the history.

So, let us start with the modules we discussed and how much, how much important questions came from. Whether it was expected. Some questions were expected, and some were quite unexpected questions. So, this we will go and revive our what are, what all things we have covered and what were the important areas. And this may help in the next coming batch to to go through the important areas because the first time INAS has been conducted.

So, coming to the questions, coming to the modules we discussed. We first discussed about approach to neurology, which is basically a basic module. Only the language, some areas we have discussed there. Remaining was predominantly about how to approach and all those things. So, there were no questions asked from the language area per se. But the sleep was the next module we discussed, and I had discussed a little bit in depth in the sleep because the questions used to come from the sleep disorders. When we were doing the last round revision of neurology also, I told you that there are some questions that might come from the, come from the disorders, particularly narcolepsy. That also has trust during the last revision. Narcolepsy's trust, and some questions I was expecting from the drugs, but there was no question came from the drugs. But the question came from directly from the narcolepsy only, and that was expected. And peripheral neuropathy, there was a, there is again an in-depth that we have discussed, but only two questions came. And those two were rather, one question was directly from our module, and the second question was a little bit, it was looking a little bit out, but that also we have discussed.

Then the muscle, I expected quite a few questions from muscle, but that area was, there was, there were no questions literally. That whatever questions I got came from muscle, but that doesn't mean that that area is not important because muscle, especially the DMDs, are dystrophies, and the new drugs in DMDs, and then about the, the, the inflammatory myopathies, the antibodies and inflammatory map. These are always the favorite questions of examiners, but they say there's no questions, unfortunately. But from neuro of tal, which I had taken a little bit in depth, and I expected few questions, that three to four questions came from neuro after. And one question came in after I had included another part also. So, there are sort of three to four questions came from the neuro of that. Thermodynamic, a little bit in-depth question scheme. And cognition and dementia, there are four questions came. And hypokinetic, hyperkinetic movement, there were three questions, and one was regarding the drugs. And the most important topic was stroke. There are 13 questions. Whether it is UG, PG, or anything, always stroke and vascular neurology, that area is very important. Here also, almost 13 questions came, and we have tried to cover stroke in depth. Put a lot of time in the stroke module, and as expected, a lot of questions has come from stroke. But again, there are some four, three to four questions which are slightly new when compared to what we have taught, what we have studied in our modules. So, that was slightly out of the box questions came in the stroke area, but it is, you cannot tell it is completely out of the box. So, we will discuss into that later.

Epilepsy, there are four questions. And headache, there are two questions. And epilepsy questions are a little bit, a little bit in-depth neurology questions, and those were practically totally out of Harrison Christian scheme. And headache, two questions. Demyelination, there are two questions. And cerebellum attacks are two questions. Spinal cord in two questions. Neuro infection, there are three questions. MND and NMG together, those two questions. And we were expecting some questions from MND. That we have discussed when we are doing the revision session also. What are things surveys also we told that we have discussed that their question may come from the smear related drugs. Then same question came. The SMA early drugs is a new thing. And so the question has came from that area only. And CSF is another area which we have not covered, but only one question that is slightly similarly, what is enormous eso pressure? That is related to that question has come. And one question from genetics has come about the, about the repeat disorder. And that also actually you can answer if you are going through the modules. We have discussed about in two places.

Now, with this, we will go and first discuss about the epilepsy. There are four questions which came from epilepsy. So, let us go through epilepsy questions. The first question was a two-year-old child with intellectual disability and episodes of atonia and false, atonic false and clonic moments. So, what are the possibilities? Options given were Lennox-Gastaut syndrome or LGS, Doose syndrome, childhood absence epilepsy. The fourth was probably given as Dravet. Actually, that was that option was not, that was not clear to me. But anyway, the answer doesn't need all the options. So, the question was, there is an intellectual disability and two-year-old child with indicativity and episodes of atonic false and clonic moments. So, when you, we have discussed this same disorder in the epilepsy, particularly in the epilepsy, epileptic syndrome by epileptic encephalopathy part two in our module. And LGS and Doose, the childhood absence epilepsy doesn't present the atonic force. Atonic force occurs predominantly in LGS, Doose syndrome, as well as in some later onset West syndromes. So, and Dravet syndrome is classically with the febrile seizures followed by febrile mac. We have discussed in our module, febrile mac, febrile seizures is onset as sesame processed meat and all those things. You are discussing our module. So, Dravet is not the answer. And childhood absence epilepsy is not associating false. So, electronic force and clonic movement, the doubt will be between LGS and Doose syndrome. But this is from the module. We have discussed about Doose syndrome where there is no tonic seizures is one thing is highlighted. And along with that, when you discuss about the same LGS and tonic, LGS tonic movement and myoclonic movement. And myoclonic is not there. A classical C type of LGS. So, we discussed status that is a code. We discussed ADPS. So, tonic, atonic, atypical, atypical absence, and atonic false, and P, the production fast activity and slow spike can discharge that as we discussed in our modules. So, a clonic predominant seizure, myoclonic or clonic seizure predominant seizure, never goes in hand with LGS. That we have rightly pointed out. We have, I have told it during the discussion on epileptic encephalopathy, LGS, when there is a clonic seizure predominant and false, it is not likely to be LGS. So, that was enough to answer this question because the two-year-old onset and there is atonic false and clonic movements. Atonia syndrome, childhood absence, that we have discussed. Dravet syndrome, status, febrile, then follow myoclonic, atypical absence, and sometimes CPS or complex muscle seizures. That was we discussed as a code. Febrile mac and LGS and the Doose is the remaining options. And Doose syndrome is something which presents the atonia with myoclonus. But LGS myoclonus or clonic seizure predominance is never a feature. That its stone exeges are predominant. So, the answer is Doose syndrome. So, that we have discussed rightly in our modules. All these things, Doose syndrome, LGS, difference, all those things you have discussed. And regarding the age again, childhood absence epilepsy, you can see this is the same slide from our module. It is four to ten years reach. So, that is also something which goes against the childhood absence. Dravet would start with several seizures. There is no extra febrile species. And atonic falls are not that common. Dravet it is more common with Lennox-Gastaut syndrome, Doose syndrome, as well as in light on stress syndrome. Okay. So, the answer is Doose syndrome. So, that is also discussed question. And we don't need to understand everything to answer it. You just need to understand that little atonic false and tonic moment goes with LGS, and clonic movement doesn't go hand in hand with Lennox-Gastaut syndrome.

Now coming to next question. Resources regarding a childhood encephalopathy. Only a two-year-old child with history of febrile seizures and later on myoclonic seizures and the gene involved. So, that is what we discussed just now, and we have discussed the same thing in the module also. A febrile seizures followed by encephalopathy and myoclonic. That febrile mac. Febrile mac is a code. We discussed febrile seizures followed by myoclonic seizures, atypical absence, and complex partial seizures. This is a classical feature of Dravet syndrome. So, this is Dravet syndrome. So, what is iron channel related Dravet syndrome? That was also discussed rightly in our module. We have discussed that it is SCN1A. This was the same slide from our module and same discussion. We have discussed that SCN1A mutation is classical for Dravet syndrome. Actually, in fact, we have discussed it in two places. Once when we are taking the module in the Dravet center, we have discussed the same thing. Then again, we have discussed about the different ion channels associated with seizures when we are discussing name sequin epilepsy. In that way, you can, this is a table directly from Harrison. You see SCN1A, 80% of Dravet syndrome, such as SCN1A. And CHRNA is an adult, I mean, autosomal dominant nocturnal frontal epilepsy. And KCNQ2 associated main feminine neonatal seizures. And LGS, when I said ADPF, all these things we have discussed. And we have discussed about table regarding the channel opening. This analogous EMC at the end also. We have discussed one table where we have mentioned that journalists epilepsy, febrile associated with SCN1A. Same gene is associated with Dravet also. That also discussed in the Dravet syndrome in the epileptic encephalopathy module part two. In the timing also, it is given here. So, that is the answer is SCN1A. So, that is also directly from our module.

And the third question asked was GABA transaminase inhibitor. This was also we discussed. This is straightforward. We discussed in the module about the module about and the epileptic drugs in epilepsy session part one where we discussed that when there is VGAP pattern, we have pattern, we discussed, we get pattern, we discussed that GABA transaminase inhibitor and associated with visual side effect. We had split it in a code and studied the same question came. So, the answer is VGAP pattern, GABA transaminase inhibitor. And we have discussed about gabapentin which acts on the, the different, different channels. One is the MAID and phenomena totally checked on sodium channel. All these things we have discussed. And this was a snapshot of the same discussion where we have drawn that VGAP pattern is associated GABA transaminase inhibitor. And which, which is again, you can remember by VA stands for visual side effect. So, retinal changes or visual side effect. The side effect of gabapentin, I mean, VGAP pattern, then it's GABA transaminase, that is GABA trend. That we get pattern is visual side effect. Government, GABA. That we have discussed. Same question came here. The next question was, in fact, directly it was the same MCQ. We have discussed in the MCQ session on epilepsy. The same question, almost same question, we have discussed. Epileptic spasms findings are all except. That is a question asked in the SS, INAS. And it was like options are generalized slow waves, generally slow waves followed by electronic criminal response, and generalized polyspike can discharge, and spindle possibly spindle. That is the fourth option. And I am not sure the fourth option. But the same question was discussed. And this is directly from Harrison. The Harrison, it is not there in Bradley or other texts. It is directly from Harrison. And they say this is a question we discussed in our module in MCQ session. We have discussed this module that the EEG called epileptic spasm in West syndrome is hyperexcitability, chaotic giant slow waves and spike and where that is option we are given. And the answer is electro decremental response. That is directly from the Harrison. And this question they, we have, we have discussed a similar question. And this question is, this is a question we discussed in the epilepsy MCQ, MCQ module. So, the answer is electro decremental response is associated with the epileptic spasm. That is directly from Harrison. So, there were total, that was the, the, this was the reference we have given during the discussion. Harrison 20th edition, page number 308. That is this is the electro decremental response associated with epileptic spasm. That is a direct question which asked in the INAS. So, in the epilepsy, there are total four questions asked. And luckily, all the four we were able to discuss in the our modules. And I hope those who have gone to the modules as well as MCQ, you should be able to answer all those things. And you don't need to know the entire literature. Question, you can rule out by using whatever you have studied from your module or whatever you studied by yourself. You can exclude the options and find out the answer. So, epilepsy, all the questions were covered.

Then coming to the next is the demyelination session. So, epilepsy, all the four questions covered. Demyelination, there are two questions asked. The first was Finger criteria and NMO MS Adam and ND Morgue were the options given. Actually, this was something which I have not discussed. Like, you cannot tell that it is, I had not completely discussed. I have discussed the criteria, but have not mentioned the name of the publisher. And this is actually the NMO diagnostic criteria, which is, which we have discussed in our module. And the name of the criteria or the, the, the publisher's name was Wingerchuck. The modified Wingerchuck criteria. This one, we are actually discussing our module. So, the answer is NMO. And actually, the question is not that tough because MS, you have gone through the criteria. It is not the answer. And whenever you see such criteria, the most criteria you have studied is Wingerchuck. Some fuse, little bit tenderness will be able to answer. But this was something which is, we have not discussed. And now I, that is a realization for me that you have to go in depth about the criteria also. So, this was discussed in neuro of tal spectrum disorder with this was a slide. And this criteria has been known as Wingerchuck criteria because this has been the publisher is Wingerchuck. And so, this was the criteria for diagnosis of NMO spectrum disorder with aquaporonic procedures. It was a couple negative.

Next question is, which of the following is not a part of McDonald criteria 2017? McDonald criteria specifically asked. And this was something which I have discussed at the end of the after discussing about McDonald criteria. I wrote on the slide that there are three major differences of McDonald 2017 and the old criteria. So, discuss at the time to 14, 43, 12. I had discussed and I wrote on the slide also that OCB inclusion, cortical and extra-cortical lesions are included. And the fourth one is, third one is symptomatic lesions in spinal cord. According to the old McDonald criteria, were not taken. But the new criteria is included. This is the three major difference of 2017 McDonald criteria. So, this also has been directly discussed in our modules. So, the answers options are OCB included. That is actually not a part is the keyword here. OCB is included in the criteria. Cortical lesions are included. Symptomatic spinal cord lesions are not included to categorize D or DIT. So, this was wrong. This was the old criteria. Old McDonald's criteria has not included the symptomatic lesions of the spinal cord and not included OCB criteria. But the new criteria, the three major difference in 2017 McDonald criteria, even if you don't study the entire McDonald criteria, at least this is the most important part. OCB is included for dissemination in time. Then cortical lesions were not included in the old criteria, but cortical lesions are included in the new criteria. And symptomatic spinal cord lesions are included in the new criteria. Spinal cord lesions, which was previously not included for counting the dissemination in space, but now it is included. So, that is also directly from this, from our modules. And this was the McDonald criteria, new McDonald criteria. You have clinical attack and number of lesions with objective evidence should be there. If two clinical attacks, and you have to, your aim is to prove DIT and D is dissemination in time and dissemination in space. For dissemination in time, the new McDonald characteristics included CSF, OCB. And for dissemination in space, previously the spinal cord symptomatic lesions were not included, but the new criteria is included. The third point is cortical as well as extra-cortical. Both have been included in the new criteria. So, that was the two questions which asked for demyelination. Both has been discussed. But Wingerchuck criteria was not mentioned in our module. That was one question which just came out of the box or out of our module or whatever I have, I have taken the classes in that. I have mentioned the criteria, but have not mentioned the name of the criteria. So, next time onwards, I will try to go into the names of the criteria. Those which are not, I thought it may not be like the name of Wingerchuck may not be that much significant. But they asked directly from that area. That was my mistake.

So, we have discussed epilepsy as well as we have discussed demyelination. Now, let us go to the cognition and dementia. There are four questions came from cognition dementia, all together. The first question is, mesolimbic pathway acts where? Acetylcholine, dopamine, glutamate, and noradrenergic. And actually, this has, I have discussed this limbic pathway. I remember like three, four times I have discussed. First, when I discussed when we were discussing about the wakefulness responses of, of the sleep-wakefulness axis. I have already told about that. Then second time when we were discussing about dementia also, I had discussed about mesolimbic pathway. And I have drawn. This was the same diagram which I have drawn during the module in managing the Parkinson's disease. We were discussing about the side effect of dopamine agonists. We are drawn above the reward circuit and median forbidden bundle, mesolimbic, mesocortical pathway. So, this is a dopaminergic part of the origin of the treatment of the midbrain and which ascend upwards and it deviates into one goes to the cortex and second one goes to the nucleus accumbens or limbic circuit. And that is known as a mesolimbic pathway. And this both are dopaminergic pathway. So, we have discussed about number of dopaminergic pathway also there. So, that was again, those who have gone through that module will be able to answer. That is dopamine is the answer. So, mesolimbic and mesocortical pathway are part of dopaminergic pathway involved in the cognition as well as behavior response. And it is part of reward pathway. That also we have discussed about it.

The next question was, abulia points the lesion to which part of the brain? Medial frontal, ventral pons, dorsal pons, and one more option was there. And abulia is actually a motivational syndrome. A motivational syndrome can range from apathy, where the patient doesn't have much adjacent, doesn't come up with answers. And abulia means they will be, there will be some motor movements, but they won't answer. And akinetic mutation is totally akinetic. So, these three are spectrums of a motivational syndrome that we have discussed in lobar function of frontal lobe. In cognition dementia session, we have discussed about this. This is the same slide, same screenshot from there. A motivational syndromes, apathy, abulia, and akinetic mutation were associated with medial frontal lobe lesions. The answer is medial frontal because medial frontal is the energization. Oscillator peripheral is executive. Medial frontal is energization. Orbitofrontal is behavioral and personality. So, the answer is easy. It is a medial frontal. As luckily, we were able to discuss the same thing in lobar function of frontal lobe, apathy, akinetic mutation when we were discussing on middle frontal lobe dysfunctions.

NPH radiology, which among the following is false? And this was again one more area which is actually in depth of neurology has been asked because this is something which is very important for a neurologist's point of view. Because NPH is a quite common diagnosis whenever there is a gait problem with urinary dysfunction. So, apex crowding, sulcus widening, makes the system effacement. So, this also we have discussed in other forms, other dementias, in again cognition dementia section. The last module, other dementias, at the end, near the end, our last discussion was on NPH where we have discussed the different signs. There are some about 11, 12 signs are there. We have discussed Evans index. We have discussed temporal horn dimension. Periodically page is there in the option. So, that is true. This is true. Which among the following is false is a question. And the next one is, the, the, next question is, why sulcus widening? So, that was there here. Widening of the third wonderland sulcus. So, there is something known as DESH, the disproportionate enlargement of the, disproportionately enlarged subarachnoid space. So, that that is what is known as sulcus widening. That means here you can see that there are some of the sylvian fissure and some of the subarachnoid space is very much wide. And the sylvian fissure is wide open. But when you see the higher cut, you can see that the apex is totally crowded together. That is because of a disproportionate enlargement of subarachnoid space. Some areas are dilated, some areas are disproportionately compressed. So, that is again the option given. Apex crowding and sulcus widening. So, those are again true. And basal cistern effacement is a wrong option given here. Even though you do not know the understand about what is basal cistern. Unknown, if you know the NPH findings, you can answer the question. Basal cistern is a space around your ventricle. That this area, the basal area around your brainstem, the pons and midbrain, periventricular as well as the peripondine and all those areas are known as the basal cistern. And NPH, it is because of increased, the, the imbalance of the flow and absorption. CSF is supposed to be the one pathogenesis. And where there will be the problems that happen in the cortex, not in the lower part. And the, the subarachnoid space, upper part of the brain is affected predominantly. So, these are different signs we have discussed. These are same slides we have put in our modules. And this is a callosal angle. The narrow callosal angle because this is, this is callosal angle is one point you can differentiate in PH from an atrophy. Because of the atrophy, then when there is a severe atrophy of the brain parenchyma, they also looks like ventricles are prominent. So, that is one extra-ventricular dilation of ventricles. The extra-ventricular dilation of ventricles can be differentiated from NPH by majorly two points. One is DESH, which you explained. Second one is callosal angle. You see here in the ventricle, here the CSF and the ventricles are applying pressure like this. In the case of an NPH, while here CSF is normal in the case of an atrophy. This is an atrophy and this is NPH. So, here what happens is the, the brain parenchyma has gone down like this because it is atrophied. So, the angle, the callosal angle here is, this is the callosal angle. That callosal angle will be widened in the case of an atrophy. While the ventricles are filled with the increased CSF, that will push the brain like this. And so, there will be callosal angle became narrow or acute. As well as there will be a disproportionately tight apex. That is known as apex crowding. Along with sulcus or prominent in the lower part. So, that is known as DESH or disproportionately enlarged subarachnoid space. So, these two are one, two important findings. This is Evans index. That is a lateral, lateral hemisphere of the, the, the lateral ventricle, the frontal horn transformed bone dimension is measured. And the maximum dimension of the skull is measured. The ratio is known as Evans index. So, Evans index more than six is another important question that can come in the coming up exams. So, all those things we have discussed. So, the answer is compact scrolling, sulcus widening, perimeter of senior NPH. The wrong answer is the basal system effacement. Wrong answer. So, that was also we were able to luckily, that also we have discussed in our modules.

So, which is incorrect match? Again, this is one area we have stressed multiple times during the revision session also. The newer drugs in neurology, especially the monoclonal antibodies and the antisense oligonucleotide group. Those two are very, very important. And when we were taking the revision session, we told that Solganesma, that is used for SMA, is there in the limelight in the news. And Nusinersen also there in the limelight in the news for a long time. And I have mentioned that these two, they may not ask. They may ask the third drug, that is Risdiplam. This is only oral drug for SMA. That also we have covered. And we have discussed in our module. So, this is correct answer here. In the map, migraine, there is another question came in the same question up regarding enmap. So, the monoclonal antibodies and migraine. That we have stressed multiple times. That is also very important. So, enmap has been true. And next two questions. Crystal is a newer drug approved for PPMS. That also we have stressed many times. Is the only drug. This latest structure is applied for approved for MS. That I had stressed once again during the revision session. And this is the question which says Aducanumab and headache. That is actually wrong. Incorrect map. Because we have discussed in our module for the treatment of Alzheimer's disease. In the module of Alzheimer's. See here, the monoclonal antibodies directed Aducanumab, Solanezumab, Gantenerumab, and Crenezumab. Of this Aducanumab is only a drug which is approved just approved in 2020. For when I was, while shooting for this module, some few days prior to that shooting only, this good FDA approval. So, ah, and that was why that is why I kept in the bold lines because it was approved just luckily, just before I was shooting for this module, just few days prior to that, this drug was approved. And that news came in the newspaper center. So, so that is that. The wrong option is Aducanumab, which is not and the headache drug. Which is directed against it is used against Alzheimer's disease. So, that is also we have luckily we have discussed. And this again stresses you that the importance of the newer drugs, particularly antisense oligonucleotide drugs and monoclonal antibodies. And these two things and the latest approved drug, particularly in MS, is important. That is the importance of this question per se for preparation. So, in cognition and dementia, there are four questions asked. More than what we discussed, it is important to understand that in cognition, there has been some questions from the basic neurophysiology. That one question, mesolimbic pathway was directly from the neurophysiology, especially when you are studying about Harrison or medicine. These things are a bit, a bit on the higher level. And the second thing, again, I want to stress is importance of Alzheimer's disease, particularly the newer drugs in neurology. Always for any neurology exam, go with the newer drugs, at least the name of the drug. And this is associated, especially monoclonal antibodies, as well as the latest approved ASOS or genetic drugs. These two things are very, very important. Then this stresses importance of those areas. So, I will tell in cognition dementia, again, is a huge area. Its very important to read Alzheimer's and NPH. Of course, is important every year. But this time, NPH MRI, they have asked in detail. Actually, this was a little bit very in-depth question directly asked from the MRI of NPH.

Then coming to the next session is, we have discussed epilepsy, we have discussed demyelination, we have discussed cognition dementia. Now, let us go to the headache. Headache, two questions asked. And one question was as expected from the newer drugs of migraine, which has been there. The previous cognitions of an option was come from that area only. So, again, that's just the importance of the newer drugs. Then the next question was, ah, the first question was, what is true regarding retinal migraine? Misnomer of migraines with schilo, unilaterally she lost with or without headache, bilateral permanent shells, and biological loss. Actually, this question was, again, we have discussed about it. But the importance of this question is, this is one area everyone will have confusion. Retinal migraine, whether it is bilateral shell loss, where it is unilateral, or whether it is an aura which is seen, whether the aura which you see in visual or you see whether that is retinal migraine. This one area where everyone will have confusion. So, this was discussed in our module. And retinal migraine is attacks of reversible monocular visual disturbance with either positive or negative visual phenomena. So, the answer was the unilateral musculoskeletal headache is answered. Not A or or is not or when you have visual aura, you will call it as migraine aura. And bilateral perpendicular shells is never seen associated with retinal migraine. That is with other laws. You need a bilateral vascular is also when you have bilateral visual loss, you cannot call it as retinal migraine or aura of retinal migraine. Even if it is transient, you call it as somehow accessible attacks because you have to rule out other proximity amino acids. You call it as hypoperfusion because of the hypervision retina or the optic nerve is reason. It can be either a pre-singapore symptom or no. But when you say unilateral visual loss with or without headache, can you, it may be a retinal migraine. But again, unilateral loss without headache, you should rule out an optic nerve head. So, that was we have discussed it in migraine session.

And then coming to the next question here. Enmap, which has come in the previous option also. We have discussed about the enmap, the CGRP related drugs and newer drugs. This is a slide from our module. We have discussed about the drug and we have told that it is given monthly injections. And we have told that the monoclonal antibody receptor and target both are different. Because this this can either target the CGRP directly or you can block the receptor. Two groups of drugs are there. And overall drugs are G-PUNS and these all things we have discussed. But we have not discussed that whether there are side effects of phenomena. We have not gone through. But you can answer if you know the other things also. Because it is given subcutaneous, that we have discussed. And it will cause us, it is a CGRP analysis, that we have discussed. One semen injection also we have discussed. So, the remaining option is hypotension. But we have not discussed about side effects of these drugs. And post-marketing trial, it has been shown that they produce hypertension, not hypotension. And injection site reaction, constipation, cramps, muscle spasm. These are the side effects with this drug. So, and there are two questions asked in headache session. And out of that, one question we have discussed. Second question we have discussed. But we have never gone into the details of this much. We just asked the question. But I think you can be able to answer even if you know. You can rule out the other option. So, you can arrive at the final answer directly. But we have not discussed about that in our modules about the side effect of enmap. We have not gone. But still, you can be able to answer it. Because the other, when you frame such a new question, the examiner who is setting the question also thinks the same way. If you keep the one option which is the answer, which is really tough, but other options if you know, you can answer it because you can exclude other options. So, that is same, the same, same basic idea of answering this question also. If you know the other three options, you can exclude the three options and find out the answer. So, we covered that also.

And then coming to the MND and NMG. The total two questions asked. One was, as we expected, the newer drug of SMA that is Nusinersen has been asked. And this is the answer is something that I think most of you will know it. And these are three newer drugs. And you see in the options, they have asked about Nusinersen directly. One question. And one question they have asked about Risdiplam. And this is only oral drug. Okay. We have covered it in one table also. We have put in the Spinal Muscular Atrophy, SMN, and B survey. How SMN1 based therapy in SMN2 based therapy. Nusinersen is only SMN2 based therapy. Others are SMN1 based therapy. That is also a possible question which may ask in the coming exams. So, that is Spinal Muscular Atrophy. And that was one question. The second question is Congenital Myasthenia with episodic attacks and family history. Semiside is associated with DOG7, Rhapsody, Chat, and Agrin. This we have discussed in our module in the query, in the MCQ. In congenital myasthenia, we have discussed the crisis is associated with either Raps and seizure and fast channel. And you need to come back to the option. These two are there. Raps as well as Chat deficiency. But this we have discussed. C stands for crisis. So, that means severe attacks are associated with Chat and childhood attack as associated with C. Chat adult also they will have C Chat associated myasthenia will have crisis or respiratory failure. But Raps usually they will present with associated childhood crisis, higher spirit, and arthrogryposis. But then adult life, they won't have crisis. So, crisis is predominantly Chat deficiency. That is C stands for crisis is what we have discussed in our module. The question came from there. And NMG, mainly the two cases. Both were, both were, we have discussed. But more important to understand is that in MND, now the most importantly, the hot topic is SMA. And NMJ again, the congenital myasthenia is one area they will ask a lot of questions. So, these two were expected important areas. And questions free from that, the same area only. So, there were actually, in fact, two questions will be able to answer if you know there's some metrics. One question was asked regarding which among the following drug is false. Aducanumab. So, and the answer there. But you should know that the importance of SMA. Now coming to the most important and most high-yielding topic for any exam, that is stroke. There are 13 questions asked. And there are four questions which we have not discussed. There are four questions out of the 13. So, that is one area we need to, I think we need to know a little bit, go a little bit further.

And this was the first question was, which among the following is wrong regarding risk reduction related risk in stroke? That is something like that. This question was not exactly what, not the same question. But the question was asked about the relative risk. That all the options are regarding which among the following is wrong related to scan risk reduction of the options. And I am not sure whether these were the options asked. But the theme of the question was from this table directly from Harrison, which we have not discussed in our module. I have not discussed this in the module. Actually, I had taken depth about stroke, but I have not discussed this table in our module. But Harrison tables for the hallway is important. And this was a question which asked from this table. So, you should by have this table related destruction of hypertension is 2.5. Atrial fibrillation 1.8. Diabetes is 1.8. It was 0.6. Smoking 1.8. And asymmetrical rotational solid risk is 2 highest. But I just, these options I was not sure. And I just, I got these options from the available options. Diabetes, warfarin, and smoking related risks are correct. But asymptomatic keratosis is not 20%. It is 2%. But again, I am not sure whether this was the exact question asked. But the question came from this table in Harrison about the risk factors of strokes. So, again, stress the importance of the tables in Harrison.

And this was the next question. The patient hemiparesis, plan for thrombolysis, initial investigation of choice. Actually, this was the same thing we have discussed multiple times during this, the managing the stroke. I was stressing to the point that there is no end of MRI. There is no need of CT angiogram. Although there is no need of ECG also. Only three investigations are required. One is BP, second is GRBS, third is an imaging is plain CT. And one thing that is clinically in the NIH score. These are four things required for thrombolyzing a patient. Nothing else is required. That has been stressed many times. And even I have framed a similar question in our Facebook page. Put a fund question. And many answered that it should go for CT angiogram. And somebody has came with the Alberta. I mean, some, some of the, some, some of the old gate lines which mentioned about in need of CT angiogram. And so, CT angiogram is optional. And similar question assassin in a CET for PG also. So, this is one favorite area because everyone is confused because each hospital has each protocol. But what a in 2020 or 2019-20 gate lines they tell that only CT, blood pressure, and capillary blood glucose. These are three investigations which is required for thrombolyzing a patient. Plus a clinical NIH scoring and clinical diagnosis stroke. That is enough. And if you meet the other contraindications and indications criteria are met, you can take directly for thrombolysis. So, the answer is NCCT, capillary blood glucose, and BP. And you don't need any other investigation. A plain CT, a blood pressure, a glucose. These are three things required for thrombolysis. Nothing more. There is no need of CT angiogram. There is no total need of MRI for thrombolyzing a patient. Your aim before thrombolyzing is to treat the patient at the earliest. Don't waste 20 minutes or 15 minutes for MRI. And your aim is to just a clinical diagnosis stroke and a contraindication indication will be met. And you need to take a CT to rule out bleed. That was the only thing you need. Then this was directly discussed in your module in the acute stroke management, investigation, thrombolysis, and monitoring at 18 minutes.

And next question was, a young male with a gas to somewhere like this. It was actually the image is not exactly similar. What I got from my students is that the question was a gastronomic saying male with decision. And what among the future, the following is false? And for answering this question, you need to understand about the image, some ideas of the image of the CVT. And from my students, what I got was it was like the image has having a dense delta sign. I mean, delta sign was there. Empty delta sign. So, this is something which I, it's not exact image. So, you can see that is a contrast image. You can see a bleed here. And this is a contrast here. And you can see the contrast is enhancing like this. And the central area you are seeing a non-enhancement. When you give a dye in the venous phase, the vein is supposed to be filled with dye. Here, in the center of the vein, there is a hypodensity or non-filling area. That is the thrombus sitting there. And this shape is delta. So, that is known as the empty delta sign. And this empty delta sign means that we were discussing about CVT. And I didn't get the exact options which has been asked. I didn't get one option was mandatory. And glycerol is not indicated. Actually, that is true. Because mandatory and glycerol is indicated only if there is edible. There is a iron. You know, it may not need again. Glycerol, antiplatelets, and anticoagulants is something which is to be given. Even if there is a bleed. That also we have discussed in the CVT when we are discussing about neurosurgeon in MCQs, MCQ session. And eurozone, we have made an MCQ at the end. We are discussing about CVT. There we have told that the different signs of CVT were discussed. And then we have discussed in the last question, we have discussed about the management of CVT where I have stressed the importance of anticoagulation to be started at the earliest without delay. And antiplatelets is never the option. I, I didn't get the other option. But you need to understand the idea. Basic idea of the question was to, the, the sign of CVT. It is very important. The empty delta sign is very important. And the treatment, basic treatment aspect of CVT. So, ah, that is something is we have discussed previously. Different signs we have discussed. This is a dense cloud sign or dense or a dense vein sign because of thrombus in the straight sinus. And this is a plain CT. This is a plain CT where you are, you can see that again, hyperdense area over the, the, the posterior area. And that is not a delta sign. Delta sign is significant in contrast CT. And these two are images of plain CT. What you are seeing is a pseudo delta sign. And here is a code sign where you see the, the transverse sinus is filled with thrombus. And the plane CT. And this is the same image which I kept there. This is empty delta sign in a contrast CT. So, empty delta sign occurs in a contrast CT.

Next question is, a 40-year-old male with hemiparesis. CT showing a basal ganglia. Prognostic score include all except. This is one area we have not discussed. So, ICH, intracranial hemorrhage, we have not discussed. That is an eye-opener for me. I will, I'll try to make something out of this. And I will put some questions regarding this area. At least. And the site of bleed, age of the volume. But you all know this criteria because you might have used it in your casualties. And I hope that most people who are doing MD Medicine will be able to answer most of the questions which comes from the ICH. Do you all know that what is the common site of bleed? You will know the ICH scoring system. So, that was the one notion. I just didn't go in detail for the ICH. And this is ICH score directly from Madison. The table is given below, which includes age, hematoma volume, and hemorrhage into fat and intraventricular location, Glasgow's coma scale. And does not include time of onset of symptoms. So, that is the wrong statement. Site of bleed is important. Age and volume is important. Because these two, interventricular, intra-parenchymal, and site of the bleed. This is cemetery volume. And this is common scale. So, the option which is among the following is wrong is actually time of onset of symptoms is wrong. And so, that is one question is came from ICH score, which we have not discussed.

The first question also, which we discussed just now, was something which we have not discussed. Normally use the mechanical thrombectomy. Which among the following false statement? Actually, the exact options I didn't get. But they were regarding the indications and contraindications of mechanical thrombectomy. Where they were given an option that is what I got. So, can these are something which I got from whatever from the students I were able to get. And these were one options. Can be done those within more than six hours. Can't be used with smaller than 4.5 hours. So, mechanical thrombectomy is done up to six hours. Level one. And after six to twenty four hours also, you can do. So, cannot be used after 4.5 hours is a wrong answer. So, that is the false statement here. Because the question asks is also false statement. So, the answer.

Was that remaining were all true regarding indications? So, this also we have discussed the slides. The same slides we discussed in our stroke module in the individual therapy chapter. We have discussed it: Level 1, A, Level 2, and Level 2B evident. So, 16 to 2016 to 6016 and 1624 meeting known and diffused criteria. We have discussed about dawn and diffuse also. And this was the goal of thrombectomy also we have discussed. So, I again stress the importance of the indications, contraindications of thrombosin, thrombectomy. These two are the favorite areas. So, stroke management part is something it is very, very important for your exams. And I believe that the stroke questions in any question paper, they come from the practical areas. The ICH score is important for practical. Uh, the risk reduction is important for practical. Uh, the indication, contraindications are important for practice, practice in your practice day-to-day practice. It is very important. So, all these various questions should come.

Another is TIA ER score. That is also a very important ABCD. That is actually not ABCD, it's an ABCD score. ABCD is two score charts. So, HAS score, ASPECT score, MRS score. So, CHA2DS2-VASc is for AF, and ASPECT score is a CT score for thrombolysis. MRS score is a disability scoring in the stroke. And this is ABCD2 score is the answer TIA, which we also discussed. ABCD2 score again, it is that from Harrison only. And this is ABC 2 score. Uh, A is B for blood pressure, C for clinical symptoms, D for duration, and D for diabetes. And ABCD2 score is a score which is used in TIA, which we have discussed. ABCD 2 score, ABC 2 I score, ABC 2 is 2 score. All the possible scores, all the possible important TIA scoring systems we have discussed in our module. And it has discussed in a stroke mechanism and pathology session in the stroke module. So, again, this stresses the importance of practical scenarios of scoring. Practical scenarios are being asked repeatedly in stroke.

Then, 74-year-old diabetic with a diabetic hypertensive with a diabetic hypotenuse with AF. No, thus with increased risk of stroke. Again, this is again the same practical scenario. So, what they mentioned is a non-valvular AF. If you have a valvular AF and non-valvular AF, non-valvular AF is based on your CHA2DS2-VASc score. And valvular AF, you will start anticoagulation based on certain other criteria. Valvular AF includes severe MS as well as mechanical replace. You will can go with warfarin only. But non-valvular, you can either go with newer oral anticoagulations or your plain warfarin. So, this was based on the CHA2DS2-VASc score, which we discussed in the stroke secondary prevention in the stroke module, where we have discussed that C stands for CCF, H stands for hypertension, A stands for uh, age more than 75, D stands for diabetes, and S stands for stroke, uh, previous episode of stroke or TIA. And V stands for vascular disorders like PVD, and A stands for 64 to 75, and S stands for female sex. So, here the question, the clue was actually a question. It is a male. So, the answer is the gender is not as because CHA2DS2-VASc score, the gender female generates. But male gender is known. Age 75 is a risk. Diabetes is a risk. Hypertension is a risk factor. A. So, this is you just need to understand the chart. So, CHA2DS2-VASc score. The practical scoring system, the TIA score, CHA2DS2-VASc score, ASPECT score, all these scoring systems are important in stroke. NIH score again, one more question has come. So, all these practical scoring systems and trials are very important in stroke session. ICH score, ASPECT score. So, this is the CHA2DS2-VASc score. And ASPECT score, you need to understand the ASPECT also because this may be the potential next coming question.

And all our thrombectomy trials, except this is one more area which we have not in depth, but I have stressed the importance of this when we're discussing revision in neurology. I told you to just remember the name of the trials of stroke and name of the trials of MS. These are two trials which are very important. Just at least a name is enough. In which it is used, whether it is thrombolysis, then it is thrombectomy. That is enough. So, next question is, what are thrombectomy trials except? Actually, uh, we have discussed in our modules about thrombolysis trial, the CHANCE trial, POINT trial, but we have forward, we have not mentioned about uh, the thrombectomy trial much. We have just briefly gone through some of the trials. But when your revision module, we are discussing in that, I have my specifically mentioned to know about MR Rescue, ESCAPE, and all. And if you read this, you know, you have if you're going through Harrison tables and Harrison, at least going through major trials in thrombectomy and thrombolysis, you will know ESCAPE, SWIFT PRIME, MR RESCUE. They are thrombectomy trials. So, the one that is standing out is HAMLET. But HAMLET is a trial for uh, decompression craniotomy. In fact, there are many trials in decompression. One is HAMLET, second is DESTINY trial. These are important trials. Then there are some hypertension trials like DIGITALITY trial and all those things. But you don't need to go into that detail. Actually, this question also framed in such a way that you need to know the basic thrombectomy and thrombolysis thrombolysis trials. And if you know the thrombectomy landmark trials, then you can answer the question by telling that HAMLET is something which is over here. Even if you don't know what is HAMLET. So, such questions are always framed like that. You don't need to study all the trials. But whatever they are in the hierarchy or whatever they are in the important major trials, you study it. And if you some some other questions come in out of the books, you can answer it with whatever knowledge you can have by eliminating the options. So, that these are the thrombectomy landmark trials of thrombectomy trials are MR CLEAN, EXTEND-IA trial, ESCAPE trial, SWIFT PRIME, REVASCAT. THERAPY, THRASH, PISTACHE. These three things are not there. Narrative. There is no need to study that also. If you know the name, it's fair and fine. But at least remember MR CLEAN, EXTEND, ESCAPE, SWIFT PRIME, REVASCAT. And DAWN and DIFFUSE. We have discussed in our uh, discussion also. MR CLEAN, EXTEND, ESCAPE, SWIFT PRIME, and REVASCAT. These are the four trials for four fight trials which are mentioned in the Harrison also, even the old areas. And also they said that the landmark trials, the new landmark trials are THERAPY, THRASH, and PISTACHE. At least from the name of the trials and where it is in thrombolysis, thrombectomy, that is enough. No need to go into further details. The questions will come in that area only.

And the trials of alteplase or thrombolysis, important trials are NINDS trial. This is very important because this is the first trial which proved the efficacy of thrombolysis in first three hours. Then came the ATLANTIS trial. And it also studied up to three hours early, but it doesn't prove that it is more than three years, it is not useful. And ECASS II also tried to study to extend the time of thrombolysis. But ECASS III has proven that the significant improvement of clinical outcome in three to three point five hours. This is one important question that can ask. So, other trials, name say something which proven less than three hours. So, three to four point five, that's just proven by ECASS III trial. Okay, that is one more important thing. So, these are two trials you should at least remember. NINDS, ATLANTIS, ECASS II, and ECASS III is very important. And in patient wake-up stroke, the stroke investigation with thrombolysis is also a newer advancement which came in 2019 guidelines, which we have discussed. A new update on the guidelines for wake-up stroke. Previously, wake-up stroke were not thrombolyzed. But his trial known as wake-up trial came up. And in that trial, it has also discussed in our modules early, in the module of stroke, we have discussed the checklist for thrombolysis indication. Same slide: age more than 18, clinical diagram of stroke disabling and NIHSS more than 4.5 hours. And it's a new entity which came up in 2019-20 guidelines, that is unknown onset with diffusion-FLAIR mismatch. So, when there's a wake-up stroke or or a unknown onset, you do a diffusion-FLAIR. And if there's a there is diffusion restriction showing infarct and FLAIR, there is no mismatch. And there is nothing in the FLAIR, a FLAIR is normal, you can take it for thrombolysis. Seemingly because they thought that diffusion restriction will start coming even within half an hour of an acute stroke. But FLAIR means the changes appear by around four hours. So, if you have a diffusion restriction there, but FLAIR is normal, that means the window is between four and around fifteen minutes or half an hour. So, that means that you can take it for thrombolysis. If if FLAIR also has shown hyperintensities, that means it has crossed four hours. So, then it is risky thrombolysis because you don't know whether it has crossed the window period of 4.5. So, diffusion-FLAIR mismatch is the answer. CT is used for other patients. Perfusion scan is not needed if it is less than six hours. Even if you are taking for a thrombectomy, less than six years, it is not a perfusion scan. That we have discussed in a module. CT angiogram is not an emergency investigation. You can do it later. So, the investigation required for a diffusion-weighted imaging in wake-up stroke is diffusion-FLAIR mismatch because the same wake-up study which used the same modality to thrombolyze and so that is a fourth indication. It's a newer indication. Again, it's a newer update. This is other indications and contraindications which we have discussed in our modules.

Then coming to the next question, that is lateral medullary syndrome. And till then, now the questions what we discussed in the stroke, the importance of the scoring system as well as the latest updates. So, that is already there which we have discussed in our modules also when we told the newer updates which are not there in Harrison and which is coming up late. So, newer updates and the practical scenario management is very important. Stroke. Then lateral medullary syndrome, which is true. This is actually a tricky question. I feel it is very tricky because the option I got is this one. One is same side pain and temperature loss, opposite side face numbness, contralateral ataxia. Say downbeat nystagmus. Diagnosis. Actually, we have discussed lateral medullary syndrome in brainstem syndrome part two. I'll tell once again. You have brainstem inhibition structure. You have midline four structures and laterally on the side, there are four structures. So, S stands for side and M stands for midline. Midline, you have structures starting with M: MLF, medial longitudinal fasciculus, medial lemniscus, and you have motor fibers or pyramidal fibers. Then motor nucleus of certain cranial nerves. So, those cranial nerves are multiples of 12: 3, 4, 6, and 12. All these come in the midline. All other motor nuclei come in the lateral. So, on the side, you have S: spinothalamic nucleus of fifth cranial nerve, spinothalamic pathway, spinocerebellar pathway, and the fourth is the sympathetic pathway, plus other motor nuclei. These are there in the lateral in entire brainstem. So, four M in the midline and four laterally. This we have discussed in our brainstem also. So, when you come to the lateral medullary syndrome in the medulla, you have the lateral cranial nerves. The medial cranial nerve is the 12th, which comes in the middle. So, 12th is unaffected. So, you take the pain and temperature, which is carried by spinothalamic, which crosses the spinal cord and goes there. So, if suppose I am having this is the right side. Suppose I am going to have an infarct which happens to be occur in my right side, right medulla. So, it should affect my right side and spinothalamic tract, which carries input from the left side. So, opposite side pain and temperature. That is wrong. Then comes the opposite face numbness. Again, that is wrong because the this side spinal nucleus will be affected or the fifth nerve. So, same side. So, that is also wrong. And ataxia. Again, the spinocerebellar fibers are affected. So, it will affect the ipsilateral ataxia. Ipsilateral ataxia associated, not the crossing. Very ipsilateral ataxia. So, all these were absent. These were wrong. And nystagmus can present in lateral medullary syndrome. That is a probable answer. But the problem here is that again, what I got from two, three students, the same, they all told it is downbeat nystagmus. But when you think in the view of a neurologist, you open braces, you will see a lot of variants of lateral medullary syndrome where you can have same side face and same side body sensation. You can have opposite side face also. So, if you take into that aspect, there are multiple true answers. You can have any type of any type of lesions in lateral medulla. And downbeat nystagmus per se. Braces, nystagmus, downbeat nystagmus to affect, you need to get affection of medial longitudinal fasciculus, which is located in the midline. So, lateral medullary syndrome can present with horizontal eye movements also. And upbeat nystagmus, downbeat is not common. So, in fact, this question, if you take in detail as a neurologist's point of view, there you cannot find an option. So, you cannot find an answer because all are either true. I feel like all these three are true, and I feel this is wrong. If I take in a neurologist's point of view. But if you think in a physician's point of view and if you think as at the MD level, you take don't go into the variants. Just take the classical lateral medullary syndrome. In the classical lateral medullary syndrome, the same side pain and temperature, opposite facial numbness, and contralateral ataxia is less likely to occur. And you can have a downbeat nystagmus. You can have any nystagmus. And there's a slight extension of midline, you can have downbeat also. So, I feel this is an ambiguous question for me. But I feel the answer what examiner might have meant was downbeat nystagmus. Just if you know the crossing cerebellar fibers. Because at the MD level, you are expected to know the crossing fibers. And you are expected to know the basic, the plain lateral medullary syndrome, not the variants. So, if you account that the true statement should be downbeat nystagmus. That is what I feel is. And this is what is discussed in brainstem syndrome two. The vertebral artery more than PICA is more common. Ipsilateral fifth cranial nerve, ipsilateral eighth cranial nerve, and ipsilateral ataxia. So, ipsilateral it will produce vertical and horizontal eye movements. And sympathetic will produce ipsilateral Horner's. And spinothalamic tract of opposite effectors are contralateral sensory. Icy, perfusory, cerebellar affected. So, ipsilateral ataxia and hiccups and diplopia can occur. And parasympathetic affection will produce hypotension, bradycardia. And the medial midbrain syndrome, you will have medial structures. So, the MLF is affected, um, and produce upbeat or vertical or downbeat nystagmus can present with MLF involvement. So, I think the probable option will be downbeat nystagmus.

Then coming to the next question, primary CNS vasculitis. Is not true. Actually, we have discussed about primary CNS vasculitis when we are discussing about the classification of stroke at the end. We have discussed that vasculitis as a cause of smaller strokes. And where we discuss the primary CNS vasculitis, we have stressed the point that they will not present with stroke. They present headache and altered sensorium is more common. And they want they'll see the stroke, for say, bleed or infarct is less common. So, these two you can tell that these two are correct. But you will be confused between these two. And we have not discussed this in details in our modules. So, actually, primary CNS vasculitis occurs more commonly in males, not females. And primary CNS vasculitis, MRI is almost 90-95 percent. MRI will be abnormal. If a normal MRI almost rules out it. Because MRA, now you may see some white matter abnormalities. That is a basis of suspecting a primary CNS vasculitis. Plus, they usually present headache, confusion, and altered sensorium. And stroke, bleed, or infarct is very less. Men are more common. It is 70:30 according to Medscape. And four to six decades is onset. And headache, confusion, and coma are the common presentation. And stroke and bleed can occur. And MRI is abnormal around 90 percent. Location and criteria. Just remember the name of the criteria. You just come in the latest Bradley. So, this is a possible another question which can come because they are they are more interested in these criteria. CAL'S-BREEZE criteria, CAL'S-BREEZE criteria, which you just remember the name. That is enough. And unexplained neurological evidence or either classicographic angiographic, I mean, unexplained headache, unexplained neurological deficit with either pathological evidence or other classic angiographic evidence of CNS. And there is no other systemic vasculitis or other explainable causes. That means that for a primary CNS vasculitis, you need to get a brain biopsy or an angiographic evidence with an unexpected neurological finding. And the gold standard is biopsy. But you don't need biopsy for diagnosis always. Uh, but other causes including other systemic vasculitis, SLE, everything, APL, everything as you rolled out. You cannot call it as primary CNS vasculitis. If those are positive, you had to call them a secondary CNS vasculitis secondary to APLs, secondary to SLE, like that. Okay. So, that was a question which is uh, which is not much discussed in our modules. I have just gone through that very, very briefly.

So, this is another question. Is again a practical question which asks NIHSS score. NIHSS score is very important score for a practical purpose. So, what is a question after NIHSS score? Again, this is for those who have practiced asking NIHSS score. Otherwise, you want you will be difficult because it will be confusing to remember and you will not revise these details of scoring system before exam also. So, those who are used this scoring system during the three years from the MD, they will be able to answer it. So, the options are name and time, name and month, name and age, month and days. Actually, this has been discussed in acute stroke management. And I had shown the NIHSS score table also. And you can see here, the level of consciousness, age and month, not name, because name, nominal affairs will be confused with it. So, age and month is asked. So, the answer option here is age and month. That is the last option. That is what is there in NIHSS scoring system. No other questions are asked for level of consciousness. Are asked by calling the patient, waking him up, alert, or going to second level of consciousness. One A, B, and C is there. A is for level of consciousness. B is for level of consciousness by asking questions. The question asks is a patient and month of birth. And what is the month? This question asked. And level of consciousness, people open and close your eyes and grip and release your hand. So, that is a question asked here. Was that from the NIHSS is a very practical question which is for those who have practiced using NIHSS score only will be able to answer. That is what I do. I am I I believe so. That was a question.

Next question is false statement regarding thrombolysis. Again, the options I am not sure with it. But the option which was false and that is the answer is alteplase not approved in India. Actually, alteplase is approved in India. And we have discussed about it in our stroke session also. A wake-up stroke can be thrombolyzed with diffusion-FLAIR mismatch. And tenecteplase. This is actually I frame these options because I didn't get the other option from the students. Which has given me some of them stored that this is the and this was the wrong answer, wrong option from all the given below. Remaining everything was regarding some indication. All regarding was true. The question was alteplase was not approved in India. This thing. And I think the examiner was pointing towards the latest update again. So, other fibrinolytic, tenecteplase has been approved. Even Indian guidelines, 2019 stroke guidelines, as well as the AHA guidelines, which proved that tenecteplase can be used. Their two doses, total dose, which is 0.25 and 0.4. This is the same slide which we have discussed in the acute stroke management, investigation, thrombolysis at the time given below in our module. So, tenecteplase is approved. There are two doses have been approved. Uh, those with minor stroke, you can use 0.4. And those who are taking for thrombectomy, it can be preferred by giving 0.25 mg per kg maximum dose. So, in the stroke module, again, stroke is very, very, very important module because the bulk of the questions came from. 13 questions out of there. Four were not discussed. CNS vasculitis, we have discussed partially. But there is a detailed question asked. Remaining everything actually were very practical questions. So, very practical and latest updates. These are the two areas which they have asked entirely in the entire question paper. The newer question, difficult questions were all from the practical aspect as well as from the updates. So, the next was ICH score. Again, directly from Harrison. Again, Harrison tables, reimportant trials and related stroke. ICH score again. So, you need to understand the importance when you are reading, reading any session. The new updates are important. And the practical scenarios, especially stroke is a very common case for any medicine fellow. So, these, the practical cases in the common scenarios, they will ask the practical things. That is the take-home message for me.

And now coming to peripheral neuropathy. There are three questions were asked. First was a cause of LUTS, all except. And we have discussed about this multiple times. One when we're discussing about the familial amyloidosis. Just we have just briefly gone through that. I had not discussed in detail somewhere in the peripheral neuropathy. I remember like in while discussing about other neuropathies. Just as mentioned about the heritage. Just just mentioned about that. But when we discussed about other neuropathies in the MDGS, we have discussed amyloidosis has been seen associated with all the monoclonal bodies. And we told that they present. I had told that they present with a male patient of CTS. Young male CTS. Always suspect the possibility of amyloid by ruling out a small fiber symptom. That is what I specifically told. Autonomic neuropathy, small fiber. That is very common with amyloid. Length and sensory motor neuropathy. They can occur. Can lamborgh. But AL amyloidosis, we have discussed in the context of contextual peripheral neuropathy. And amyloid angiopathy, we have discussed in stroke. Amyloid antibody occurs because of A beta 40 deposit. We have discussed in Alzheimer also. We have discussed A beta 40 and 41. 40. So, that has nothing to do with AL amyloidosis. So, the AL amyloidosis, the peripheral nervous system is not a brain. Doesn't affect brain. So, almost differences from this reference is actually from Bradley. It affects all the individually. Commonly affects either individually together in kidney, heart, liver, and autonomic nervous system, peripheral nervous system. CNS is not mentioned. So, stroke is not associated. But stroke is associated with A beta 40 amyloid dominant Jupiter. Both are different entities. And familial amyloidosis also presents with predominantly say peripheral neuropathy. So, we have discussed about the different manifestations of AL amyloidosis in other neuropathies. We have discussed people from CTS, they present with small fiber neuropathies and other neuropathies. Whenever a young male person with CTS, there should be a possibility of this also should be considered and should be evaluated. Especially for autonomic neuropathies. So, autonomic neuropathy, always a male is one thing we have to evaluate. And this was a table. This was a chart. We have discussed about other neuropathy. I'm not going into details in that. All the monoclonal gammopathies can present with amyloid-like presentation. And we have discussed that they present with CTS and peripheral neuropathy. So, um, this introduces venous affection and produce probably stroke. And this was a bit out of the way. We have not discussed about in detail about amyloidosis in our modules. And the next question is to show that not the neurosupply of urethra. That was an interesting question. Because you may think that this is something very new. But it is actually, in fact, not new. One. This is a practical question. Again, we have discussed about neurogenic innervation of bladder. In that, we have told that bladder innervation: sympathetic, parasympathetic, somatic, and higher center control. You see the hypogastric neurosupply, sympathetic, parasympathetic, pelvic splanchnic, and somatic by pudendal nerve. And we have shown the same figure in that. And you can see that pelvic splanchnic supplies the internal sphincter, internal urethral sphincter. And you can see the hypogastric and vesical plexus, which supplies again the internal urethral sphincter. And pudendal neurosomatic supplies external. So, that is urethral sphincter is part of urethra only. So, question is directly from the bladder. You make it simple. It is directly in the bladder. Uh, so, pudendal nerve supplies. Hypogastric nerve supplies. Will be expanding. Ilioinguinal has nothing to do with the urethra. It is just something which comes in the lower part of the abdomen and the perineum area. So, it has nothing to do with the urethra. So, that the answer is ilioinguinal. That is actually, in fact, a simple question. Even if you don't know the supply, feeling, you can leave. No, if you know the bladder innervation, you can answer this. So, that is actually discussed from our question.

And second question is actually, in fact, directly from our module on the upper limb. In that, even in the revision, as well as how to prepare for NEET, I have mentioned specifically that these signs are very likely to ask. And I have told that during the revision, I have attended the DNB exam. They have put a Phalen's sign, similar figure of Roman sign, and asked what is this sign and which nerve. Same question came here. And they have put the somewhat, it's not exact image, someone image like this and asked which nerve is affected. And this is an OK sign. So, we have discussed about it when we are discussing an upper limb nerve. So, you can see that we, this is the same drawn by me during the discussion. So, that is OK sign. That is associated with median. And that is anterior interosseous nerve, is a branch of median. Posterior interosseous of radial nerve. Ulnar nerve has nothing to do. The OK sign is because when you hold like this in OK position, you need to flex the flexor pollicis as well as the digital phalanx. So, these two are supposed to be median by the anterior interosseous. If this is weak, you can show like you cannot flex. You can just hold like this. You cannot able to. You can see here, this is straightened here. And here you can see the bend is very sharp here. But here you can see it is more or less less flexed. It is flexed in interphalangeal first in the front. Distal is not flexed. So, that is a classical feature of anterior interosseous nerve. Because distal neural phenolic and joint is affected. As well as if peel is affected. So, anterior interosseous is the answer. The sign is OK sign. I am not sure exactly this question was asked. But it was OK sign which is kept for example. So, OK sign, we have discussed in upper limb nerve in our modules. So, peripheral are three questions asked. All were discussed. But I will tell that AL amyloidosis was a little bit out of the box. And we had not discussed that much detail. But if you know that we have discussed it in the peripheral nerve. That is enough to answer it. Because we are not discussing AL amyloidosis in the stroke. Stroke, we discuss A beta amyloid deposition. That is a different one. So, that was about peripheral nerve.

Now going to hypokinetic and hyperkinetic disorders. Total three questions asked. The first question was which I has been stressing during the module as well as during the revision session. I have told that newer drugs are important in Parkinsonism. Again, I have stressed about safinamide, rivastigmine, ropinirole, and opicapone. All these were the options. And MAO-B inhibitor is safinamide. Safinamide is not uh, it is not there. Is safinamide is an MAO-B inhibitor which has been discussed when you're discussing about management of Parkinsonism. You can see that I have written on my own handwriting. This happened. I made. So, safinamide is a newer drug which has been approved. And it is again stressing you whether we have discussed or not, that is nothing a matter. What is important is is again stressing you that newer, latest, and approved drugs is always, always, always whatever is a neurological decision, that is very important. So, always go and revise before the exam. The newer drugs, and especially monoclonal drugs, especially the uh, the uh, and the synthetic and the ASO drugs. So, those genetic drugs and newer drugs, always, always revise before exam. This again stresses the importance of that. Okay. You see, rasagiline is another new drug. All these things we have discussed in the management of Parkinson's.

The next question was again, 21-year-old female, restoring posture, behavioral symptoms. And I have mentioned that whenever there is a there is a young patient or any patient comes with behavior, a lot of dystonic symptoms, unless the story, always rule out Wilson's. And if you see the options, so it is clear. It is an autosomal. Which one of the following is true? That is the question. Autosomal dominant inheritance. Wilson's disease, we have discussed. We have discussed that it is an autosomal recessive. I am not going into the actual image. Image of script. Even if without image, you can answer it. Image kept as something like a panda sign was kept. And actually, we have not discussed about images of Wilson's. That is actually something. It's an eye-opener again for me. You have to go in detail about the MRI images. We have tried to put almost all possible images in the different modules. But this thing actually we have missed it. And I think I have told the image. I have not shown the image. And autosomal dominant inheritance. That is wrong. Even if without this, we can answer it. Because I have mentioned that dystonic posturing, generalized dystonia, always, always rule out Wilson's. And I don't know. It is dietary supplement of copper. Because copper deposited disease, you are not going to supplement it with restrict the copper. That is wrong. This is true. Because restrict copper is true. And this is something which you all will fall for. Because genetic defect of copper transport or protein called ceruloplasmin. Is not its a low ceruloplasmin defect. It is ATP7B defect. And that will reduce the amount of ceruloplasmin. So, low ceruloplasmin gene is not affected. The answer is restricted copper. And what you are seeing here is a panda sign. So, in there is two signs. One is face of J and panda. And double panda sign. J and panda is something you see in the midline in the midbrain. Where the eye of the panda is formed by the red nucleus. Which is here. The red nucleus. This hypodense. The face. I.e. of the panda. And the ears are produced by the preservation signal. Single signals of the substantia nigra pars reticulata. Ears. This is the substantia nigra pars reticulata, which produces ears. And the chin is produced with a low signal. Let's say superior colliculus. So, this is a chin. Genius producer. Low signal density of hyperbolic. Many hypo signal intensities of superior colliculus. So, that is the panda sign. You will see the panda sign where panda sign you will see in midbrain. While the the the miniature panda sign. Club panda sign is seen in the pons. So, there are these two pandas. Similar sign is seen in the pons. These two ponder together. It is known as double panda sign. So, one panda sign is seen in the midbrain. And second panda is smaller panda is seen in the pons. And this smaller panda plus bigger panda, you will call it as double panda sign. So, these two signs, especially panda sign, is very important in the context of Wilson disease MRI. They will keep protein panda sign or bright claustrum. These two are very important. So, that was the giant panda sign. Second sign is miniature panda. That is seen actually. Just remember it is seen in the pons. So, in the pons, miniature panda. And in the midbrain, you will have a giant panda. Together known as double panda sign. Another sign is a bright claustrum sign. You can see that claustrum is hyperintense on T2. So, that is the three signs of your Wilson disease. So, that is one question. Actually, even if you don't know the MRI, you can answer the question. Because it is a restoration and options that are all regarding the Wilson's. So, Wilson's disease is just a basic question. I think most of you will be able to answer. Even if MRI. And next question asked was example of complex tic. This is actually again something which is quite, uh, different, difficult question for me. But for MD, little easy. Because in Harrison, it is clearly mentioned. The options were sniffing, slugging, your shoulder, hand movements, and shaking. So, this is statement from Harrison. Complex tics are with coordinated movements of multiple muscles. Latest Harrison, jumping, sniffing, head banging, echopraxia. So, sniffing is given in Harrison as a complex tic. But in American Academy of Neurology, Continuum Journal for Movement Disorders, 2019, they had mentioned that simple vocal tics include grunts, balls, photos, moans, groans, sniffs, and throat clearing. So, vocal simple tics. There concludes sniffing is a complex tic. So, you can go with sniffing is a better answer. I feel struggling of short, simple hand movements is simple. Hand shaking is simple tic. A complex tic is something which include coordinated movements of multiple muscles. So, sniffing is moving like this. So, it's a coordinated movement of something like records. More complex and coordinated movement. So, the answer is a complex tic. And this is also I have discussed my modules. Sniffing as a simple tic. But that is a motor motor simple tic. I had mentioned because I just got to the reference of the Continuum Journal. But when I go on to the Harrison, they had mentioned that sniffing is a complex tic. So, the answer is complex tic. So, hyperkinetic, hyperkinetic. There are three questions asked. Out of that, one was regarding the newer drugs, safinamide, expected. Second was Wilson's, expected. And Wilson's, actually, even though slightly out of the box from our modules, but it is easy and we can answer it. The third question was again, actually, it was easy. But there was a little bit confusion regarding the option for me, at least. So, I will regard as two questions probably out. But you can answer still all the questions. But the importance again stressing hypo, hyperkinetic. Again, stressing the importance of Wilson's is very, very, very favorite topic, favorite area of all the all the examiners. And most of you will go to the Wilson's. So, Wilson's, there is nothing. I think there is nothing much to confuse in Wilson's. And second is a newer drugs of Parkinson's. That is again very important. Okay. So, uh, that was about hyperkinetic disorder.

Next is we will go to discuss about one genetics related question came, which was actually I didn't get the exact question. The question is to the following is a pentanucleotide repeat. That was a question. And options. One more option which is probably the answer, which I exactly don't know the option. I didn't get. But you can answer it without even going into this. We have discussed in our module two times. One we have discussed when you are discussing about hyperkinetic movement disorder and MCQ discussion. Second time in the discussing about dystonic metronome. We have discussed this like trinucleotide repeat disorders. Trinucleotide disorders can be referred to polyQ and non-polyQ. PolyQ means those with CAG repeats. And those without CAG repeats are polyglutamine disorder. So, this if you know the trinucleotide repeats, you see DRPLA, Huntington's are trinucleotide repeats. You can see that ERPLA is there in the polyQ repeat. Huntington is a polyglutamine. Non-polyQ, that is non-CAG. Plateless. This is a triplet repeat disorder. All these are triplet repeat disorders. So, this includes fragile X, Friedreich's ataxia, and myotonic dystrophy type 1, that is CTG repeat. So, that is MD1. So, the fourth option is supposed to be there. That might be in the answer. Even if you don't know the pentanucleotide repeat, you will be able to answer if these were three options which is given, which is what I got. And when you come to the this is the same slide which we have discussed in the cerebellum ataxia. Ataxia and cerebellum. In that, the hereditary ataxias are autosomal recessive. At the end, we have discussed this slide where you can see that CAG repeat ataxia. Yes, includes SCA1, 2, 3, all these are exons. SCA12, and you can see that this is a pentanucleotide. SCA31. Then SCA10, and SCA37. So, like that, you can add and SCA36. So, I don't know exactly what was the other option kept. But still, you can you can easily answer that if you know that is a triplet repeat disorder. Because triplet repeat disorder is something which you remember. And SCA, and obviously you have to study. And if you got gone through these modules, it I think you will be able to answer. But still, I don't know exactly what is the options. But the question was pentanucleotide repeat. So, that again stresses the importance of genetics in neurology. So, uh, these are repeat disorders which we have gone through multiple times. So, in the hypogenetic, hyperkinetic, there were I mean, in the genetics, one question asked for pentanucleotide repeat. I think it is not a tough question if you know the other option.

So, again, the genetics in neurology at the base, the repeat disorders, you have to replace the the different mutations in genes because they will ask lot of questions from genetics. Genetics is very, very difficult and very, very important in neurology MCQs. So, the next question will discuss about neuro-ophthalmology. There are some three questions. Junctional scotoma. Junctional scotoma. We have discussed in neuro-ophthalmology. Optic nerve. We have discussed that there is a Willbrand knee which comes in a cell which can slightly go into the opposite nerve and come back. So, a lesion in the distal part of the optic nerve junction, if there is a compression, they can produce optic damage of the left side. That will produce left central and the damage of the nasal fibers which carries temporal temporal vision. So, it will produce lesion like this. That is known as junctional scotoma. I my students are stolen the insurance scotoma or something. You just kept there. Glaucoma is not the answer. Pineal gland is located. This is a corpus callosum. And this is a brain. The pineal gland comes here posteriorly. So, pineal tumor has nothing to do with the chiasma. The anterior part of the chiasma, optic nerve, and the chiasma. Lesion and diaphragm sella meningioma. And I have mentioned also that the diaphragm sella meningioma or the meningioma compressing the optic nerve and chiasma junction is the common cause for this. So, the answer is that diaphragm sella meningioma. If that was option kept. This is what I got. The options are. So, question was bro. Although the theme of the idea of the question is junctional scotoma, which we have discussed in optic nerve session. At this timing and we have drawn this figure also. How to make out a junctional scotoma? So, that is a direct question. In a more or less application-based question. And AION, which is true. We have discussed about ischemic optic neuropathy. Separate module. When I was keeping that module, I was thinking that whether this was so important for medicine. But when I gone back and with the certain areas, I find out that it is one of the common clinical picture you will see. Acute onset of visual loss. AION versus IA, arteritic and non-arteritic. So, I had included ischemic optic neuropathy in a separate session. Steroids can bring the complete visual improvement. Visual loss. Which of the following is true? Or acute onset of visual loss is in the vertical meridian. And optic disc is hyperemic. And I didn't get the actually I go to the two options. I didn't get the next two options. I didn't get. But the question was all together from ischemic optic neuropathy. Ischemic optic neuropathy. Uh, and it was a question was about arteritic. That is what I got. Arteritic versus ischemic optic neuropathy. Question. And whether it is arteritic or non-arteritic. Steroid one bring the complete vision loss. Vision improvement won't be produced with zero. But it will produce reduce the progression. And if you know about the visual occurrence in vertical meridian. Is actually true. Because it is altitudinal hemianopia. Altitude and visual loss. That also we have discussed. Carton-like vertical meridian vision loss. That is something which if you know that ischemic optic neuropathy will produce vertical. That is enough to answer this question. So, visual loss question. The vertical meridian. And this option I am not sure whether this was option because I go to a subject arteritic ischemic optic neuropathy is what I got. But I'm not sure about the option. But the true statement should be a visual loss occurred in the vertical meridian. Because it is it is the most simple thing among all together. Like in practice, it's again a practical point of frequency. Whenever a patient comes to altitudinal visual loss, you should think of ischemic optic neuropathy. The second appear practical oral question. And again, the junctional scotoma is also a practical oral question. When the visual field is like this, you should think of a mass lesion compression of pigment and the chiasma junction. So, this was a difference of AION from AION arteritic and non-arteritic. And arteritic is mostly in more than 60 years. And non-arteritic, more than 50 years. Non-arteritic is more common. This whole things we have discussed in the module. But for answering this question, you just need to understand that this occurs in altitudinal hemianopia, which is vertical meridian. That is only the thing you need to know. So, there where the next question is 50-year-old female, third decade, blurring of vision, pupils bilaterally sluggishly reacting over 6 days. Reacting and vision loss was over 6 days. With image of the fundus was given. I'm not sure what image is given. But I personally feel for answering this question, doesn't need an image. Because there is a visual loss. That is something which is going again or particular reducing duration. Producing an acute acute visual loss is less likely to have. And you can the image what I got from my students was that is an optic neural testimonials kept. But even if without that, you can answer. Because papillary also doesn't produce visual loss like this in six days. So, that too are not the option. Blurring of vision of pupils and visual loss in six days is less likely to do because of papilledema. And even if you glaucoma, there is no history of any headache or anything. And fundus changes in glaucoma is different. Even if you don't see the fundus properly, if you the common sense, you can answer this question is bilateral optic neuritis. Because blurring of vision of pupils bilaterally and the given image was of blurring of the fundal margin. Was I didn't get the exact image? So, this answering, I don't think the image is not that much for answering this. If you just don't go into a confused major. If you take it that headache and visual loss can occur. Glaucoma, obviously it can occur in glaucoma. But here it is like a headache, blurring of vision, and bilaterally and within six days. And image of the fundus. So, the fundal image is given. Glaucoma, you won't see an acute fundal changes like that. So, you will see is a papillary. Usually visual loss is not a classical feature of papilledema. And blurring of vision can present. But this much which is affecting is less not than that common with papilledema. And optic nerve initially classically doesn't produce visual loss. So, and papilledema is different. We have discussed in our neuropathy session on papilledema and papillitis. And typically in the last session, last slide was I think this was a slide. The same slide I had kept here. So, papilledema. The difference in the disc. It is red and red with the marked hyperemia. Two to six diopter swelling. You cannot make up the diopter and roll in the image. But what you can see is there is there is no bleed. And it is less marked edema. And you won't see much bleed or any more all those things there. So, and visual.

Loss is there, so those things favor more of papillitis. So I will go for bilateral optic neuritis. This has the option because, again, here, if we shall lose is not a classical feature of papillitis, that is enough to diagnose that. So neuro often all the three questions for a practical, clinically oriented question. So again, in this exam, you are seeing a lot of practical, a lot of clinically oriented questions.

So next was neuroinfection. There are three questions asked. Once first was achievation with the visual uh, again a clinical question. We still showed the sermon since last six months, left a pareto-occipital like this was actually a major script and unilateral. So it was something like this. This is an image, this is not the exact image, something like which is contrast non-enhanced. English can see that hyperdensities. And this is a contrast image against the contrast here, but it is non-enhancing. That is what was given. And so it is said, achieve a patient with this one, you should in a symmetrical peripheral occipital lesion, you should suspect that progressive multifocal leukoencephalopathy. That also we have discussed in our MCQ session on infection. This this was the same image we discussed uh, and almost similar image. Pareto-occipital was given in the image slide also, but whatever I had given, I got was the same person. I kept in the MCQ, just a right pareto-occipital, but the question as was left parallel is only different. So the question is basically to identify the image and think of a PML. That is the first thing you need. And you don't need much. If you read about the options, you will get totally confused because a lot of statics is being asked. But always, always think that the common things they will keep that you should know something which is practically important. They will keep in the option. It occurs in the early course. That is wrong, actually. HIV and PML aldosterone occurs nearly course. Jesse, whereas antibodies are commonly seen in the normal population also. Though that is all these are strategic questions. You don't need to confuse with that. If you just remember this is the same slide we have discussed and we discussed that PML occurs when the CD4 count is less than 100, when the immunosuppression is severe. So by that time, it is not in the early phase. It is in the later phase. So that is enough to answer this question. So it doesn't occur in the early phase. It occurs in the uh, late phase of HIV. And to identify PML, I am I think this is a this was the answer just given. And to identify this, you need to have a basic idea. Basic idea about PML. That PML is asymmetrical, pareto-occipital, and it is non-enhancing in in the background of an HIV. But PML iris, which is associated with natalizumab, and that can be a slightly enhancement. And we have discussed all those things uh, in the the session on HIV uh, in the infection MCQ2 in CQ 102 that we have discussed in infection secure the same vision. So ah, PML is an infection of oligodendrocyte and are dealt roughly around 55 to 85 percentage as zero positive. That was the second option. Around 70 to 80 percent is normal. So it is JSC virus antibody is very commonly seen in this one. PML is caused by JC virus, which is a polio virus. And 85 percentage of total cases are HIV. So it is very common with HIV. And it usually occurs in immuno-recovery following heart and particularly those with CD4 less than 100. So it is not seen in the early phase. They can will be seen when the CSF CD4 count is very low. And CSF is normal at the mild pleocytosis. PML is due to immunocompromise. No contrast enhancing is seen. Contrast enhancement is seen when PML iris is there. And diffusion restriction on the leading edge is one more feature. No specific treatment is there. Murtazapine, interlocking seven, topo, they can are used for trials. Are all these are off-label trials. So these things we discussed in the our MCQ.

Then clinical picture of three days fever, altered sensorium, and seizures. What is false? NCCT and CSF prior to antibiotics, steroids prior to antibiotics, and intercity before CSF. So one more option I just didn't get it, but the answer is there are these three options. So this is a patient with fever, altered sensorium, seizures. So whenever there is a there is a management of already suspected, we have discussed in the module of meningitis. We have discussed towards the end where the treatment is discussed. The treatment of antibiotics should be given within 60 minutes or one hour of admission to ICU. So you cannot wait for an NCCT or CSF to get an antibiotic. If you cannot shift for uh, this is not a cut-off to start antibiotics. Preferably CSF to be get before giving antibiotics. But it doesn't mean that always you have to wait for CSF and NCCT to get antibiotics. Is totally wrong. I'm not sure the what is fourth option among the available option. This is a seemingly wrong answer. Steroid prior to antibiotics is seemingly correct because steroid should be initiated prior to antibiotics to reduce the inflammatory reaction at least 20 minutes prior to the antibiotics. And NCCT before CSF is not always a must. But here there is an altered sensorium, seizure. When there is an altered sensorium, seizure, focal signs, you should always get an NCCT before CSF because uh, it can be a possibility of abscess that can herniate on doing a CSF. So that is something which is seemingly true. So among the available option which I got, I feel this is the wrong rash. But if there is a totally wrong option is there, I am not sure because preferably CSF and CSF should be done prior to antibiotic. Preferably NCCT should be done prior to CSF. But in this clinical scenario, you cannot get a CSF without NCCT because patient has altered sensorium, seizure. And you cannot wait for a long time more than 60 minutes for antibiotics. So it should be better to go with this option among the available options. So again, this tells about the importance of management. Again, a clinical scenario. The focal signs, seizures, raised ICP. Optimum patients immunocompromised. Then imaging should be done before CSF. This is what we are discussed in managing this session. We also told that within 60 minutes of arrival, you should give antibiotics. SSP. The false statement is again. This is something which we have not been discussed in detail of SSP. But I have told only two things important about SSP while we are discussing about the prion disease uh, that the same question came here. CSF medicine antibody issues and diagnosis. Reactivation of means is a reason versus me. I just created. I cooked up these options. Only option which was given. This answer which I got was a short environment. A periodic disaster scene that was the answer of this question. So the the theme of this question is you need to understand uh, the SSP EEG changes. That I have told the two things important about SSP. One is a CSF antibody and this is Sandy Wood. And second is the EEG. And these are two questions they will ask in SSP. Usually in all questions. So this is what we have discussed in our modular prion disease. A short duration periodic complex has seen CJD where a long duration is in SSP. If it is that periodic complex are repeating less than four seconds, you will call it as short duration. If it is more than four seconds, you will call it as long duration. So long duration uh, this is in radar maker complex. Long duration complex. That also the name also we have mentioned in this same module uh, so long duration is a uh, seen in SSP. So the wrong answer is short duration. So again, the idea of the question is to understand two things. One is EEG and second is the CSF. EEG IgM CSF IgG measles antibody. So these two are something is important in the case of SSP. And remember slow myoclonus of question speed. These are three things which is very important in SSP. So that also as we have discussed.

So neuroinfection, three questions asked. All were discussed. But all their more important is all where practical oriented questions. All their practical oriented questions and almost were expected, except that question from PML. Just not that quite commonly asked. Remaining where expected, expected questions. CSF and treatment of managers is routinely asked. SSP something is important in neurology. SS questions most probably the EEG. Other some EEG radar maker complex and the CSF IgG miso scientific. These three things routinely they used to ask in different neural questions. So that also not that tougher and more practical question.

Then spinal cord. There are two questions asked. One was a patient of the lower limb weakness of lower limb and neither is excited planned. There is extensor. So that means knee-jerk, the root value is L2, L3, L4. So the lesion should be above L2, L3, L4. And a sensory level at umbilicus. So umbilicus sensory level means T10. So lesion should be above T10. So options contains T7, T8, which vertebrate to look for an imaging. Actually, the exact options I didn't get. T10, T11 vertebra, T7, T8 vertebra, and L1, L2. So this was the thing we discussed in our MCA in our session on spinal cord anatomy. So this is the vertebral level and this is a spinal level. So in T10, the spinal level is L1, L2. Here the patient is sensory level at umbilicus, that is T10 segment is affected. So the lesion should be above the T10 spinal segment. So the MRI should include a session above T10 vertebra. Because 10 vertebra, the spinal cord segment is L1, L2. Clear. The T10 vertebra, spinal cord segment is L1, L2. So the upper cervical cord, it is same level. Lower cervical cord, add one. T1 to T6, add two. T7, T9, it is add three. So suppose it is T10 spinal segment. So it will be located around T7. Spinal cord, ah, spinal level T10 segment of spinal cord will be located around around somewhere around T6, T7 and a vertebra. So the imaging should include T7, T8 vertebral image should be looked for is T7, T8. Actually, in fact, it can be any level above it. If you think in a neurologist's point of view, but from the options given below, all the options are below T7. You should at least image a T7, T8 level. Because T7, T8 vertebral level, you will have a spinal segment of T10 will come. Because at upper cervical, spinal level is same. But global cervical, add one. Upper thoracic and two or three are added. To lower thoracic, add three. And T10 vertebra corresponds to L1, L2. And you see L1 vertebra correspond to sacral segment. If you take L1, you will see a sacral spinal cord. If you take T10, you will see an L1 spinal cord. So you are supposed to take a T7, T10 is the answer. Because this question is based on the basic anatomy of spinal cord and the vertebral level and coordination with its spinal level. This was something which you see practically when you see a practical spinal case which is kept for your exam. This is a routine casino.

So again, it is a pure clinical oriented question. So spinal cord, two questions asked. Again, it is clinical orientation is very, very, very, very, very highly a clinically oriented question. So keep on asking. Both were discussed. One was regarding the vertebral level. And the second question is actually uh, the neurogenic bladder relation. That has actually asked in the peripheral nervous. But I kept in the peripheral. But that question was directly as neurogenic bladder. Because they you need to know the bladder infection. Again, it is very practical area.

So ah, the next question was again coming from the sleep. There are two questions asked. We are expecting to ask questions from the newer drugs as well as the tree disorder. Particular narcolepsy. He gave the both questions for narcolepsy. One was 20-year-old male, 14 while laughing, immobile for a while, hallucination while waking up in the sleep. What is the diagnosis? Again, it is very clear. We have discussed it in the sleep session that narcolepsy occurs during the positive emotions, not negative, not during the cry, during the laugh. Similar question, similar clinical scenarios we have discussed. And he has laughing followed by immobile atonia. And then hallucinating well asleep. And what is a diagnostic test? Muscle T is a diagnosis test for narcolepsy. We have discussed different types of archaeology. One, two, three is a slide from our discussion. Narcolepsy one, two, and three. One, two, and idiopathic hyposomnia. Narcolepsy one has narcolepsy and cataplexy. Here uh, he has ah atonia is there. And sleep paralysis plus or minus sleep hallucinations. Hypocretin decrease. And MSLT with less than eight minutes sleep latency. And sleep onset REM sleep more than or equal to two minimum two circuit. So that was the next question was based on MSLT. Which of the following is false statement? If you have gone through this table, it is easy to answer. Should do an overnight polysomnogram. So before any MSLT, you should do a baseline polysomnogram. Because before labeling as narcolepsy, you should rule out OSA or other sleep disorders. Then average sleep on a sleep onset less than eight minutes. So that is used for diagnosis of using MSLT for diagnosing narcolepsy. Next question is sleep. What's the drum sleep disorder in one sleep is required for diagnosis of narcolepsy? If this option was exactly this, that is answer. Because narcolepsy requires two sleep. Minimum two sleep pawns at REM. This is an REM REM early onset narcolepsy where or your hypocretin is less. So that hypocretin is a weak promoting hormone. So what happens is you will get early sleep. Because hypocretin needs less. So REM is onset. This early. We have discussed about the pathophysiology, all those things detailed in a sleep module. And that is something which you request. If you want to explain for again, it requires a lot of time. Because sleep at visual is something is very complicated. We have tried to make it much simpler. If you watch the basic modules, then go for the sleep disorder, you will understand it better. So that was the importance of narcolepsy. Again, telling you that the importance of sleep disorders, particularly in archaeology. And the newer drugs is important. Sleep. The question asks both from narcolepsy only.

So next question is just completely new for our modules. Because this would be something which we have not discussed. When you will tell the CSF pressure is raised. But this is a very again a practical question. Because all the CSF when you're checking the CSF, especially for NPH or idiopathic hypertension or during a meningitis, you will measure the pressure. So how much millimeters of mercury is significant? So this is 150 to 150 to 150, 150 to 200. And what you remember is something around 180 is normal. Less than 180 is normal. But when it is more than 200, you will call it as raised SAP. Because up to 200 can be normal, particularly in obese patients. So especially when you are evaluating a CSF for IAH, you should keep in mind above 180 to 9 200 can be kept normally. If it is obese and if there is abdominal pressure inside, you can have a mild raise. So the range. This is a sparring statement from eighth edition. Broadly, brain edema disorder. A normal CSF pressure range from 80 to 180. But that may go as high as 200 in an obese patient or those who are not relaxed. So you should take him more than 200 abnormal. So that also the question was slightly outside our discussion topics. But this is directly from Bradley and directly a practical oriented question. Because you would learn everywhere 180 is normal. You have an attempt to predict 150 to 200 as abnormal. But more than 200, you should take it as abnormal. If the option was like that, the option doesn't have this. And the value you send this. But the value above 180, user you can go for that also. Depend upon option. But actually more than 200 is supposed to be taken as abnormal.

The next topic is cerebral and attacks. At two questions came. And actually one was expected. I was telling that SCAR one question will come. I didn't get the exact options of this. Which of the following is false? But I got the three true answers. One is SCAR three extra-pyramidal skaters. Machado-Joseph, which has extra-pyramidal. SCAR seven, we have learned that's carcinomas. Visual loss. SCAR two has slow circuits. That also we discussed. So the fourth option might be the wrong. I exactly don't know what is the fourth option because I didn't get that option. But without knowing that also, if you know the three right answers, you can go with the exception. So the questions were all the questions. If you see, the most of the questions which looks like tough. But what they meant was if they are given four options, one will be something high fit. And remaining three is something if you know. And if you know there are three options and you can go with the fourth by using excluding the remaining three options. So that is the basic, basic, basic idea of the examiner who has kept the exam. That is what I think is uh, some of the tougher question also. Tougher question comes like that. If you question seems to be tough, there will be some clue in the options. So this is a slide from our session on SCAR. SCAR one has pyramidal, extra-pyramidal. SCAR three is slow circuits, which has three types of variation. One is with uh, one is with extra-pyramidal. And SCAR four has pain. SCAR five is lingual ataxia. SCAR six is downbeat nystagmus. Pureness, pure, pure ataxia. SCAR and SCAR seven is macular degeneration. So you with knowing this only, you can answer that the fourth option, whatever it was, that was a false statement because of the three statements are true. So slow circuits classically in SCAR two, but it can also occur in SCAR one and three and so on. But it will eight once earlier. This is the same slide from our uh, discussion on SCAR. And III and 17 because they are associated basically angle involvement. And they are associated extrapolating involvement. But some movement disorder can present with SCAR seven and 17. Classically 17. Seven also sometimes they can have chorea and myoclonus tremors with SCAR tall and twenty. Twenty remember palatal trauma is important. So we have gone through what are the importance in SCAR in that session. Each, what is the most prominent features? And this is different types of Machado-Joseph. SCAR III, see also type one Parkinson and dystonia. SCAR my childhood type two is ataxia. Type three is ataxia, trophy. This as we have discussed in detail on module. I am not going into details because it will take taught of time.

The next question was uh, sub back. You combined on the following is false. This is something which slightly outside the module. Because we are not discussing this detail. But it is easy to answer. See, we if you have discussed that subacute combined degeneration can be associated with vitamin B12 deficiency, hypocupric, vitamin E. All these can be a subject recommended degeneration. So it is associated always with anemia and macrocytosis. Raw sometimes it can be associated with third anemia and macrocytosis. Because the causes can be not even better, vitamin E, hypocritical. These can personal subject will come in. So that is obviously looking like wrong. So that is the answer. This question. Vitamin beta sublimation will stop the progress. That is obviously may be true. If it is write down beta deletion. See posterior lateral cord is involved. That is all correct. The fourth option I didn't get. But obvious wrong answer. I feel it is uh, as always supposed anemia and microcytosis is strong.

So cerebellum attacks here. There are two questions asked. One was discussed. One was one was about SCAR which will discuss. One even though we are not discussed in a detail, but I think it was able to answer. But again, it is so everything was more practical oriented questions. Most questions were and many of the questions were on the expected area. So they not from unexpected areas. Most were from the expected areas.

So these were the questions asked. Total 46 questions available. To I was able to recollect the help of some of my students. And I am thankful to them to get me the questions. And one is the the again stressing the importance of stroke. Stroke is one area which is lot of questions came. And I will try to stress the importance of clinical. Stress the importance of one is clinical questions. Whereas a lot of clinical questions were asked. Second thing is there has been a lot of questions asked about updates, especially treatment. But newer drugs. And most questions I feel like most from the expected area. So not from the unexpected areas. And again, stressing the importance of newer updates, newer drugs, as well as the clinical. And the stroke is particularly important. Even epilepsy is one area. They have gone into little bit depth about childhood epilepsy. Is a paleptic encephalopathy. They kept on asking two questions. And one from the drug. And so that is epilepsy. Something which is where they have been dead uh, from the sleep. They asked two questions. Both were from narcolepsy as expected. But I was expecting some questions from the newer drugs of sleep. I hope one question will come in the need from the newer newer drugs of sleep. Then peripheral neuropathy, two questions asked. One was alarm melodious. Just little out of the box. But still you can able to answer if you apply some logic. And second question was actually from the bladder urethra. The question looks like weird. But when you go and check your bladder, which is like near supply of bladder is something all medicine people will study for their long case. Because paraplegic is one long case for medicine exam. So that was about peripheral neuropathy. Muscle. I was expecting some question. But there was no augustine as from muscle. That was something unexpected for me. But I think muscle again, it is important. You cannot skip muscle. Because especially the dystrophies and the inflammatory memories. Particularly the antibodies. That our favorite areas.

Then coming to neuro-ophthalmology. There are three questions asked. Neuro-ophthalmology is something which they are asked like something very practical, very clinical. Like they are put junctional scotoma. And they have put some fondness images. And fundus images. I was expecting. But even without the fundus images, with practical knowledge, you can answer that. When cognition dementia, again Alzheimer's, the newer drug they have asked. And the cognition, some of the slightly deeper neurophysiology like mesolimbic pathway they have asked. Then hypokinetic and hyperkinetic. There are a few questions out of the box. But but they were all expected only. Like Wilson's disease. Even though we thought images, you can answer without knowing much about relations, you can answer. Then not that tougher questions. Then stroke was one area. There are four questions out of the box. And there are new questions came in. But over from Harrison tables. And that stress the importance of Harrison tables. As well as the at least over the major styles. And uh, very practical oriented. Very new updates also. Scores were asked. So that is something which you need to understand from the stroke. And images were come from stroke, epilepsy. Or from the your hyperkinetic movement disorders. And the fourth area I want to stress is even though muscle is not us. But I feel either inflammatory or from muscle dystrophy. There will be some questions will keep on coming. So that was about the innacity recall. And I hope you have done well. And if there is any queries, you can put questions either to directly to Marrow or through the Facebook. Thank you. Thank you.