Transcription
start discussing about the neurology recall sessions 2023 neat. So, coming to the question paper, there are actually, in fact, a good fair number of questions came from neurology. And I had included some of the topics are not neurology. Some two questions are from Psychiatry, actually, and that is not related to neurology. There are few questions which are common, like they have some involvement. They may be covered in infection as well as in neurology. But, uh, predominantly, there are 23 questions which are predominantly neurological questions which I could, uh, collect. That is 28 questions. And see, first of all, I want to tell you that any recall, this is not the exact questions. This is something we got from multiple sources, and we did a, uh, Zoom call, Zoom video, video conference to get the proper questions. Then also, we had some confusion regarding the options. So, this may not be the exact questions.
And coming to the question, coming the pattern of the NEET this time for neurology part, there has been a difference from the previous pattern. There are some unexpected areas. Questions kept on asking from, like, particularly from, uh, pain area. There are few questions coming from that area only. And the majority of the questions were not complicated. That, like, usual pattern of clinical scenarios or usual pattern of questions in the stroke. All those things are not there, actually. In fact, there is no question in the stroke area. So that is what, every year, if you take the last two recalls, the third recall, last three recalls, if you take, uh, there is a lot of difference, uh, in the the pattern of questions. So you, you cannot expect a similar pattern every time. But although your basic knowledge will help to answer these questions.
We'll go to the questions. This is the first question that is, which of the following is Central area of sensitization of pain? That is, uh, initially I got the option question as Central area of sensation or Central perception of the pain was the first, uh, question I got. Then it has been corrected by some of our students that it is Central area for sensitization of the pain. So, what is pain sensation? Pain sensitization is a phenomena by which, uh, you, the the recurrent or chronic pain, uh, the body becomes more, more, more, more available for the pain, or the body senses the pain even with a slow threshold and a severe pattern. If a non-noxious stimulus can produce a pain, that sort of exacerbation of the pain experience, that is known as a sensitization. That happens basically in the peripheral as well as central area. And if you take Harrison, one sentence is given that Central sensation of pain happens in dorsal root ganglion. So, actually, in fact, the pain sensitization or the neuronal plasticity to the chronic pain, that is known as neuronal plasticity to the chronic pain. There's a modulation or modification of the of the the chronic pain. Happen, the recurrent pain happens. The, if you have a radiculopathy, slowly what happens? If you touch in that area, he will get a pain. Even without touching, the pain will increase. That means the threshold for stimulus has decreased. So that is known as sensitization. That is known as neural plasticity. This is broadly, and they have three steps: activation, modulation, modification. If you see this side is a peripheral system, and this side is a central areas. The central area predominantly happens in the dorsal root ganglion. The activation, initial process, which is reversible. There is not much need. Details are not required, but I just tell you because this question has come up. Next time, some question may come from this area. That is why I just try to cover that area. So, this is activation is a reversible process. That is the initial process. And then you have the modulation, and then you have the modification. There are three steps: activation, modulation, modification. These are the neuronal plasticity by which the body became more sensitized to the pain. So activation can happen in the peripheral area as well as the central area. When it happens in the peripheral area, that is known as autosensitization. This happens in the peripheral, happens in the peripheral receptors. The central happens in the dorsal root ganglion, predominantly the dorsal root ganglion. This is because of the protein conformational change because of repeated stimulus. There is a protein conformational changes are happening. Conformational changes happening that is responsible for the activation. They had autosensitization, wind-up phenomena. Wind-up phenomena is happening at the dorsal ganglion. That is because of again, because you remember we were discussing in the learning module, the the memory, memory, memory module, we discussed about long-term potentiation and long-term depression, which is a synaptic process of plasticity. The same mechanism happens here because of recurrent stimulation. You have glutamate. Glutamate has three types of receptors. It has NMDA, not three, has two types: metabotropic and non-metabotropic. One group is NMDA, kainate, and AMPA. Okay, kainate and AMPA, which we have discussed again. This is important in epilepsy drugs. We have used it. So, of these, just take over the kainate. Remember NMDA and NMDA and AMPA. The NMDA has a calcium channel, while AMPA is a sodium and potassium channel. Normally, the calcium channel of NMDA is blocked by magnesium. When recurrent stimulation happens, this calcium channel opens up, and the calcium goes in because magnesium is removed. So, recurrent pain stimulation, magnesium is removed, NMDA channel opens, calcium goes in. When calcium goes inside the cell, there's a lot of changes happening to the dorsal ganglia, like there will be some, some, some, some protein kinase activation, new protein production, hyperactivity, the receptors will come, all those things we have discussed in the module. Ultimately, what happens is glutamate-mediated, I mean, the NMDA-mediated calcium influx, and which causes exacerbation of pain. This is just like your long-term potentiation of synaptic velocity. That is known as a wind-up phenomena. But these two, peripheral as well as central wind-up and autosensitization, are reversible processes.
Then modulation is where the question came, that is from the sensitization media. The modulation has heterosensitization and central sensitization. Heterosensitization happens again in the peripheral receptors, while central sensitization happens in the dorsal root ganglion. This central sensitization, this is because of phosphorylation of protein. Phosphorylation of protein. The first one was protein conformational changes, but this one is phosphorylation of the protein. It's a much more long-lasting pain. This is reversible, but it is long-lasting. Okay. So, central sensitization happens in the dorsal root ganglion, predominantly the dorsal root ganglion, because of phosphorylation. And your pain became more sensitized. Heterosensitization happens in the peripheral. And the modification is the final and chronic process where the change happens at the genetic level. This happened again centrally as well as peripherally. Centrally, it is again in the dorsal root ganglion, predominantly, and some of the cortical fibers or the upgoing fibers also. Changes will happen. Your A-delta, C-delta fibers also change. So that is a much more complex process. So, just remember neuronal plasticity of pain or includes one is activation, modulation, modification. Modulation is not on sensitization where you send and peripheral. Almost all central processes happen in the dorsal root ganglion, while the peripheral happens at the peripheral receptor level. So, central area sensation, just directly given one sentence is given, not any details. One sentence is given in Harrison that central sensation happens in DRG. This is also the same thing is given in broadly or any text you refer. That is a process of neuronal plasticity to pain. That is how your chronic pains like your trigeminal neuralgia, chronic chronic migraine, or even your sympathetic dystrophy, that is your complex regional pain syndrome, these all happen because of the neuronal plasticity. One mechanism of neuronal plasticity is central sensitization, which happens in the dorsal root ganglion. So, the better answer, answer is spinal cord because dorsal root ganglion is situated inside, near the spinal cord. I, I don't know what are the exact options asked here, but this is the answer for that. The ideal answer is DRG. I don't know. I'm not sure whether DRG was given in the option. If DRG is given in the option, that is the answer. If that is not given among the following, the best answer goes to spinal cord. That is, uh, what my inference is. There may be a difference in opinion because I don't know the exact options and I don't know the exact question. This was an almost nearby question. That is why I want to discuss the entire area. Okay. If I know the exact question, I won't go in such detailed discussion.
Okay, so coming to the next question. The placebo effect of the pain is mediated at what level? Again, there's a confusion regarding the options. Some told cortex is there in the option, while in Zoom discussion, some told thalamus was there in the discussion. Some told some thalamic, cortical flow. Let us discuss the topic rather than going into the option because I don't know exactly what option is given. So, this is something which is given a figure in Harrison, but this is quite commonly discussed in other areas. Like, this is when you give a placebo drug, that will produce some analgesia. That is because of the cortical modulation of the pain pathway. Because, uh, this placebo effect is a neuropsychiatric or psychiatric modulation, psychosomatic modulation. If they ask a pathway, at what level it is not psychosomatic modulation, it is a level or the pathway at which it is happening. This is happening at the cortex predominantly. These are the areas involved. These are the periaqueductal gray, uh, your hypothalamus, periaqueductal gray, and rostral ventral part of the medulla, and dorsolateral prefrontal cortex. This is a dorsolateral prefrontal cortex, and this is your, uh, rostral anterior part of the anterior cingulate. Again, these two form the part of the frontal lobe. Okay. Dorsolateral prefrontal cortex, anterior cingulate. I had discussed during the module that these are the areas, frontal lobe area of the limbic system. Pain and emotion is processed predominantly in the limbic system. So, again, the areas are in the same areas of the limbic system. Hypothalamus, that is also a major area of the limbic system, and periaqueductal gray, and rostral ventral medial nucleus of the medulla, RVM. Rostral ventral medial nucleus, and hypothalamus. Hypothalamus. Sorry, this is not hypothalamus, this is periaqueductal gray, and this is hypothalamus. Okay. And this is rostral ventral medial nucleus of. These are the areas concerned with placebo analgesia. So, it has brainstem structures, and it has cortical structures, of which the major part is actually the cortical structures. There was, as much as I know, there was no option like brainstem. Actually, it has areas of brainstem like medulla, as well as other areas involving the cortex. So, I feel if cortex was the was there in the option, that is the best possible answer. But this mechanism is not only happening at this level. It has some thalamic activation, thalamic inhibition, thalamic activation also. So, that is why if thalamus was there, that is also an option, you should answer depending upon what is the option. We will see the subject. What is happening? So, you can see that this, uh, whatever is given, that these are the areas concerned with pain, and these red lines are the ascending pain. The pain is ascending from here, and these green lines are the descending pathways which inhibit this pain by or descending pathways. So, you can see that you can see that there is, uh, there is blue things are increased activation. So, these are increased activation of prefrontal cortex, dorsolateral prefrontal cortex, and some part of the nucleus accumbens, which we have discussed in our module. Uh, I'm not going into details of that here. That is that we have discussed multiple times in Parkinson's as well as dementia. And there has been some inhibition of the areas of medial thalamus. That red thing is where the pain, or red thing is where the decreased activation. And these periaqueductal gray, rostral RVM of the spinal cord and medulla are this RVM and spinal cord where you have either increase or decrease activation. These are the areas involved with psychological, neuropsychological effect of the placebo effect on pain. So, you can see that medial thalamic nucleus is involved. So, even though thalamus is not a major part, some part of the medial thalamic nucleus, which forms part of the limbic system again, are also can be involved, can be connected to the placebo. But as much as I got from the majority of students, thalamus was not there in the option. Cortex was there in the option. So, if cortex is there, placebo effect is mediated to cortex. That is, in fact, not only cortex, it is predominantly frontal lobe, that is, rostral prefrontal and your anterior cingulate, plus some areas of hypothalamus, some areas of the periaqueductal gray, and some areas of RVM and spinal cord, plus minus medial thalamus. So, that is what is the placebo effect of pain. I discussed it again because it's a new topic, and there is a lot of confusion regarding the options.
So, next was a clinical scenario. Is given a 42-year-old male patient who has scored dystonia and depression. And they give it is a slowly progressive process. And they had given a family history of anticipation. I don't know exactly what is the statement, but this was what is given. So, anticipation in family history means repeat disorder. So, it is a repeat disorder. That tells you that a repeat disorder. And you can see that depression, psychiatric depression is there, and chorea is there, and dystonia is there. Very, very, very clear answer. The answer is Huntington's chorea. I don't know the other options. Sydenham's chorea will not have family history. Sydenham's chorea is secondary to rheumatic fever and depression. Dystonia, chorea, psychiatric plus movement disorder in a young male or an old day, psychiatric plus violent movement disorders and extrapyramidal symptoms. You should think of Huntington's chorea. Okay. So, that is the answer for that.
The next question is also very simple. Patient had history of fever, diarrhea, later developed oculomotor myoclonus, something like that. They're given whether they're given myoclonus or myorhythmia. I'm not sure actually. It is not oculomotor myoclonus, it should be myorhythmia. Myorhythmia, which we have discussed in our module. We discussed it twice. First, first, we discussed in cerebellum also, and again, we discussed somewhere in the movement disorder session also. Oculomotor myorhythmia is a classical, classical, classical movement disorder which is seen in Whipple's. So, Whipple's presents with GI involvement, arthritis, some may have dementia, psychiatric symptoms, seizures, cognitive impairment, and movement disorders. Myoclonus, all those things are part and parcel of triad of Whipple's. So, uh, that the options which is given here is, it's not paroxysmal. It was triphasic. It was given as triphasic. It was given as Whipple's. This is actually, whatever there is a error in the slide. So, the answer was triphasic Whipple's was the answer because the classical movement disorder which we have discussed, oculomotor myorhythmia, and oculofacial skeletal myorhythmia is a classical movement disorder which is seen in Whipple's. It is not seen, not explained in other conditions classically. So, that itself is a diagnosis. You just see that supranuclear gaze palsy is also there. I remember some students told that was there in the question option. That makes it more clear because progressive supranuclear palsy, Parkinson's disease, and Whipple's disease. These two are differential diagnoses. We have discussed it again in our module on PSP also. So, the answer is triphasic Whipple's.
The next question is, they given a patient diagnosed with Parkinson's disease, develop hypertonia, rigidity after treating with low-dose paroxetine. And they given some angle or something. And which of the following is a mechanism led to this feature? So, this is very clear. This is very easy question. Anyone can answer it. Levodopa is notorious for causing movement disorders, particularly perioral dystonia. And this is classically because of dopamine receptor blockade. That is also very easy and straightforward question. There's nothing to think about it.
Where and epileptic drug causes weight loss? Again, there is a confusion regarding options. Some told topiramate was not there in the option. Some told some of the students told that topiramate and zonisamide both were in the option. Anyway, levetiracetam and phenytoin are not the answer. Topiramate is a drug which is used for weight loss in other ways also. Like, a patient with migraine with weight gain, you give topiramate because topiramate has affected migraine as well as in the weight gain. And if a patient had want to go for weight loss also, you can give topiramate. And in epilepsy patients, especially females with obesity, you can give topiramate. So, topiramate is the answer. If both are there, if suppose the option topiramate is not there, then you can go with zonisamide. If you compare topiramate and zonisamide, topiramate is a better option for weight loss. And zonisamide is much lesser, but it also causes weight loss. So, we discussed about the side effects of topiramate and zonisamide in our module, where you discuss about drug side effects. I had repeatedly told antiepileptic drug side effects are very, very, very important. It causes weight loss and kidney stones. In 1.5% kidney stones are much more in the case of zonisamide, approximately about 4% in zonisamide. And weight loss. Zonisamide also causes some amount of weight loss. So, that is there. Zonisamide also remember that causes angle closure glaucoma. That is another question which is coming in the next question. Topiramate causes angle closure glaucoma and myopia. Hyperammonemia when used with valproate. Valproate itself causes hyperammonemia. When you use topiramate with valproate, hyperammonemia is high. Then coming to zonisamide, it causes weight loss again. So, that is why I told you can answer zonisamide or topiramate. If both are there, topiramate is the first answer. If only zonisamide is there, you go with zonisamide. Antiepileptic which causes angle closure glaucoma. We just discussed that is again topiramate. Zonisamide, that is not classically described. So, even though both are almost similarly acting, not classically described. So, the answer is topiramate. Phenytoin, levetiracetam. Another drug which causes angle closure glaucoma quite frequently used in neurology is amlodipine. That can cause.
Tricyclic depression. Again, this is another confusing question. I'm not sure what was the option given in the last one. Some told magnesium, some told calcium. And I will give you the reference also which I got from Bradley, which is higher in CSF than in plasma. Remember sodium, chloride, protein, and magnesium. These are higher in CSF than plasma. While calcium, bicarbonate, and glucose, these are low in CSF. So, I think it was option given was calcium. If magnesium and sodium was given, I will go for sodium only. Because that is something which is definitely given in all textbooks. But Bradley has given that see higher level of sodium, chloride, magnesium, and lower level of potassium, calcium, bicarbonate, glucose is one CSF than ultrafiltrate. So, higher level of sodium, chloride, magnesium is on the and, I mean, what I told this wrong actually. So, not protein. Sodium, chloride, and magnesium. Okay. So, lower level of glucose, calcium, and bicarbonate. So, potassium, calcium, bicarbonate, and glucose are low. Okay. Sodium, chlorine, magnesium is on the higher side in CSF. So, I think what I got from majority of students is that some tell that in the option, some told that in the options calcium or some told that in the option magnesium or whatever. The answer, I feel it should be sodium.
Female on vitamin supplement. This also a tricky question. Female on multiple vitamin supplementation complaining of symptoms. They told some tingling or something like low-level symptoms of peripheral neuropathies. So, vitamin A toxicity, vitamin D toxicity, hypervitaminosis, vitamin B6, vitamin E toxicity. Again, pyridoxine toxicity is known to produce sensory neuropathies. So, it has nothing to do with myopathy. So, hypervitaminosis produces peripheral neuropathy. Vitamin B6. Vitamin A toxicity has nothing to do with neurology. It causes fat-soluble vitamin. And vitamin D also is a fat-soluble. That doesn't have much neurological symptoms, but they can cause aches and pains. And vitamin toxicity. If vitamin deficiency can present with myopathy, myeloneuropathies, subacute combined degeneration. By hypervitaminosis B6 is the answer, which causes peripheral neuropathy.
Okay, so coming to the next question. Which among the following is a non-sedative anxiolytic? This is not a neurological question. Even though we neurologists use these drugs, these drugs are not more used by physicians. And almost everyone uses it right and left. Anxiolytics are something which is very out of the box. I'm telling you. And anxiolytics is one group of drug which is grossly prescribed unnecessarily from level to higher. Whatever symptoms if you cannot localize, you give anxiolytic. That has become a practice in many places. That is not correct. But we'll come back to the question. Chlordiazepoxide, diazepam, clonazepam, alprazolam. All benzodiazepines are sedatives. The only non-benzodiazepine drug is buspirone. So, the answer is anxiolytic which is non-sedating is buspirone. This is a table from Harrison. Diazepam, lorazepam, alprazolam, chlordiazepoxide, and all these things are benzodiazepines. Buspirone is that non-sedating drug. Okay. This is non-benzodiazepine. So, that is the answer for that question.
Coming to the next question. What are adverse effects of clozapine? Again, it is not a neurological question. Either medicine or psychiatric question. And you all know that clozapine is a drug which is given for movement disorders, especially drug-induced dystonia in a Parkinson's patient, in a psychiatric patient. Only drug you can safely give clozapine, withdraw the drug and start with clozapine if your drug-induced movement disorder is not controlled. And you want to give treatment for psychiatry, go with clozapine. Clozapine is safe in all ways. But clozapine causes severe pancytopenia. That is why nowadays, majority used to give quetiapine instead of clozapine. Quetiapine also the the the dopaminergic blockade or the side effect because of movement disorders are much lesser than many other antipsychotics and doesn't have much side effects like clozapine, like fatal syndrome, severe fatal syndrome is not seen with that. That is why you used to prefer quetiapine with clozapine. So, the answer is pancytopenia.
The next question again, it is a very, very tricky question. Migraine treatment during lactation. If you come to migraine treatment, you know that all these drugs are used in migraine treatment. Okay. So, migraine treatment in pregnancy. What will you give? In pregnancy, you cannot give any drugs for prophylaxis unless risk-benefit is beneficial. So, majority, 19, majority, almost every patient with migraine in a pregnant lady, better not to give prophylactic agents. Not of the drug is 100% safe. If at all you want to give, you can give beta-blockers. You can give tricyclic antidepressants. And if you use common sense, the answer is very clear. If you want to see which one of the following is safe, which among the given options is safe. You know that there are postpartum depressions. So, antidepressants are quite frequently given postpartum and prepartum ladies for postpartum depression. So, amitriptyline should be safer during lactation. That is why they used to prescribe that. That is one option you can think. So, pregnancy, you cannot give any drug. Then coming to lactation. What about lactation? Lactation, the problem is majority of the drugs will secrete into the breast milk. The drug, the best drug is beta-blocker, particularly propranolol is the best drug for migraine prophylaxis in lactation. But beta-blocker is not there. So, when what will you give? Verapamil is not proven. It is not even approved by FDA. So, you cannot think of verapamil. Secretion is in the milk, and a child can get sedated. This is not absolutely contraindicated. All, but there are studies are lacking. The amount of studies are lacking. And sodium valproate again, that is not that safer. You can have a secretion into the milk. So, not that safer. And all reproductive female, we preferably don't give sodium valproate. And verapamil is relatively safe. So, confusion remains between amitriptyline and verapamil. But you see that we have discussed our module. We had given this table in our module where you can see the American Society of Headache has classified level A, level B, level C, level U medications. The verapamil is not even in the level B. Level A contains antidiarrheals, sodium valproate, topiramate, metoprolol, timolol, and triptans. Amitriptyline comes in the level B. But there is amitriptyline in the level B. What do you see? The calcium channel blockers are here in the level U, where you have inadequate or conflicting data for support of use of medication. So, you don't have a proper data for giving verapamil for migraine. Leave or or leave that patient is pregnant or lactating or whatever. You don't have enough data to tell that verapamil is a good drug for migraine. Leave the side effects also. Everything. It is level U. So, among the options, level B drug you have is amitriptyline. But beta-blocker is a level A drug, and particularly propranolol is a level A. Metoprolol and propranolol and sodium valproate are level A drugs, and it is safer in lactation. So, and, uh, again, American Society of Headache Society also recommends that the first, first choice is a beta-blocker. If not possible, tricyclic antidepressants can be given in lactation.
So, now coming to the next question. MM and CB. What is the treatment of choice? This we have discussed. MMC is a drug-induced disease of multifocal motor neuropathy with conduction block. A disease of middle age around 40 years, male, affecting median nerve, IGM GM1 ganglioside antibody. And the drug of choice is IVIG or immunoglobulin. Immunoglobulin is the drug of choice. Plasma exchange is not proven. Steroids can sometimes worsen MCB. As never studied, never, never given. So, the answer of answer is IVIG. So, that is a very direct question, very easy question.
Next question. There's something which we have discussed. I have discussed it twice. Once I discussed in cranial nerves, which is recently added before your NEET PG exam, where I have discussed numb chin, numb cheek, and numb cheek-lip syndrome, and trumpet player's neuropathy. All four peripheral nerve branches involved. I discussed because I hope that some area, some question may come from this area. This is very, very important syndrome in neurology. A numb chin syndrome or Roger's sign, where you have a numbness of the lower lip and the chin area. That area you have numbness is known as numb chin syndrome. Well, numb cheek syndrome is where you have cheek and upper lip involvement. And numb cheek-lip syndrome. I'll show it. Numb cheek syndrome, numb chin syndrome, numb cheek-lip syndrome. And lip syndrome. That is nothing to do with malignancy. But lip syndrome, trumpet player's neuropathy. Numb cheek syndrome is where the infraorbital nerve, where you have the, uh, infraorbital nerve, which comes from the foramen, here, inferior, uh, infraorbital foramen. There is a malignancy, cancer, invading into this area. The nerve coming out will be affected. That produces numbness of the cheek and the upper lip, sometimes upper gum also. That is known as numb cheek syndrome. The question asks is numb chin. So, numb chin syndrome is where the mental nerve or the mental foramen inside your mandible is infiltrated by tumors, most likely because of a solid tumor malignancies like carcinoma of breast, lung, or even lip malignancies. The mental foramen is involved. You will get a numbness of the lower lip and the chin area. This is very important because sometimes a patient comes to your OPD with this numbness of this area, persisting for few days or few months, and you evaluate everything, MRI, everything is normal. You give some drug and the patient won't respond, sometimes may respond also, but again comes back to you. But if such a syndrome is there, you should evaluate for the primary malignancy. You should take an MRI brain, not only the brain, you should take facial cuts including the mandible. Maybe maybe sometimes you request CT cuts also along with that to see that whether the mandible is invaded with a malignant tumor. So, that is known as numb cheek, numb chin. What is numb cheek-lip lower limb? Numb cheek is infraorbital foramen, infraorbital nerve is involved. If the tumor has progressed and involved the facial nerve, you will have numbness along with the lip. This area is paralyzed because the branch of facial nerve is involved. That is known as numb cheek-lip syndrome. So, this is numb chin syndrome of Roger's. Mental or inferior alveolar nerve. It is related to malignancy. It is very, very, very important. In such a patient comes with such a syndrome, you should always search for malignancy because numb chin is more associated with systemic malignancies. But numb cheek, numb cheek is more associated with local squamous cell carcinoma. So, numb chin is more important because numb chin, you may not find a malignancy here. It may be somewhere. You have to do a PET scan. Sometimes you have to do a PET scan. Sometimes you have to evaluate for the males. Numb limb, lower limb is very infraorbital nerve involved in the distal facial nerve. And trumpet player's neuropathy. Somebody who plays a trumpet, you have pain in the upper lip because of anterior superior alveolar nerve involvement. That is a different entity. The answer here is a neoplastic entity. Numb cheek syndrome is associated with neoplastic entity.
Next question is antibiotics not precipitating myasthenia gravis. That is actually very easy question. And this is very straightforward question. One liner question. Aminoglycosides, fluoroquinolones, macrolides, and tetracyclines. These are drug classes of antibiotics which can worsen myasthenia gravis. Aminoglycosides, teicoplanin, fluoroquinolones, macrolides. These all will cause worsening. The answer is cephalosporins, which is quite commonly used in myasthenia gravis patients with respiratory infections. It's quite common phenomena like seen things in respiratory infections. Myasthenia gravis can worsen because of infection, not because of drugs. So, this is some table which I had given in the module. Statins, procainamide, amiodarone, chloroquine, hydroxychloroquine, botulinum toxin, aminoglycosides, corticosteroids, immune checkpoint inhibitors, iodine contrast, magnesium. All these worsen myasthenia gravis. See one thing important you have to remember is corticosteroids. Just use the treatment of myasthenia gravis, particularly myasthenia gravis crisis. When you give IV methylprednisolone, you can have a worsening initially, then later it may improve also. But that worsening is usually covered in such scenarios by giving plasma exchange along with IVIG or I mean along with the corticosteroid or IVIG along with corticosteroid. So, corticosteroid-induced paradoxical worsening is also seen in myasthenia gravis. But the answer here is these macrolides, fluoroquinolones. These three were in the option. Answer here is cephalosporins.
So, next question is opioid uncommon side effect. Again, this is not a neurological question. Don't think too much. It's very easy thing. Opioids are well known for physical dependence and tolerance. Somebody was selling in somewhere and Harrison, it is given like that or whatever it is given. Opioids are well known for its physical dependence and tolerance. Addiction also is there with opioids. Quite common. That is why opioids, many of opioids, you cannot prescribe that easily. And coming to hyperalgesia. Normally, opioids are given for treatment of pain. But sometimes, paradoxical and chronic opioid therapy, you can develop paradoxical opioid-induced hyperalgesia. This is very uncommon. But that is the answer of this question. That hyperalgesia. Exact mechanism is not known. Some, some alteration in the pain pathways where opioids act is supposed to be the mechanism. But it is develops. Confusion of hyperalgesia between tolerance because in tolerance, when you use repeated opioid dose, initial sign what you see in tolerance is the duration of the effect comes down in tolerance, and patient requires more dose for this. Similarly, here also you will see initially you may see that either duration comes down or the pain starts coming early. That is sometimes difficult to differentiate. That is opioid-induced hyperalgesia. And that is an uncommon side effect. That is the answer for that.
Next question is actually the only question asked from dementia, but it is very easy question. 30-year-old female patient presents with internuclear ophthalmoplegia, who was treated for optic neuritis before investigation diagnosis. Again, optic neuritis means previously treated. That increases the risk of MS, which we discussed. And internuclear ophthalmoplegia, which means it is a brainstem involvement. There are two sides are there. Investigation for diagnosis, not VP, because it is not an acute episode of optic neuritis. VP is not used for diagnosis of MS. But it can diagnose optic neuritis. That's all. The disease is actually multiple sclerosis. You need MRI brain to look for the other areas, classical MRI signs of multiple sclerosis, and spine and brain to look for dissemination in space and dissemination in time. You can localize by using your MRI. So, the answer is MRI brain and spine should be done. Okay. That is clear.
Next question is impulsive petit mal. This is again, I feel it is not a good question. Actually, these classifications, petit mal, which is a childhood disease or a childhood fear. That things are way old entities that is not at all used since years, maybe in decades. This is the oldest name. So, petit mal is a focal seizure. Impulsive petit mal was or Jan syndrome. These are other names for juvenile myoclonic epilepsy because of the jerky myoclonic jerks in the shoulder. It was initially called as petit mal because petit mal was the initial name given for complex partial seizures. The initial phenomenon of staring look and all they will call petit mal initially. So, this is impulsive petit mal is another name for JME. This is something if you know, you can answer. If you don't know, you cannot answer. The answer is JME. JME, other names are Jan syndrome and impulsive petit mal. And these questions are actually very, not at all useful question, I will say, because this, this knowing this, you are not getting any benefit basically, because this is something which is not used nowadays. Who is going to call a patient as petit mal or impulsive petit mal? Nothing like that. It's not there. But still, for the entrance, you can ask all those sorts of questions. And the answer is juvenile myoclonic epilepsy. Other names are Jan syndrome and impulsive petit mal.
So, next question is question number 19. A 48-year-old patient who is a carpenter by profession. This is also again, a very tricky question. Carpenter by profession, presents with tremors involving head, voice. This is important. Head, voice, tongue, and impairment of activities like drinking. Okay. Impairment of activities like drinking. There's a family history of similar complaints. And patient is able to perform activities if he concentrates for the same. And the diagnosis. Okay. So, um, this essential tremor can have a bimodal peak from 30 years above and 60 years. There are two peaks. You can see the age is 48, which falls in the criteria for diagnosis of essential tremor. Whatever you tell, essential tremor. We had seen hundreds of essential tremor patients in this age group also. And essential tremor is 19. Till now, we don't know whether it is a pure ET only or whether it is some pathology growing inside the brain. Because many of the ET patients sometimes they may develop. I had seen some, they may develop some other signs and later may develop parkinsonism also. So, parkinsonian features also. So, that is why the entity called as ET plus has come up. Again, the the understanding of ET plus or even the the existence of ET plus is again a controversial topic. So, we will leave all those things. Let's come back to the question. There's a head tremor. I had discussed in our module. Whenever the patient is having head tremor, your diagnosis is very less. Head tremor, you have only very few diagnoses. One is dystonic tremor, and second is ET or essential tremor. Clear. So, either dystonic tremor or ET tremor. Then he has a voice tremor. Voice tremor is typically seen in essential tremor. Voice tremor is not a feature of Parkinson's. Sometimes you can get dysphonias in laryngeal spasms and dysphonias associated with breathing difficulties in dystonia. In a generalized dystonia, but when the patient has tremor, tremor means it is involved in the hand. You can see that it is involved in the hand. And if that tremor, if you consider as dystonic, suppose a confusion happened between dystonic and essential. If you consider that tremor which is happening here is a postural component. A postural component can sometimes be dystonic also. If dystonic postural component with a head tremor and with a voice tremor, it cannot be an isolated dystonia. It should be a syndrome or it should be a generalized dystonic syndrome. So, in such a patient, you won't see him working as a carpenter. You will see him difficulty in walking. He will not be doing any activities. And he will have when you have voice tremor in dystonia, that is actually not a voice tremor. This is because the laryngeal spasms, they will have breathing difficulties, they will have stridor. So, those things are not there. It's a very benign thing what they have given in the history. A carpenter, because he requires very fine activity, he is able to do it. He has a head tremor, voice tremor, and tongue tremor. Tongue tremor occurs in eating. And impairment of activities like drinking, because eating, the tremor will be more. While doing fine activities, holding the glass, drinking water, when reaching the face, the tremor will worsen. So, it's a classical phenomenon of an essential tremor. There is no confusion at all. It should be. So, the answer is essential tremor. The confusion when we had discussion with students was dystonic tremor. It's never a dystonic tremor from the question whatever it is available. Because to have a head tremor with a limb dystonia with a hand tremor, the patient should have severe dystonia of all limbs and he will not be unable to walk also. That much severe dystonia should be there. So, it is not a dystonic tremor. It is a very benign thing. They're telling he's a carpenter. He's 48 years old, having a head tremor, having a voice tremor. That voice tremor is a clue. Tongue tremor is a clue. These two things are classically telling that is essential tremor. And I feel the best answer here is essential tremor.
Patient on treatment with fluoxetine at 10% with recurrent thunderclap headache and angle closure glaucoma. MRI showed vasogenic edema in the parietal and occipital region. BP, I'm not sure whether BP is given or not. Even if BP is not given, the answer doesn't change. So, we'll leave that BP thing. Patient on fluoxetine. That is very important. Present with a recurrent thunderclap headache. So, what just take the symptoms there. When you analyze a question, if there's a clinical question, take the symptoms and take the cues. So, he's on fluoxetine. That's the first cue. Second is thunderclap headache. So, what are the causes of thunderclap headache? When the patient comes with thunderclap headache, I had explained multiple times. Thunderclap headache, you think of RCVS. You think of subarachnoid hemorrhage. Then you think of a CVT. Then you can sometimes also occur in older age group with a metastatic. But classically, these are three things you should consider when you have a thunderclap headache. Or the fourth one is an idiopathic or a primary thunderclap where you don't know the exact mechanism. And if you take the etiologies of thunderclap headache, if everything is ruled out, even migraine can cause thunderclap headache because of RCVS. So, RCVS are reversible cerebral vasoconstriction syndrome. They present with thunderclap headache. And this RCVS come under a spectrum of hypertensive encephalopathy. Hypertensive encephalopathy, RCVS, and PRES. Both come from the spectrum of hypertensive encephalopathy. RCVS because of it can cause stroke, it can cause cortical edema, it can cause vasospasm. So, the next part of the question, they are telling that the patient had a vasogenic edema in the parietal and occipital region. What is that vasogenic edema in the parietal region? Vasogenic edema means it is not a cytotoxic edema. Cytotoxic edema is seen in MRI as diffusion restriction. Vasogenic edema, there is no diffusion restriction. But vasogenic edema is seen in FLAIR and T2. So, vasogenic edema means this is classically PRES. They're telling posterior reversible encephalopathy syndrome. Classical PRES, you don't have a diffusion restriction. You will see FLAIR hyperintensity in the parietal area. This is something which they're telling is a PRES. So, that is a PRES. And patient is on fluoxetine. For RCVS, it is one etiology. Second is drugs, particularly antipsychotics and tricyclic antidepressants and SSRIs and SNRIs. These are the drugs which produce PRES. And some of the chemotherapeutic agents are drugs which produce PRES. RCVS spectrum. So, and even if they are not given the BP, the answer is reversible vasoconstriction syndrome. Why it is not PRES? They are not given an SAH in MRI. That is a simple answer. NMS. They are given some angle corners to confuse you with NMS. But there may be some NMS component may be there. But whatever they are given in the history and MRI finding is favoring of reversible cerebral vasoconstriction syndrome. That is classically seen with your SSRIs and SNRIs.
And 17-year-old female presenting with perioral sensation, bilateral upper limb tingling sensation, recurrent histories of perioral and a bilateral upper limb tingling. EEG was done during activation phase of EEG. They doing some activation process in EEG. The symptoms were recreated but without EEG changes. What is the cause? The confusion between all three exists among the candidates. Hyperventilation spells, functional sensory seizures. First of all, take the sensory seizures. What is sensory seizure? Means you have right and left cortex. And sensory seizure means it is from the, suppose I'm having a sensory seizure from my right parietal. So, what will happen? I will have sensory symptoms on my left side of the body. It cannot be bilateral. It cannot be perioral. Perioral and bilateral upper limb means it should be spreading to the bilateral cortex. That is very unlikely. When the seizure spreads to bilateral cortex, patient will not have consciousness because it became generalized. Clear. So, sensory seizure according to history, it is not at all. You will not think of sensory seizure. This is not the classical presentation of sensory seizure. Sensory seizure, one side of the body you will see that is clear. So, then coming to the next, next, next options. There is an easy taken. The event of good. But EEG shows normal. That means it is unlikely to be epileptic. That also tells you that it is unlikely to be epileptic. But sometimes in the deep-seated temporal lobe and all, you may not see any EEG changes. But when the seizure patient had a clinical changes or a seizure during the event, you will see some slowing at least a slowing or a fast activity. So, there is nothing is there. That tells you that it is not an epileptic event. That also rules out your sensory seizure. So, it should be either hyperventilation or functional. During the activation, you will do what other mechanisms you will do activation of EEG? One is sleep is an activation process. Second is you will do hyperventilation. And third is a photic stimulation. These are three classical things you will do in EEG for activation. Normal EEG. Any routine EEG will do all these three things. So, during hyperventilation, the patient might have shown this event. That tells you that the event was provoked by hyperventilation. The answer is hyperventilation spells. The next confusion the students was why it is not functional. See, the definition of functional neurological syndrome is different from hyperventilation spells. Hyperventilation spells may be part of a functional spectrum or a conversion disorder. But hyperventilation spells can also be triggered by the patient. Can also be triggered for malingering by the patient. And it is a different. Functional is never means that it is malingering. Functional is actually a disease of neurological disease only. It is not a normal thing. Functional disorders are not malingering. It is not a normal thing. They are a disease only. Functional describes that the possibility that there is a functional change in the brain circuit, not a structural change. Understood in the nervous system. There should be a functional change which you cannot make out by your imaging or any test available right now. But there's a functional change. There's no structural change. So, functional neurology is a different thing where you get a psychogenic non-epileptic seizures, which they demonstrate like a cure. That can be functional. But hyperventilation spells is somewhere in between. So, among the options, there should be a confusion. But I think the best answer is hyperventilation spells. Functional, the definition is slightly different.
This is again an ambiguous question. But I feel the answer is hyperventilation spells. Functional, the definition is slightly different.
This is again one of the question which asked from the muscle. Actually, I had been telling like LGMD, the naming and the protein. Every time one question is coming. Last time also one question came. So, I told you to study the new name and all. But the question doesn't need a new name and all. The defective protein. LGMD 2A. That is a direct, direct, direct knowledge-based question. That is calpain-3, which we have discussed in our module as well as we discussed in high series also. Like LGMD2 is a CAPN3. 2B is a dysferlin. 2C is sarcoglycan. Alpha-sarcoglycan protein. These all things we discussed in the other dystrophy in the muscle disease module. So, LGMD1, we have discussed myopathy, laminopathy, caveolinopathy, HSP40 proteinopathy. All those things we have discussed. So, LGMD2A is calpainopathy. Okay. This is a repeat question. This is like from this area, one question every time they will come. You should always in any exam, whether it is a NEET or it is INI, you should go through this area.
Induction therapy for cryptococcal meningitis. I don't know exactly what options was there. The induction therapy is actually a fluconazole.
Cytosin with Oten B Lial OT with fluc. Cytosin as induction for HIV patients and immuno-competent. It is Oten B plus flu for four weeks. But in immuno-deficient HIV, it is for two weeks. Then consolidation is the dose. Is given. We have discussed it in our infection where we have discussed MCQ on infection. We have discussed about this uh two three questions we discussed about in the beginning only. Uh, you can watch that. So the answer is fluyen plus Oten. I think there was one option on flucytosine plus Oten. Was there? I don't know the exact option, but I that is where I explained the details. The answer is Oten B plus flucytosine for two weeks in immuno-deficient and four weeks in immuno-competent is the induction phase. Then consolidation phase, you give fluconazole 800 milligram per day in HIV patient. While it is 4800 milligram for eight weeks in the case of uh, a uh, normal patients. While in immuno-competent, a maintenance for about one year is given at 200 to 400. While in HIV patient, you continue lifelong. And usually cryptococcus infection happened in a CD4 count of less than 100. That also we have discussed. So that is the induction therapy. Is again a straightforward question. There's nothing confusing that if you know, you can answer it. And HIV, there's a clinical case given. HIV patient with the CSF showing presence of fungal spores and lymphocytosis. What is the diagnosis? I exactly didn't get the entire of the question. I think uh, the question was framing for a cryptococcus meningitis. So there are two questions on this.
Manus. This question is again an interesting question and there are some confusion in this question that this actually not a pure neurology question. Uh, it has some infectious part also because they given black tar heroin. This black tar heroin is a crude form of heroin which looks brown or black in color which is used for IV drug abuse and all. When they use this, this contains botulinum toxin. So you can have a botulism because of black heroin. And whenever you have black heroin, the first thing is botulism should come to your mind. So botulism can be wound botulism, infant botulism, or through the food. Food-borne usually present with GI symptoms and later neurological manifestation. IV or uh, IV drug abuse associated with botulism. They classically present with the facial and pharyngeal weakness or bulbar weakness. So they present with facial paralysis and bulbar symptoms. So next DD is a GBS. Pharyngeal-brachial cervical variant or some variant of GBS. GBS versus botulism. So the black tar heroin is a clue for that. If black tar heroin is not there, it can be GBS also. Then they are given a CSF report of zero cells and 75 somewhere around 75 milligram per DL protein. This actually shows an albuminocytological dissociation. And there are some students telling me that in Harrison, it is given if it is 100, it is given as albuminocytological dissociation. But in Harrison, it is never mentioned. Albuminocytological dissociation is 100. They given is albumin-ratio protein usually bracket they given 1 to 100, meaning 100 above. But uh, Harrison is not the last word for everything. You understand that the concept of albuminocytological dissociation rather than mugging up what is albuminocytological dissociation tells you that the protein is elevated when compared to cells. You usually, usually when cells elevated, you will get some protein elevation as in infection or sometimes in traumatic tap. But here when the cells are not increasing and protein is elevating, that means that there is an inflammation happening happening in the CSF or happening in somewhere in the nervous system in the in the that area of the nervous system. So that tells you that it is not a typical finding in GBS. You can get albuminocytological dissociation in many conditions. GBS is one among that. So here also you can get a raised protein in botulism also. So that is why this protein is raised in this one. This also tells it shows albuminocytological dissociation only. Always in GBS, botulism is a DD. Okay. Botulism is something which causes descending paralysis of body. I told body, botulism, diphtheria, tetanus. These are three things which produce descending paralysis of body. Start from downwards. While ascending paralysis produce many conditions. One among that is GBS, CIDP, GBS, everything is starting the lower limb goes upwards. So descending paralysis of the body, that is tetanus, botulism, and diphtheria. So that type of starting with the pharyngeal and facial can also present some variants of GBS. But here they are given black tar heroin. That tells the clue that this is not a GBS. The answer is botulism. Clear. That is actually a combined question of neurology as well as from infection. But that is a pure infection question in fact because they given particularly botulism. The classical presentation only confusing thing was albuminocytological dissociation. Just that understand that that dissociation can present even in many conditions. It tells you that there is increased immune production of protein.
Okay. History of dermatomes is given and I don't know what is the exact history and I don't know which area or which rash they had shown. They can have a heliotropic rash around the eyes. That is more pathognomonic. Heliotropic rash around the eyes. Then you have a butterfly rash around this area, around the cheeks. Then you have a shawl sign, where you have on the posterior part of the neck where you wear the shawl. And the V sign in front of the neck. That is in front of the chest. Anterior chest. Then you can have Gottron's papules and Gottron's sign. Gottron's sign is on the extensor aspect of the MCP joint of the knuckles as well as the extensor aspect of the elbow and sometimes the knee. You will see erythematous macular rashes. Then Gottron's papules are when these rashes become papules. Gottron's sign thing become papules, it is called Gottron's papules. And mechanic's hand. Mainly on the radial surface of your hand, basically more on the index finger and the thumb area. Hand and the palmar surface. You will see the mechanic's hand. I remember that. I mean, from the students told heliotropic rash was given. That is around the eyes. Gottron's was there on the extensor aspect of the hand. Heliotropic perioral butterfly rash in the face, that is the cheeks. Shawl or V, the posterior neck and anterior neck is a V. Posterior neck is a shawl sign. Gottron's sign and macules, extensor like knuckles, elbow and knee. Gottron's papules are when the macules become papules. Mechanic's hand are classically not classical of dermatomes, but also seen. Dermatomyositis. It is seen in. I discussed about particular antibody positivities in some of the inflammatory myopathies.
The last question which was treatment of listeria meningitis. In elderly, meningitis is very simple. Which we discussed that in a patient up to 50 years of age, you will give a third-generation cephalosporin plus vancomycin as a drug of choice or empirical therapy. Why? Because you want to cover Streptococcus pneumoniae, you want to cover Neisseria meningitidis and Haemophilus influenzae. These are three drugs, three bacteria you are planning to cover. In those immuno-deficient or an old age, more than 50 years, alcoholic, nutritional deficiency, less than two years, you will think of another possibility of Listeria also. Listeria, you cover with ampicillin. That is 2 gram IV Q4H is recommended. But remember, even though they are recommending cephalosporin, vancomycin, majority of the patients, especially in India and particularly in South India, you can treat with only cephalosporin because pneumococcal resistance is much, much, much, much lesser. Even if you are not able to give ampicillin, like the patient is having renal dysfunction, you can treat with ceftriaxone 2 gram also. Neonate, you give ampicillin, gentamicin. 250 years, third generation cephalosporin. This is directly from our module. The slide is from the module. You can go and watch the module where I discussed about all those things. So ampicillin is a drug of choice for Listeria monocytogenes and 2 gram IV Q4H. And there was one question regarding substance P, which I didn't get the answer. So I mean, I didn't get any of the options because it was a huge question. But there was a question regarding substance P. So regarding substance P, I don't, I didn't get the options. It is a neuropeptide. It is a neuropeptide which is relating to neurokinin in a family. And this substance P is involved with pain, particularly and pain to that to a slow pain. That is mediated through fiber C. You have A fiber and C fiber. A delta fibers carries a fast pain. This carries a slow pain or it carries a chronic pain. It carries a chronic pain. It has a role in inflammation, neurogenic inflammation. It has a role in vomiting and nausea, particularly when seen with pain. Can sometimes trigger nausea, vomiting that can be triggered with this. It also involved with some behavioral response including mood, anxiety. It has been known to be associated with some learning and regeneration also. So all these are together the function of the substance P. And substance P produces chronic pain. Substance C produces slow pain. Substance C acts through fiber C and they are located in the dorsal root ganglia. They are mainly located in the ganglia. And because it's chronic pain and it is relation with mood and anxiety, that is why many of the chronic pain patients will have anxiety or depression as a component. And that is why antidepressants act. That is one mechanism why how the antidepressant act in such pain also. And it causes neurogenic inflammation. It triggers nausea and vomiting. It causes some of the regenerating mechanism. It causes vasodilation. So it has multiple mechanisms of action altogether. Remember that substance P is a molecule which is a neurotransmitter, neuromodulator released from the nerve, particularly dorsal ganglia. It has some involved the pathway. I think there was the option was regarding dorsal ganglia and other areas. It is present mainly in the dorsal ganglia. So this question I didn't get the end options and answer. I tried to multiple sources. I didn't get exactly what was there. But the only thing what I can provide you is you just go and read about substance P and particularly in relation to pain. These are the actions of substance P. And substance P is a neurokinin related peptide. So that was about the 28 questions which was asked in the NEET SS. And as I told initially, this paper is rather different from the last two sessions. But even if there are only very few clinical things, those clinical things were easy. The questions were not that tough, but they made you confused with few ambiguous questions and they made you confused with the options. And from the entire review, what I want to tell you is that I didn't get the exact options. So there may be some difference in the options and questions, but the areas are same and discussions are same. So this will be, I hope this will be fruitful for all those who are planning for the next NEET SS. And before planning NEET SS, make sure that watch all the recalls first. Okay. And like any time, this time also, like all the times, this time also, a lot of questions came from neurology. Out of the entire questions, 28 questions are from neuro, which is something which I got. It may go up to 30 also. So that was about the NEET SS 2023 recall. Thank you all for listening.