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and most of them quite sure, quite well rested, my dog. But those If you do want to join Quest Med, please use skis 20 to get 20% off. So if you do this, do subscribe. Don't forget to use our ski. See 20 to get 20% off the subscription, the Oscar, the communities and amazing space for you to just share any ideas, questions, whether you regarding to medicine, not medicine research projects. So please do join the Oscar. The community, I think moving. Put the link on the chat and you can just voice any doubt or any thoughts which you have, and one of us will be there to answer them or, if we can't answer them, will sign post you to a person who can. And some of the ground rules were all medical students. So please, if on it's all based on you care guidelines. So if you do a recheck your local guidelines as well, without further ado, today's session is gonna be presented by our president Really want on? He has an amazing session planned. You guys will be mesmerized by the end of it. I'm sure. So yep. Girlfriend leave it to prevent. Misha wants to do the show first. No, I do it. My camera. Okay. Um right. Hi, guys. We are final season, and today we're gonna be covering the neurology topic. It split into two sessions, so today will be covering, um ah. Few neurological conditions. It's gonna be a heavy session, and it's gonna be covering majority of the predominant conditions that we need to know. It's medical students. Um, on Yes. So let's let's get started. A seizure. This is the final season session, and every every topic will be preceded by a question. So the session is about 1.5. I was long, and we have 10 questions plan. Better that you guys know before we start in case we run over. Um, so let's start off with the first question. Could someone launched a pool, please? We'll take about about 40 to 50 seconds per question. All right, let's end up. All right there. So majority of you guys have gone for dive, I think diabetic neuropathy, followed by my senior gravis and want a Popsicle or OSIs. So the the key points in this question itself is that yes, it presents. The keep on that I wanted to highlight is that multiple sclerosis and the right answer here is multiple sclerosis could present similar too many different conditions, such as CIDP, such as my Stina Gravis. But the key thing is that although she tires a bit, uh, fasted in, uh, although she tires when she walks, it's always important to remember all the types of symptoms that you see now both off pins and needles. It's not usually classic off my senior gravis, although you get diplopia and mainly with diplopia get ptosis as well. Now the tiring phenomenon is usually common. Ah, on exertion with many, many different conditions. And that's it's the same with multiple sclerosis, that's all. So the the key points being about off pins and needles over over the past two years, and it being a rather progressive kind of episodes followed by the, uh, tiring out Turning out is the most common and first symptom off multiple sclerosis. Um, that that people complain off, And that's why this this kind of question points towards multiple sclerosis rather than myasthenia gravis or diabetic neuropathy, um, with diabetic neuropathy, which we would cover in the in the next few slides, you do get pain and loss of sensation in usually the glove and stop stocking distribution. So that's not really mentioned in the question here. So it kind of rules diverting your neuropathy, but out So multiple sclerosis. Sclerosis, What is it? It is a demyelination off these Neurontin, the central nervous system, and it happens over time and space and the keys over time and space. The reason why you say, over time in spaces, because it is a diagnosis off, uh, ruling out, which means that it should be the last diagnosis that you consider after kind of ruling on every other thing or working on your neurological conditions. Um, the key feature, as I mentioned, is fatigue. And that's the first symptom on the main symptom that people present with optic you write this and optic neuritis usually presents with color vision loss, and if you use a fundoscopic, be able to see the optic atrophy as well, or the kind of inflammation there internuclear ophthalmoplegia and a bilateral internuclear Ophthalmoplegia is usually pathognomonic for multiple sclerosis. Now some people might be wondering what exactly this is, and this will be I'll be going over this in the next slide Now good worst off phenomenon, which is a kind of increase in body temperature, especially after going through a bath or doing exercise a high, rapid, increasing body temperature limit. Sign our limit syndrome, which is when in next election, you get shooting spinal pain. Uh, just briefed, uh, that last for a few seconds. Spastic weakness has seen in all upper motor neuron lesions, numbness and pins and needles being one of the main symptoms, usually in the periphery is urinary, incontinent and sexual dysfunction being part of the autonomic nervous system. So Internuclear internuclear ophthalmoplegia I know is basically a lesion in the medial longitudinal nonanginal for sick list. And what this is is that it connects. This isn't a brain stem now, and it connects cranial nerve six and criminal of three, if you recall Cradle of six innovates, the lateral rector's and cranial of three innovates the middle of practice. So when there's a disconnect between the lateral actors and the middle rector's, the ice one legs before the other. So assuming that does it does it? It was a lesion in the MLF here. Uh, it would cause this criminal of green in the six to kind of lack of four. The So when, when abducting, maybe adopting the I hear it would like as compared to when adopting the I hear if that if that makes sense now, together with that, because of this lag between the to me directors and the lateral rectus, you notice double vision. So let's nystagmus. And usually the double vision is horizontal double vision. In fact, I asked a patient how they feel. The patient had a primary progressive multiple sclerosis with horizontal nystagmus heart nystagmus is basically the pulsating nature off the eye on you be able to see when they abduct or adducted isis, and it could happen in a horizontal or a political plane. And the way that they see the image is basically it is moving for them as well on a slight amount. But obviously, after a long time, they able to come compensate for that movement, and they don't see they see only double vision, but initially it moves around for them. And so that's what identifies this sort of the standards that you'd be able to see you as a clinical features. Well, Let's double vision Now. They're three different types of multiple sclerosis primary progressive, which is diagnosed initially. And it just it's just a rapid increments off the inflammation or the demyelination in the brain relapsing remitting. Which is it sort of episodic inflammation boats. And the reason why this sort of episodic information about happens is because when you're young, as you can imagine, your inflammation is caused because of this demyelination, and the brain is able to compensate for this neuro inflammation because you're young and you have a good immune system. So it's able to kind of go back to this sort of, Ah, baseline, Let me just move this. If you guys could not annotate, that would be great, right? So this sort of neuro inflammation there's a compensate re effect by the brain and eventually, once this compensative century effect is not being able to be met by the brain, that it progresses into secondary progressive. That is a so called relapsing remitting pattern with a consistent increase over the years. And now multiple sclerosis usually takes about 15 to 20 years to develop and and move across, at least from a relapsing remitting to a second progressive stage where it's a primary, perfect progressive stage could be anywhere between 10 years to 30 years. It depends on the pathophysiology an individual basis, right? So there is a criteria for determining the diagnosis of multiple sclerosis, and it's called the McDonald's criteria. It is really what, memorizing this because it is tested upon and it has been tested about in the past. I wouldn't I wouldn't go through this. But I've left this as a kind of simplistic, uh, guide by you guys. It's it's kind of a condensed version off the McDonald's criteria. Um, yeah. Ah, few other features that you might see in your investigations are you do a MRI t two flat to see the neuro information in the brain and what you know usually notice our periventricular lesions right here. So this is a lateral ventricle all over here, and you can see this sort of periventricular e lesions. And these are called Dawson's fingers. If I can convince you that they kind of look like fingers, it's a it's a stretch, but yeah, these are called Dawson's fingers and the lateral ventricles again. Very ventricular e lesions. But what what they basically mean is just on the outskirts of the ventricles. You see this stuff? A demon demyelinating process together with that you see oligoclonal band band an intrathecal i g on a lumbar puncture in the CSF. Now, oligoclonal bands are not pathognomonic for multiple sclerosis, as you can get it in many different disease processes. But intrathecal i, G and oligoclonal bands are usually seen highly in, um, multiple sclerosis in the CSF, so a lumbar puncture also is worth doing. Now the management off multiple sclerosis varies from person to person and depending on what type of m s. But they have. Firstly, they used the expanded disability status scale. It's also called the EDSS kind of stratify, which the amount of support you need in terms of a social scenario. And obviously there's a package of care and all those stuff that skated depending on the patient's needs. But in terms of an acute relapse, where you get has spasticity increase of a sudden increase, plasticity or pain? Suddenly you do is you use high dose IV corticosteroids, steroids in the form of methylprednisolone on. As you can imagine, corticosteroids dampen the immunosuppression by changing the protein protein functioning in the adrenal glands to secrete more cortisol. So it actually immunosuppressive is in the central nervous system. Now, in terms of disease modifying treatment, you that they do their many different types of disease modifying treatment. To be honest, if you are interested in that, you can take a look at the multiple sclerosis official website. But the two main ones that I've come across and are majority really used in the, uh, in very be practice. Oh, are we in medical students? Are is ah, gravis and fingolimod. And these are indicated for highly relapsing remitting m s here as well s here active relapsing m s. Um, and this this is done about six months, uh, every six months now, in terms of side effects that you get. As you can imagine, this is a, uh promoting urine lesion or a cortical lesion. So you get 50 and you use amatidine to treat the 50 spaciticity because it's an upper motor neuron lesion. You get baclofen gabapentin and Dantrolene with baclofen being the first line for this spasticity, which you can titrate up according to the patient's necessities. A neuropathic pain you get, you use gabapentin in terms of lifestyle modifications. Smoking is a huge risk factor for M s. Um, and increasing exercise also helps that kind of support This m s in terms of recovery. It increases the serotonin in your brain, and it increases the blood flow there also. So it allows for a prolonged recovery period s or less decreasing stress that that helps. Too cool. Let's go on to the next question. Now, if someone could launch the multiple right, let's end the ball there. And so majority of if you guys have gone for 82 81% have gone for B, which unfortunately is in the right answer here. But it is important to note and let's let's try to work this question out together slowly. So a man presents with weakness in his distal lower limb. So he's presenting with weakness currently to your neurology clinic. He has diplopia, which started two weeks ago, so there is ocular symptoms. He mentioned that he had a viral in illness about two weeks ago and a gastroenteritis about a week ago, and the weakness seems progressive over the past weeks, and it's only now affecting his limbs. So the limb limb weakness has been secondary, with the diplopia being the primary symptom. Now, with Diplopia being the primary symptom and the limb weakness being the secondary symptom, it seems that there is a progression from up, up or or in the ocular symptoms. And it's moving down words the symptoms And this sort of indicates that it is the syndrome called Miller Fisher Syndrome, and we will go through the difference between GBS and Militias syndrome in the next two slides. So let's try to rule out what it can't be. Now. It can be diabetic neuropathy because there's no history of any diabetes. It can be multiple sclerosis because there's no history of upper motor neuron signs of cortical signs. And there's no Myskina Gravis symptoms because it doesn't say anything about muscle contraction or anything like that. So let's talk about neuropathy, and it's key to understand. What, exactly in Uropathy is a neuropathy is a distant approximate weakness because the distant and of the neuron is affected before the proximal end. And so in GBs GBs is it is a syndrome that could be caused by either a viral illness or a bacterial illness. But most likely in a stem, you'd see a gastroenteritis stop a picture. Uh, usually by campylobacter judge and I And it is it's caused by immune complexes that attack the myelin sheath off periperal nose. And the reason why this happens actually is because antibodies is produced against campylobacter. June I and these same antibodies have the appetite. Oh, that can bind to this myelin sheath as well. It seems like a flood design, but that's how it works. And so the same antibodies go and recognize the myelin sheath s a foreign body and go on a tack it. So the clinical features of GBS is that it hasn't a sending paralysis. So as you can imagine, it's a neuropathy, so it's always a sending. It's progressive and symmetrical, and you could lose reflexes very, very quickly. And it usually happens anywhere between 1 to 4 weeks after an infection, and usually it is a stomach event infection, and there is a cranial of involvement. Now, the diagnosis. You do it. Obviously, you work through the diagnosis to do a F B C, because it could affect the respiratory muscles as follows the diaphragm. You do it with critical scientists neurological examination and in a lumbar puncture, you notice a soul race protein with nothing else affected and finally, with nerve conduction studies. As you can imagine, the nervous being demyelinating because the immuno immune complexes are attacking those peripheral nerves. And so there's decreased conduction. Now the treatment for this, um, GBs is IV IgG intravenous immunoglobulin that going by and stop these antibodies from binding to the mile and she plasma exchange if this ideology doesn't work, or if the patient has a in fact, not infection. So anaphylactic reaction to i g a immediate that stuff or is not compatible with a V i g ventilate resupport. If the F B C is decreased as well as cardiac monitoring, just to make sure that there's no signs of arrhythmias or um any any any cardiac dysfunction know comparing this to Miller Fisher Syndrome mill Official syndrome is a variant of GBS, but it kind of progresses with my muscles being affected first and then a decent, causing a descending paralysis as we saw in the question earlier. The usual antibodies that are affected are anti Jacob one B antibodies, and it usually precedes a viral illness And that was the red herring in. The question is, Well, I put that he had a viral illness about two weeks ago, as well as the gastroenteritis about a week ago. It usually causes ophthalmoplegia, which is kind of pain and disorder, and moving the ice a reflex here, a tractor know decreased reflexes, absence of reflexes and decrease or a wobbly gait. Um, and, of course, descending parallel paralysis. As we've mentioned now, the diagnosis for this would be a F B C. Again cause it could affect the diaphragm or respiratory muscles, clinical signs and symptoms, neuro examination, cranial nerve examination and, of course, checking. If this anti DQ one B antibodies are present and similar to GBS do intravenous immunoglobulin as well as plasma exchange, right, this is the next question here. Run. Could you explain the key difference between TVs and look Fisher again, as I was asking you? Well, I'll do it after this question, since people are asking, uh, already time in answering the question already. Sorry, I meant in the previous military she I meant that it supersedes are succeed. A viral illness doesn't precede a viral in. Sorry, right? Let's stop the older and majority of you guys have gone for B, which is the right answer here with other. I think about 40 30 people, 30% of people going for a now. The reason why it be here is because, and again with every question it gets, it gets. It gets easier if you break it down. So he's a diagnosis diabetic with increased numbness and pins in increased pain in his limbs. And this is a common diabetic neuropathy on the present, a shin so so far, uh, we think you have a diabetic neuropathy. He's under lawsuit, in which kind of confirms that he's on it's. It's similar to diabetic neuropathy, although it could be a could be because of a mental illness as well. But usually duloxetine is given for pain relief in diabetic neuropathy, and he also says that it's very friendly. Neuropathy and bouts of urinary retention and gastroparesis is which is which Castro Paris is, is quite common in diabetic neuropathy and, you know, often present with vomiting and stuff. So now that we know that it's diabetic neuropathy and he's asking for increased amount of pain with pain relief, the next step after duloxetine is usually amitriptyline. But then, in this case, because he has urinary leakage, that retention amitriptyline actually causes, uh, stopping the autonomic or a kind of a depression of the autonomic autumn autonomic system symptom. And it is notoriously known to cause an increased amount of urinary retention, and so we can just skip right to amitriptyline. We need to go to gabapentin next, and that's why gabapentin here it's the correct answer. So let's talk about diabetic neuropathy here. Diabetic neuropathy occurs because off inkley increased amount of glucose in the blood stream or serum that causes increased amount of oxidative stress to the neurons. Um, which slowly kind of packs at the neurons and stops them from reacting towards sensation and pay any and produces increased amount of pain. Now, the clinical features that you would notice with diabetic neuropathy is a glove and stocking loss of sensation that just means it's start distally in the fingers and moves in poor in the toes, and then it moves up with peripheral pain. This painful can be really, really painful on that. So you tried tend to give a strong pain killers for this gastroparesis, which is the stop or in the working off the enteric nervous system. And so what exactly happens is that this patient might not be able to kind of, uh, eat or keep stuff down and constantly moments. And it is key to know that that could be electrolyte imbalances. Because of this due to the gastroparesis. And together with that, you could get in Europe a thick also and a diabetic foot, which diabetic foot could cause many different problems include including the neck necrotizing fasciitis as well as a neuropathic. Also, which is one of the most painful else is that that people can experience if they can experience it because of the uh, given that there's no loss of sensation there. I know the diagnosis. Diagnosis has recovered in Mary. A session last week on Tuesday would be actually even a one c and O. J E T T A random and fasting on two separate occasions. I'm sure you guys know the criteria of seven or above 11.1, and the treatment here would be to do diet control educated. The patient on how they can kind of improve diet control would be for weight loss, given that the person is overweight or back to diabetes, diabetes, duloxetine, amitriptyline and government. In in that order are the, uh, the pain relief used for diabetic neuropathy. Um, yeah, And if anyone wasn't placement with me, we we recently saw a case off this condition called diabetic. Um, your trophy, which is over the the increased amount of glucose kind of attacks a plexus rather than individual nerve causing, complete muscle wasting, distally and proximately on. If you guys want to know more about it, it is a condition, that's what Yeah, researching and the difference between GBs and Miletich I'll come back to you once I've kind of finish this. So then we move on to these two conditions off acute and chronic inflammation demyelinating the myelinating polyneuropathy. And this is also as we mentioned together with m s is a kind of diagnosis off exclusion where you can't really find a cause, and it's presenting with the stuff of symptoms that you classified under the IDP or CIDP. So the idea being a rapid or slow CIDP being a rapid demyelination of the neurons resulting in a loss of function and the key is loss of function and for chronic. The symptoms must be continuously there for over at least eight weeks. Now the clinic clinical features for a i D p. R C O D p could be fast or slow. Progressing a zit says in the name on. The key point is that pins and needles are often the first symptom that a person notices and then slowly increase implemented. Demyelinating polyneuropathy. You know this slow sensory changes going from distant approximal, and this affects the motor neuron sees. Also, you notice, uh, motor changes after the sensory changes. So that diagnosis off this would be nerve conduction studies, and you can. There's not much you can not much else that you can do. You try to rule out all the other conditions, such as M s. Um, can really be a mess because it's it's It presents us a more of a lower motor neuron, uh, sort of wasting and stuff. So the treatment that you offer for people suffering with a IDP or CIDP would be cycle psychological Support IV I G. As you can see, it's a recurring team in many off this inflammatory conditions. Plasmapheresis, which is just plasma exchange as well, cyclophosphamide, which is sort of immunosuppression that they use over a prolonged period as well as in the cute setting. You notice you notice that they use steroids to kind of dampen down the inflammation, as we explained earlier. So let's move on to the next question now. Could someone launched a pool the right? Let's stop it there. All right, so the the results. It's interesting to see because it's and actually it's a intermediate mixed between B and D, with both being 38% and the right answer here is actually be, which is anti acid. I called in antibodies. Now the reason. Let's let's again break this question down. And the way that this person presenting is key and understanding why it is be over. The this 59 year old man presented doses and diplopia, and actually the first line actually gives it away. Tosis and diplopia. So, uh, concerning the majority of the people have been selecting Be already, you're considering between my Stina Gravis and Lambert Eat and Syndrome and the other if you don't really make sense. Rheumatoid arthritis, this one as we saw Mill Official syndrome and this one is um, show guns syndrome? No, sorry. It is Dermatomyositis. Um and so we can see here that we're considering between lumber eating syndrome or my senior gravis. The first sentence Tosis and Diplopia. And it has gotten a week over the past few months. He does have a history of small cell lung cancer which is treated for chemo radiotherapy, and he struggles to breathe. And on examination, he has reduced fbc. So this person could go into respiratory arrest any time soon. So it is really, really important. And you manage him by giving oxygen and supporting this sort of respiratory dysfunction with a bypass. Um, and not the CPAP. Um and so the reason that it's it's a cycle in and he s tackle in antibodies of us limbs, which is a presynaptic about educated culture and channels because there is ocular involvement. Usually, Lambert Eating Syndrome does not present with ocular involvement. Where's my Stina gravis kind of presents with ocular involvement. And so that's the difference in fact, differentiating factor between these two. So we're talking with myopathies now and myopathies. It tends to be with muscles, Uh, and with muscles, it's more off approximately. I know it's a hard concept to understand because it took me really long to understand. But it tends to be a proximal muscles affected before distal muscles, and I know it's a bit hard to comprehend. But that's out. That's how it works, So the shoulder girdle will be affected before the brachioradialis are real. Muscles on the hip girdle will be affected before the gastrocnemius as an example, so myasthenia gravis it is antibodies against the acid. I call in, uh, receptors here, and it affects deep purple nervous system. Approximate better feel nervous system because it's a myopathy by the clinical features, is that you noticed doses unrest for dig on exertion, such a muscle fatigue ability on exertion. So this is a key feature. Ocular involvement. You notice a blood or the patient would notice a blur diplopia this formula, which is a dysfunction in speaking and normal reflexes because it's affecting the testicle in channels and it's not affecting the reflexes, which are kind of based on nerve roots. So you notice all this stuff, and so the diagnosis that that that point you to it's myasthenia gravis out, that kind of, uh, get you to a small senior gravis, Uh, and before, before it gets you to my myasthenia gravis, you need to do a CT thorax, and the reason why you do it is there's another condition that could present as a myasthenic feature, and that condition is called a thymoma, which is just a tumor or a counter off the thymus gland. And and if you recall back your pre clinical days, the thymus gland, it's what producers be in December. And so it would make sense that these antibodies are being produced in overdrive and going and attacking this off this antibody on this acetylcholine receptors. And so you do a CT thorax first toe rule out a thymoma, followed by, uh, this electromyographic. First you check for FBC, also to make sure that there's no sort of respiratory depression because the diaphragm could be affected. Also, the experience tree or inspiratory muscles could be the intercostal muscles could be affected as well, and the key 0.2 no, tia is that on an e mg repeat, it's repeated stimulation causes a decreasing contractility. That basically means that the more you work, the weaker you get and the reason why I'm trying to highlight this is this is because it's the exact opposite in Lumberton syndrome, and we'll talk about it in the next slide. Now there's a Tensilon test also where they inject IV a door for me, Um, which is similar to pyridostigmine. It's just a a surgical industries inhibitor and to see whether it the condition improves. And it kind of helps to see if increasing amount of acid I Colin improves their muscle kind of contractility and stuff so that it leads are points towards the diagnosis off my Stina gravis. Now the treatment for this would be your period or stick mean, which is a A surgical industries inhibitor. It basically increases the amount of acid I color called acetycholine that stays in the synaptic laugh cleft. Yeah, allowing for more binding to happen, and a more likely postsynaptic you're on your own to be activated together with that being an inflammatory condition or a myopathy, you do immune suppressions with azathioprine or cyclosporin, and if it is a time on, you do a time ectomy and in terms of an acute treatment, you do IBIG as it is with all inflammatory conditions that we have seen so far you'd give oxygen because the F B C could be really low because of the depression of the diaphragm. You do a bypass. Well, you know, one continuous pressure, but you want by level pressure because that you still want them to activate their respiratory muscles. You do plasmapheresis and off. Of course, you stop precipitating drugs Now there are many different precipitating the drugs that could cause a myasthenia gravis crisis. Um, could you guys name in the chest? What a few drugs that you guys know that could could kind of precipitated a myasthenia gravis condition. Yep, that's right. So be WGA's are one of the biggest class of drugs that caused this myasthenia gravis. Quinolones also, or penicillin means as well. Lithium also causes, yes, anti muscarinic. Yes, all of them helped cause, uh or cause myasthenia gravis or an exacerbation in my senior gravis. So differentiating with Lambert eating syndrome, the pathophysiology is that it could come from a paraneoplastic small cell cancer, or it could occur independently as an autoimmune disorder, but usually in stems. You notice a small cell cancer being the precipitating factor, number it and syndrome, and it's specific to small cell lung cancer. It is antibodies against the presynaptic vote. Take it the calcium channels and so the culture cannot be activated on it affects the peripheral nervous system again, proximal as it is a myopathy. You notice limbic nous. You know this mild autonomic involvement, including heart rate, bladder and bowel control, BP, control. You go. You experience hypertension. You do that sort of autonomic dysfunction being affected. There is rare ocular involvement, as we saw in the question since that was ocular involvement, it leads towards my Stina gravis as well as the opposite off. My sonogram is being repeated. Exercise or muscle contraction brings back the strength and reflexes. So that being said, the MG again opposite to my senior gravis. Repeated stimulations increases the contract with the contractility off the, uh muscle, and it almost becomes spastic, which means it's it's a very stringent It's very stiff and contracted, and the treatment for this would be managed underlying cause if there is one, which is cancer. Small cell lung cancer to be specific immunosuppression and acute relapse is you. Could you go for IV IgG Cool. Let's go into the next question skin someone launch upholstery. All right, let's stop it right there. Um, so majority of you guys have gone for 45% of you guys have gone for a less, um, you traffic lateral sclerosis. And this is a relatively mean question, I would say. But it is worth knowing the distinguishing factors between different types off motor neuron disease. Um, and the next few slides were kind of highlight that. So the right answer here is actually primary lateral sclerosis. And the reason why this happens is because if we break down the question, that's increasing weakness in the lower limbs. So it could be both an upper motor neuron or a little lower motor neuron lesion. Our disease, it's increased over the years. So it's progressive, you know, you should have a motor neuron disease in your head. There's difficulty with balance and salary A which is just drooling on examination. She has increased tone, and this points towards, um, a more of a upper motor neuron because increased tone is is allowing the lower motor neuron to constantly stimulate, causing a kind of spasticity are increased tone. And she mentioned that her father, her father, passed away with motor neuron disease. So it's something that could be a heritage, the component as well. The reason why it's primary lateral sclerosis is because this pls constant most more common than not present as a upper motor neuron lesion rather than lower motor neuron. So motor neuron disease, the fact that we need to know is that the main domain are majority off. The patient's presenting would be a mixed up and lower motor. Sorry, it's intermittently motor, but motor neuron picture because air less is the most common motor neuron disease. Uh, generally upper limbs, the flex is would be stronger than the accent, extensive and in lower limbs. The extensors would be would be stronger than the flex is. There won't be any sensory loss because it's the motor neurons that are being affected. Nose, finger. This provinces because a new ocular involvement and know swing that disturbance. Because thieves the, um, autonomic nervous system is not being affected. It's only the corticospinal, which is the mortar mortar tract. Cool. So, um, let's go through. All the different motor neuron disease is that are going around the most common ones, at least with primary lateral sclerosis and heritage very spastic paraplegia being up majority really upper motor neuron ls being somewhere in the middle of Cialis. Aggressive muscular atrophy, spinal muscular atrophy, bulb a palsy and as a pseudobulbar palsy as well, presenting as a little more than you're on, as you can imagine. Multiple Z in walls, the cranial nerves on so cranial nerves, a little motor neurons. Generally it's affecting long, but in your arms. Now I spontaneously Drew drew a diagram here just before we move onto the next. Lights are just kind of specified. I'm not sure if it's if it's clear because of my drawing that this is an upper motor neuron. This is an upper motor neuron, and this are lower motor neurons supplying the face and the rest of the muscles in the body as a graphic. So a less was this progressive above the proposed E ls being the most common one the mean survival age. Or arrange for this. A less is due to five years, Um, and it involves dysphagia dysarthria, respiratory involvement and limp muscle wasting. Because both the upper and lower motor neuron are being affected. That's where you get a mixed upper and lower motor neuron sign you get for situations and weakness, which are lower more than you're on science, a brisk reflexes and spasticity, which are upper motor neuron site. Now there is a kind of medication that could help delayed, uh, Ventolin later independence. But that's not much that we can really do with motor neuron disease in general. But Reilly's all is there. It tends to usually evidence say that it extends the so called dependence by about three months. But usually the prognosis is quite bad. Unfortunately for this disease, the next one is progressive all policy. So it affects the lower motor neuron supplying the cranial nerves off the off the face. It affects cranial nerves 9 to 12, which is ah, which is usually located in the middle of off the brain stem. Um, and that what you usually see is tongue wasting, wasting of muscles off mastication and a decrease amount of swallowing. The swelling kind of, uh, reflexes is not present, um, and facial muscles being kind of atrophied. So it could carry the worst problem, since the reason is because the patient eyes eyes not being able to kind of support themselves as you can see the vagus nerve criminal of 10. It's all to be involved. So the so called trick drink you're being supported by the vagus nerve, recurrent laryngeal nerve and imperious superior laryngeal nerves. Um, are you can't really be a suppress cannot be really supported. And so it leads to infection aspiration, pneumonia and breathing difficulties in as s the progressive about the political aggress progresses on it also has a very short kind of expectancy. So the next two are the last two kind of motor neuron disease is that they were gonna be talking about today is primary lateral sclerosis as well as progressive muscular atrophy. Now, primary lateral sclerosis, as we saw, saw the answer to the question, Oh, is a upper motor neuron sign. It's usually the beets cell in the motor neuron card cortex that have been affected. And so it being a upper motor neuron sign you notice marked like weakness and no change in Congress cognition. The reason I'll go through the reason why I put no change in cognition is because I'll go through in a in a bit. What happens to people with more than you're on this and the cognition Um And so you notice upper motor neuron signs here predominantly, as we saw in the question. And finally, progressive muscular atrophy as this wasting off the muscles in the in the body. It needs to be a little more than you're on sign just because the long motor neuron not supplying the muscle so I'm being able to be activated and it atrophies. And in this case, distal muscles are affected before proximal muscles. Uh, for just this case. So in terms of management of motor neuron disease, we can go. We can control the risk factors. We can ask the patients to kind of stop smoking. Surprisingly, obesity is considered protective in motor neuron disease, with industrial exposures to industrial community chemicals, resulting in a worse prognosis. Males have a higher frequency off motor neuron disease compared to females, and more likely than not, at least in recent years. Athletes tend to have more, more, more chances of getting more than you're on disease Now. The diagnosis generally that we need to know for medical school, is that it's a mixture of upper motor neuron and lower motor neuron science. Just a heads up. All these kind of differentiation off motor neuron disease is mainly supported in the UK, whereas in the US degenerate call the bracket umbrella the whole damn as a less, um, so it needs to have a progression in time and region on there. There's a scoring system to diagnose airless, which is ls Korea criteria. We don't need to know that. But if you're interested, you can google it imaging works. And it is he to rule out any other precipitating factors because this diagnosis could be really, really kind of, uh, it could take a stink in their mental health on and psychological psychological well being. And so you tried to rule out infective causes terror toxicosis hypocalcemia my senior gravis before giving a diagnosis of a diagnosis of motor neuron disease. Now, in some in terms of support. As I mentioned social care support and mental health support, you know the reason as I as I mentioned the previous light. No change in cognition is that many of the people experiencing motor neuron disease experience emotional lability. What this means is a quick fluctuation in their moods, which means at one time they could be laughing and just the next time it could be crying because of the change in happiness to sadness emotions. So that's emotional lability. And they're given this SSRI citalopram for that. And in terms of silent, uh, they're given given sialorrhea is excessive drooling, and they given atropine eyedrops. Estrellas amitryptaline as we discussed earlier, it causes a autonomic dysfunction. Uh, it started kind of suppresses start of nomics up nervous system atropine, parasympathetic nervous system so it causes a dry mouth are a dry ice. And so you need to be careful when prescribing this, especially a hostel to watch out for infections because there's no more lubrication. The suction machine for sialorrhea. So less Botox similar to amitriptyline affecting the acetylcholine, uh, kind of receptor. This channels right, Let's move on to next question. Just five more questions left, but someone launch the pool. But someone said, I don't understand why it's pls and not airless. A less present as a mixed upper and lower motor neuron sees symptoms, but the previous question kind of specified as upper motor neuron symptoms. So it points towards most likely diagnosis of pls rather than a less right. Let's stop it right there. Fantastic. I think majority of you, 30% of you have gone for the right answer down. So here is actually see on dairy is a reason why I put this question, and it's not exactly a neurological kind of pathophysiology, but it's because, uh, straight up this person is on bisoprolol and verapamil, which causes complete heart block. So that's the reason why this person has become kind of stiff. And the reason why this this this is a key point of highlight. It's more cardiology related. Is that, um when when people kind of collapsed in this position or they go into awkward positions because of hypertension or heart blocks or arrhythmias, economy is diagnosis epilepsy on it. It's socially limits that the patient from driving, and that's a huge chunk off people's lives because they need to get places they need to drive around. And the moment you're you get a one time incident off off a cliff. See, it's six months off driving. Next time it's one year of driving, so it's key and majority many of the patients who we saw you we had to exclude as syncope first, before kind of going to diagnosis off epilepsy and so you need to consider the patient's social factors as well. Try to investigate whether this could be syncope and then go on to kind of, uh, try to find out the diagnosis of epilepsy. Obviously, this is a very extreme incident because the sacral and verapamil this shouldn't be happening, but it cost a complete heart block. But it's kind of to highlight a point that that we need to kind of understand. So syncope was his epilepsy that's combated to usually syncope has no aura. Where it's epilepsy has an aura. Both of them are a cute, and syncope happens between seconds two minutes. Whereas epilepsy happens for a few minutes, both have variable incontinence on. Both have implicational trauma. As you can imagine, falling down could result in traumas. Syncope is usually not nocturnal, so it doesn't happen when you sleep, whereas epilepsy could happen when you're sleeping. Um, and that's why you kind of put monitors and stuff to notice whether they're epileptic fits at night and syncope has a rapid returned to baseline virus. Epilepsy has a post. It'll state, which is a confusion, usually confusion or headache and a slow return to baseline and the order here is generally for generalized seizures or temporal seizures, which will go through in the next few slides. So think of be the main do syncope. Is that happen? Are cardiacs and syncope in off orthostatic syncope? Context Syncope is caused by arrhythmias, bradycardias tachycardia, supraventricular tachycardia beat, even tickle a tachycardia atrial fibrilation. My cardio infarction or sick Sinus syndrome are structural. Could be back. Valvula hokum are pulmonary embolism. Where is the orthostatic syncope? Could because off hammer itches, volume depletion, a primary autonomic failure. Such a spark. Instance for Lewy body dementia. Secondary autonomic fail. You're just diabetic neuropathy and amyloidosis or drug induced, which is orthostatic hypertension, Right? So let's talk about an epileptic attack that the $2 off epileptic attacks that could happen and epilepsy itself or a pseudo seizure. So it's important that we distinguish between these two. So an epilepsy usually has a prodrome. A feature that means something happens like an aura. Or something happens before the epileptic attack. This natural tongue biting contrast to anterior tongue biting and pseudo pseudo seizures as an increased serum prolactin. About 15 to 20 minutes. Post episode where it's a pseudo seizure, doesn't have increasing prolactin as possible cyanosis because of respiratory depression and a synchronous and rhythm is jerking moment. Obviously, does this difference from the different types of epilepsy that you could get? But the generalized epilepsy has this sort of synchronize and rhythm make jerking motion, whereas a pseudo seizure has hyperventilation. So this is how your distinguished within a plastic attacks. So this is the broad kind of classifications of generalized seizures. Generalized seizures can be classified astonished clonic, myoclonic, atonic and absence seizures. So tonic clonic seizures and the reason why it's generalized seizures is because the whole brain is being are the whole The whole brain is being activated. Uh, now, keep going to remember is that the other time, which is focal, which is a specific lobes of the brain being affected 10 progress and move into a generalized seizure. So that's that's something you could you could start off as a focal onset and then generalized into a tonic clonic clonic or a grand mal seizure. So tonic clonic has this sort of abrupt seizure activity, a drop seizure initiation. It has stiffened limbs, uh, and symmetrical rhythm. It jerk it. So tonicity and clonus city clonus being symmetrical, Rid Emmett Jacking and tonicity being this different names, there is a loss of awareness, mostly in general seizures. You will see a loss of awareness except for absence seizures. You could do Focalin pad or Focalin impaired or in bed awareness or non in part of an issue for absences from Ondas urinary incontinence. There's this phenomenon college, actually in March, which is the activation off the motor fiber. Slowly, as you progress down the neck down to the pectorals and slowly downwards, and it's like the so called contract shin of muscles that moves down with. And that's what it Jacksonian marches because it slowly trickling down. Now a myoclonic seizure seizure is the also happens with a sudden loss of consciousness. There's sudden jokes of movement, and that's in contrast with a tonic clonic weather's symmetrical, joking, joking motion with stiff and limbs. Where is this is sudden moves? Uh, sudden jokes of movement and what you see on an E. G is Polly Spikes. The next one is a tonic seizure, which is a complete loss of tone, as it says in the name, so you see a sudden freeze with a complete, complete loss of tone, so they the muscle can't really be activated. So the patient just drops down. And because this happens such that the patient just drops down, the patient is highly prone to trauma, and there's a complete loss of muscle top knowing absence, seizure. So that was sort of an absence. Seizure. It was It was yeah. So I was trying to highlight the point of that being absent seizure Where you just kind of staring the blank space and forget about everything that that's happening in around your surrounding you. Um and so, yeah, so that's exactly what happens. I blinking head bobbing, and you kind of just lose your concentration and just look around and don't focus on any one particular thing. There is lots of awareness, but as a quick recovery, and it usually lasts between 10 to 15 seconds. As we saw it as they saw you in this, uh, kind of episode and the usual thing that you see is three hearts spikes on an e e g. And that's kind of the exam that you notice. Um and so the key generalized point, I think, one person said, doesn't Jackson in March occur eyes a focus issue. You know it can occur in both a tonic clonic and a focal seizure. As you can imagine, that part of the brain the motor cortex is still being activated in a tonic clonic or a generalized seizure so it could happen in a pre frontal frontal. A little seizure, which is a focal seizure, as well as a tonic clonic one on. Do you notice both sides of the brain is being engaged as loss of consciousness immediately, and it could be divided into motor or non motor functions? No focal seizures are divided according to the lobes that are present in the brain, the frontal lobe being the one for Central executive processing. You know this abnormal posturing because the motor cortex is there's well, Jacksonian march. Also, in the frontal lobe seizure, you noticed this kind of significant on guard position that the person takes and towards paralysis, which is a small boat off about a minute or so off complete. Corral assist after the seizure because all of the muscles have been activated. Now the parietal lobe. You notice parasthesia because the primary sensory cortex is there, and that's the majority of the symptoms are parasthesia basically hospital lobe because it communicates with the ice. You know, this floaters that could be a temporary loss of sight was called, um a which is, um, just a a black circle in the middle. I'm and finally, temporal lobe seizures are the ones that we commonly know it because it's caused by I mean, the symptoms are lips smacking. Bradycardia is sisterly olfactory cost a tree, auditory or hallucinate? Auditory hallucinations because the auditory a primary surgical tech space in the temporal lobe, the old factory and dusted the cost. A tree, which is which is your taste is just in the temporal lobe that is below the front frontal lobe, Um, and the, uh, an auditory hallucinations. Because surgery and olfactory of the old factory probably is also in the temporal huge, normally no notice this phenomenon off the deja vu all jamabo, um, and a feeling of anxiety, also known as impending doom. Now, many of this kind of episodes yeah, often often presents with an aura. Can someone name what the general or a description is? Basically, um, what people usually characterized as an aura? Exactly. Nice, but It's usually a smell. And what exactly do you think that they smell? Cripples? Put in the chart. But what's the most common smell that they report? Yeah, I mean, yeah, correct. So someone has said butterflies about, if less in the stomach is actually one of the first symptoms. So you notice a kind of a a a knees in in sort of queasiness in the in the stomach? Yes, so that's right. Bundle of the smell is usually what they want to stop. One troubles know that's what they kind of noticed in this type of aura for seizures, and the activity is dependent on the lobe off brand. It's being affected. So let's go into the acute management of seizures now. Could someone launch the pool? You're doing well, that's just three more questions after this, right? Let's stop it there. So majority of you have gone for B, which is the right answer here, and the answer is IV lorazepam. And the reason why if we break down this question is that this person has come into the emergency department for an acute seizure. And so the paramedics mentioned that it's lasted over six minutes and you have tried. The initial therapy for the woman is over six minutes. Orders multiple seizures over six minutes. This person is in status epilepticus. And so since this person is instead of epilepticus and the buccal middle, middle, Um, and the rectal diazepam has been tried, which is the initial therapy you have in your administered one dose of IV lorazepam. That the key point to notice that you need to redoes are re administer this IV lorazepam about 10 to 15 to 20 minutes, post the first dose. If that still doesn't work, you could either keep it at the same titration off slightly, try to titrate it up, and that's really dependent on your local guidelines. So this is the sort of acute management for seizures that you notice prehospital you you give a rectal diazepam or buccal midazolam on. And when there's an established data status was just a seizure for above five minutes in the hospital setting. You give IV lorazepam and you repeat this in 10 to 20 minutes. Now, if that still doesn't work, you could give me find a do in our down here, as it is in our guidelines, they use Levitra system as an IV infusion, also known as keppra, and you do an aesthetic support. If this doesn't work again, you do anesthetic support and escalate care. Now. One important thing to do just in a pre hospital setting is one small feature that helps them. Is the head still lift maneuver on? That really helps because it helps to keep their airway painted and protected. And that really is something that it's going to compromise any acute seizures. So the management of seizure varies from dependent on which different type of seizure. You're kind of targeting, uh, and so a generalized seizure would have sort of operate and or as the first option. Oh, if the if the person is a female off childbearing age should give a day lamotrigine of a massive pain. Actually, you give lamotrigine or Levitra is a time for an absence. Seizure. That's the That's the different, different kind of, uh, management guideline that you give it a sodium Velcade. Yes, but usually what exams ask us this, either section might that you give for absence seizures and sodium valproate issues fel if tonic clonic seizures or the generalist agents is co existent now myoclonic seizures. You give sodium well, or if it's contraindicated, you get clonazepam lamotrigine with focal seizures, you give a carbamazepine or lamotrigine with libertarian system or sort of apparatus, the secondary. And finally, in pregnancy, you give lavatory system or lamotrigine, as this is safe in pregnancy. So as you can imagine, antiepleptics I don't not all easy going to do is they just don't solve seizures to come with many different side effects. So then valproate it causes. It's the first line for general seizures. It causes an appetite. Increase appetite and weight gain could cause alopecia. But one key thing that you need to notice just a for 50 inhibitors. So if the patient is on warfarin or the c o. C. P. You need to understand that this kind of drugs will last longer in the blood system. So you need to titrate every single drug that it could have a potential effect on, because hepatitis off and cryptitis as well as thrombocytopenia and it has teratogenic effects, so you can't give it to women off child bearing age or if you, if you really want to give it to women of childbearing age, they need to have a pregnancy education to make sure that they shouldn't get pregnant on sodium operate. And if they're thinking of getting pregnant, they need to be removed of sort of operate 46 months. Um, carbamazepine is the first time for focal seizures. It is a P 4 50 inducer opposite off. So dumb bell on it could cause dizziness, ataxia, drowsiness. Uh, because SIADH Yes, well, visual disturbances and Stephen Johnson syndrome, which we'll talk about in just a bit. And these are all safe to use in breastfeeding. Only barbiturates are not safe to use in breast feeding. Lamotrigine um, this second line in general seizures and it could cause this'll phenomenon called Steven Johnson syndrome and finally found it. When you say for 15 years, I just like of a message been I could cause peripheral neuropathy, dissidents, ataxia, drowsiness, good cost megaloblast economy. It started swelling mistake lymphadenopathy, and it could cause this phenomena colostrum relation, which is vitamin D deficiency, which causes kind of calcium. To be re absorbed from the bones. It causes a weak bones which could be prone to fractures. All right, so there is the symptom called Steven Johnson syndrome syndrome. That is a side effect off. Many off this that you, you many of this antiepleptics that you noticed. And it is a substance off this syndrome called toxic epidermal necrolysis. Um, the only difference between these two is that this is less than 10% skin involvement. But this is about 30% or more skin involvement. You notice a maculopapular rash that could develop into a bully or vesicles, as you can see here, it's You can see a few vesicles here. Continue bicycles here. You know this fever ultra Leah out a tragedy. And so what you do is you to stop the drug, you administer IV fluids and you do a non a TC of dressing cause you don't want to just pull out the kind of skin that's come loose there and you increase their dietary intake to promote the healing In terms of toxic epidermal necrolysis. This rarely occurs with anti a pellet epileptics. But since as yes Waas a subset, I thought it would be good to like distinguished both of them. It is usually a kind of a scalded appearance over the extensive surfaces are, you know, despite Rexy and tachycardia with systemic features as it's similar to a bun, a positive Nicole ski appearance. That's basically when you can oppress it and it removes the sort of dumb. A dermatological layer kind of just peels off. And that's what a positive Nikolsky appearances I do IV fluids, and if it's a lot, I mean kind of condition. You give IV IgG again nonadhesive dressing for the reason I mentioned earlier, and you increase the dietary intake from what? The healing In terms of seizures, they could have a A if they ah, huge impact on people's driving. And that's our social life. And that's really important to know the Viagra isn't always assist in in examinations. Eso it's it's good to know these. So when the seizures are awake and there's loss of consciousness, you can really, really light for a license when you're one years seizure free. If there's only a one off seizure seizure, you need to reapply after six months, Um, seizures. When awake and asleep, you can only play after three years. Um, uh, if seizures have been asleep only after three years antishistamine asleep, you can only play if the last It's more than 12 months off the first sleep since seizure. And if it's only asleep that this and seizures that do not affect the consciousness or driving again its job so you can see that if there's a one off seizure, it's usually six months. And if there's more than one off seizure, it's usually 12 months that you're affected. And that's why I said that The hypertension question that it is really a huge impact, especially on people who rely on driving for their livelihood. So it is a really key to consider this. And finally, for those drivers who drive a bus, Laurie coach want greater than one seizure is straight up Kenya disqualification and one off seizure is a five year disqualification, so you can see that it has a huge impact on people who kind of do this with your livelihood to right last three questions at 9 10. So just just a bit more and be almost done. Can someone launched upholstery called, Um, let's stop it right there. And yes, majority of you guys, 74% have got this right. You've correctly identified that this is Parkinson's disease on a person. Presenting with food takes loans and movement. It's slightly stiff, and you notice it reduced sense of smell, the reduced sense of smell being the first effect of Parkinson's disease. So it's all extrapyramidal symptoms on, so the sort of rigidity gives it away. So the correct answer is carbidopa. And it's a component combination off Ah, levodopa as well as a carboxyl the sorry a decarboxylase inhibitor, and we'll explain what exactly that is in just a bit. So the three key features off Parkinson's disease is bradykinesia resting tremor solids, rigidity, and it is key to understand the difference within spasticity and rigidity. Spasticity is an upper motor neuron lesion where you notice a complete stiffness. Where it originated is a progressive or a a lesson degree of spasticity. That's that's the best way I can highlight it. But the best way to learn about it is to see patients and understand what exactly is going on there is mentioned off a lot of it being velocity, velocity dependent or velocity independent. Um, I try to find a few papers that kind of highlighted this but couldn't find too much or night on it. So if someone knows, please do post in the chair. But these are the three main symptoms, as well as the stuff that's seen in this picture being the classic presentation of Parkinson's disease. So what do you exactly give for Parkinson's disease is a a sliver Toprol, which is a dopamine agonist as well. I say dopa, the carb carb oxalate inhibitor. The reason why this happens is because you don't want the dopamine active being acting on the peripheral document receptors, especially now God or in your hands to give the expert extrapyramidal side effects. And so you wanted to be concentrated in the CNS, so you wanted to be converted when it crosses the blood brain barrier barrier. This dopa decarboxylase inhibited, cannot cross the blood brain barrier. And so all the all the liver don't go straight into the brain. So the four systems that affect the the Ms Olympic infundibular and and dose of systems that the substantia nigra that affect Parkinson's disease. So let's go into the next question. Um, we we need to talk about Parkinson plus syndromes, which will be after this question. I kind of changed the order because the that if I put it earlier than that side might give away this answer. Um, so could you guys please relaunch the pulled the books, right. I'll stop it right there. Fantastic stuff. Sees the right until you guys have completely smashed it. Um so see is the right answer, because Lewy body dementia usually presents with this sort of hallucinations that has seen. And she tends to mention that he sees things that don't seem to be present at the moment. You see that hallucinations is a key differentiation factor off Lewy body dementia. But also, it's the fact that dementia is an earlier onset compact to the um this is called other other features. So we will go through the body dementia in just a bit. Uh, but yeah, So Lewy body dementia. It happens. Uh, hallucination is one of the key examination topic, but dementia because before the Parkinson symptoms. And that's how you distinguish between Parkinson's as well as dementia. Because in Parkinson's, uh, dementia, because together or after the Parkinson's syndrome, symptoms have been experienced. So these are Parkinson's plus syndrome is the reason why they called Parkinson's plus syndrome are because they emit it, the so called Parkinson's parkinsonian features, and they could be easily misconstrued as a pockets and syndrome cortical basal. These generation occurs because there's muscle stiffness, stiffness, tremors, slow start, slut, speech shaking and difficulty swallowing. Multi multi system atrophy or multiple cystometrography causes bladder dysfunction, which is on sexual dys innovation, which is the autonomic syndrome postural hypertension, cerebellar, ataxia s or less bradykinesia. So this bread it can you can use that could kind of suggest that it's a Parkinson's syndrome. So it's important to remember that in the moment you see pretty convincing you don't go straight for Parkinson's syndrome, you look at different pockets and plus syndrome as well as the the antipsychotics that people might be on because this could. This could activate the D two receptors well. And finally, there's progressive supernuclear palsy, which is a dysfunction and walking loss of balance. A moment there in the early stage of the disease. This's as a stiffness bradykinin centrum this constant, so you can imagine why it's closely relevant, are related to Parkinson's syndrome, and the key thing is that they tend to fall back where a spark it in syndrome, they are leaning forward with a kind of the parkinsonian gate where us If you pull people with progressive supernuclear palsy backwards, they kind of lose balance and move. Tend to fall backwards. So dementia? No, they're different types of dementia. I've talked about Lewy body dementia already, but, uh, Lewy body dementia is because Louie bodies are alpha sign you cleans in the substantia nigra. We will skip that because we just talked about it. Vascular dementia happens because of ischemic injury. Did you lifestyle? Lifestyle factors are, uh, kind of conditions that you might have. It causes confusion, disorientation, poor balance are unilateral numbness or paralysis. If that's a stroke and executive and frontal and semantic this dysfunction as almost disease A similar to vascular dementia. Except it is because off, um allowed clocks and your February tangles. And that's the kind of key fact obviously does weigh more happening. But as the ky fact that we need to know for examinations, that's memory impairment and confusion, and it's very progressive. It's hard to distinguish between vascular dementia and Alzheimer's type dementia, but a kind of testing to see if MRI to see whether this amyloid plaques on your formulary, tangles and present could help distinguish this and finding front of the temporal dementia as the frontal look kind of controls our executive functions. A loss of this executive functions would cause inappropriate behavior, lack of judgment, loss of inhibition, loss of empathy and loss of interpersonal present personal skill and lack of appetite to kind of distinguish between certain situations. So, yeah, so these are the different types of dementia, and the key drugs that you can use to treat dementia would be a mounting and donepezil donepezil being more indicated to it's Alzheimer's dementia where it's memantine being in more indicated to it's vascular dementia. Cool. Um, the final question. Now we are contract to finishing at half feet. So let's just launched a pool. And while you guys are doing the pool, our next session urology part to cover many different conditions, especially neurosurgical emergencies, headaches, um, headaches and tumors. So that's on Thursday at seven PM the same time. So please to join us for our first the expression right? Let's stop the ball right there. Um, majority of the people majority of you guys have gone for see 44% followed by A, which is 2027% and see is the right answer here. And the reason why it is C is because this person is presenting with serotonin syndrome. Um, the reason why is presenting with serotonin syndrome is high fevers. My address is, uh, on, uh, confusion. Uh, my address is being blown out. People's and confusion and hyperactive bowel sounds. And rigidity is kind of the symptoms. The main symptoms off serotonin syndrome. Um, with hyperactive bowel sounds being one of the key features a serotonin syndrome in your distinguishing from neuroleptics malignant syndrome, I presume. The other 27% we went for Dantrolene thinking of neuropathy, neuroleptic malignant syndrome. It's their differential diagnosis. This was any sense, and sertraline on has chronic kidney disease. The reason why I put chronic kidney disease is because this person is taking a pretty painkiller for the for his knee shall ask you guys What? What pain killer Do you think this this person took? Uh, yeah, NSAID, but specifically which are specifically which drug? Um, not exactly. So this person being on chronic kidney disease cannot against it. Um, yeah. So this president, being on chronic kidney disease cannot really take insets because answers affect the different story. A different artery consider cause a different reconstruction, Uh, and so disperse in contact insides. This wasn't as actually taken the first line that's indicated in, um, chronic kidney disease for pain, which is Tramadol Tramadol. The reason what happens in Tramadol is that it has a a few SSRI properties. Uh, and so this has caused this so called, um serotonin syndrome. And that's why that's a chronic kidney disease, and a pain killer comes into play. So the difference between serotonin syndrome and you're elected malignant syndrome serotonin syndrome is a high, really high amount of serotonin in your body. It's caused by mouth is monoaminoxidase inhibitors, SRS, Tramadol, Ecstasy and amphetamines. It causes the neuromuscular junction activation. So as we continue as confusion autonomic activity, hyperactive bowel sounds this being, uh, kind of significant because it's only seen in certain syndrome, so has management. You give IV fluids, and benzodiazepine is to kind of calm the body down. And if it's really severe, you give Cyprohepadine as well. Ask your approach now, in terms of newer left in malignant syndrome, usually notice it after starting an anti epileptic um, the antipsychotic Sorry on usually results in pyrexia muscle rigidity, confusion and autonomic activity. Um, it causes a race credit and kindness because of rhabdomyolysis. There's a slow onset off. This order is normal or slow ball, so that's the difference. So for both, you stop the medications, you start IV fluids, but you could give Dantrolene or bromocriptine for the management off your elliptical malignant syndrome. This neuroleptic malignant syndrome could present as a kind of dystonia as well. So that's a complete loss of toll A Tonia or dystonia, which is a partial loss of tone. Um, by the patient, kind of just drops down or or kind of loses their function as well. So they're different types of presentation of neuroleptic malignant syndrome. But it is a very, very key differential that we need to know the final sort of slide that I'm sure many of you we, us, as students are doctors would have seen is this thing called a functional neurological disorder. Um, this usually happens, and and I'm going to be really, really careful with my choice of words here. Functional neurological disorder is the, uh, it's less talked about, but it's the second most diagnosed a neurological disorder in the UK It's a group of the starters cost by abnormalities in the brain. So there is abnormal abnormality in the brain, and it shouldn't be assume that it's a a psychological factor and it needs to be sent it he a psychiatrist. It's caused by biopsychosocial disorders and as a range of symptoms, which kind of doesn't really fit into any picture for a syndrome. It could be on and off. It could be It's not really progressive. It's on enough. It doesn't really follow a neurologic pattern, and no one can really pinpoint why, exactly happens. And just the other week, I I heard I heard of a syndrome that causes it's usually affected. It usually affects young females, and it causes complete bladder retention over 1000 ml. I'm forgetting the name off it, but if anyone knows, please put in the chart. But that's one of a functional neurological disorder, because people don't really know why there's such a high retention, Uh, but it is a good differential, Um and yeah, I think that brings me to the end of today's session two minutes early. Please join our our session on Thursday. I'll be doing that, too. It's going to be focusing on many different conditions. Such as, um, uh, neurosurgical emergencies called a queen A That stuff. And we'll also be focusing on headaches, which is a huge part off, uh uh, medical school curriculum. Yeah, and please fill in the feedback for me. Follower. Yes, that's right, Ellen. Perfect. That's follow syndrome. You're right. Follow syndrome is the diagnosis for the bladder. Attention. Uh, you get access to the slight and the recordings once the once it's uploaded or metal, it should be in the next day or two. If you guys have any questions, please to stay back. You know, one person asked about the, um difference between GBs and limbs is no, no, no injury juice and, uh, official. Let's try to go more So GBs is antibodies that affect the myelin sheath off the peripheral nerves. It is a a sending paralysis. So it goes from so it being a neuropathy, that means you need to start distally and move approximately. And so it's a sending palaces. So it goes to the distal ends and it slowly moves up. It is symmetrical, and you could lose all your reflexes quickly. It's usually after the his After history of stomach infect infection usually caused by campylobacter. Judge. You know, now in terms of enough conduction studies as it is, it's kind of demyelinating or it's against a mile. And she, um it causes a decreased enough in the conduction, and the treatment is ventilatory support. There is criminal of involved involvement. Um, but it's not pronounced, uh, at the same time Miletich a syndrome. The eye muscles are the first to be affected. As we saw in the question I muscles. Ocular muscles were first to be affected, followed by the distal muscles proximately distal muscle. So there's a descending part of this is so it goes from the ice and then slowly spreads across. And that's Miller Fisher syndrome. It's, uh, it's a variant of GBS. It's It's quite rare, and it's cause of antibodies against NTG. Q B one antibodies. Um, it's caused by these antibodies. Sorry, and the eye muscles is It's keyed. My muscles are the first to be affected. Asparagus. I noticed on all the case studies that I read. It was the eye muscles that were the first to be affected. So again the diagnosis would be to monitor the F B C for both because of the depression off the diaphragm on expiration inspiratory respiratory muscles. Um, your examination, cranial nerve examination. You could do nerve conduction studies as well, but I think the main thing that you would do is test for these antibodies. Um, and you do IV idea plasma exchange in this case, Uh, the reason I think one of the questions was the reason why we need to distinguish this is because this could be inherited, whereas this is caused by a pathogen. So if it could be inherited and we need to do genetic testing to make sure that the descendants of the Children off this person might not have the same kind of anti GOP one antibodies Cool. Uh, I hope that explained your question. Um, bunny, just point the acute inflammatory demyelinating polyneuropathy That's basically referring to GPS. It could just be clear. It's DBS placing subset of a I. D. P Um uh is a subset of sorry 80 pieces. Subset of it when you talk about a i. D. P. R. Basically referring to the most common presentation of TVs that when you when you talk about all the ascending paralysis something that's basically what it's, that's what your affair and as a I D. You just meet here on that cool. It's anyone so sorry. So burn expense. Corey Burning smell usually correlate with the temporal lobe seizure, but it could be a generalized seizure. A swell because the temporal lobe is affected in a general seizure, too. Um, eso and Oskanian. Oscar examination is a kind of a practical examination that people in the United Kingdom on. I think Australia also do it. It's usually at the end of the year where they're different stations and stuff like that. It's not something that you do as a test, uh, in a clinical scenario, it's It's an assessment for medical students. I hope that answers your question. Who? Let's stop the