Computer generated transcript

Warning!
The following transcript was generated automatically from the content and has not been checked or corrected manually.

Light first day, I wanted to say, um, I hope everyone had a good holiday break and everyone's feeling rejuvenated and ready to, yeah, and feeling ready to tackle the second half of the academic year. Um, before we start just a few kind of general introductions. So Neuro Spotlight is a revision series, um from Western Neuro. So, and it's aiming to kind of help supplement medical students no matter what year you're in or which university you're from to kind of get a good grasp of understanding of common neurological conditions, especially the high yield ones that they commonly like to kind of ask us in exams. Um, we are joined by kind of doctors that deliver the sessions and they've given up their Monday evenings to kind of help us do that. So we're very thankful for them just to briefly mention the team. So there's me, Iran, um I'm joined by Ola sued and so we're a group of less term medical students who have a keen interest on clinical neuroscience and clinical medical education as well. Um So you'll be seeing us kind of take turns moderating future sessions. So today's topic is your, um, neuroinflammatory conditions and just a few kind of housekeeping rules before we begin, please keep your microphones off and cameras turned off as well whilst the speaker does their um lecture. And if you have any questions, just type it in the chat, you can just go through them throughout the sessions when we have many breaks or especially at the end, we have allocated time for that as well. Um And near the end as well, I'm gonna send in a feedback form. There's a link that I'll send for a feedback form. Um And that's just mainly to kind of help us get a gauge of how we're doing in terms of anything we can um make changes in the future. But also, um get back to the speaker that we have because they've given up the time as I mentioned earlier the Monday evening to help us and answer any questions that you have. So without further ado I'm gonna pass the floor on to Doctor Envier. Hi. Um Can you hear me? Yeah, hi. So my name is uh I'm an fy two currently working in the West Midlands North region. Um I'm currently placed on GP and um I have a very keen interest in neuro. Um It's something that I want to pursue in the long um in the long term. So I was very happy to deliver a session today, especially um on a very important topic, a topic that comes up very very often. Even in my final year exam in Leicester, I had a question on, on, on one of these topics. So I'll elaborate on that when we get to it, but it's something that's really important and, uh, hopefully you guys will, uh, would enjoy and, and learn something if there are any questions, just put them in the, uh, put it in the chat and then, uh, we can answer them at the end or as we go along. Um So yeah, so without wasting more time, we'll, we'll, we'll start. So the, the topics I'll be covering today are guillain-barre syndrome, myas gravis and M SS or multiple sclerosis. So, so the first one is uh guillain-barre syndrome. So, guillain-barre syndrome is can in, in medical terms, be described as an acute paralytic polyneuropathy. So, it's acute and onset, it comes on suddenly it's paralytic, it leads to paralysis of your muscles and it affects more than one nerve. So, so that's something that we need to remember. Um The most important thing is, and, and we'll see why that is later is that GBS only affects the peripheral nervous system. So you don't get any upper motor neuron signs, you only get lower motor neuron signs as it only affects the peripheral nervous system. And it presents with acute onset, ascending symmetrical motor weakness and sometimes you may have sensory deficits. And what that basically means is that again, it's acute at onset and it's ascending So it starts at the, at the peripheries, that's where you start to get the, the weakness and then it ascends up in a symmetrical fashion. So it happen, it will happen bilaterally. Um and it will be uh it will happen in a similar pattern and it will ascend upwards and it's usually a motor weakness, but sometimes you can also have some sensory deficit as well. If you look at the picture on the right, it just shows you exactly what's what's happening. Uh So your axons are covered by myelin sheath, uh which is basically the uh the Schwann cells wrapping themselves around and um your uh it's an autoimmune condition. So your antibodies attack the myelin sheath and cause demyelination of the um of the axon. So, usually, um it's preceded by an infection and commonly uh infections with Campylobacter, uh which causes um diarrhea and vomit diarrhea, mainly cytomegalovirus or EBD. So, usually patients would have had um about four, you know, about a history of either a, a upset tummy or some sort of um sore throat, um uh approximately four weeks before the symptoms um come on. Um and, and basically your immune system goes into a bit of an overdrive when it's fighting those infections and it leads to B cells in your body producing antibodies against the antigens that are specifically found on the um on the Schwann cells or the myelin sheath. These antibodies. Um uh antibodies basically can um So they, they don't only just attack the, the anti um the antigens on the Campylobacter or the CME or the EBV virus. But they also mimic um uh the antigens on these viruses. They also mimic uh the antigens present on the Schwann cells. So, so you um when these antibodies are produced against those antigens, they, they don't only attack the, the antigens on the, on, on the infective organism, but it also starts to attack the antigens on the myelin sheath. And this phenomenon is known as molecular mimicry, which basically means that the antigens, they look similar um uh in both uh the um uh the the infectious virus as well as the uh the antigens found on the myelin sheath. This leads to destruction of the myelin sheath and will lead to issues with nerve conduction. Um Other things that can trigger it are trauma, surgery, immunization and other immune activating events. And I remember in my fourth year, um I saw a patient who um at that time, uh had had a flu jab and then she presented with symptoms of uh GBS. Uh So it just shows you that any, anything that can activate your immune system can actually lead to GBS, um being initiated in your body. So it presents with an ascending symmetrical motor weakness. So firstly, it's usually it's mostly motor and it ascends from the, from the periphery. So from your toes upwards towards the legs and, and then it can also start in the tips of your fingers and upwards towards your hands and arms. And so we describe it as a gloves stocking distribution. So, uh, gloves on the hands, it seems it, it just goes upwards from the tips to the arms. Um, a key feature is that you have absent or reduced deep tendon reflexes. That is something that's very important if you see that someone has motor weakness in the peripheries in their, in their lower legs or in their, in their forearm or their hands. And they also have depressed or absent tendon reflexes such as the ankle jerk or the knee jerk. Then GBS is a very, very likely diagnosis in that patient. Uh Some in some patients, you can also start to get loss of sensation and paresthesia and this can present with neuropathic pain. So the sharp stabbing, burning pain in the peripheries, um it can also eventually progress and, and as it's ascending upwards, it can ascend into your, into your um facial muscles. So once the uh once the facial nerve starts to uh to demyelinate, you can get a facial nerve, cranial nerve palsy, uh which can present with uh drooping of the, of the face of the one half of the face. Um and you will also not get forehead sparing because it's a low motor neuron um condition. So, as I said earlier, um GBS usually is preceded by an infection. So it could be uh you know, any of the Campylobacter CMV, EBV, just a few to name. And this can be about 44 weeks before the onset of these symptoms. Symptoms will typically begin in the feet and progress upwards. Um And it will ascend uh symmetrically. So you'll have the same weakness in both your peripheries. Um And then patients will sometimes complain of a backache and or muscle cramps, symptoms will generally peak at about 2 to 4 weeks. Um So that's when you'll have the, you know, the the extent of the weakness will, will reach its peak and then recovery will begin. And this can take from months to years and, and usually most patients will recover pretty well uh from GBS. So the main thing is is that GBS is usually a clinical diagnosis. You can also do um have some tests such as nerve conduction tests or you can also do a lumbar puncture which sometimes shows a raise protein, but generally, you'll see that they'll be diagnosed based on examination findings. So this is the criteria. So there are required features. The required features are progressive weakness in both arms and legs and aflexia. As I said, aflexia is, is very important if uh aflexia or hyperreflexia that needs to be there for you to diagnose um GBS. Um Other associated features may be mild sensory signs or symptoms, uh cranial nerve involvement, especially bilateral facial weakness, uh relatively symmetric. So the um it will be as symmetric as it can be the, the the weakness, um autonomic dysfunction, uh you can get, so you can get uh changes in postural drops or, or urinary retention and things like that and reduce nerve conduction or a protein in CSF. So those are the other things that if you are not sure about the diagnosis, you can always do a nerve conduction study which will show demyelination and reduced velocity of the of nerve conduction. Um And on a lumbar puncture, you may see slightly raised protein in the CSR. So management wise, um it's quite, it's quite conservative. Um I would say so you observe closely, you um you, you monitor the weakness. Uh and what I saw on the wards was the big mark um to see how far the weakness had gone up. Um Just to keep uh keep an eye on it. Another really important thing is, is bedside spirometry. And this is because it can um if this, if this weakness spreads to the muscles of the diaphragm or the intercostal muscles, it can start to cause uh cause respiratory depression and eventually respiratory arrest. So it's something that's very important to look out for um ECG and cardiac monitoring, um DVT prophylaxis because these patients will be immobile for a long time. So they need good DVT prophylaxis with either um not so much tens where you can give them lots or you can give them enoxaparin. Um uh As uh as per the guidelines, uh they may require catheter if they are unable to control their bladder or if they can't walk to the toilet, which would probably be the be the case. And very importantly, good pain control with opiates. And you know, to, to make sure that these patients are not suffering with, with neuropathic or pain related to um uh to, to the to the condition itself. Specific management, however, is uh mainly um IV immunoglobulins. So you give them IV IgG and another one is plasmapheresis. Um but this is only useful within the first two weeks of onset. Um studies have shown that there is no benefit after three weeks. And so you basically uh in essence, you're trying to go to the plasma and remove all these uh these antibodies are attacking the myelin sheaths, steroids are not effective. So, steroids are not used in the treatment of GBS because the studies have shown that they have um no effect on the prognosis or the um or the course of uh course of the disease complications wise, GBS has uh has uh two or three main complications um autonomic dysfunction, as I mentioned earlier. So if, if those uh those nerves start to uh demyelinate, you can get cardiac arrhythmias, which is why it's important to do regular ECG S or if patients have any palpitations or um or chest pain, it's important to do it easily, quickly postural hypotension, it can lead to hypertension and urinary retention. So, these are important things to look out for and be aware of um pain. As we, as we discussed earlier, you can get a lot of neuropathic pain, um DVT and P because of prolonged immobilization um and the import on respiratory failure. So, it's really important that patients with GPS undergo um undergo regular spirometry. Um and, and spirometry. And the main thing you're looking at is the F VC, if the F VC is starting to fall, um as compared to the um the uh the spirometry figures from the fall, uh you need to involve it. Uh as a patient may be going into respiratory failure and then eventually respiratory arrest. So at if we see below 20 mils per kg uh or about one point uh or, or one point or 1 L, I think um is uh is, is indicative of an it referral and patient may need to um may need to be intubated and ventilated as a result. So the next topic. So this again is a very important topic. It's uh called myasthenia gravis. And this also is an autoimmune condition, but it affects some a a different part of the of the nervous system. It affects the uh the neuromuscular junction. So where the, where the nerve endings are meeting the muscles. Um in essence, what happens is that you get muscle weakness and it progressively gets worse with activity or how patients will describe it, that, um, it gets worse through the day or it's worse at their symptoms are worse at the end of the night, but they're quite good. They, they, they feel ok at the, at the beginning of the day there is a strong link between my gravis and the thymoma, which is a, a can, uh, which is a benign, usually a benign tumor of the thymus. Uh, and they say that it's, it's to do with uh the maturation of the immunoglobulins, which I eventually end up attacking the uh uh the um the receptors that we'll talk about. And there is a bimodal age distribution. So usually it happens in men uh around the age of 60 women generally affects under the age of 40. And uh it's also associated with other autoimmune disorders such as Graf's uh rheumatoid arthritis. And uh sle the pathophysiology is quite simple, autoantibodies are produced against the acetylcholine receptors that are found on the muscles or the muscular membrane. Uh Usually what happens is that your, your um at the uh at the synapse, uh your uh uh um your presynaptic bulb uh will release um will release acetylcholine and this acetylcholine that attaches to these acetylcholine receptors and it allows the passage of sodium ions um and uh and to flow through and cause another action potential in terms of nerves. But in in um in the case of muscles that causes contraction, um however, antibodies can start to block the receptor sites and reduce muscular stimulation as a result. So, no longer can the acetylcholine molecules attach to these receptors because these antibodies are just sitting in the in the receptor sites and eventually increased stimulation leads to more receptor sites being blocked, blocked. And because these acylcholine receptors will also block the receptors. And so this causes progressive muscle weakness with activity and eventually with time um in myasthenia gravis, the complement system also gets activated. So your C one C two C three C four complements and they can start to attack these receptors and destroy them um uh for uh destroy them completely. So, um so you have uh firstly, you have those antibodies and then now you have reduced receptors. And so myogram is quite progressive um in that sense presentation uh for myogram is so, hallmark is usually muscles um uh that are affected on the proximal muscles, the muscles of the eyes, um uh usually bulbar signs like um like voice becomes weaker or or swallowing problemss. Uh So usually it will affect the extraocular muscles and they will with diplopia. Um so the eye muscles, um the intrinsic eye muscles will get affected um eyelid muscle weakness. So you get uh you can start to get orbicularis oris weakness. And so these patients may present with progressive um ptosis. So they, they, they've noticed this, that their eyes become more droopy as they go through the day or towards the end of the night, um, difficulty in swallowing. So maybe they might present a little bit of dysphagia, food, getting stuck, not being able to swallow completely, bringing food back out, um, or this artery. So the voice, they feel they might describe it becomes weaker. Um And by the end of the night, uh it's quite hoarse and quite weak. So, so those are the kind of symptoms to look out for. But the most important thing is that it's, it will be uh the, the symptoms will not appear at the beginning of the day, but they will become progressively worse through the day, especially at the end of the uh uh towards night time, examination wise. So you can do a couple of examinations to elicit uh myasthenia gravis, uh or the size of my gravis. So you can get them to blink. So repeated blinking, uh get them to blink for a minute or two and you will see that suddenly, uh towards the end, they'll start to develop ptosis as the muscles um around the eyes start to start to fatigue. Um You can get them to abduct their arms, you can get them to do it 20 you know, up to 20 times and it will cause um you will start to see that their, their ability to raise as far as they could earn at the beginning reduces and their abduction becomes weaker. Um You can get them to just look upwards and it's called prolonged upward gaze. And eventually they'll start to say that, oh, we're experiencing, it looks, you know, we're experiencing double vision or we're feeling a bit dizzy. Um, and that's because the, the muscles of the, uh, the muscles that are causing the eyes to be pulled up are starting to fatigue. Um, you can also check for a thymectomy scar. So you might see a scar around here. Uh, that's where the timer sits. Um And if you have, if you have a scar there, and if there is a history of a time over that, you can be quite, quite sure about your diagnosis of, of myia gravis. Uh Usually you won't see any loss of reflexes as we talked about GBS, there will be no sensory signs. It's a purely motor sort of presentation and no autonomic dysfunction. So it's very different from GBS in that sense. And one thing that is similar is is that you need to perform spirometry in these patients, especially when they're acutely unwell because just like the muscles that we talked about, the muscles controlling the, the, the diaphragm or the, the intercostal muscles. Um, myasthenia gravis can affect these muscles and eventually lead to fatigue. Um especially in, in patients who may have um infections of the chest. Um and they may be breathing a bit more uh a bit more than usual. So the resp rate is high. So eventually you'll start to see that they will start to fatigue. Um, and so it's really important that you, you measure their FBC and you want to make sure that if it's falling, um, uh, in terms of its pattern or if it's going below 20 M per kg, you need to escalate to it for ventilatory support, like intubation and ventilation investigations wise. Uh, the main thing that you're looking for is the, the autoantibody. And, uh, the common one is the acetylcholine receptor antibody. Uh So that's one that you can look out for other less common ones are a muscle specific kinase. And uh I think lipoprotein related uh protein for which is also slightly less common. But generally, you'll see that uh acyl receptor antibody will be positive in these patients. You can do a CT or an MRI scan to look for a possible thymoma if you're suspecting uh that as a cause. Uh you might see on a chest X ray, you might see a wider media side of which could be indicative of the time over. You could do electromyography. If you are unsure of your diagnosis, then you can use this, uh this this investigation to, to check um uh check for muscle fatiguability. And another one of those tests that um we rarely use a medicine that you know, is to treat and see if uh if the patient gets better. So it's called an edrophonium test. So you give the medication that actually helps with myasthenia gravis and see if it relieves the symptoms. If it relieves the symptoms, then it means that myia gravis is most likely the cause. Um, but this needs to be done in a, in a controlled setting and it's not actually done as commonly. Um, as you think, management wise. Uh, there is medications that you can use and the main medications that you need to know about are called acetylcholine Aase inhibitors. If you remember, um, in the, in the, in the synapse, you find acetylcholine erase, which is an enzyme which breaks down acetylcholine into acetate acetate and choline. Um If you, if you block this enzyme, this means that you have a greater concentration of acetylcholine in the synapse, which means that there is uh you know, a greater chance that you won't fatigue or you'll have enough acetylcholine to uh to help you um, stimulate the neuro uh stimulate the muscular junction. Um, examples of these are pyridostigmine, which is the most common one that's used and neostigmine, which is used usually in it settings in patients who are undergoing a crisis. You can also use immunosuppression. So you can use um prednisoLONE low dose and azaTHIOprine and these are usually used for acute cases just so that um uh it's safe for that time. Um And sometimes ay toy even on a normal, thus can, can improve symptoms. So that's something that they can consider if myasthenic grass is getting, uh you know, quite extra, uh quite bad at a young age. Uh, a thymectomy might improve the symptoms. Complications are very similar again. So, a myasthenic crisis is what you are looking out for. And in this, you know, um, you will get symptoms such as slack facial muscles. So they're, they can't smile or they look very fatigued and, um, and tired a weak neck. So they're unable to control their neck, uh, drooling so they're unable to control the muscles of their tongue, uh and their mouth or, or a bit of a nasal speech. So these are things that you're, you're looking out for and making sure that, you know, uh these patients are not developing any of these symptoms because if they are, it can eventually lead to weakness of the muscles of respiration. So the muscles that are controlling the diaphragm and intercostal muscles, which can, then if they are fatigued, can lead to reduced respiratory rate and eventually respiratory failure. Um as I said, it can be triggered by a respiratory tract infection when, when patients have uh nrtis, they start to breathe heavier and they start to either respirate goes up or in an asthmatic patient undergoing an asthma, an acute asthmatic attack. So you wanna make sure that they are not fatiguing and if they are fatiguing, you need to refer to uh the specialists who can provide these patients with ventilatory support uh with either bipap or intubation, bipap is, is um is a type of niv uh which gives uh pushes air in and takes air out. Um at the same time, um in a myasthenic crisis, you would treat with IV renal. So IV IgG and you would also use plasma exchange to remove those acetylcholine receptor antibodies and improve symptoms. Another complication with myasthenia can be the opposite. So, um as I said that we use these acetylcholineesterase inhibitors, you can, you can use too many of them. And sometimes if you know, if you're not getting the dosing right, or if someone has overdosed, they can develop um they can develop an an excess of acetylcholinesterase inhibitors which will lead to increased amounts of acetylcholine in the in the neuromuscular junction, which can also lead to respiratory failure. Um Back in year one, I remember it was a slug syndrome which is uh what um uh what is described in a cholinergic crisis. So these patients, if they're undergoing one, they might present with hypersalivation, uh increased or profuse sweating, increased lacrimation, urinary incontinence, diarrhea, gi upset and emesis um or vomiting. And they also may have a meiosis of the, of the pupils. So these are some things that you need to look out for, especially on the patients are using pyridostigmine as a as a regular medication. So, the last topic that I will be covering is uh multiple sclerosis. So, multiple sclerosis is um is quite a vast and quite a big topic and um it describes a chronic and progressive condition which involves a demyelination of neurons. But the the the main thing is is that these neurons are usually only found in the central nervous system. So it only affects the brain and the spinal cord. If you remember earlier, I said that GPS only affects the peripheral nervous system. But in this case, in the case of multiple sclerosis, it only affects the central nervous system. So the brain and the spinal cord, it mainly affects the CNS. So the cerebrum, the brain stem, the cerebellum and the spinal cord. And it's also caused by um activation of immune cells which um which attack myelin uh which is usually powered around the oligodendrocytes in the CNS. Uh typically the patients are young adults and uh for some reason, it com more commonly affects females. You cannot diagnose MS based on one episode. So, you know, if, if there's one thing that you wanna take about uh take away about MS is uh it's, it's a, it's a condition where um where if you have one sort of episode where you think that MS may have triggered it, you cannot uh diagnose it based on that you need multiple episodes at different times. Um If someone just experiences 11 episode of MS through their life, it's called a Clinically isolated syndrome. So it's just a one off thing, but you cannot diagnose it as a chronic or a progressive condition. The pathophysiology is very similar to GBS. So in the CNS, you have uh the oligodendrocytes which actually uh wrap around the, the nerves in your CNS. And um you basically get um you basically get antibodies which are activated against these oligodendrocytes and they destroy the myelin around the um around the, around the axons. Um and this leads to impaired electrical nerve reduction. And then that is what you see as the symptoms of MS as a result. Um early disease will usually improve. So usually you see your body is able to recover. So, if there is demyelination, your body can uh remyelinate. However, with time and with age, uh your ability to remyelinate reduces. And so the symptoms become more progressive and permanent. The one thing um uh one key statement that you will always see with MSN is one to remember is that the lesions are disseminated in time. So you get, you get different presentations at different times. So as I said, you can't diagnose it based on one presentation, you have to have more than one. So it has to occur at different time and then they need to be disseminated in space. So the region that affects in the brain or in the spinal cord or in the CNS, they need to vary. You can't diagnose MS based on uh on just 11 lesion occurring in 11 place of your, of your brain. So, demyelination occurring, let's say around the optic nerve just once, cannot be diagnostic of um of MS. You must have other um other areas in the brain or other nerves in the CNS which must get um uh must get uh demyelinated for you to diagnose MS. So there's the lesions need to be disseminated in time. So they need to be more than one uh one lesion and they need to come on at different times and they need to be disseminated in space. So you can't just diagnose it based on this one lesion um or 111 process of a demyelination. Um You need to have multiple ones in multiple different regions in the brain. Um Another uh common thing that you can see is internuclear, intranuclear ophthalmoplegia. And this is caused by the demyelination of the medial longitudinal fasciculus or the MLF, the MLF basically, it connects the cranial three and the cranial six. So, the cranial of six usually abducts um the eye and then as it abducts it, it sends a message to the cranial L3 to ADT uh the uh the um the uh the opposite eye. Um So let's say if the right eye is affected um when you get, when you abduct your left eye, um the right eye will fail to abduct because um the, the LR so the lateral rectus on the um on the left eye is able to pull the um uh pull the left eye to the um uh to um laterally. However, um the the signaling pathway uh from where it connects to the uh to the cranial nerve three of your, of your right eye, which will then lead to auction of the right eye is now destroyed. So this will abduct um in in isolation, but the it cannot send a signal to the other eye to um adduct. And so this is called intranuclear ophthalmoplegia, which is commonly seen in um in patients with MS. And it's, it's, it's called a disorder of conjugate lateral case because both two are both two pupils cannot move laterally. Um Only one of them will um under manifestations. So you can get lots of places where, you know, you can get these, these areas of demyelination. Uh common ones are, you can get motor weakness in the face. So you can develop Bell's palsy, you can get Horner's Syndrome. So your p your partial ptosis meos and anhydrosis. If, if um if um that sort of sympathetic nervous system gets um demyelinated, you can get full limb paralysis. If there is some lesion in the um in the, in the um in the um uh in the anterior portion of the brain or in the middle, uh uh middle portion of the brain, you can get sensory weaknesses. So you can get trigeminal neuralgia. Um you can uh you can get random areas of paresthesia and numbness. Um ataxia. If it affects the, if it affects the cerebellum, you can get cerebellar ataxia or you can get sensory ataxia um as well. If um if sensory nerves that provide sensation are are demyelinated, other symptoms that you need to be careful of um before diagnosing. Um MS are things like migraines. So you need to be, you need to be sure that you're not missing a migraine and diagnosing it as MS uh strokes. So, if there's any limb paralysis, you know, you need to rule out stroke as a more um acute concern. Um encephalitis can also present with um similar symptoms and Lymes disease, which can also present with facial, facial nerve weakness. So you need to make sure that you're uh you know, you are uh excluding all these reversible causes before you can jump into something as something like um MS as a as a diagnosis. So, the disease course is, is quite variable in, in different people. So, the most common one is this uh the one that you see at the um at the bottom, it's called a relapsing and remitting multiple sclerosis. So, so you get symptoms, uh you demyelinate, then you suddenly, then you eventually start to remyelinate, but you don't ever return to that same level of function. And these will happen with time as time progresses, you'll get these episodes of remyelination and demyelination and the symptoms that you experience. But with time you will just, you, your symptoms will progress, your comorbidity will increase. Uh So, so it's a bit of a chronic disease. In that sense, you never really go back to baseline. You can get primary progressive MS where it's just progressive. From the beginning, you get, you get gross demyelination of the, of the neurons in the CNS and it will probably eventually lead to death or you can get secondary progressive. So it starts as a relapsing, remitting sort of disease where you get demyelination and remyelination. However, with time in a couple of years, you start your symptoms just progress, they never get better. Um And uh uh and, and the a slightly less common one is a progressive relapsing, a sclerosis. So that just progresses after each stage, you just get, you just keep getting worse and then you're getting worse, but you're also getting these episodes where it flares up. Um So yeah, so, so you, you have to figure this out. This is something that takes um you know, you, you observe a patient over over a few years to see which part of that cycle they might be in investigations wise. So it's usually a clinical diagnosis made by neurologists. But what supports and the main sort of like way to diagnose it is is an MRI scan of the, of the brain and the spinal cord. And usually you will see these typical lesions, you will see areas of demyelination and you can do these uh t one weighted images with gadolinium enhancement, which will, which will point out areas where you can see demyelination. And remember, you can't just base on one area of demyelination in one part of the CNS. You need to see another area of demyelination, let's say, you know, there is uh a bit of demyelination in the uh in the middle lobe of the brain. Um But you have to wait for another, another time for um some other symptoms to appear to redo the MRI scan to see uh the lesion in a different part of the brain. Uh just to make sure that it's disseminated in space as well. You can do lumbar punctures and uh you can see these oligoclonal bands in the CSF, which can also be, which can also help point towards the diagnosis of um of MS. The management for MS is uh is mainly symptomatic management. So it's carried out by the multidisciplinary team. There are some um some medications called such as B2 Interferon and, and some monoclonal antibodies, but they, their effects are quite um quite limited and they're not reversing in any way. So, so the main thing is is to manage these patients um uh manage these patients symptomatically. So, exercise can decrease muscle strength, neuropathic pain. If you're having um uh sensory um uh sensory loss in pain, you can treat that with DULoxetine, pregabalin, gabapentin patients may become depressed. Um So, you know, with a chronic disease, there's always a risk of that. So counseling CBT or the use of SSRI S is always useful um diet. Um There is some link with uh low levels of Vitamin D and so Vitamin D supplements may help with symptoms. Apparently it's, you see more as far away you go from equator, you see a greater rise in the number of MS cases. Uh So they, they recognize to do with Vitamin D hypertonia spasticity of um of muscles, you know, due to upper motor neuron signs, you can treat with physiotherapy or baclofen. But there are, there are drugs out there, there are monoclonal antibodies such as Bengali or beta interferon. But um but their, their use is quite limited. Um if patients present with a, an acute flare up as we discussed, the, the primary progressive. So you get these flare ups, you can treat them with um IV um IV corticosteroids. So you can give them methylpred um uh uh A methylred IV or you can also give them oral corticosteroids and to maintain remission. As I discussed, you can use um immunomodulators such as we tend to be on off in cood um and biologics uh to, to help um keep the patient in remission. Um But eventually you'll see these flare ups and the disease will progress. So, yeah, so that's basically the end of my presentation and I have a very small quiz and I was wondering if you could just put the answers in the chart and then I can go through through the answers with you. So the first question is what is the characteristic feature of lesions in multiple sclerosis? So I mentioned this in, I think the first slide on MS if you could put an answer in the um in the chart, I would um be grateful. So, so what is the characteristic feature? What is the key, key word uh or the key statement that we use when we describe lesions in multiple sclerosis, you put down in the chart. That's perfect. Yes. Yeah, that's it. So, the the lesions are disseminated in time and space and just to explain that again. So usually, MS presents with um the, the first presentation of MS. Uh most commonly is is with a condition called optic neuritis, which is a demyelination of the optic nerve. And so, and so these patients will present with um optic neuritis and you can suspect that this patient may have MS. But the main thing is that you have to wait and see if there's going to be another episode of um um another episode of demyelination. Now, if the patient develops optic neuritis in the same, in the same nerve again, um at a different time, you still cannot diagnose MS, it needs to be a different symptom in a different place. Uh So, so let's say optic neuritis was the first sort of symptom and then someone develops um facial weakness or, or Horners syndrome in the left eye or a sort of like AAA neuropathic pain in their, in their leg. So at that point, you can, you can say that this patient is more likely to have MS because they've had multiple lesions at different times and they have occurred in different parts of the CNS. So, question two is what type of tumor is associated with myasthenia gravis? So, a teratoma ba leiomyoma, c thymoma or ad lipoma. That's perfect. Yes. Uh So see thymoma. So, thymoma is um uh is a, is a tumor or benign tumor of the thymus. Um It is thought that uh the thymus is where antibodies or the the cells, the B cells, they usually mature. And so uh B and the T cells mature. Um and, and it is thought that some dysfunction in the thymoma can lead to the of these um acetylcholine receptor antibodies. So, uh thymoma is actually strongly associated with myasthenia gravis. And as you said, it can actually be therapeutic even if you don't have a, a cancer of the, of the thymus, just doing a thymectomy may help with the symptoms of myasthenia gravis in the long run. Um What kind of ventilatory support would you offer uh to someone undergoing a myasthenic crisis? Would you, so, so these are patients that we discussed that their are falling and their respiratory um respiratory function is going down. Would you leave them on room air? Would you employ CPAP? Would you employ bipap or nebulized salbutamol how would you help this patient? Yep. So, so c is the, is the right answer. So, bipap is a type of N IV and it's called BL positive airway pressure. Uh It, it differs from CPAP in the sense that CPAP just pushes air inwards. But BIPAP is able to, to uh put air in and take um air out. And so basically acts as a, as a vent, um uh uh as a, as a way to ventilate your lungs. But the best thing is that it's not invasive and you can do it on someone who's awake. Um And, and you don't need to sedate them. Um uh you know, which you would have to in the, in the, in the case of intubating and ventilating them. Um Question four is, is the following statement, true or false. Steroid treatment has shown to be effective in the treatment of GBS. So, are steroids? Uh Would you use steroids uh in a patient presenting with GBS? Um Yes, true or false. Yeah, that's perfect. So false is the, is the right answer. Steroids. Um have uh you know, many trials and studies even though we think that, you know, it's a, it's a sort of immune, immune, immune modulated. Um uh it's an autoimmune disease and usually we see that um steroids do help in, in suppressing the immune system in um in immune uh in autoimmune conditions. Uh But in GBS, many trials have shown that steroids actually have no role. So there is no point, you know, putting someone on steroids and obviously starting them on complications such as gastric ulceration, diabetes or, you know, all of those osteoporosis, there's no risk, there's no reason to put the patient under that sort of risk. Um So it's really important that, you know, you avoid steroids in GBS. Uh what drugs would you recommend for treatment of spasticity in multiple sclerosis? Um So, as we discussed, you get upper motor neuron signs, you can get spasticity. Would you treat that with sertraline, amitriptyline, botulinum toxin A or Baclofen? Yep, that's perfect. So D baclofen, so, Baclofen is an antispasmodic and it can help with um upper motor neuron spasticity that may be caused by uh demyelination leading to um leading to upper motor neuron spasticity in let's say the legs or the or the arms. So, Baclofen and also physiotherapy, physiotherapy can be very, very useful in, in retiring function or retaining some sort of function in in areas of spasticity. Yeah. Thank you for listening. And if you have any questions, please just put them in the um in the chat and I'd really appreciate if you can fill in the the feedback form that is um put in the chart. Yeah. Thanks again everyone for coming and thank you doctor for doing the session for us. Um Please um do fill in the feedback form by doing that. You can also get the copy of the slides from us. Um, here's a QR code as well. Um, and then just a few, um, other announcements, um, there's, uh, Nick kind of the group who's like a national kind of group focusing on students getting into kind of neuro neurology or your surgery. Um, they're holding a conference in, I believe on the third of February, which is Saturday. Um, that was, that's planned in person, but there's also an option that you could do it online. And that's the QR code for that. And then another thing that they're doing is um an undergraduate prize, which is an essay kind of competition. There's three kind of categories. So if anyone's interested just scan that uh QR code. Otherwise, if um everyone's happy, we'll see you in the next few sessions. We'll be covering other things like UR anatomy, um cranial nerves and stuff like that. And we'll provide the announcements through um our Instagram and for the students, we send out emails as well. So, thank you, everyone. I think that finishes the session today. See you soon.