Computer generated transcript

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

Hi, everyone. So it's around seven or sixish now. So I think I'll start, um, my name is Rose and I'm af one doctor currently and I've just finished Imperial Med School. So, um, I've just been through finals and have somewhat of an idea of, um, um, what's the process of pa exams and what things they like to bring up and what things they like to assess for. Um, so today I'll be going through neurology basis and going through some of the more common, um, tested, um, exam, examination presentations and conditions in cases for neurology and it's very informal. So feel free to unmute yourself or, um, type in the chat any questions that you have throughout and I will, um, check regularly and answer them. And, um, and, um, there's a II don't have a mentee, so I'm just going to be informally asking questions and if that's the case, then please feel free to put it in the chat. Um, and, um, so I know what most of the common responses are and if things need further explanation or not, um, or you can also just, um, write it in a piece of paper as well because it's kind of uh uh I, I'll ask a few questions and then I'll go through the questions based on what I've talked. Ok. Um So to start off with, um I'm going to go through some brief um um neurology um sort of overview of common um thing, uh common things to just to be aware of and remind ourselves about. Um So to start with um the neurological systems are separated into the central nerve system and the peripheral nerve system. So the central nervous system is basically composed of the brain and the spinal cord and the peripheral nervous system is everything else, including cranial nerves and spinal nerves in the peripheral nerves. And um the main main main um things to be able to sort of differentiate between in patient examinations is between the upper motor neuron signs and the lower motor neuron signs. So, um the main differences are that one causes spastic paralysis, whereas the other one is flaccid paralysis. So it's essentially floppy. Whereas the other one is almost um increased in tone and very rigid, uh increased reflexes for upper motor neuron lesions. Whilst the lower motor neuron is decreased and positive upgoing babinski scan um and reduced, sorry, it's meant to be increased power in the upper motor neuron lesions not reduced. Whilst in lower motor neuron lesions, it's reduced. You also get some fasciculation, some muscle wasting in lower motor neuron disease as well as decreased tone as well. Whilst it's increased in the upper motor neuron. And um the way we can classify is most upper motor neuron lesions are stroke, multiple sclerosis, brain tumors or spinal cord. And most lower motor neurone lesions can be to categorized as GBS Gilla barre syndrome, peripheral nerve lesions. So, this would include things like diabetic and alcoholic neuropathy, carpal tunnel syndrome, any kind of traumatic nerve injury and neuromuscular junction conditions as well. So, this would be, for example, myasthenia Gravis bottle, which is caused by which is caused by a toxin produced by the bacteria. Um Clostridium Botin and also the Lambert Eaton syndrome as well would be would form part of the neuromuscular junction conditions. Um And um so those are the two ways you can categorize between the upper conditions for the upper motor neuron and low motor neuron. Um problems and motor neuron disease is a weird one because it kind of fits in the category for both. So you can have upper motor neuron signs and a combination of lower motor neuron size as well for motor neuron disease. And that's why it's in the middle of the two circles. Um And finally, we talk about increased tone, but what does it actually mean? And you can actually categorize it into two different types of increased tone. So, spasticity, which we talked about and rigidity. Now, spasticity is commonly associated with cortical lesions. So this is kind of lesions with the lobes of the brain and this includes um stroke, for example, um it's also velocity dependent resistance. So as the speed increases, the spasticity tends to increase as well. And um the spasticity also varies in terms of flexion and extension movements as well. Whereas rigidity is a more of an extrapyramidal um lesion. So it's commonly associated with Parkinson's disease, for example. And uh the resistance is um throughout uh same throughout all kind of um motions and also uh speed as well and often is described as a lead pipe rigidity. And um often we often hear with Parkinson's Parkinson's Parkinson's disease, for example, where we hear the word cog wheeling and that's basically this rigidity of increased um tone alongside a trump tremor that happens um um together with the rigidity and that produces a cog wheeling, um a sign symptom that you can see in patients. Um And finally, just a, a brief overview of all the different kind of main conditions you'd need to be aware of for Britain's and ps. Um and where in the brain, these lesions are so mostly um main ones to know in the spinal cord, the main problems you can have is um multiple cirrhosis cord compression and hemisection of the spinal cord as well. Um For cerebellum, it tends to be stroke related, alcohol related. Um and um Parkinson's plus symptoms as well. Um brain stem tends to be stroke and Parkinson's um meninges are typically meningitis and subarachnoid hemorrhages and cerebral stroke. Um um basically um involves the cerebral cortex which is divided into various multiple lobes and it contains stroke, multiple sclerosis, tumor, brain bleeds and venous thrombo embolism as well. And the basal ganglia is mainly involved in motor and motor coordination. So, and it's found underneath the cortex and um it involves lack and a stroke which we'll go through about what exactly it is. Um Huntington's Parkinson's um Parkinsonism and um, lack of a stroke which I've mentioned before. So that was just a brief overview. Um, does anyone have any questions at all? Um, if so, feel free to ask now or if not, we can move on to the next section. OK. Um, so the first SBA is, um, I'll give you all about 30 45 seconds to have a read of it and answer it. Um, please feel free to put it in the chart so I can explain things further as I mentioned before. Um, based on what answers you guys give. Um, but otherwise, um, have a read of it and I'll give it about 30 to 40 seconds per question and then move on. Ok. OK. Moving on to the next question. Now again, feel free to, um, put in the chat. What do you think the answers are moving on to the next question? OK. I hope everyone had time to answer those three questions. Um, so now we'll move on to some of the explanations for that. So um to start off with stroke. So, stroke, as we know is a sudden onset of focal neurological deficit, um which is presumed to be of vascular origin and lasting for more than 24 hours. And that's kind of the basic criteria for defining a stroke. Now, stroke can be categorized into an ischemic stroke which is the majority of the strokes. So, between 80 to 85% of strokes and essentially, it's due to lack of blood flow in the brain. And it can be caused by various mechanisms which include thrombosis, which is basically an arc plaque that narrows the blood flow to the vessel, an embolism which is basically a blood clot formed elsewhere somewhere else in the artery that gets migrated in the circulation to block a vessel in the brain and systemic hyperperfusion as well. So this would be, for example, during cardiac arrest or instances of very low BP, hemorrhagic stroke forms the remaining 20 to 15% of strokes. And they can be categorized into intracerebral, which are the ones that happen inside the brain and the subarachnoid, which happen in the subarachnoid matter. And a stroke can be classified by the Bamford classification. So basically, this divides stroke into where the lesion is in the brain. And often when you in cases, when you see presentations of people presenting with symptoms of stroke with motor neuron lesions, often the question they ask is which where in the circulation is which part of the brain is affected or where in the circulation is the, is the blockage or the incident uh or the rupture. So, um they can, these can be categorized into four different areas which are the total anterior circulation, stroke, or a partial anterior circulation, stroke, and posterior circulation stroke and lack in our infarcts as well. Um So um talking a bit more about the anatomy. So the um in order to sort of understand where the lesion is in the brain from um symptoms, you kind of need to understand the um the anatomy of the blood vessel supply in the brain. So the brain receives blood from two sources, which is the um internal carotid arteries. Um and um and posterior vertebral arteries, which is for the posterior circulation. So right now, I'll talk about the anterior circulation, which is the purple circle at the top. So the anterior circulation, you receive the blood sources from the internal carotid arteries which arise from the common carotid carotid arteries. And then the internal carotid arteries branch into two major vessels, which is the middle cerebral artery and the anterior cerebral artery. And these two vessels which is the middle and the anterior cerebral arteries form the anterior circulation and they supply the blue area and the orange area. So that's basically this area and this orange area here. So that's blood, those two vessels supplied are supplied by the anterior circulation. Now, the posterior circulation arises from the vertebral arteries down here and they, they originate from the caly subclavian arteries from the aorta and the posterior vertebral arteries of the that supply the brain essentially supply the, the occipital lobe over here, the cerebellum and the brainstem. So those are the three regions supplied by the posterior circulation. Whilst the anterior circulation supply most of the local area and the blue and orange pals here, I hope that makes sense if not just feel free to message or unmute yourself and ask any questions. Um So, in terms of uh defining um anterior um circulation, um strokes um that you can, you can call it tax, which is the total anterior circulation, stroke or partial anterior circulation, stroke. And the requirement for this is to meet either all three or two of out of the three of the um the symptoms. So this includes a um contralateral motor or sensory deficits, hermonis eminia and um higher cortical dysfunction, which can be categorized as either dysplasia or neglect. Now, um the anterior cerebral artery um can uh as we mentioned, the anterior circulation contains this anterior cerebral artery and the middle cerebral artery. So, in the anterior cerebral artery, it specifically contains um contralateral motor and sensory loss that's worse in the legs. Um And alongside behavioral changes and the behavioral changes occur because um the anterior cerebral artery supplies the frontal lobe which is associated with the individual's behavior. Now, the middle cerebral artery. The, the sort of the highlight thing is that it causes contralateral sensory and motor loss in the arms more so than the legs. And uh it was also associated with quadranopia um which is shown in this picture above where it's basically a, a quarter of your vision is um is absent and also aphasia as well. And this could be one AEA aphasia or Brocker aphasia based on whether it's receptive or expressive aphasia. Um So that's basically the main sort of learning point from here. So, if the arms are more affected than the legs, then it's a middle cerebral artery, anterior cerebral artery, sorry, middle cerebral artery. And if it's the legs more so than the legs arms, then that's the anterior cerebral artery and the criteria for defining anterior circulation. Um um um problems would be contralateral motor sensory loss, hoops, he anopia and higher cortical dysfunction as well. Um Now, moving on to the posterior circulation. Um so, as mentioned before, the posterior circulation is supplied by the ventricle arteries which supply three main areas including the occipital lobe, the cerebellum and the brainstem. Now, the cerebellum, the symptoms associated with cerebellum can easily be sort of remembered through the acronym Danish, which basically contains dyskinesia ataxia, nystagmus, intention, tremor, blurred, slurred speech and hypotonia. And um and the brainstem um is it contains um symptoms of reduced consciousness. They will often present with cranial nerve damages. And that's often because um the um the, the, the cranial nerve nuclei are found and uh originate near the brain stem and then they move their way upwards to the supplying um the rest of the brain. Um And also you get crossed signs. Um And what we, what we mean by this is they have contralateral signs on the arms, legs and the body, but on the face and areas associated with the cranial nerves, you get ipsilateral signs. So it's on the same side of the lesion. Um I'll explain this a bit more in detail in the next slide. Um And finally, with occipital lobe, you get visual agnosia, which is basically an inability to recognize an image. So you're able to see it and you can see the fact that you see it, but you're not able to label it as whether it's a pen or a pencil or a jug or whatever it is. And it can also cause um her contralateral heia. So this together forms um um forms the typical symptoms associated with a posterior circulation stroke. And um to which degree um you see these symptoms depends exactly which part of the vical artery um is affecting, um which sort of region predominantly more. So sometimes you can get symptoms of um causing more cerebellar symptoms as opposed to brainstem. Um see you and um just to explain the cross signs that we see in brainstem injury, the reason why we get cross signs in the motor and contralateral um um symptoms in the motor and sensory modalities is because of the cortical spinal tract and the spinal thalamic tracts. And these two tracts essentially cross over after the brainstem. And so when there is a lesion in the brainstem, because these tracts cross over the symptoms present themselves on the opposite side. Whereas in the cranial nerve pathway, the um the, the, the, wherever it is, wherever the nuclei is, that's where that's how the nerves migrate upwards. And therefore, it's ipsilateral, it doesn't cross over. And so if there's a lesion at one part of the brain stem, then the cranial nerve dysfunction will happen on the same side. Whereas for the other two, because the nerve fibers cross over after the brain stem, the lesion happens on the opposite side with motor and sensory functions. I hope that makes sense. But again, feel free to um unmute yourself to ask any questions or message on the chat if there are any queries regarding that. Sorry. Can I just quickly confirm? So you said corticospinal is contralateral spinal thalamic is contralateral and cranial nerves ipsilateral. Yes, that's exactly. And what about what the small gap? Um There's a gap before it becomes uh before it decussate. Do we need to know anything about that or that? That's I think beyond the level of paces. Yeah. Um The main thing is just that brainstem injury will cause cross signs of where partially it's contralateral and partially, there are ipsilateral symptoms whereas for most other forms of um um the um strokes, for example, anterior circulation, it's always contralateral motor and sensory loss. Ok. Thank you. Any other questions at all? Ok. Um So now moving on to la in our infarcts, so these are um small uh perforating arteries that supply the subcortical structures, which we mentioned before as the basic anglia. And also others include t the thalamus and internal capsule. And they tend to present with mild or smaller symptoms because they are very small injuries to the small, very small perforating arteries in these regions. So these tend to present with very pure motor hemiparesis, for example, or very pure sensory stroke or an ataxic one and sometimes a combination of sensory motor ones, but tends to be more pure motor sensory ones. And they generally lack cortical signs, which are, for example, hem anopia or agnosias or apraxia, which is a difficulty in initiating movements. And the reason why they lack these cortical signs is because they don't involve the cortical structures. Um It's subcortical, it's, it's affecting the arteries that supply the subcortical artery, um um parts of the brain and um that as I mentioned before is the basal ganglia thalamus and so on. So those are the lack or infarcts. So now, um going back to the first question I asked uh which was about um this man, a 70 year old who's admitted with a facial droop and slurred speech. Um and his right arm is kept in a flexed position. Power on the right side is um less on the upper limbs and more um more on the lower limbs and the fields are intact. So this is basically a left middle cerebral artery stroke. And as we mentioned before, with middle cerebral artery, the arms are more affected than the lower lower limbs. And that's why it's a, it's a middle cerebral artery stroke. And we can establish that this is an anterior circulation stroke because of the, because of the the symptoms of the facial group. Um and the Sla Beach and the um the effect in the effect happening on the contra lateral side of right side of the upper limbs and also in the right side of the lower limbs. Um It's not an anterior total anterior circulation stroke because it doesn't contain all three categories that are required for a total anterior circulation stroke. It only contains um two of them. Um It's not a uh right anterior cerebral artery stroke because again, the legs are affected um less so than the arms. Um It's not a right middle cerebral artery stroke because um it it would affect the left side and these are all right sided symptoms in this presentation. And it's not a left brainstem stroke because there's no sort of evidence of any cranial nerve palsies or ipsilateral symptoms of the face that we mentioned before. Alongside the contralateral symptoms of the motor and sensory functions on the body. Does that make sense for SBA one? Any questions? I had a question? Yeah. With the slurred speech counts as the higher cortical dysfunction in this case. Yes. Yeah. Thank you. Yeah. Any other questions at all? So moving on to the next part. So in terms of investigations for stroke, so um anyone presenting with any symptoms of a stroke, the urgent, urgent, most urgent important investigation to do is a noncontrast CT head. And the main reason for this is basically to rule out an hemorrhage not to look for the presence of the stroke. It's basically just to rule out an hemorrhage. And the most important reason for this is because um you need to distinguish between whether it's a hemorrhagic stroke or an ischemic stroke because the management of the ischemic stroke can actually make the hemorrhage worse if it's a hemorrhagic stroke. And um uh you need to do a noncontrast CT head because um if there is a um that's the only way you can sort of find the hemorrhage, it does not rule out the ischemic stroke if it was normal. And you can see here the difference in presentation of um um how a ischemic and hemorrhagic stroke appears on the CT head and um which one is more hyperdense and which ones more hypodense. So, in terms of management for stroke, um they, the after ruling out whether it's a hemorrhagic or an ischemic stroke through the CT head, the main sort of differentiating factor is duration. So, was it, did the patient present within less than 4.5 hours or did they present after 4.5 hours? So, if it's less than 4.5 hours, then the main treatment is basically thrombolysis with IV alter places. Um and then you give them um 300 mg of um aspirin orally. Now, um if they present with uh after the 4.5 hours cut off frame and they have contra or they have contraindications for thrombolysis, then you would immediately just start off with the aspirin 300 M GS um for two weeks and then they will be continuing on lifelong clopidogrel, 75 mg. And if they can't have clopidogrel, then that would be a combination of Dipro and aspirin um and um contraindications for thrombolysis. Um Some of them, these are not all of them, but some of the most important ones I've listed here, but there's more to the list are essentially an onset of more than 4.5 hours if there's an acute trauma or hemorrhage that you're suspecting and you've not been able to rule it out. Um Symptom subjects suggestive of any sort of subarachnoid hemorrhage. So things like raised intracranial pressure, um thunderclap headache, that kind of description um and um deranged clotting as well if there's any kind of indication of this person is very likely to bleed out, for example, um or cause a a hemorrhage into the brain as well. And the whole aim of these sort of reperfusion therapy, which is either thrombectomy or thrombolysis is basically to restore blood flow, to reduce that irreversible damage that could happen. And that's why this 4.5 hour time frame is very important and knowing when the onset of symptoms was, was really important and in your history taking, you should definitely ask for the patient. When did the symptoms start? Do you know when it started? Because that kind of aids, the treatment management plan later on? And um finally, another treatment treatment option is basically thrombectomy, which is removal of the thrombus. And um um this is basically when there is a very large occlusion of the proximal anterior or posterior circulation when you do a CT or an MRI. And um um so yeah, that's, that's basically stroke management. So I guess to summarize it, main indications would be essentially to find out whether it's within the 4.5 hours at that time frame. If so, then you go with thrombolysis, if not, then you go with aspirin with lifelong clopidogrel. Um And then you just need to think about the contraindications for thrombolysis. And if they do have a contraindication, then you wouldn't um do the thrombolysis. And also it's quite useful to ask um in your history for questions to sort of show that you're thinking of whether the patient does have contraindications for thrombolysis. So for example, you could ask them about um like symptoms and symptoms of subarachnoid hemorrhage. But you could also ask them for any kind of bleeding tendencies that they've had in the past. Do they have any sort of blood hematological conditions that could derange the fact that they will not be suitable for thrombolysis? Are they on any warfarin that could potentially cause a bleed? So that kind of questions would be useful to ask in your history just to show the examiners that you're thinking of the contraindications of thrombolysis as well. So you're just kind of thinking one step ahead as opposed to just finding out what the diagnosis is. Um So yeah, um any questions about that at all before we move on to the next SBA explanation? No. OK. Um So moving on to the explanation for the next um question. So this was basically someone who's presented with um signs and symptoms of basically a stroke. Um And what is the next management um for this patient? So the answer here is 300 mgs of aspirin. And uh the reason why it's not a carotid Doppler is because it would, it wouldn't be an immediate treatment to investigate this. Um This would definitely be done. Um And it's one of the follow up investigations for someone who's presented with stroke. And this is basically to look for um any stenosis of the carotid arteries and if the stenosis in the carotid arteries is more than 70% on the Doppler ultrasound, then this patient would essentially be suitable for a thrombectomy. But this would not be the immediate treatment that you would do. Now, um as I mentioned, 300 mg aspirin is the immediate treatment. If the patient presents with more than 4.5 hours in this question frame, she we don't really know exactly when she was presenting, but we know that she went to bed and she was normal and then she woke up and she had these symptoms. So we don't really know whether this fits within the 4.5 hours time frame or not. And when you don't know that you don't go for the thrombolysis, you go for the aspirin management. Um 75 mg clopidogrel question answer c would not be suitable because that's more of a secondary prevention and a long term management following the initial acute management of the stroke. An ECG um this should have done, this should have been done way before. So during the acute collecting in A&E wherever the patient presents, the ECG forms part of the baseline investigation and even, you know, before the CT and everything that the ECG should have been done. So it's not really a management per se. It's just an investigation that should have been done prior. And then, as I mentioned before, thrombolysis um would not be suitable because we don't really know if the duration of symptoms was less than 4.5 hours as it's not specified. And that's why it's really important to ask that. When did you, when did the symptoms start? Um Because that really aids the management. So that was ba two any questions with, without that tool or in terms of management or investigating um, stroke? Yeah, I have a question actually. Um So on, I think maybe two slides ago you mentioned about CT Angio. Um if you suspect it's a large thrombus um point in your kind of your initial management, would you consider all that? What would happen to make you consider doing the Ct Angio from your Clark? I mean, so um CT Angio would be considered. So for example, when you do a stroke, um a CT head, a non contra ct head, it will definitely rule out a hemorrhage, but it won't necessarily sometimes won't show if there's a stroke or sometimes if they have a tia it's resolved. So again, you can't see if there's an ischemic component to it. So the next line sort of higher definitive investigation to see if there's any kind of ischemic stroke would be um A and or an MRI scan or an M angio. So those would be the next line if the CTT head does not show anything ischemic, whereas if there was anything hemorrhagic, it will definitely show and that's why we can use it to help rule out hemorrhagic strokes. But we can't really, it doesn't necessarily rule out an ischemic stroke. So if you can't see an ischemic stroke, then the next line would be, for example, if they had a tia and it's already resolved, the next line would be doing an MRI or a CT Angio an Mr Angio. Oh Yeah. Thank you. That makes sense. OK. Any other questions at all? OK. So I move on to the next question. So um Vertigo um we're not going um someone else. No, CT Angio, you would not necessarily do it for every patient. It would be, it would be dependent on whether you can see the cause of the, is whether you can see the ischemic stroke on the non contrast CT head. And if you can't see that, then the next line of steps would be um would be um CT Angio or an MRI and so forth. Um And also if you're thinking about a Tia and if you do an MRI, that would be the kind of process for it. You wouldn't necessarily do it for everyone. No. Does that answer your question? Yeah, lovely. Um So, vertigo um in terms of vertigo, I'm not gonna go into too much detail about it, but just, this just helps to summarize the um third question that we asked um for S B3. So Vertigo essentially is just a, a sensation of spinning um of the or movement of the room around you. And um essentially, you can categorize vertigo as central causes and peripheral causes. Now, central causes are when there's a lesion in the cerebellum or the brainstem and peripheral causes are when there's a lesion in the labyrinth. And um that's essentially the area responsible for balance. Now, the way to differentiate between whether the vertigo has been caused by a central cause or a peripheral cause is, is to think about whether there, there is an associated nystagmus. Now, if the nystagmus is horizontal, then it's likely to be a peripheral cause and associated with some sort of um uh labyrinth problem or whether it's associated with um menorrhea disease or B PD, which is benign paro positional vertigo. Now, if there is the nystagmus, it's multidirectional. So essentially, it could be horizontal, it could be radical, it could be rotationary, then it's associated with a central cause and affecting the eye, the cerebellum or the brain stem. And typically, it's either a stroke of these regions or it could be multiple cirrhosis. And um and so that's just the brief overview of where to go and how to kind of classify whether it's a central cause or a peripheral cause within the peripheral causes. The main ones to be familiarized with and have an understanding of is B PV, which is um um basically when there is small crystals, crystals of calcium carbonate, they basically form and shift in the inner ear falling from one position to the next and that can affect, um, um, the sort of, um, vertigo and the, um, symptoms, um, based on which part of the little air, air components that they fall into the crystals and, um, it can last for seconds. Um, so it's very short lived. Um, it's particularly worse with head movement. So they will complain of the vertigo being associated with moving the head or waking up from the head and turning around and so forth. Uh And the ley and help maneuvers are essentially to, helps to sort of diagnose them. Um, menorrhea is um unilateral symptoms. And um the way to kind of differentiate it from B PV is that it's a bit more long, long lived. Um So it's lasting for a few minutes as opposed to seconds. Um And it's associated with tinnitus, which is basically that ringing sound in your ears and hearing loss, hearing loss as well. Um Labyrinthitis or vestibular neuritis, these are basically inflammation of the labyrinth or the vestibular nerve. And um it's often occurring after an infection. So you could, in, in your history, you tend to, you'd want to ask about any kind of preceding viral or infections um in the body. Um Again, it's associated associated with tinnitus. Now, um the way to rule out um between labyrinthitis and vestibular neuritis is basically to see if there's any associated hearing loss. Hearing loss only occurs in labyrinthitis because it contains the cochlear nerve. And um and in vestibular neuritis, neuronitis, there is no hearing loss. So that's just a view view on the vertigo. So now moving on to the question three. So this is someone who's presented with vertigo associated with nausea and vomiting. Um She's got a history of um past medical history of hypertension and um some clumsiness in her right arm. Um and also a um droopings of her right eye um alongside some multidirectional nystagmus. Now because it's not multidirectional as nystagmus, we can kind of quite quickly say that this is a sub peripheral cause um affecting the cerebellum or either the brainstem as opposed to being a peripheral cause. So that way we can easily rule out the A B and D because they are um peripheral causes and they would have a horizontal nystagmus as opposed to a multidirectional one. between C and E. This is a really hard question. So the reason why it's ae is because there is a component of cranial nerve, palsy, cranial nerve injury um associated with it because of the droopiness of the right eye. Um that can be associated with the cranial nerve three palsy. Um And um and also um uh the clumsiness in her right arm that could be ataxia. So that doesn't really help to rule out between cerebellar or brainstem. But essentially, I think it's a cranial nerve involvement that causes that, that justifies it being a brainstem stroke as opposed to a cerebellar stroke. Um because cerebellar strokes don't tend to have um any cranial nerve involvement. It tends to be the Danish symptoms. So, just diag um ataxia, nystagmus, tremor, blurring of the speech and so forth. Does that make sense in terms of S B3? Any questions there at all? Yeah. Ok. Um, so, um, now we're moving on to a different set of um, topics and conditions. So this is the next SB, so I'll give you a few um seconds to have a read of that and answer the question and then we'll go through that. Ok. So I hope everyone's had a chance to have a read of that and um think of what the answer might be. Um So essentially, we're talking about Parkinson's disease at the moment. So it's a neurodegenerative disease and it's affecting the basal ganglia, which we, as we mentioned before is a subcortical structure. And it's really important for motor coordination and control as well. And um it's a, basically the sort of pathophysiology is associated with deposition of alpha nuclei into the basal ganglia and the loss of dopaminergic neurons in the substantia night growth. And um in terms of the sort of three cardinal symptoms of Parkinson's disease would be bradykinesia rigidity. And as we mentioned before, a lead pipe and cog wheeling, and that's because of the increased rigidity alongside the tremor as well. And specifically with Parkinson's disease, the tremor tends to be unilateral and when they're resting. Um Parkinson's disease also presents with a few varied nonmotor symptoms. Um And these commonly tend to be sleep disturbances, depression and autonomic um um symptoms as well such as postural hypertension. And um just to mention that um there was no motor weakness per se um in the um uh Parkinson's disease. And this is mainly because the cortical spinal tract is not affected. It's um um it's in fact because of the loss of the dopaminergic neurons in the substantia nigra um in the basal ganglia. And that's why you get these um symptoms and not promotor weakness. Um So, um this again, just kind of shows um typical presentation of Parkinson's disease and um it's also often um associated with um um the shuffling, the classical shuffling gait. Um and um everything else kind of we've mostly mentioned as well, but also this duped po posture tends to be common in um Parkinson's as well and loss of facial expression and something that's not mentioned here. But actually, one of the common sort of first presenting sort of indications of Parkinson's disease is loss of smell. Um So that they tend to have that probably months to years before they actually develop Parkinson's symptoms. So that's kind of an early, very early sort of nuance of potential development of Parkinson's when they lose their sense of smell. Um So, in terms of diagnosing um Parkinson's disease. So, um um it's usually a clinical diagnosis. Um So, based on history of presentation most commonly the presentations because it's very marked when you examine the patient, um when you feel the bradykinesia and the rigidity. Um and um another way sort of to kind of confirm the diagnosis is if you're suspecting and Parkinson's disease, then you tend to give a trial of levodopa and uh those with Parkinson's disease, uh tend to have a good response to Parkinson's and this is a good, a good enough for formal diagnosis of Parkinson's. However, if there is an um diagnostic doubt of Parkinson's disease, then imaging is used and this tends to be an MRI or a DA scan, which is a dopamine transporter scan. And um as we can see in this image, um compared to the normal dat scan, the, this one is abnormal and that's basically shown by because of the reduced um uptake of the uh dopaminergic neurons of the um in the scan um due to the loss of the dopaminergic neurons in the basal ganglia. And that's how you'd confirm that. Um So Parkinson's disease um often has a lot of differentials. So you can categorize it based on the various cardinal symptoms of um um of Parkinson's. So, in terms of tremor, um what other conditions can cause tremor. So um there are sort of two main categories of this. So there's intention tremor, this is when it's worse at the end of movement. So when they try to do something and towards the end of it, they notice that the tremor gets worse. For example, they aim to, um, reach out for something. Um, and towards the end of it, the tremor gets worse. So they try to press something and towards the end of it, the tremor gets worse and this is different to, um, Parkinson's disease because the tremor is at rest when they're not doing anything. And, um, intention tremor is often due to cerebellar damage and this includes things like multiple sclerosis, strokes and alcoholism as well. Um And in terms of postural um uh cause of tremor. So, um this is basically worse when unsustained posture. So when they, for example, have their hands um held out like this for a very long time. And um the causes for this can be a essential tremor. It can be associated with um beta agonists. So, for example, if you're using like salbutamol, um and also in um when there is a high amount of thyroid um in the whole body. So, if they've got thyrotoxicosis or hyperthyroidism, then they can also cause this kind of postural tremor. So, in terms of tremor and the differential, the main ways would be either Parkinson's which would be resting tremor in tension tremor, which worsens towards the end of movement, um which would be kind of cerebellar damage and um postural when um which could be caused by various components like essential tremor or hyperthyroidism or beta agonist. Um moving on to further differentials um So you can also get um symptoms of Parkinson's that are very similar um um as uh due to um drug induced ones. And that's because a lot of drugs do affect the dopaminergic pathway and cause extrapyramidal side effects. So, um these tend to be um antipsychotics, particularly the um atypical ones which are for haloperidol and, and the first generation ones and metoclopramide as well. So, metoclopramide is an antiemetic, which can also work as a prokinetic agent. So, for example, if they've got gastroparesis, then you tend to give prokinetic agents to sort of help with the bypass of food. And, um, and that can cause symptoms that are very similar to Parkinson's disease basically. And this would be drug induced parkinsonism and the way to sort of differentiate between an idiopathic Parkinson's disease as opposed to a drug induced. Parkinson is basically the symmetrical, symmetrical nature of the symptoms. So, in this drug induced ones, the the symptoms are always symmetrical. Whereas in um uh idiopathic Parkinson's disease, it's unilateral symptoms, you will not get symmetrical symptoms. And um, um, so, um, if someone does have Parkinson's disease and they come into hospital for some, anything that requires um, metoclopramide or like an antiemetic, then you, it's really important that you do not give them metoclopramide because it will worsen their symptoms. And um, instead, for example, for nausea or vomiting or even as a prokinetic agent, you can give something called do domperidone and the reason why you can give this as an alternative is because domperidone does not cause the blood brain barrier and therefore does not worsen the symptoms and does not cause the extra pmal side effects, which metoclopramide does because it causes the blood brain barrier. I hope that makes um clarifies any kind of confusion or anything. So if anyone does have any questions, please ask um just a quick question is essential tremor from your previous slide. Is that the same as postural tremor? Yes, yes. Postural is essentially a type of called benign tremor essentially. Yeah. So it means the same thing. Yeah. Thank you. As in I would say essential tremor is a form of postural tremor. It's not the same thing. Oh OK. So a partial tremor would be the umbrella term and then everything associated with that. For example, as, as I mentioned, the tremor from th hyperthyroidism or the tremor from medications like beta agonists or the tremor from essential tremor would be classified as an postural tremor if that makes sense. Yeah, that makes sense. Thank you. Yeah. Yeah. So we just any other questions at all? No. OK. So um so now we're moving on to Parkinson's Plus syndrome and this is essentially a group of neurodegenerative diseases which present with features of Parkinson parkinsonism, but also um or have other features that differentiate them from typical Parkinson's disease. So the key features that they have that's relevant to Parkinsonism is the tremor rigidity and the brady cream easier, but they also have added symptoms that differentiate them from typical Parkinson's disease. Now, I don't think you need to know sort of a huge amount about these, but main things I'd say to know about is that there are four different types. So there is progressive supranuclear palsy, multiple system, atrophy dementia with lower bodies and corticobasal degeneration. And I guess the main thing I'd say to sort of um uh memorize or uh understand about these conditions would be. So for our PSB progressive supranuclear palsy, it's associated with um um vertical gaze in uh issues, issues with the gaze, especially vertically and also um postural instability. Um um Now, for multiple system atrophy, the main thing to know about is it contains a lot of autonomic symptoms. So things like incontinence and postural hypertension and that tends to be sort of predominant problem as opposed to the rigidity or the bradykinesia or the tremor, for example. Now, with dementia with lower bodies, it's basically the way to differentiate. It is basically they have a cognitive decline um before they actually develop the motor symptoms of Parkinson's disease. So, before they develop rigidity and so forth, they will have a cognitive decline alongside some hallucinations as well before they actually have the motor symptoms. And then um for corticobasal degeneration, this one is a bit more of a complex one. I don't think there's any kind of markedly specific thing that helps to differentiate it, but it's basically a whole combination of things like apraxia, anosia. Um um And um and the other symptoms that's mentioned on the table. Um So I guess just to summarize progressive supranuclear palsy is particularly associated with gaze problems, especially vertical gaze and instability, postural posturally, multiple system atrophy contains a lot of autonomic nervous system problems like incontinence and so forth. Dementia with liver bodies has a cognitive decline and hallucinations before the motor motor symptoms start developing. So this is a secondary and then corticobasal contains, I think it's kind of more difficult to kind of find out one specific thing that can differentiate between Parkinson's disease and corticobasal degeneration. But um I guess it contains things like agnosia and apraxia, which is not really common or normal for Parkinson's disease. So that's kind of Parkinson's Plus syndrome. Um um in terms of management for Parkinson's disease. So um if levodopa is often the first line management, if motor symptoms are affecting the patient's quality of life and the way sort of the mechanism of action is basically is um so when levodopa is decarboxylate, so when it gets metabolized, it forms as dopamine and this increases the amount of dopamine in the brain, which is what's deficient because of the loss of the dopaminergic neurons. And so it sort of replaces the dopamine that's lost and therefore helps improve the symptoms that they are experiencing specifically regarding motor symptoms. Um it's usually given with carbidopa, which is a basically a peripheral decarboxylase inhibitor. And this essentially helps to prevent a metabolism of uh metabolism of levodopa into dopamine in the peripheral system before entering the Maria. And help this essentially helps to reduce the systemic side effects of levodopa as well. So it's C and given together um levodopa and carbidopa. Um and in terms of um side effects. So despite giving it together with carbidopa, there is some substantial amount of side effects, I guess the main ones to know are the ones that I've listed on the um, on the um slide here. So, um, it would be end of dose wearing off. So this is when, um, so towards your, so towards the end of having um, the whatever dose it is before the next dose is given towards the end of sort of the, um, the timeframe of when they, towards the end of the beginning of the next dose, they tend to typically have um worsening of symptoms. And that's because the, the, the medication tends to not work as time progresses. And before they have the next dose, if that makes sense, um, on and off phenomena is essentially when they, despite being on the medication, sometimes their symptoms are very well controlled and sometimes it's not so much controlled, even though the dosage is optimized and, and even even if they are compliant and so forth, they can have random times where it's really well controlled and sometimes when it's not so well controlled. Now, dyskinesias at peak dose is essentially when they've got the involuntary erratic movements of the face or the arms legs or trunk. And essentially, it's kind of similar to sort of the extrapyramidal side effects when patients take antipsychotics and they have that repeated movements of their lips or tongues or whatever it is. Um And, and the others such as dry mouth, anorexia, palpitations and postural hypertension as well. Um So, yeah, these are the main sort of side effects for levodopa that you'd want to know any questions about management for Parkinson's disease. Yeah. No. Ok. Um So now moving on to the, the last question I asked, which was about the Parkinson's disease. So this patient is presenting with tremor in their hands for the last three weeks and she um she has a tremor which is not, not noticeable at rest in both hands. So this kind of immediately indicates this is not typical of Parkinson's disease because Parkinson's disease is unilateral symptoms and this is symmetrical symptoms. Um And um the symptoms are also associated with increased tone. Uh She's also got a past medical history of gastroparesis and she's been treated for that with metoclopramide. Otherwise she is well. Um so given the likely diagnosis, what is the most appropriate next step in the management? So, um so the fact that she has bilateral symptoms kind of rules out typical Parkinson's disease and we'd be suspecting more of an atyp atypical one, which could be drug induced ones or the Parkinson's plus syndrome ones or the, um, sort of the differentials for the tremor that we talked about earlier such as, um, um, the essential tremor or the postural tremor or the intention tremor. So, reassuring and discharging is not going to be viable for this patient because it's not going to help with anything trial of levodopa. you wouldn't really do this because this is not, we are not suspecting an idiopathic Parkinson's disease as it has got atypical symptoms, switching metoclopramide to domperidone would be the answer correct answer in this case because as we mentioned before me, metoclopramide passes through the blood brain barrier. Domperidone doesn't. So therefore, it doesn't have much of the extra paramid or side effects that metoclopramide produces um trial of ropinirole. Again, ropinirole is a drug class. It's a dopamine receptor agonist that's used to treat Parkinson's disease of idiopathic origin. And also CINO is also a monoamine oxidase type B inhibitor, which is also a drug that's used to treat Idiopathic Parkinson's disease. And these two types of drugs can be given in together with Lepido or it can be given as a monotherapy as well based on how responsive they are to the different drug classes. So those are treatments for essentially normal Parkinson's disease. And the right answer in this case would be switching metoclopramide to temper any questions about Parkinson's disease as well at all before we move on to the next section. No. OK. So next SBA I'll give you about 30 40 seconds just to have a read of that before we move on. So I hope you guys have had enough time to um have a read of that question. So now we're moving on from central pathology um to peripheral neuropathies. Um So, um in terms of um helping to sort of differentiate between peripheral neuropathies, um there are some specific questions you could ask. So the first one is, does the, does the neuropathy follow a specific nerve distribution? So the common ones to be aware of particularly for pas is carpal tunnel. So medium median nerve, radial nerve palsy, which commonly presents with a wrist drop and a sensory loss in the back of the hand and a common perineal nerve palsy as well, which is, which basically um is a presentation of a foot drop. So they're not the patient is not able to Dorsey flex their foot. And um so those are kind of the specific nerve distribution, um injuries and neuropathies that you need to be aware of. Um And then um next one is um does it follow a dermatomal or a myotomal distribution? And if it follows a damato or myotomal distribution, then we'll be thinking about something along the lines of a nerve root impingement. And this is basically where the from the site where the nerve leaves, the spinal cord, there is an impingement. And therefore, as patients often present with sharp pain in the back or the arms or legs or shoulders that may worsen with certain activities based on whether it causes further impingement of the nerve. And then the last question is about, are there many nerves affected? So, is it one nerve affected or one distribution of nerve affected or is there many nerves affected? And if it's many nerves affected, then it tends to be peripheral polyneuropathy and with peripheral polyneuropathy, it tends to be sort of a symmetrical presentation that worsens from distally and ascends upwards basically. And the way you could categorize, this is basically essentially as the patient presenting with predominantly sensory symptoms or are they predominantly presenting with motor symptoms? If it's motor symptoms, then it tends to be, for example, Kian Barson or ACI P, which is basically chronic inflammatory demyelinating polyneuropathy. And it's basically just a chronic version of G GBS. Um polio, which is very uncommon nowadays. So don't think that would be a presentation for you guys to overly sort of worry about in um in cases and ch married tooth as well. So this is basically a rare hereditary cause of both sort of sensory and motor symptoms, but predominantly motor um no neuropathy when it comes to peripheral nerves. Now, when it comes to sensory neuropathy, um it tends to be um things like diabetes, alcohol B12 deficiency, amyloidosis and um CKD as well, and um II think it's quite easy for me to remember that these are symmetrical symptoms because diabetes is not going to just affect one leg. It's going to affect both legs or um alcohol, drinking alcohol is just not going to affect one leg. It's going to affect both legs, same with B12 deficiency and so forth. So this is how it's kind of mostly symmetrical symptoms that affect distally and then move upwards. So this is a good kind of framework you can use to sort of classify different peripheral neuropathies as you are taking the history in patients or examining the patient and seeing um kind of the distribution of the nerve injury and in patients. Um so we'll talk about GBS or Guillain Barre Syndrome. So what is it, it's basically an autoimmune demyelinating polyneuropathy that's affecting the um the peripheral nerve system. And just to sort of differentiate it from CIDP, the difference is that Guillain Barre syndrome is an acute onset, whereas the other one is a very chronic progressive loss of the myelin teeth, essentially, whereas GBS is very acute onset. So within sort of a presentation of about 2 to 3 weeks, essentially. Um So um what is the pathophysiology? Um essentially patients uh before they develop GVS, they tend to have a pre um pre pre episode of some sort of infection, whether it could be a gastro uh some sort of gastroenteritis or any kind of infection really. But typically the causes would be Campylobacter CMV and HIV. So they have a sort of procedure infection. And what happens is once when the immune system attacks and removes the infection, it mistakes the antigens on the mile sheath of these peripheral nerves as the antigen, that's the same or similar to that of the infection. And so essentially what, what the immune system does is it starts attacking the myelin, um, because it sort of because of this molecular mimicry between the antigens on the myelin sheath and the antigens on the infection that we just recently cleared off the body. Um And so, what it does is it's an autoimmune process that attacks the myelin sheath as a result of molecular mimicry due to a preceding infection, um typically caused by Campylobacter CMV or HIV. Um So that's what sort of the pathophysiology of GBS um in terms of how it presents with. So, um as I mentioned before, they'll have an infection and then 2 to 3 weeks later, um they'll start developing with symptoms of peripheral neuropathy. So, um so it progresses very acutely um and it goes ascending. So it starts very distally and moves upwards. Um and it's a progressive extending peripheral neuropathy and they have both symmetrical symptoms. So, symmetrical limb weakness, reduced reflexes. So, hyporeflexia or aflexia, and they also have sometimes autonomic nerve system symptoms as well. So things like incontinence or postural hypertension and um the sort of most dangerous part of Guillain Barre syndrome is that it can progress upwards to affect the respiratory muscles, including the diaphragm and so forth. And that can cause respiratory paralysis, which can cause breathing difficulties and potentially cause death as well. So I think that's kind of the the major worrying part about GBS. Um There are some something important to know is there are some variants of GBS. So one such example would be Miller Fisher syndrome, which is a triad of ophthalmoplegia, aflexia and ataxia, but there's essentially no muscle weakness. So that's quite useful to be able to know. So you can ask for these symptoms or check for these symptoms in a case to see if they've got ophthalmia, for example, or if they and I think it just shows to the examiner that you're thinking of the border aspect as well just as opposed to just the basic GPS. Um So that's GBS and the variant Miller Fisher in terms of investigations and management. So the main important investigation for Guin Barr syndrome is nerve conduction studies. And if you think about it, so my what it does is it allows fast conduction of electrical impulses across the nerves. So when this gets damaged, the speed of which electrical impulses that are transmitted decreases. And therefore on a nerve conduction study, the velocity, the conduction velocity decreases. So that's kind of the cardinal way of understanding GPS and diagnosing it. On a nerve conduction study, there are however, other investigations you can do as well. So lumbar puncture is another important one. And on lumbar puncture, what you see is an albumin cytological dissociation. So this is basically a discrepancy between the amount of protein there is and the amount of other cells as well. So there is an increased amount of in GBS. And that's because of all the inflammation from the autoimmune molecular mimicry mechanism that's happening. But the glucose and the cell count such as the white cell count so forth, that remains the same and normal, it doesn't change, it's not deranged. And that's because there's no infection that's causing it. There is no, the trigger is not an infection, it's just an inflammatory process. Um Spirometry again, as I mentioned before. One of the really scary things about Guillain Barre syndrome is that it can affect the respiratory muscles. That's why spirometry is really important to check for respiratory weakness. And if there is evidence of respiratory weakness, then you need appropriate excalation to it and so forth to give that extra support with ventilation. And you can also do um some bloods as well. So, um things like anti gangly antibodies, for example, in Milleria in Miller Fischer variant, um that's not sort of the first line investigation. The main ones you'd want to do are nerve conduction, lumbar puncture and spirometry. Um in terms of management. So this is sort of an autoimmune inflammatory process. You'd give them IV immunoglobulins plasma exchange to remove the antibodies and supportive management, which would, for example, be respiratory support and including ventilation and intubation if they are having breathing difficulties. So that's kind of the management and investigations for Guillain Barre syndrome. So, going back to the question that we asked earlier. So this is a very 20 year old woman. Um And um so the reason why I've highlighted that 20 year old woman is because autoimmune conditions typically present in women and also younger women as well. So, if you're thinking about a young young woman, you're thinking young person, um especially a woman presenting with sort of aberrant symptoms, that's not necessarily a stroke, then you'd want to be thinking about Guillain Barre syndrome or autoimmune problems as well such as like myasthenia gravis. Um So she's got a four day history. So it's very acute um um low extremity weakness to the point she's unable to immobilize low extremity extremities. And um basically, the main key thing is two weeks ago, she had diarrhea and vomiting. And um so the answer in this case is um c because it's a guillain-barre syndrome. So she's got normal CSF white cell count, normal glucose because there's no infection and raise protein because there is inflammation. Now in AMB, they are representative of if there was an infected picture of either bacterial or viral meningitis, for example, origin and um DNE. So people tend to get DNE quite confused. So in um um guillain-barre syndrome, typically, it's the myelin sheath that is damaged. And because the myelin sheath is damaged, you tend to have a decreased velocity, as I mentioned before in the nerve conduction studies, sometimes. However, the disease progression can be quite bad that the axon itself can also start developing to get damaged. And if that's the case, then the amplitude can also start to decrease on EMG S. Um when you do the um nerve conduction studies, um it would just be velocity, it would be the amplitude as well if that changes and decreases. So that's basically the answer to that. So I hope that clarifies everything. But if anyone has any questions, feel free to unmute yourself or um mention on the chat. OK. So uh moving on to the next question, um I'll again, I'll give you a few minutes to just have a read of this. Yeah. Mhm OK. So I hope everyone's had some time to read the question and um have a think about the answer. Um So now we're moving away from sort of peripheral neuropathy and peripheral lesions to sort of neuromuscular junction disorders. So essentially, there are three main causes um that you need to know about. So, Myasthenia gravis being the main one in association with Lambert Eaton syndrome and Botalli um as I mentioned before, bottle is, is basically um due to a toxin that's produced by Clostridium bottle and um that can cause um symptoms um associated with neuro muscular junction disorders. Um So all three of these have common features which are essentially lower motor, lower motor neuron signs. Um And um specifically what's really important is that there are only motor science symptoms, there are no sensory symptoms and the reason and why that is because it's motor neuron that's being affected, the motor neuron to the muscle, that's what's being affected. Um So there's no sensory involvement in it at all. Uh Often patients do have a very normal tone. So when you examine them, it will just have a motor deficit but no sort of um changes to their tone per se and usually the proximal muscles are affected more so in particularly sort of the eyes and the facial muscles as well. Yeah. So that's kind of common features of all um neuro muscular junction disorders. Um We're specifically going to focus on Myosin or gravis. So, myosin or gravis is essentially another autoimmune disease affecting the acetylcholine receptors in the post synaptic side of the neuromuscular junction. Um And importantly, what's importantly, something to be sort of familiarized with is that it's very strongly associated with thymus hyperplasia and Thymomas. So if you sort of are invest thinking about my gravis in someone with sort of symptoms and signs of raised hyperthyroidism, then you want to think about that too. And it's really important to know if they've got a thymoma or a thymus hyperplasia because in the management removing the thymoma, for example, and removing that hyperthyroid state can help with the symptoms and cure the symptoms without any further intervention. So, just being aware of the large association between thymus hyperplasia and thymoma in association with myasthenia gravis. So, what is the presentation? So it's all the presentation that we mentioned before in terms of um here, um the common features, but also specifically there is this element of muscle fatiguability. So what's muscle fatiguability is essentially when your symptoms get progressively worse as time passes and as you're using the muscle, more and more, and um this is because the antibodies are attacking the acetyl coline receptors, the more you use the muscle, the less binding sites are available for the acetylcholine to bind onto. And so essentially what you need is you need more of the receptors to be available, more acetylcholine to be present. But because of the antibodies, it's not available, it's not present and therefore the symptoms worsen as you try to move and use the muscle a bit more and more. Um so this is sort of very specific and cardinal to myo gravis. And um what differentiates it from other neuromuscular junction disorders, for example, again, as I mentioned before, proximal muscle weakness, and often there's an element of sort of ocular muscles and facial muscles as well. And you can get symptoms when you look at them, examine the patient, you can often see um sort of flattening of the eyebrows and ptosis. Um because of the involvement of the proximal muscles. Um and in uh um neuromuscular in myo gravis, um you you get normal reflexes, so there are no changes to reflexes per se. Um um In so, so in terms of investigations and management, so, um basically, um you would want to do an EMG which looks at the sort of the nerve conduction through the muscle fibers. Um you'd want to do um antibody testing to look for specific antibodies that bind to the acetylcholine receptors. And as I mentioned before, because of the massive association between Thymomas and mast, obviously, you'd want to do a CT chest as well on emg um what you'll see is this decremental response. Um So the more as you use the muscle, more the the results on the EMG gets worse, you can see on this image that the amplitude sort of decreases with time as the muscle is being used more and more and more. Um So it starts off with relatively high and then towards the end, it's almost half the amplitude of the original um response. So that's what you would see in a emg with the decremental response. Um Antibody testing, we mentioned ct chest, we also mentioned and um and if the ct chest it comes out positive for a thymoma, then removing off the thymoma can basically improve the symptoms and cure the patient without any other intervention or medication. So that's why it's important to do to be aware of that association. Um So, in terms of management, so essentially, you treat the patient with um an uh acetylcholine esterase inhibitors. An example of this would be pyridostigmine. And what it does is basically, it breaks down. Um um So acetylcholine esterase basically breaks down the acetylcholine. Um and um and this prevents the, so the inhibitor basically prevents the breakdown of the acetylcholine so that there's more available in the neuromuscular junction. Um You can also because it's an sort of autoimmune inflammatory process, you can give them steroids and plasmapheresis and IVIG as well to help with the inflammation and reduce the inflammation. And if there is a thymoma that's evident causing this, then you'd want to do a thymectomy as well. So that's essentially the management for myasthenia gravis. Main one being pyridostigmine, which is an acetylcholinesterase inhibitor, which inhibits acetylcholinesterase, which essentially breaks down acetylcholine. And so by inhibiting that there is more acetylcholine available in the neuromuscular junction. So more of it is available to bind to the receptors and prevent that the the the complications associated with the problem. Any questions about my steno gravis at all? So I have one question. So if in the question stem, they say that as the chest revealed like a wider me media like a thymoma and one of the options was just a thymectomy. Would you choose that over? Like let's say given, you know, pine or IV, done. So, if there is clear evidence that the cause of it is, um, sort of a thymoma, then one of the first line treatments would be to do a thymoma. And if we to do a thymectomy and if that doesn't improve in the patients, um, um, still have ongoing symptoms, then it would be pyridostigmine and forth and so forth. But because of the strong association of 60 to 70% having a Myosin gravis, um having Thymomas in association with it, you'd want to think about doing that first. Um Without before giving potos. Yeah, cool. Thank you. Any other questions at all? Um Is there a difference between EMG and nerve conduction studies? Um So, yeah, nerve conduction studies is um so EMG is essentially for muscle fibers particularly and a nerve conduction study is for any peripheral ner nerves or any nerves. It's not specifically for the conduction of nerves within the muscle groups if that makes sense. Ok. So nerve conduction studies is just used to test how fast a nerve is working basically. So it's used in MS and things like that. And then EMG is for muscle fibers specifically. Is it just in myasthenia gravis that its user? Is it? So any sort of neuromuscular condition that you're suspecting? So, as I mentioned, Lamberton, for example, Myasthenia gravis botulin is so those kind of conditions you'd be thinking about emg. All right. OK. Thank you. Any other questions? OK. Um So um moving on to the next part. So this we mentioned about the decremental response on an emg that you see um to LA syndrome. So when, when you think about Myo gravis, this is a very important differential to consider because they kind of are very similar but also quite different at the same time. So Lamberton syndrome essentially is caused by antibodies that attack the calcium channels at the neuro muscular junction. So these calcium channels are in the pre synaptic nerve. And when they become attacked, essentially, there is less release of acetylcholine. So essentially, there is less acetylcholine similar to myo gravis. Um And um a really important thing is um whilst myasthenia gravis had a huge association with Thymomas and um hyperthymic thymic states. Um Lambert Eaton syndrome has a massive association with um cancer. It's often a paraneoplastic syndrome associated with cancer and especially small cell lung cancer. So, if you are suspecting someone to have Lamberti syndrome, likewise, you'd do a CT thymoma, a CT A CT to look for thymoma and Myo gravis, you'd want to do a CT CT test um to look for sort of some sort of lung cancer that's ever present because that's a co a common association between the two. Now, in terms of differentiating between Mycena Gravis and Lambert Eaton Syndrome, both of them essentially cause cause proximal muscle weakness. But um with mycena gravis, it gets worse, the symptoms worsen with repeated use. However, in Lambert Eaton Syndrome, essentially the symptoms improves with repeated use. And this is because as you use the muscle, more and more and more, there is more calcium channel, more of the calcium channels become engaged. And therefore, there is more release of acetylcholine. And so there is more functioning within the neuromuscular junction. And so that's why in Lamberton Syndrome symptoms significantly improve and there is more activity and more action with the muscle. Um my steno gravis um causes doesn't really impact is not known to impact um normal reflexes. So, therefore, reflexes are normal. But um Lamba Teton syndrome is known to affect reflexes and reduce reflex. And I suppose that's because it affects the calcium channels, which is involved in the, in the sort of nerve um nerve conduction process and the sort of triggering of the nerve impulse. So that's why the reflexes get affected uh um when it affects the calcium channels. So that's kind of the main differential between uh la syndrome, myosin gravis and a big differential to consider if you are thinking about Myosin gravis and neuromuscular injection disorders. Um ok. So, um so yeah, so going back to the question that we asked earlier, so this patient was presented with fatigue and double vision. Um and her symptoms are worse at the end of the day, which is kind of um expressing that there are there is more activity happening. Um The symptoms are worsening which kind of fits in line with myasthenia gravis. Um she has a history of hyperthyroidism. So, the reason I included this was because um as I mentioned, myasthenia gravis is a um autoimmune condition. And in hyperthyroid, there is a main kind of um like the main cause of the hyperthyroidism is essentially graves disease, which is an autoimmune cause as well. So when you tend to have one autoimmune causes, you tend to have, you're more likely to develop other autoimmune conditions as well, like hyperthyroidism plus myci gravis or multiple sclerosis plus B. So that's just kind of just to remind you that if someone does have one set of autoimmune condition, then they are sort of slightly more predisposed to develop other um autoimmune conditions as well. And uh this patient also has bilateral mild ptosis. So, um how would you um sort of appropriately treat this patient? Um And, and pharmacologically would be to give pyridostigmine, which is the um acetylcholine um esterase inhibitor and that increases the amount of acetylcholine in the receptor to um um compensate for the damage to the receptors as because of the autoimmune response. Um Interferon is usually only given in multiple cirrhosis, um particularly increasing levothyroxine dose is not really going to do much because the symptoms are not due to poor poor hyperthyroidism. Um And atropin is um um something that will worsen the symptoms essentially because it's an anticholinergic antimuscarinic. And so it actually reduces the amount of acetylcholine. So, it will worsen the entire symptoms and the presentation and stopping levothyroxine is also not going to do much in terms of helping their symptoms. Um, but yeah, that's, um, that's, uh, Mycena Gravis slash Lumberton syndrome. Um, any questions at all about that? No. Ok. Um, so I know time is coming to 830. I did have one more. Um, SB uh, let me just go find it. I did have, yeah, one more SB so I don't know if you want to, it, it's just going over one more condition. So I don't know if you want me to carry on or if you, what, what whatever you're com you guys are, are happy with. Um um I'm happy to stop here, but I can also go on if you want me to. So carry on. Ok. Um So in that case, I will go through to the next SBA. Um So again, I'll give you a few more minutes or seconds actually to um read through this and then think of an answer. Ok. So I hope you guys had some time to think of the answer to that question. So now we're moving away from all the muscular problems into um, headaches. So, um e essentially headaches can be categorized into primary causes and secondary causes. Primary causes is when, um, I guess primary, I guess it originates within the brain and it's not associated to a secondary presence of a tumor or a secondary presence of an infection or a secondary presence of anything that causes raised intracranial pressure that causes the headache. So that's why it's primary because it's of primary origin with no other cause triggering it. So essentially these can be categorized as migraines, tension, cluster headaches and trigeminal neuralgia and then secondary headaches. As I mentioned before, something is triggering it. Some, there is some pathological process behind it that's causing this. So, um meningitis and cephalitis, hemorrhages or all the three different types of hemorrhages, um tumors and cerebral sinus venous thrombosis as well. So, these are the kind of ways to classify everything that could potentially cause a headache. Um So, um so we're going to be talking about migraines. Um So what is a migraine? Migraine is essentially a chronic condition that causes attacks of headaches. And um there's a million different various triggers to it, but some of them. So there's an easy way to remember it. It's essentially chocolate, the acronym. So um things are like chocolate hangovers, orgasms, cheese, caffeine, contraceptives, lying, alcohol, travel exercise, all of this anything really can trigger um trigger of migraine. So, in your history taking, if you are suspecting, you know, if someone is presenting with migraine, um sorry, headaches and you want to sort of rule out migraines, it's good to ask them for sort of specific triggers that are specific to migraines. So I'd specifically ask for, does any food, particularly cheese or caffeine or wine for example, affect your worsen, your headache, um and so forth. Just to show to the examiner, you are thinking of all all possible headaches, including migraine to rule it out. Um So those are the triggers often and in terms of symptoms. So we can think of it in, in terms of Socrates. So it's often unilateral. So migraine does not cause bilateral headache, very rarely, but usually just lateral. It, it's perox. So it just comes and goes um randomly. Um it's not persistent really. And um in terms of character, its very pulsating, throbbing in nature. Um in terms of radiation doesn't really radiate to anywhere, particularly. Um and alleviating factors are things that help with the pain and the headache would be lying in a quiet room, dark room because often associated with photophobia and photophobia as well and the timing. So duration migraine can start last anytime, any duration between 4 to 72 hours. Um And within that period, it can be consistent, but it's also it's usually coming and going proximal. Um in terms of things, exacerbating factors that worsen the pain would be things like physical activity, stress, noise, light, anything really. And um it can be moderate to severe pain, quite debilitating to quality of life and activities of daily living. So in terms of other associated symptoms to do with migraines would be aura. So they often have a preceding aura before they develop their headache, which could be lights, tingling sensations, usually kind of visual aura of like flashing lights or shapes or whatever. Um but also associated with photophobia, photophobia, nausea, vomiting, visual changes, so blurry vision, for example, and paresthesia. So, tingling and numbness and it does have a significant consequence on activities of daily living and quality of life. So, in terms of um uh management, so essentially three lines of management. Um first you start off with conservative management. So things like having a headache diary to help identify what the triggers are and trying to avoid those triggers. Um um and um kind of controlling, you know, having a better sleep hygiene and making or you're eating on time and so forth and avoiding what could be triggering those headaches. Um If those are not working, the second line of treatment would be a sort of acute medicals to treat the acute onset of the pain. So that would be starting off with paracetamol or Ibuprofen or Nsaids. And then if that doesn't work, you would move on to the next line would be Triptan. So like Sumatriptan, for example, and then um pre preventative. So if the acute medical treatment is not helping with the pain or it's not working, then you want to think about preventative treatment which helps to prevent the onset of the pain. So as soon as they feel like something is going, um as soon as they feel like the pain is coming up, then they will take the medication essentially. And um this is basically a propranolol which is a beta blocker or topiramate, which is an antiepileptic. So you start off with propranolol or topiramate. If that doesn't work, then you think about starting um, amitriptyline, which is a form of an antidepressant essentially. And that would be sort of the, within the third line. That would be the second line. So essentially, for management of migraine, it's always stepwise approach with starting off with conservative then acute medical. Within that it's paracetamol first and then Triptans and then preventative would be starting off with propranolol or topiramate and then moving on to amitriptyline as the sort of the last result. Um So uh going on to the um final spa that we asked earlier. So this patient, a 40 year old man coming with a headache is more on one side of the head. So it's unilateral. Um and he's got a bit of photophobia associated with it and he's got a history of headaches in the past. But um so it's not a new one. So it's kind of chronically going ongoing and it's similar as well. So this is the thing, if someone has chronic headache, you need to in your history, it's really important to ask whether this current presentation that they are having is similar to their usual headaches or is it different? Something different is likely to indicate some, some other sort of acute pathology or something like meningitis or whatever it could be. However, if it's similar, then you can think of in the same lines of it could be their manifestation of their just chronic headache. So it's really important in your history to ask, how is this headache different or similar to the one that they already have if they already have something and we already know that this patient is taking Ibuprofen and Nsaids as well, which is not helping them. So, um the next appropriate management would be Sumatriptan. So like I mentioned, conservative management followed by acute medical management which would be um paracetamol, NSAID Ibuprofen, all of that, then within that next line would be the Triptan. So the answer here would be simp it would not be codeine because um step up from Nsaids and Ibuprofen is Sumatriptan not codeine diclofenac. They are already on an NSAID. So adding another NSAID is not really going to make much of a difference unlikely. And um topiramate and amitriptyline are essentially prevention of migraines as opposed to treating their um um acute presentation of the headache. So that was migraine in a nutshell. Um Does that make sense any questions about migraines at all? No. Ok. So within um headaches, um so I'll just go back to this page. I've not um I've not really spoken much about trigeminal neuralgia, but that is something you'd want to think about for patients because that's something that can come up um in terms of all of these I've not mentioned them because it's unlikely for you to have acute presentations in patients like meningitis, encephalitis and hemorrhages are not. I mean, if, if they are real patients, particularly, like in the case that we had very unlikely for you to, for someone to be presenting with a subarachnoid hemorrhage, for example. So I've not gone into two much depth about them, but they are definitely very important for your writtens exams. Um CNS tumors, this could potentially come up um as it's more of a chronic presentation and similar to cerebral sinus venous thrombosis as well, especially within your sort of history taking component, this could potentially come up. Um So I'd say just to, I've not mentioned them in, in the powerpoint, but those are some three to be aware of um for patients, but otherwise that comes to the end of the presentation. Um I hope it was useful. Um Please feel free to ask more questions if there are any questions. Otherwise, I would be really grateful if you could fill out the feedback form. So you could just scan the QR code. Um And I'll just wait around if anyone has any questions. That was really great. Thank you very much, Rose. Um If there's no other questions, I mean, we'll wait for a few more minutes. Um But yeah, thanks. Thanks for taking the time out to give the lecture. I really appreciate it guys. If you could fill out the feedback once we get enough feedback we can um, release the slides in the recording as well. Thank you very much. Thank you. Yeah, I 1 g didn't. All right. Thanks Rose. Um I think I'm gonna head off now. Have a good evening. Thank you. Thank you. Have a good evening as well. Bye.