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Hello, everyone. Welcome back to the year four cabinet revision tutorials, which is a week long series that covers all the specialties relevant to the Edinburgh medical school curriculum. We're covering neurology today and we're very lucky to be joined by Magdalena, a final year medical student ever to you Magdalena. Thank you so much for that introduction, Lucas. Um I know people will be coming in um over the next few minutes or so, but we'll just make a start and, and they can join um as we go. Um So first of all, what to expect from this tutorial, it's impossible to cover all of neurology and one tutorial. So we will just go through the main conditions and presentations and this will not be a lecture. It will just be a case of highlighting the key points to know for your upcoming exams. There will be a lot of empty cues throughout and you can vote for the right answer using the pole function. Just a note that the polls are completely anonymous. Uh So don't worry about getting the answer wrong. Just please have a go and these slides will be made available to you after the tutorial, I've included some additional notes on some of the slides and also the M C Q s, I've included the correct answer and, and a little bit of an explanation as to why the correct answer is the correct answer. So after this tutorial, you can go back for the M C Q s if you wish so and do them again or have a look for the ones that you perhaps got wrong and, and take another look at them. So, starting with an M C Q. And so after the death of an 82 year old patient, an autopsy was performed and his mid brain is shown in the image on the left compared to a normal midbrain shown in the image on the right. So what is the most likely diagnosis? And I launched the pool now, I'll give you a few seconds. Answer Lucas, I'm not able to see the polls. Are you? Yep, I can see it in the chat. Okay. I can see that now too. Thank you. So just a few more seconds. Okay. We'll stop there. So the correct answer is see Parkinson's disease, which the majority of you got correct. Um So what you can see on the autopsy is you can see the discoloration of the substantial lycra due to loss of the pigmented nerve cells that happens in Parkinson's disease. Moving on. We've got another MCQ. So a 65 year old male presents the G P with stiffness and poor balance. You notice a course tremor in his right upper limb, which is worse as he sits at rest during the consultation. What is the most appropriate next step? A few more seconds, last few people to get their votes in? Okay. So the correct answer is the and refer to neurology. So a diagnosis of Parkinson's disease and which is the most likely in this case should only be made and and management should only be initiated by a specialist in movement disorders. So that will typically be a neurologist. Um but consultants, for example, in medicine of the elderly might also have um interest in Parkinson's disease and movement disorders. So they might also be um the ones that these patient's see. Um but a GP would not be able to make that diagnosis. So nothing. So Parkinson's disease, I'm sure you're aware is a progressive degeneration of the document allergic neurons in the substantia lycra and which is a part of the basal ganglia. And it presents with a classical triad of radical in Asia tremor and rigidity with the bradykinesia. You might also see hypokinesia, which is a poverty and of movement. And patient's will typically have your shuffling short steps with reduced arm swings and they'll have difficulty initiating movements, they'll have difficulty and turning and when you walk in one direction and then turning to walk in the other direction, the tremor is worse at rest and it becomes better with voluntary movement, but it can also worsen what things like stress and fatigue and it's usually a pin rolling tremor and the rigidity is all described as cold, real rigidity or lead pipe frigidity. And if you've ever felt and the tone in the limbs of a patient with Parkinson's disease, it really does feel like that. And so if you ever do come across patient with Parkinson's disease, definitely do examine them and look for these signs. These signs are characteristically in asymmetrical and and they can also have other features such as mask like facies. So um they don't show much emotion or expression on their face. They can have micrographia. So they're writing becomes smaller and rem sleep behavior disorders, especially in later stages of the disease. And patient's will often act out their dreams and it appears as though they're sleepwalking, but they're really acting out their dreams and that can, as you can imagine, be quite dangerous. Um they can trip and they can fall postural hypertension is also quite a big issue in these patient's and depression, dementia and psychosis are also very common in the later stages of the disease. So the diagnosis is purely clinical, you can do a spect scan, but only if there's difficulty differentiating between essential tremor and the tremor seen in Parkinson's disease. So if there's any doubt in the can do aspect, otherwise, it's completely clinical diagnosis and like we mentioned, diagnosis should only be made and management should only be initiated by specialists in movement disorders. The management is complex and as with pretty much all neurological diseases, it requires an M D T approach, levodopa. I'm sure you'll be aware and is commonly used, but there's also things like dopamine agonist and M A O B inhibitors and COMT inhibitors. I'm just seeing a message that you're having trouble hearing me. Is anybody else having that issue as well? Okay. Um Let me just turn my mic off and then back on and see if that improves. Is that any better? Look at, do you have any suggestions as to make as to how to make the audio better? Is it any better after I've refreshed my mic or people still having difficulty hearing me? Still the same. Sorry guys, I'm really not sure how else I can improve it. I'll maybe try and switch my camera off and see if that improves things, but let me know if you're still having trouble hearing me. Um So we were just talking because, ok, if you bear with me one second, I'll try and, and put my headphones on and see if that works. Is that any better? Now, are you guys able to hear me? Ok, great. I hope that's better. Um And I hope that's better. Um So let me know if it's not. Um But we'll just keep going. So, uh we're talking about the management of Parkinson's disease and the fact that it is complex and the key decision to make is when to um start leave the door open, when to start supplementation of the dopaminergic signalling. Because the efficacy of levodopa it reduces with time, meaning that patient require larger and more frequent doses which of course comes with worsened side effects. And so you can delay um starting leave with the pub are using dopamine agonists. Um so you can start to leave it open later. And the disease, meaning that you can use lower doses as the disease progresses and you should never stop the medication abruptly. Um Even if the patient is in the hospital and also think about situations where the absorption of the medication might be reduced. So for example, if a Parkinson's patient is having abdominal surgery or if they're having um an episode of gastroenteritis, you might want to think about how else we could supplement the Dublin allergic signaling if they're oral intake is not great and or their absorption is not great. And that might be for patches. So for transdermal rather than oral medications, and whenever you're prescribing medication for a patient with Parkinson's disease, really think twice and be careful because you do have to avoid antidopaminergic. So things like medical provide them paradyne haloperidol and lots of other antipsychotics as these can cause um neuroleptic malignant syndrome and these patient's which is uh life threatening and it can cause lots of different issues with their movements and, and it can cause other movement symptoms. So, moving on another M C cure this time, it's a 74 year old male who presents the GP with his wife. And you noticed that the patient box of an ataxic gait, his wife is worried as he has been more forgetful over the past few months, he often appears to be confused and is struggling to follow conversations. And the wife reports that he has also had a few episodes of urinary incontinence, which has never happened before. He has no recent weight loss or headaches. Also, what is the most likely diagnosis? A few more seconds, people are a bit split on this one. Uh So somebody has just asked what is a ataxic gait? Um So an ataxic gait is when people have um issues with their balance. So if there's a uh for example, at cerebellar lesion, and you'll see people walking and I always kind of imagine it like a penguin walk and their gait will be wider and they're kind of wobble from fit to food. I hope that makes sense. Please do ask questions as we as we go along. Um Okay. So the majority of you have gone for answer, see normal pressure hydrocephalus, which is the correct answer as the patient in this case has all free of the classical symptoms of normal pressure hydrocephalus. So number pressure hydro catalyst, I'm not sure if you guys have come across this very much, but it's something that actually comes up and MCQ is quite a bit and it's a unique form of non obstructive. So communicating hydrocephalus, and it's a reversible cause of cognitive impairment. Seen in the elderly. It's thought to be secondary to reduce CSF absorption, which in itself might be secondary to head injury, a subarachnoid or meningitis. And it presents with this classical triad of urinary incontinence, cognitive impairment and gates abnormality. And these symptoms develop over a few months. And as you can imagine, because they happen in the elderly, most commonly normal normal pressure hydrocephalus can often be mistaken for Parkinson's disease because of the abnormal gait or Alzheimer's disease. Um but it's always worth having normal pressure hydrocephalus on your list of differentials. If you see a patient presenting with these sorts of symptoms and for the diagnosis, you do a CT head which shows hydro catalyst with Mark facilitation of the ventricles, but with the absence of Selkoe enlargement and the management is a VP shunt and that reverses all of these symptoms. Okay. So another MCQ, a 33 year old male presents to his G P with a six month history of reduced libido and erectile dysfunction, which is starting to have a negative impact on his long term relationship. With further discussion that the G P discoveries that he suffers from headaches and frequently bumps into things which visual field defects are you most likely to find on examining this patient okay. So lots of people going for answer eight bitemporal hemianopia, which is the correct answer. So this is a K osmo vision. Most likely the patient has a pituitary tumor which is pressing on the chiasm and causing a bitemporal hemianopia. So another M T Q you are on the stroke ward and examine a patient who has the visual a defect to an image below. What's the most likely location of the lesion Waiting on a few more response is okay. So the majority of people have gone for answer e left optic tract, which is uh correct. So this is our right homonymous hemianopia. So it's a lesion of the left optic tract, another visual field um MCQ. So a 62 year old male suffered a cerebral infarcts six months ago, you perform a visual field examination and note the presence of our rights superior homonymous quadrantanopia. What's the most likely location of the lesion? A few more seconds? Okay. So a bit of a split on this one but the majority have gone for answer D which is the correct answer. So this is a postcard asthma lesion. It's a superior homonymous quadrantanopia. So remember everything in the brain is the opposite. So superior, um homonymous quadrantanopia. Therefore, it's a lesion of the inferior optic radiation and and it's in the temporal lobe. So the acronym it pit which you may have come across uh parietal inferior, um temporal superior is really useful. So this is superior among the MS quadrantanopia. Therefore, temporal lobe, I hope that makes sense. Um Hopefully the next phase slides will help to clarify things as well. So visual pathway lesion's come up and emcee case all the time, you can appreciate that. They are quite an easy questions too, right? So they do appear quite a lot. So pre Ks Malaysians are straightforward because ipsilateral unilocular visual loss chiasma lesion's caused by temporal hemianopia. If the upper quadrant defect is greater than the lower quadrant defect, then it's an inferior chiasma compression. And that will commonly be a pituitary pituitary tumor. But if it's a lower quadrant um defect being greater than upper quadrant defects, then it's superior chiasma compression and that's commonly a craniopharyngioma and then your post K as Malaysians cause homonymous hume anopia. So if it's a lesion, it's a lesion of the contralateral optic tract. For example, if it's a left homonymous hemianopia, it's a lesion of the right optic tract. If it's in Congress, it's a lesion of the object tracked. But if it's Congress, then it's a lesion of the optic radiation or occipital cortex. If there's macular sparing, it's a lesion of the occipital cortex and I'm just coming onto pits on this slide. So, homonymous quadrantanopia. So if it's um superior, then it's a lesion of the inferior optic radiation in the temporal lobe. And if it's inferior, then it's a lesion of the superior optic radiation in the parietal lobe So it's Parietal inferior temporal superior. And I find that acronym quite helpful because things do get confusing. Um these slides, as I said will be made available to you. And I hope that those slides have summarized visual pathway legion's. And for you, I think this is really all that you need to know if you learn these few slides and if you learn the content of them, you should be able to answer pretty much any question that comes up on this topic. Okay. So the next MCQ, a 32 year old female presents to your clinic with a four month history of diplopia on examination, she is unable to abduct the left eye and develops a coarse nystagmus on abduction of the right eye. What is the most likely diagnosis? So we're getting quite a split. I think this is more of a challenging question. I'll just give you a few more seconds. Okay. So the majority going for be internuclear ophthalmoplegia, which is the correct um answer. So, if you haven't heard of this before, it's an inability to congregate eye movements because of a lesion involving the medial longitudinal fasciculus. So it classically manifests as impaired adduction it to last year up to the lesion, an abduction, nystagmus, contralateral to the lesion and moving on. So, following from that question, which neurological disease is most associated with this eye movement disorder. Okay. So majority going for A D multiple sclerosis, which is um the correct answer. An internuclear ophthalmoplegia is associated with M M S. There's some other clues in this question as well. So the fact that the patient is female um and middle age also 0.2 more towards M S. Uh So M S is chronic sale cell mediated auto immunity. My alienation of the C N S, there are different types but the relapsing remitting um is the most common type. So patient's will have these acute episodes lasting between 1 to 2 months and that will be followed by periods of remission. And the other subtypes are secondary progressive and primary progressive. But relapsing remitting is seen in I believe, 85% of patient's. So the vast majority and epidemiology is important in M S. It's relatively common in the UK. You will definitely see patient's with M S whilst you're working and you may have seen patient's already on your placements. It's more common in females. There's a free to one female to male ratio. It's more common in middle age, patient's 20 to 40 years and much more common at higher latitudes. Um So patient's present with non specific features making it quite difficult to diagnose. For example, significant leverage e is very common. They have lots of visual symptoms. So, optic neuritis very, very common. I appreciate that you guys haven't done ophthalmology yet. But optic neuritis is inflammation of the optic nerve. It's very painful, painful eye movements, red eye, um painful eye movements on examination and they'll have repeated episodes of optic neuritis. So if you see that, think about M S um like we said, there's internuclear or film a plasia and lots of other visual presentations as well. They'll have numbness, pins and needles. Trigeminal neuralgia is common as well. Um weakness, a taxi, a tremor um and lots of other symptoms like urinary incontinence, sexual dysfunction and intellectual deterioration with time as well. So the diagnosis requires a demonstration of two or more lesions which are disseminated in time and space. And that is the key. So you most likely you will be doing an MRI brain and spine and it will show these high signal T two legion's um periventricular plaques are commonly see, you'll see that in an MRI in the next slide. And also this Dawson fingers sign, there's also oligoclonal bands which I found in the C N S and um there's also increase intra fecal I D D synthesis. So you can see the periventricular plaques there uh in the MRI and it creates the appearance of these Dawson fingers, these oligoclonal bands seen in the CSF management. So, unfortunately, their area is uh no cure. Life expectancy is reduced by approximately 5 to 10 years. But you really have to think about the quality of life especially as the disease progresses. Um And again, an empty T approach is required for the acute relapse is that I mentioned um you use high dose steroids So, oral or IV level methylprednisolone was commonly as long term management as disease modifying drugs. There's lots of them. Um but there is, there is no cure, the disease will progress. And as it progresses, specific problems arise that you need to address. So, um spasticity you can use back within or gabapentin patient will have intermittent self catheterize ation for their urinary incontinence. And a drug called amantadine is often used for the fatigue, that patient's experience moving on to eye movements. Um So six muscles involved in eye movement. This diagram is just to remind you of those. So that superior oblique, inferior, oblique, um lateral, superior, uh medial and inferior rectus. And it's worth knowing these muscles. It's worth knowing which cranial nerves control which muscles because it will help you to understand creating nerve policies and I'll just go through the main cranium there of policies. Again, this is something that comes up quite a bit of exam. So I would make sure that, you know, these cranial nerve free palsy or oculomotor policy. So this nerve controlled eyelids, the people to inferior oblique and all of the rectal muscles except the lateral rectus. So if you have a a cranial er free Paul's day, that I will be deviated down and out, you'll have tosis. So, dropping, dripping off the upper eyelid, the people will be dilated and there will be no direct light response in the affected eye, but an intact consensual like response in the unaffected eye cranial near fall policy. So, cranial nerve fall for controls, the superior public. Therefore, a policy causes vertical diplopia uh due to the defective downward gaze. And typically patient's will notice this when they're reading or walking down the stairs. There's also Torshin all diplopia. So sub patient's might tilt um their heads um and they might be aware of doing that or completely unaware of doing that and that I will be deviated upwards and rotated upwards in the cranium. Therefore, policy, cranial nerve six. Um So this cranial nerve controls the lateral rectus. And because of that, um if there is a policy, patient's will have horizontal diplopia due to defective abduction. So another MCQ for you, a 35 year old male motorcyclist is brought to any following at high speed collision with a lorry. He has suffered polytrauma. He has a reduced level of consciousness and you assess his eye response on doing this. He noticed that his right people is dilated and his right eye is deviated down and out. So what is the most likely cause of his eye defect? A few more seconds to answer this question. Okay. So the majority, although there is quite a split, um the majority are going for answer be uncle brain herniation, which is correct. So the patient has a cranial nerve free policy. Um that's most likely due to displacement of the Incas of the brain due to increase intracranial pressure in this case, intracranial pressure is most likely to be increased because of some type of brain hemorrhage which has taken place. Um And that uh fungal her nation is compressing granule nerve free causing a policy. So there we go. I think this diagram illustrates that quite nicely. It's life threatening. Compression is a life threatening um condition, cranial nerve free is compressed by the Incas of the temporal lobe as it's displaced under the tentorium, cerebelli do to raise Andrew cranial pressure. Um And I've seen this come up quite a bit as an M C Q. So it's just something to be aware of. Another thing to be aware of is Horner syndrome, which is damaged, the sympathetic nerve supply and presents with a classical features of tosis, the dripping of the upper eyelid, eyelid, my osis, a smaller people and film osis, sunken eye and anhydrouse iss which is loss of sweating on one side of the face. There's lots of different causes. Um The one that is most likely asked about is a pancoast um long trimmer. So that's a long trimmer that's at the top of the lung. Um Brain trimmers can cause this as well. M S carotid artery dissection and encapsulitis, stroke, trauma covered this sinus thrombosis and lots of other things. Another M C cure, you perform a lower limb examination on a patient who is scheduled to legal lumber spine surgery. You find that the patient has a poor ankle jerk reflex, which nerve balut is most likely to be affected. Okay. So the majority of people going for answer is C as well, which is correct. Um And this question really is just simple recall um worth memorizing which uh nervous are responsible for the different reflexes. Another MCQ for you, a 35 year old male presents with painful numbness and tingling in the upper lateral aspect of his right by you suspect a diagnosis of meralgia, paresthetica, which nerve and they're fruits are most likely to be affected. Okay. Um My headphones have just run out of charge. So I'm hoping that you can hear me. Um I'll pop them back on once they charge. Um So the majority of people have gone for answer. A the correct answer is actually d the lateral femoral cutaneous nerve and the nerve root is L2 L free. Okay. So there are some key mono neuropathies um that I've listed for both the upper limb and they're lower limb. I think they're worth learning again. It's a very easy question too, right? Therefore, they do come up quite a bit. So, um axillary nerve will cause a flattened deltoid. And that typically happens with a humeral neck fracture or dislocation. The radial nerve will call's wrist-drop and that's typically a humeral midshaft fracture. The median nerve will of course cause carpal tunnel syndrome. Now, um a key thing to know is that damage at the rest will cause paralysis and wasting of the thinner eminence muscles and the opponents pollicis muscles along with sensory loss to the palmer aspect of the lateral 2.5 fingers. If you have damage, further up damage at the elbow, you'll get all of these things. Um, plus loss of foreign pronation a week, risk fraction and ulnar wrist, deviation, ulnar nerve. Um We'll call the claw hand that's typically medial epicondyle fractures and a long thoracic nerve neuropathy will cause a wind scapula and they're lower limb. Um Two key wants to know the lateral cutaneous nerve will cause meralgia, paresthetica and the common peroneal nerve will cause foot drop. And that's very common with neck of fibula fractures. And I put this in. Um just to remind you of the key dermatome, I don't think you need to learn all of them, but these key ones showing here, I would um make sure, you know, so another MCQ, this time, we've got a 32 year old male represents with rapid onset excruciating headache around his right eye on examination, you note that his right eye appears watery, it's bloodshot and there's visible tosis, there's no foreign body in the eye. And he tells you that he has been having several similar episodes in the past few weeks. On further questioning, you find that he has taken paracetamol and codeine buddies have had no effect and he has no other medical conditions. He is a current smoker and he works as a software designer. So what is the most likely diagnosis? Okay. Lots of people going for e cluster headache, which is the correct answer. There's lots of typical features of cluster headaches in this question. The other one you might think of is medical medication, overuse headache. Um It's possible but much less likely and you would really need to find out the dose um and the frequency and how long he has been taking paracetamol and coding for. And I think this is just a reminder to not jump to medication, overuse headache as soon as you see, that patient's have been taken analgesics for their headache. So, um following on from that question, you give him some subcutaneous um sumatriptan and his headache resolves. But what is the most appropriate long term management to avoid the recurrence of his headaches? Ok. Vast majority of you going for C verapamil, which is the correct answer is the prophylactic treatment of um cluster headaches. So, headaches, um a very common problem that you'll come across in clinical practice and therefore very common and MCQ. So definitely, no, this before your written exams and for your Oscar these um I quite like this image. We are about halfway through the tutorial. I'm hoping that you're not getting this bottom right, revising neurology headache. Um like I said, we're halfway through. So let's keep going. Um I just wanted to run for the different types of headaches. So, first of all, medication, overuse headache is the commonest type of headache. Um, a lot of people think it's migraine but it's not. And the examiners often ask if you do get a headache stent station in your office keys. They often ask what's the most common cold of headache. And people say it's migraine, but it's not. It's medication overuse headache. So it has to be present for 15 or more days of the month and it develops or worsens while the patient is taking regular. Key thing is regular symptomatic medication. And it most commonly occurs with opioids and tripped hands, migraine. I'm sure you're all very well. Affair aware. It's a severe throbbing pain, typically unilateral, but it can be bilateral. It's associated with nausea, photophobia and photophobia. So the patient will tell you that they need to go and lie down in a quiet dark room and headaches may be precipitated by aura and they can last up to 72 hours. Tension headache feels like a tight band around the head or a sensation of this pressure around the head. It's typically bilateral. Unlike migraines, it's lower intensity and it's still very painful and it's typically not associated with um those symptoms of nausea, photophobia, phonophobia or aura. They can be related to stress and they often do coexist with migraines. So patients can have both and in cluster headache. So intense sharp stabbing pain around one I it's very intense and meaning deputy patient will be restless that be agitated during the attack, they'll be walking around and not being able to find a comfortable position and stay still. It typically occurs once or twice a day and each episode lasts between 15 to 2 hours. And as the name suggests, they do occur in clusters, these clusters can last any length between 4 to 12 weeks. Patients will often also complain of nasal congestion, um redness in there, I and watering of the eye and swelling of the eyelids. It's more common in males and more common smokers and it can be triggered by alcohol. So I've included this um table uh which does have quite a bit of information in it. But I just wanted to summarize the acute and the prophylactic management of each of those types of headaches. Um like I said, this comes up all the time in MCQ. So um just to briefly go for medication, overuse headache and in acute term, you want to withdraw whatever medication their own. You withdraw simple analgesics and triptans abruptly that can of course worsen their headache initially with opioids. Um don't ever abruptly withdraw them. That has to be a much more, a gradual thing for prophylaxis. You want to educate the patient um on why they're getting these headaches to make sure that they avoid over using medication in the future. For a migraine and the acute management with um oral tripped in and an insight or you can use an oral triptan and paracetamol. If the patient is a child, if they're under 18 years old, they cannot take an oral tripped in. So you have to use um a nasal triptans instead. So that's your first line if that doesn't work. Um You can offer them um non oral medical, provide preocular prima seen and, and you can consider adding a non oral NSAID or tripped into that as well for prophylaxes. Um you want to try and identify what is triggering the migraines. Some people will have very obvious triggers like stress alcohol, cheese, chocolate, red wine, and also be aware of women on the combined oral contraceptive pill that can cause migraines and a lot of people. So for prophylaxis, it's a case of avoiding those triggers, propanolol can be effective and to permit. But you want to avoid that in women of childbearing age because it is teratogenic amitriptyline is also used and I'm not sure how effective this is, but it is recommended by nice and acupuncture tension headaches. And in the acute term, it's aspirin, paracetamol or NSAID as first line for prophylaxis again, acupuncture, um and also low dose amitriptyline, but there's not as much evidence for that. So it's a little bit controversial for cluster headaches and you can use 100% oxygen or a subcutaneous triptan acutely. And for prophylaxis, it's verapamil. So the next MCQ, a 19 year old female university student represents the GP with a 24 hour headache. Um It's severe, it's associated with photophobia and phonophobia. She has vomited twice. She has no relevant past medical history. Other than a recent upper respiratory tract infection, you examine her, she is Perec Shiell. She has no rash or popular Dema and G P calls for an ambulance right away and while you're waiting for the ambulance to arrive, what is the most appropriate management? So just waiting on a few more people to answer. Okay. So it looks like people are touring between a and see. The correct answer is see um am benzo penicillin. So the most likely diagnosis in this case is bacterial meningitis. A key point is to always have a high level of suspicion with bacterial meningitis. We don't need to have the neck stiffness or the rash um for it to be bacterial meningitis. Um You want to transfer this patient to hospital as soon as possible. But in the pre hospital setting like a GP practice, you can give I am Benzo penicillin as long as that doesn't delay the transfer to hospital. So next MCQ um is the same patient and did you be does go avoid the ambulance, the patient's take into hospital. And further investigations do show a diagnosis of bacterial meningitis. The patient lives with two flatmates who she was last in contact with this morning and they both feel well um at present with no symptoms. But what advice would you give them a few more seconds to answer. Okay. So majority going for e which is correct, they do need oral ciprofloxacin. Um So those who have been in contact with patient's with confirmed bacterial meningitis within seven days of that patient developing symptoms need either oral ciprofloxacin or overall revamp isn't as prophylaxis. So even if they don't have symptoms, they do still need to treat them prophylactically. Okay. So meningitis, like I said, have a high index of suspicion because it can be quite difficult to diagnose. It can be quite subtle. Um key things in the presentation are a headache, pyrexia, not even vomiting, photophobia. Um They can be drowsy, have a reduced level of consciousness or they can even develop seizures and neck stiffness is very characteristic of meningitis, of course, but it doesn't have to be present and the prepared crash again characteristic, but it does not have to be present. Um The most common cause is useful to know common mcq as well. So in an infant, less than three months old, it's group, be strapped, patient's age between three months and 60 years. It's an N Meningitidis S pneumoniae if they're aged over 60 and Listeria mon on site of genes if they're immunocompromised. So in terms of the diagnosis, you to get bloods and blood cultures right away, um a lumber puncture can be useful. Um It can be useful to confirm the diagnosis and to guide your antibiotic management. But the key is that it must not delay management. Um If it will delay management, start antibiotics and right away, don't, don't waste time doing the lumber puncture. Um The antibiotics are the priority and also be aware of the contraindications for um for the number puncture. So if there's any signs of race, intracranial pressure, if they have a reduced G C S, um if they have papilledema, vocal neurological signs, those are all signs of race. ICP. So do not do a number puncture, do not do a lumber puncture if there is signs of bleeding, um or high bleeding rest and if they have a signs of sepsis or a rapidly spreading rash, um and CT is typically not required unless they do have signs of the race, intracranial pressure. I see that somebody has um asked about the management. Bear with me. I'll explain that in the next slide. So the management, um like I said, most important thing is to immediately transfer the patient to hospital in the pre hospital setting. You can give I am Benzo penicillin, but it is not really uh the transfer once they're in hospital, it's an A B C D approach. You want to give them IV antibiotics as soon as possible. And that's typically IV and keep politics seen or IV kept Jackson if they're aged between three months and 50 years. Um It can be IV K F or kept Jackson plus amoxicillin or ampicillin if they are at the extremes of the age range is two, less than three months or more than 50 years. Consider I'd be DEXAmeth is um especially if they do have a raised intracranial pressure. If you see signs of severe sepsis or a rapidly evolving rash, you want to involve critical care. Um The patient might need an intubation and ventilation in that case. And like we mentioned, or else ciprofloxacin or every fan person and as prophylaxis for close contacts of patient's. Um So this is a slide just to summarize there, red flags of headaches. It's not an exhaustive list. It's very important to be aware of these. So key things are a history of malignancy or a history of recent head trauma changes in your headache characteristics. So if they tell you the headache is different to, to what they usually what they usually um feel if they have changes in their headache with posture or if it's worsened by an exertion by coughing or sneezing or the valsalva maneuver. That's quite worrying if they have um symptoms like vomiting, pyrexia, neck stiffness, photophobia, rush, or local education empire, level of consciousness, um new onset neurological deficits. So any sensory deficits, any new onset weakness and any changes to their cognition, um changes from their normal headache, like we mentioned changes in personality, which will be noticed more so by relatives and those around. Um and rather than the patient themselves, a funder club headache and also if the patient is immunocompromised. So another MCQ, a 78 year old male presents to agony of sudden onset weakness in his right upper limb changes to his vision and difficulty speaking, you examine him and you find that his power is two out to five in his right upper limb and five out of five in all of his other limbs. His sensation is, is normal, is intact and you find that he has a right homonymous hemianopia. You refer him for an urgent ct head and what is the most likely location of his pathology? Okay, a few more seconds. So majority going for be middle cerebral artery, which is correct. This is the most likely um a stroke in the left middle cerebral artery. So next 82 year old female presents to any following sudden onset loss of vision in her left eye whilst she's gardening, she is frightened and worried as this has never happened before. You examine her at her left eye and the examination is completely unremarkable. She tells you that she is now feeling well and her vision has returned to normal. She had a past medical history of hypertension, hyperthyroidism and hyperlipidemia. So what is the most likely diagnosis last chance to get your votes in? Okay. So vast majority going for be Amoros isf you get which is the correct answer. So this is the most most likely T I A in the right retina or ophthalmic artery, which is also known as a neurosis you get. So this side is really just to remind you of the cerebral blood supply, um remind you of the circle of Willis. Um And which part of the brain, the supply by which artery that's important. And of course, in stroke and determining where the stroke is. Um This table summarizes the Oxford stroke classification. Um It's, it's a lot of information but definitely something I would learn as it does come up quite a bit. Um So a total interior um circulation infarct, middle and anterior cerebral arteries are involved and you'll see all free of unilateral hemiparesis is under hemisensory loss of the face, arm and leg, homonymous hemianopia and some form of higher cognitive dysfunction. For example, at dysphasia, if it's a partial into your circulation, infarct is the smaller arteries of the anterior circulation that are involved. And you'll see two of those features. If it's opposed to your circulation infarct, it's the vertebral basilar arteries that are involved and you'll see anyone of cerebral or brain stem syndrome, loss of consciousness and then isolated home one with hemianopia. If it's a luck inner in part, it's perforating arteries around the internal capsule, the thalamus and the basal ganglia and its anyone of unilateral weakness on the face and arm or their arm and the leg or, or, or of all three of those um or pure sensory stroke or a tactic, hemiparalysis and other patterns of stroke to be aware of. Um the lateral medullary syndrome. So it's a posterior inferior cerebellar artery that's involved. And patient presents with ipsilateral ataxia, the stag mus dysphasia, facial numbness, and also a a cranial nerve palsy, for example, Horner syndrome, which we went over earlier. And they can also have contralateral limit sensory lost Weber syndrome and they were present with an ipsilateral cranium. They're free policy and the contralateral weakness. These are much fairer and they're much fairer in terms of empty cues. But the imparts that we went through on the previous slide um commonly asked about. So to make sure that you know that classification. So the management of stroke, um of course, a CT head first to make sure it's an ischemic stroke and not hemorrhage. It before you go ahead and from belies the patient and with IV out phase, which which you can do if the patient presents within 4.5 hours of their symptom onset. Um but be aware of contra indications for this. Um So that might be a recent history of head trauma, recent history of a stroke. Um some sort of bleeding disorder if they're already on anti coagulation as well. From beck to me is quite a new treatment. She's being used more and more. There is a strict criteria that is used and I haven't included here. But if the patient's do meet that criteria, they can go on to have from beck to me. And as soon as you exclude hemorrhagic stroke. You want to give the patient 300 mg of aspirin and that will be continued for two weeks. The patient will then be on anti coagulation for life. And that's usually clopidogrel. You can use aspirin with the program middle if the patient does not tolerate the clopidogrel. And of course, think about your secondary prevention measures. So controlling their BP, controlling your cholesterol, making sure their diabetes is well controlled, giving them lifestyle advice and using medication. And um also of course, a long period of rehabilitation will follow most strokes and the patient will regain their function to um varied extents R T I A. Um the CT head is typically not required unless you suspect that there might be a different diagnosis. Um And similarly, you give aspirin 300 mg as soon as possible and anti coagulation thereafter. So that's usually clopidogrel. If they don't tolerate clopidogrel, then aspirin and Emperor middle with A T I A. Um you want to consider coratids imaging and if there is some sort of clot in the carotid artery, then and an in dark tecta me to remove it. Um Again, there's strict criteria that the patient must meet and again, that secondary prevention measures really, really important. Um And the key thing is that they cannot drive for at least one month after the T I A. So your next MCQ is a 22 year old male with a history of epilepsy, which is usually well controlled on sudden caltrate. He presents to any following a generalized seizure during which he sustained some bruising and some small cuts to his face. This is his first seizure in two years. He does not smoke, he's not drink alcohol. He works as a waiter at a local restaurant and he drives to get to work. What is the most appropriate advice to give the patient regarding his driving? I'll give you a bit more time with this one as I realized that the answers are a bit more the year. Um And I see that somebody's asked a question which I'll answer in the meantime, um It's a good question. So if they have a F D add Apixaban to clip of the grill or you only use Apixaban. Um So I guess that kind of depends and you'd be guided by neurology. Um It's a risk benefit ratio. Um And most of the time, I believe that you would just keep them on the Apixaban um because they are already anticoagulated with Apixaban. So there's usually no need to add the clip of the grill and, but neurology would guide you with that. Okay. So 83% of me going for answer D which is correct. This is a really important question. Um and something that definitely I got asked about in a Noski. Um So if the patient has had a seizure, they cannot drive for 12 months and they must inform the D V a way that they have had the seizure after the 12 months, they might be able to return to driving if they have had no further seizures. Um So, epilepsy. Um so the diagnosis typically you do an E G and some form of neuro imaging. So a CT or an MRI usually following their first seizure, their management. Um you always want to consider reversible causes first. So does the patient have, for example, some type of electrolyte imbalance that is causing the teachers rather than a diagnosis of epilepsy? Um So you typically start antiepileptics following the second seizure, lots of different antiepileptics, um which be aware of them, be aware of some of the key points about them, for example. So to evaporate, you want to avoid in women of childbearing age, but you definitely don't need to know how to play with the different anti epileptics. Um As that is quite specialist knowledge and with antiepileptics, you must consider you're driving other medication that they're using. Um uh some of the anti epileptics will be contraindicated or they'll affect um absorption of other medications. So, pregnancy like I said, um contraception and breastfeeding, you cannot breast feed on some of these anti epileptics. Um question coming through and what order of importance are the investigations listed as? Um So I'll just go back to that start uh to that slide. Um They would usually be done at the same time. I'm not sure if you're referring to the investigations in the case of epilepsy or just investigations in general listed for out the presentation um for epilepsy, the E G and the CT and the MRI, but typically be done around the same time. There's nothing to say that one should be done before the other for epilepsy. Okay. Another question coming for, are we likely to get aspect provoked seizures in year four? As I know the guidelines for those is must not drive and must notify D V L A in most cases, driving with stays for six months after the provoked seizure. I think you're, I mean, I don't know what will come up for you guys, but from my experience, they can definitely ask you about provoke seizures, but I think it's much less likely um that they do will most likely be in the case of a diagnosis of epilepsy. I hope that answers your question. So the next MCQ 29 year old male with no one epilepsy is brought any by ambulance. He's having a seizure which started around 35 minutes ago. And this partner gave him some become midazolam at home, but unfortunately, this has had no effect. Um And once in any, he had received two Bullis is of IV LORazepam, but again, this has had no effect and he's still seizing. So what is the most appropriate next step in his management? Okay. So lots of people going for e phenytoin infusion which is correct. So, the patient is in status epilepticus. And the next step after he's had two bonuses of IV. LORazepam would be a phenytoin infusion. If that still doesn't terminate his seizure, you want to involve critical care. And the next step would really be to um induce a general anesthetic um to paralyze his muscles and the seizure. So status epilepticus, um it's a single seizure lasting more than five minutes or two or more seizures that occur within five minutes of each other. Without the patient retirement returning to normal in between those seizures. It's a medical emergency. You use an ABC approach. Um So make sure the patient has um venous access, make sure their airways save um use airway adjunct if if needed and so on in the pre hospital setting, Pr diazePAM or mcmichael Midazolam can be used and relatives of patient's are often taught how to do this and patient will have these at home just in case they do go into status epilepticus in the hospital. The first line is IV diazePAM or IV LORazepam and usually give up to two doses of this second line is offended to an infusion and third line. Um like I said, it's involved in critical care and interesting general anesthetic. So next MCQ, a 24 year old female presents to any following a road traffic collision. She has polytrauma, she has an open left tibial fracture and a presumed head injury on examination. She opens her eyes when he speaks to her but isn't confused and is asking you where she is? She localizes to pain. What is her dcs score? Okay. So people are quite split. Just a few more seconds, get your answers in. Okay. So the correct answer is D her G C S is 12. So if we break that down because GCS 12 doesn't really tell us anything. We want to know what she's scoring for the individual components. She opens her eyes when you speak to her. So she scored are free for eye movement. She is confused but she is speaking to you. So that's a four for variable response and she's localizing to paint. That's a five for much of a response adding up to a total of 12. And there we go. That's the Glasgow Coma scale there. I put it in really as a reminder, I think it's something that people um don't really revise um when they're going through things, but it does come from time to time. So it's just useful to remind yourself um after the components and um discourse for each one. So just make sure you, you know your Glasgow coma scale. So the next MCQ um CT head of a 24 year old female is showing what is the most likely underlying pathology. Uh huh. Okay. Yep. So majority going for C rupture of middle meningeal artery, which is correct. So this is most likely an extradural hematoma. You can see that there's a biconcave or a land shaped collection of blood because the tough dura matter layer keeps the blood and more localized. It doesn't spread as much as an other hemotomas. And extradural hemotomas are usually due to rupture of the middle meningeal artery in the temporal region because of skill fractures. I believe that this is the last M C Q. So 73 year old male is brought to A and E by his daughter as she feels that for the past few days, he has not been himself. He has been more confused with fluctuations in his level of consciousness. He has a past medical history of hypertension, chronic alcohol abuse and back to diabetes. He lives alone and has been previously limited due to recurrent falls that have been unwitnessed. He requested a CT head. What is the most likely diagnosis? Okay. So the correct answer is the patient does have all the typical signs of a subdural hematoma. So um here is another little table just to summarize all the different types of head injury and bleeding. I think the most important thing is to um just know which type of injury is associated with which clinical features and have an idea of your head of the typical patient that would present with these ones with each type of head injury. So an extradural hematoma is bleeding into the space between the dura matter and the skull. Um majority of these occur in the temporal region where the skull fractures cause rupture of the middle meningeal artery. It's typically um your patient's that come in after road traffic accidents, they've had some sort of acceleration, acceleration injury, or perhaps a blow to the site of their heads. They might have this lucid interval um where they appear to be okay and then they suddenly deteriorates and quite rapidly and they're likely to have a raised intracranial pressure because of all that bleeding, a subdural hematoma is much more subtle. It's bleeding into the outermost meningea layer. And it's most commonly around the frontal and parietal lobes. It can either be acute or chronic and it typically happens in the elderly. It's quite common with patient's that have a history of chronic alcohol use. Um and it can happen when patient's are on anticoagulants as well. It's a much slower onset and patient's can have these fluctuating, um fluctuating confusion there, fluctuating consciousness. So it's more difficult to diagnose but always on your list of differentials with a patient is presenting with confusion um and their early, early a subarachnoid hemorrhage. It's usually spontaneous bleeding from a rupture to rebuild aneurysm. Um but it can also occur in the context of traumatic brain injury. And patient will have this sudden occipital headache or a thunderclap headache. And the last one is interest liberal hemorrhage. So it's collection of blood anywhere within the brain substance. There's a number of risk factors such as hypertension, um any vascular uh legion. So any aneurysm or arterial venous malformations, trauma tumor and impacts as well. And it's similar to an ischemic stroke. But so that's really why you do the CT head. It's differentiate between the hemorrhage and the ischemic stroke sometimes are very similar, but they can have um much more reduced consciousness and I would definitely learn this table very common to come up. Okay. Um So to finish off, I've just got this CT spot diagnosis um quiz. Um I don't have poles for this, but I'm hoping that some of you will feel brave enough to pop an answer in the chat box. So I'll just give you a few, few moments to take a look at the CT and think about the diagnosis and please just pop in the chat. What you think the diagnosis is if you're not sure what the diagnosis is, perhaps just put what abnormalities you can see. Yes, it's an acute subdural hemorrhage, well done Diana. Okay. So what you can see here is this crescent shaped or a sickle shaped collection of blood and you've got midline shift as well and this is acute because the collection of blood um appears bright, it's hyper dense. Um So blood on the CT is bright and if it's a cute, it will appear brighter if it's chronic and it will be hurt in this my sides. There we go. Uh So this is the next one again, just pop in the chat. What you think the diagnosis is or what abnormalities you can see. Yes. So this is a chronic subdural hematoma. So you can see how that compares to the previous CT scan. Again, you've got this crescent shaped or sickle shaped collection of blood and some midline shift happening. But this time you can see that that collection of blood is not as bright. Um Meaning that it's more chronic, it's been there for some time. Okay. The next one. Yeah, well done. So it's a subarachnoid hemorrhage. Um So what you can see as you can see these bright areas indicating um acute blood and you can see that in the basal cisterns and also in the sulk. I so this is a subarachnoid. Um and the South Korea and the basal cisterns would usually be dark because of the presence of the CSF. Uh But in this case, you can see that they're appearing bright and the last one a bit more challenging. Anybody want to hazard a guess or just say what abnormalities they can see. Yeah, well done. So this is an acute basal ganglia, intracerebral hemorrhage. So again, you can see this bright area in the basal ganglia indicating an acute collection of blood so well done. Um That's really everything that I had prepared for you guys. Um For tonight, the last slide is just some general pieces of advice. I know a lot of people don't like neurology. But I think you can be very well prepared for a lot of the neurology questions. There's a lot of things that you can just learn and you're more or less guaranteed to get those questions right, if they do come up. So I think neurology questions are your chance to do well. No, your main conditions and presentations, there's adult in neurology. Um but make sure, you know, the, the main ones, the management of the main conditions and the presentations to an extent that would be expected of a generalist. So there's a big focus now of um us being more generous rather than specialist. So nobody is expecting you to be playing around with um medication for epilepsy or Parkinson's disease. Like I said, that would be done by specialists, but you do need to have some knowledge. Um perhaps the knowledge that would be expected of um of a doctor in a G P practice that would be seeing these patient's, but would it be changing their medications? And it's really all about pattern recognition um doing lots of M C Q s and recognizing those patterns. I would also say that remember that this is a neurology exam and not a neuroscience exam. So think about the clinical things more rather than um the all the neuroscience things have some level of awareness. Um But think clinical neurology um and passing it and Oxford Tam pick of clinical medicine are really all that you need. I've used them all for it, my clinical years. Um and they've, they've been everything that I've used and I've done okay. Um So have those two resources uh and use them and you will be absolutely fine. So, thank you so much. Thank you so much for answering the emcee cues and the little ct quiz at the end. I'm sorry about the technical difficulties at the beginning. Um Thank you for bearing with me. So I hope this was helpful. We do still have a few minutes left. If anybody wants to ask any questions about anything that we cover their neurology in general or exams, I'll hang around and I'll answer any of those. Um But otherwise, thank you so much and look as I don't know if you want to say a few words. So somebody asking, is there an easy way to remember the motor supply of medium ulnar and radial nerves? They get very confusing. I agree with you. They do get very confusing. I'm afraid I'm not aware of any easier way to remember them, not aware of any acronyms to use. So unfortunately, I think it's just a case of trying to remember them. Um May I quickly see the slides on cranial nerves and I muscle supply again? Yes, of course. I'll just go back um bear with me as this can be a bit slow. Um And somebody else asking if the size will be available. Yes, I'll pass the slides onto the case and they'll be uploaded onto Medal and as well the recording and, and on the side you do have a few more notes and answers the Insuk use with explanations. I'm still trying to get that slide for you. It's just moving along. Yeah, slowly. Do you have any tips on CT head interpretation? Um I think just know the appearance of an epidural, a subdural and a subarachnoid on CT. Definitely. So that value concave lens shaped, collection of blood versus um versus that crescent or sickle shaped. Um Remember that blood shows up right in the city? Um I think that's really all I need for forward here. I think it would be a bit me enough time to give you anything else. Um Of course, you want to just have a look for, see, always check if there's any skill fractures, any uh trimmers. Um Yeah, but those would be my top tips. Just take a good look at a few CTS and know what the appearance of a subdural epidural. And so Barack Odus, sorry Tom, I'll get to the side that you're asking for eventually. It's just taking its time to flip back for you.