Clinical Crash Course - Neurology 1



This on-demand teaching session covers the different types of multiple sclerosis, definitions, key terms and how to differentiate between them. It also goes into how they present, what symptoms they can present with and how they are diagnosed and managed. There are also discussions on different investigations and novel therapies. This is a great session for medical professionals to attend and stay up to date with the latest information and treatments for multiple sclerosis.
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Learning objectives

Learning Objectives: 1. Identify the definition and characteristics of Multiple Sclerosis and its associated medical terminology 2. Identify common symptoms of MS and distinguish them from other conditions with similar presentation 3. Describe the imaging techniques and investigations used to assess MS 4. Identify potential treatment options for patients with MS 5. Explain the multi-disciplinary approach to managing and supporting patients with MS.
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The following transcript was generated automatically from the content and has not been checked or corrected manually.

that. Thanks. Um, back to really, Um, So I get a free Amazon voucher just to let you talk with first time minutes of my lecture. I wish. I wish I could always get Dylan. Oh, yeah. Okay. Next time. Oh, it would help any further there Selves or covering urology. There's a lot to cover in neurology. Yes, but a whole years to be in your hood, She s o split it with two parts. Uh, so the first part cables in passing to clip. There you go. So the first part is, Ah, basically, I'm going to bring that mobile school says Parkinson's disease. And let's see, So multiple sclerosis. I'm trying Get rid of this. The bar on the talk. His mother s so multiple sclerosis. So the definition for multiple sclerosis, it's a inflammatory disease. So it's in your inflammatory disease and involves demyelination across multiple sites in the central nervous system. On that, lesions are disseminated in time unspent. That that's the definition for multiple sclerosis. Every demonology wise, I mean age. Usually it comes on around 30 ages 13 to the young girl, um, more common in females and many effects like white caucasians. Scandinavian community on, UM, 15% of patients have confined to a wheelchair within 10 years of diagnosis. So keep Pixar. That is, that it's a neuro inflammatory disease involving demargination across multiple sites in the central nervous system. And it's disseminated in time and space. That's the main bit. So again involve some environmental things people think maybe consequence. Multiple sclerosis, the viruses, the latitude rave wrong diet, vitamin D levels. Um, but the key terms, they're Teo. Some key times you might hear what when you read in a medical school. Sister is, uh, but you might hear clinically isolated syndrome and radiologically isolated and girl so clinically isolated syndrome is you might have symptomatic m s with a radiological lesion, but which isn't explained. How about any other causes such as infection or fever? Um, but again, that's a single in absorbed, and it's not disseminated in time or space on grade. A logical statement is that you might see a lesion on a scan. Oh, posing no symptoms. So again, like, say, going back to disseminate in time and space. This comes from the McDonald's criteria, which is used to diagnose multiple sclerosis. Another thing you might find him a little scratches. Theirs may do a little puncture. You see a legal corner bands. If there are legal clonal bands in a liver puncture, this can be this is evidence off dissemination in time because the illegal contraband that caused by the breakdown of the myelin, um and therefore that can be evidence of dissemination in time. So you will connect castle eight syndrome and radiological isolation grow, and then you have a mess. And for diagnosis off a mess in Mississippi to 70 times space. And if you do have the illegal colon bombs on, see a chef and that could be evidence for this. Okay, so if you look at em, Esther, different types of a mess, courses of a mess, the first one you see, probably most common one is the relapsing remitted m s on. This is where you get reluct, and then you get some Rick full recovery or some recovery. You get no symptoms, and then you get another relapse. Another one is primary progressive, Ms. Primary progressive. Unless she gets symptoms, and then you might have a period of time with no symptoms. But you don't get any resolution of symptoms, and then you get symptoms again of a mess. So the difference between the relapsing remitting is you do get your symptoms improved to get better. I really completely go away or partially go away. Where's the primary? Progressive. The symptoms remain, and we don't go away in between a relapse. And then you can have the secondary progressive MS, which starts always relapsing, remitting that mess, and then it becomes secondary. Then it becomes progressive a mess, and then you have progressive relapsing a mess again. It's not as common that one, so relapsing remitting ms is more common. One, uh, relapses last usually 12, at least 24 hours and the different severity on again. A steroids are used in treatment of relapses to speed up recovery from really patients using the average of one or two relapses a year and recover in between anything you would get full recovery, but then, later on, in the condition you might get a look. You partial recovery secondary progressives or developed after relax in remitted. Um, the disability starts accumulate more rapidly on dream Ishan from relapse remitting remission, bases lost and again, this is helping that different rates of progression for for people primary, progressive, no remission could get periods of more stable disease. That's the less common one in progress. Simply, that's a mess. So again, that's a bit of an overlap between prime progressive and relapsing remitting that minority of patients present in this way. Um, it's hard to tell the difference between this one and a primary progressive ms until they have their first real uh, so we've mentioned this relapse spells what? What is the definition of a relapse? So there's a strict criteria of in order to diagnose a relapse. So usually a relapse arises over hours to days and worsens over several weeks and then gradually subsides over several weeks or months. That has to be a relapse for us to be over 30 days apart, to be classified as a new relapse. Um, yes, that's the definition of the relax. So our eyes are the hours two days on, in order for today was new. One has to be 30 days apart, so most patients like the Remicade, will present you have optic neuritis for the first symptom of a mess. So what is optic neuritis optic neuritis that weight presents is you get periorbital pain, which is worse than I movement to get reduced visual acuity and blurred vision. And they have loss of color vision. So usually it's the red color that they lose. It's you have a positive relative afferent pupillary defect, which I've been covering on the next line. Um, again, it's usually one eye unilateral on symptoms. Peek at about two weeks, but and resolved by weeks for instate thought fixed. So a quarter of the best patient presented looked in your aunt. This essentially most patients Captain Ureters at some point in their disease course so well, a TiVo Afrin pupillary defect. So this is an example of our relative afferent pupillary defect. Then this is our APD in the left eye. So when the light is shows China shown in the right eye, you get through people reconstruction in both eyes. Where is when it showed in the left eye? Um, you will not get constriction, and that's because you've got inflammation of osteo, which is the Afrin's nerve when you do the people reflex. So that's example of a left sided R a p D. And it's the swinging light test R e p t. Another eye condition that you might get with, um, a mess The might see is we'll call intranuclear ophthalmoplegia So internuclear ophthalmoplegia happens when there's a lesion. The medial longitudinal fasciculus. So the medial longitudinal fasciculus is a connection between the abductions nerve and oculomotor. So abductions nerve. If you remember that innovates if you came to my cranial nerve teaching innovates electoral rectus, um, it causes the eye to abduct. Um And then oculomotor nerve surprised me directors because it's adult and honestly, when we abduct one idea, there are adults and bites first. So they have to have some salt connection between them. Where to make the two muscles work together. And this is what we called the medial longitudinal fasciculus. Now, if you get a lesion in that, then like in this example, there's a lesion right on my left. So what you get is the eye on the natural. I will get nystagmus the eye that's going abducted, the presenters nystagmus, and there's absolutely I will get will not be a adopted. So that's an example of the right and the left lesion, at best, what we call intranuclear ophthalmoplegia. It's the optic neuritis is most common one. But patients can also get into neutral help, leisure and a mess. So, like the early symptoms of them s would be optic neuritis get altered sensations of paresthesia burning sensation, numbness and also trigeminal neuralgia. And again, the consent with fatigue. And it's important with these symptoms that you will go out all the conditions that can mimic a mess such as our underactive thyroid anemia. And we'll call the some of the other, um, s minutes later on and again slower process. So again, depending on where this lesion is, the demyelinating to present different things So usually several hemisphere will cause things like parasthesia paralysis. Spinal cord lesions can cause plasticity. Sexual dysfunction sink to dysfunction, bladder and bowel. Um, optic nerves can cause kidney writers again. If you had a medulla or palm time lesion, get this artery a duplication vertical stuck with again cerebella signs as well get a cerebellar lesion crystal part of central nervous system. If you remember the new morning Danish a cerebellar conditional so dysarthria a taxi, a nystagmus intention tremor, slower speech hypertonia so that they're all good presentation of cerebellar problems. And again Central nervous system, usually upper motor neuron signs of spasticity, brisk reflexes, weakness and then autonomic dysfunction as well. And then the single you toss phenomenon. So again, don't confuse this with a relapse, so you toss phenomenal. It's simply when they come out a hot shower in hot control and they have been activity, we'll get an exacerbation of their symptoms of a mess. Special visual sentence. That's what going you toss Phenomenal. No, a relapse because you got remember the definition really last familiar. And another sign we call it might get Lhermitte's sign. Now that one is when they bend their neck to get this electric shocks electric shock sensation down the spine. It's a type of neuropathic pain. Um, and this kind of a colonel, the things about well as the best so normally the investigation. So we could do, uh, MRI to look at these lesions. That t two weighted MRI, you don't have and find new lesion from the old lesion. Then in the MRI scan, you can add gadolinium and gadolinium. It will show new lesions. No. Got much experience in radiology. So car questions of them not Oh, yes, he can. I didn't gadolinium to look for new lesions. You can have visual evoked potentials on again, like, say, a lumber puncher, to show all the little band which can show dissemination in time and they go, That's an example of, um um, a row. So classic MRI findings that we get in a mess is that jokes the cortical lesions periventricular lesions, which is also known as doors and fingers in front. Sentoryu lesions aren't aren't a corporation. These are classic areas. Lesions you get in the pathology, please. White matter lesion, the political inference sentoryu all uncle and the optic nerve as well the management of a mess to use. It's a multi different team approach when you managing a mess and involves off the more metal desk. Consultants and specialist nurses visit Therapist Fault E M Charities. That is a mess society speech, language therapy, social services and then symptomatic management. Um, so, uh, again relapse. Usually you can give him a steroid relapse. And then there's some disease modifying agents that are listed there. And then this new novel therapies, which was made in hometown Sheffield at the bone marrow transplant. And so that was worth looking into. If you're interested and then symptomatic management as well, Like a mentioned so lax tissue constipation. You know, retention. You can give oxybutynin or Internet itself. Capitalization and muscle spasms could be treated with Is your Botox injections baclofen pumps? Gabapentin does pump. And then there's always. There's also a scope for cannabis, which is an interesting and it's offensive interested the spasticity and again. So the poor prognostic factors that mess would be male gender lay a john, sir. Multi cerebellar seem to involvement early on a disease. And then, like I say, some of the mess mimics so one of them is neuromyelitis optica. So now that is antibodies against the myelin protein anti aquaporin four on D um, mold again. In this world, I mean near my life is optic. It's usually bilateral optic Neurontin was investigate unilateral spastic weakness in lower limb century problems. Bowel, bladder. So you get spinal cord lesions and you get optic nerve relations. Transverse myelitis is over three or more beautiful segments. The other things you want to look like sle so Lupus sarcoid acute, disseminated, incur for my lighters. And again it may be 12 deficiencies and on presents with neurological symptoms. Weakness? Uh, parasthesia than it's a sensible Just check that B 12 levels before referring neurologist. Yeah, that's M s the next week of a Parkinson's disease. So again, the definition for Parkinson's disease is it's a neuro degenerative condition, this time a mess. Is it in your inflammatory condition? Packets of diseases in New York, degenerative condition of the basal ganglia? Um, they're they're representing effects, initiation and execution of ultra movements. So this symptoms are classic for classic symptoms. I remember truck tremors, rigidity a kind easier or bradykinesia in postural instability. So trap tremors. So this difference just going off. The traumas separate do Parkinson's disease. So this essential tremors essential tremors is when you get tremors, when you're holding things, trying to hold a position or when you're trying to do with the hands, you get a tremor. That's an essential tremor. And then there's also on intention, tremor and intention tremors When you get all the shooting or under shooting, when you're going to reach for things, this is a problem with, um, cerebellum. So remember the eye in Danish, the intention tremor, and then the tremor you get in Parkinson's disease is we call a resting pill rolling from, and this occurs at rest. Um, weather. When you know not doing anything to just start at rest will start getting his pill rolling. Tremor. So it's different to the central tremor and intention tremor. We're looking over rigidity versus plasticity, so rigidity is Was this since the passage joint movement. So again, in Parkinson's disease you get lead pipe rigidity. So that's sustained. Was is it resistance? The passive mirrors throughout the whole range of motion and you don't get a fluctuation. Quite. There's a lead pipe. Richard seizures throughout the whole passive movement and then called real rigidity. Is jerky resistance, the past improvement? So that's when your muscle tensions and relaxes defenses of relaxes. You get this call wheeling effect in rigidity the two times with lead pipe majority. Where is the sustained resistance throughout the passive movement and called Trulicity is we get jerky resistant spaciticity. It's like difference of spasticity is something you might get someone after they've had a stroke, and that's what we call a class knife a spasticity. So initially there's a lot of resistance, and it's suddenly you get a lot of distance, like when you open the clothes and plus knife this lofty dependent. It can affect either agonist antagonist that muscles and there's no tremor and is usually your hyperflexing a a positive cloners, which is again or promoting your lesion, and you can get a stroke. Patients Final one is the difference in Bradykinesia, a disk kind of easy and hypo coming the bride. It kind of eases slowness of initiation of volunteer movements with a progressive reduction speed. Example. When you repeating an action like tapping your finger or thought they eventually get slowness, this is what we get. We get Parkinson's disease. A coney is loss of ultra movement. Um, the Hypo Kinesis is movements or produced in scales, which is micrographia. I pull phone. Yeah, again. That can also happen in Parkinson's disease. And then this kind of eases separate is dimensional ct for vantas movements of what's well, it's presence of indulge millions. So they did. You get lots of on treatments, but I'll talk about to get the involved movement. Then this can happen in Parkinson's disease, the side effect of the dopamine medication. So that's the difference. This is a classic or Parkinson's disease. Um, again must like blank expressions. Do the posture, the pill rolling tremor, um, Coke? Well, legit, um, the slow shuffling gait. But he can easier depression to the classic symptoms of Parkinson's disease, and they're also non motor symptoms of Parkinson's disease. And this could be things like nausea. Uh, Ram sleeps the rapid eye movement Sleep Behavior Disorder, which presents the acting out that dreams visual hallucinations and, again, visually, stations congee. Since in Parkinson's disease. It can also be a side effects with the medication depression and an autonomic dysfunction, which is awful static hypotension, constipation, you know, recent and erectile dysfunction. Hyper celebration on dystonia for the pathology in Parkinson's disease. So you get the loss of document Arctic neurons and you stop stanchion. I grew apart compactor. Um, the surviving noble neurons contained what we call a little body societal president inclusion. It could contain gluten body and the main component that nobody is what we call off my nutrients. So abnormally folded protein called Alpha nuclear, which is in the founding Louis body. And that's where we get in Parkinson's disease. And you also get loss of Nordgren Aleve, which is producing book all look, the local Screw this of the ponds and I just is a picture that show you where the locus cruel assist. So lots of doctors Minuteman ergic neurons in the foot finish Niagara. Um, lots of nortriptyline production and lockers crew less on the living bodies on a little bunch of things. Uh, contain office on you today. There you go. That's Parkinson's subsidized. I bring back disease. So just going over the direct the an indirect pathway of basal ganglia. Just a recap have been no relevant in clinical exams, but it's always good. I like to listen for about two physiology and my talks and just trying the read cut back to that 1st 2nd year when we did the the science side of mentioned. Um, so the direct pathway is a excited to report switch. The cortex was the indirect pathway. Is the inhibitory afraid to the quarter? Now that direct pathway again, the cortex excite. If we look at the dark part of the insulin, the doubt But the cortex excites the stratum. Because this right, um, it is excited. It has an inhibitory effect from the global politics. So inhibits ago with politics now because the goal is politics is no inhibited. It can no longer going inhibit the thalamus that between the both Protestant turn and pharmacist inhibitory pathway. No, because of those person sent, it can no longer inhibit. The thalamus columnist is able to go and exciting the court tests because again, it's an exciting probably not for the the the direct, possibly big sites to court. Looking at the indirect pathway now, the cortex excites the stratum. The stratum is excited. It wants to go on. Inhibit. The girl was part of sex Turner. So it goes inhibits of those parts of 6 10. Now the girls products external is inhibited. Now it wants to inhibit its off balance, but because it's inhibited, it can no longer still been having this with balance. So the stool family then was excitement, levels, price, Internet, Um, and because it goes first extent has not inhibited. Sometimes that's a bonus. Condemn going, Excite the clothes off the Internet. Well, gold stars, in turn at this time, is excited, and therefore it wants to go on inhibit the thalamus. So this time it can go on a but the thalamus. The thalamus inhibited. So now, because it's inhibited. It can no longer excited court. That's how the indirect possibly inhibits the cortex. Now, when we want to initiate movement, we've got this dopamine. Now the dopamine, the way it works is it work from the direct pathway where it excites these straight? The strike times already excited. It will go on except strikes again. And therefore there's been there's no further changes to the diet pathway. So our oh, where's that in dark? Possibly it actually inhibits the pathway between the stratum and with those past external. It's now because that pathway was originally inhibitory on. Um, it went and inhibited the gold prospects Turner. Now, because of the adult me, that pathways now inhibited. And it no strike no longer inhibit because plastics dinner so therefore now now is that part of it is inhibited. The broad was passed. External could no longer inhibit the supplements to the silk. Thomas let me get that right again. Story That pathway comes down and therefore because not no longer a big change that's X that that can go on inhibit, be subthalamus, sometimes in a bit, so so Thomas can no longer inhibit the girls. Probably that in turn, a global policy in turn it. It's exciting. So because that's no inhibited close past Internet, no longer excited it inhibit the thalamus. And because the goal for us in Turner Canola inhibited columnist, the thumbs can then go on excitement cortex and therefore it hasn't it. It becomes an exciting injury. So therefore, when you want to initiate movement, you get this double whammy from the direct and indirect, possibly fix of dope me, and therefore you can go on initiate movement. So, no, there's a lot to take in there, but I can always There's any question that noise could with that again. So just the risk factors for Parkinson's disease that age on the history, the racial origin there's a table risk factors, so age, gender, female, white, Caucasian and from Mr Parkinson's disease. Um, and again it practices days before the age of 50. But thinking is there a genetic, uh, had injuries? So again, there's some conditions that called Parkinson's. Plus, these are other conditions that can cause Parkinson's symptoms. And that's like Wilson's disease drugs such as antipsychotics, um Metoclopramide stroke in the basal ganglia, multi system atrophy and progressive supernuclear palsy and 5 to 10% of Pakistanis of familiar. So again, like, say, if there's a family history of parks is these all happens before the age of 50 you were thinking, is a familial component, and these are things we have to go into details part of my urology course for obviously undiscovered it just for a bit of interest so you can get also on dominant Parkinson's disease, or especially depending which gene has the mutation a sense. See a GI at the L. R K. Two gene again causes dominant and her tip access to these Where's the park in Jean Pink? One. They're all recessive. Parkinson's disease investigations. There's no single day, if not it tested parks. Is these this clinical diagnosis? You wanna do blood test to rule out other causes of tremors and things like that or function MRI CT is without with the structural causes of Parkinson's symptoms. And then you can do a duct imaging, uh, which demonstrates the loss of dopamine new ones in the profession. I will treatment so treatment, normally in both replacing striatal dopamine um, in her enhanced transmission of go from anergic. New rules on stimulate the document receptor the classic treatments with treatments. Again, the treatment you might see is leave it open, please. Carbidopa. So Carbidopa is adult pretty troubles in theater for most common treatment used might have also heard it called Mother Par. So that's the Leave it open carbidopa. You can use Dove for me in this, but you want me. These come used for younger patients because you you want to delay starting. Leave a dog, but you because we leave the door when you get reduced. Efficacy of times. If it's the younger patient with Parkinson's disease, you want to try and use something else instead of leave it open. Um, and these things could be Doc me and agonists. However, there are some side effects of dopamine agonists, and they can cause cardiac, um, pulmonary fibrosis get increase in risk of impulse control disorder. Um, especially patients have had a history of impulse disorders or alcohol abuse. You presented visual hallucinations and again daytime sleepiness, and again we leave it up. But you should know if some of that it should not stop it abruptly because there is a risk of called neuroleptics malignant syndrome. If it is stopped abruptly, um, they can have a dog mean agonist patch, if you can. Can take believe it overall. Really? Um, some of the side effects relieved, talking for his nose. He had diarrhea to get g I upsets everything is yeah, that's the problems with Don't leave a doper is what is Pete up this kind easier. So this is the peak dose. They get these involuntary withering movements called what we call Alpha Tosis and then later on, when you have been taken, leave it off for two years. They can get a local on off effects where the symptoms of Parkinson's disease come, Come back towards the end of the dose. So again, that's where you want to reserve. Leave, Doc with the later on in the disease. If you want to try and use things that don't mean agonists early on in the disease, these were the after Tosis movements you get. And then there are the adjunct as well. That confused. And this is the model a me knocks days being hitter can. This can be used to reduce the dose a little darker. Side effects. It's causing problems on again. Uh, there are this increases long term effects is legal. Compton emitters on the amantadine and then symptomatic treatment again. You've only daytime sleepiness. Would, like, say, side effects. Office started hypertension again with plants. The injection treatment with Metrogel found again. Excesses, elevation. That game proxies you in treatment? Black of irony. Um, bromide. Back in a second. Okay. Yeah. So, uh, I'm in the final bit. I'd like to cover is a seizures and epilepsy. So what's the difference? Within a faint and fit? Might be something you might test on, You know, ski again If you have an A any job is from the patient presents, you might say I had a fit. Do you want to try and work out whether it was a genuine seizure, whether it was just a faint or syncope fill again things that might suggesting he will be if there was a triggering factor. So the site of blood or anything? Um, if there was a distinct programs where they felt a bit nausea, vomiting, dizzy before the event, and again, if they were conscious that there's loss of consciousness, if they if there was, um since just seizure versus fit, shorter duration, quicker recovery on an ongoing left the GI, but no confusion, because just think so. And then a seizure could be recurrent. They might have some aura before 100 visual or order tree. My particular smell automatisms convulsions at the onset of the loss of consciousness. Where's the other one is convulsion after the loss of consciousness, um, longer duration and then posted through that very tired and confused, tongue biting incontinence? There's some of the different screen syncope and a seizure, But again, a syncope is a transient loss of consciousness and Institute of Global super hyperperfusion, so they get reduced. Blood supply to the head usually lasts a couple of minutes, and it's usually a warning sign before, like patient was pale sweaty, the legs go wobbly. They can get a few jerky movements when it does happen. But this rapid recovery no postictal confusion. So the most common one is reflex syncope that could be raisel vagal. So this can happen when patients eases out of blood, get sudden drop in blood pressure, heart rate situational. So after a coughing fit after going for a week and then again could put pressure on the carotid Sinus cause you seem to be, and then you want to rule out cardiac causes. Well, so it was really skinny. CG could be heart blocks. Bradycardia of stocky heart is in structural problems. Like a little external system course syncope. Um, so, yeah, or farsighted hypertension can cause syncope. So this could be also things like alternate fairly from Parkinson's disease. Diabetic neuropathy. Um, after vogliamo lost my goal to start a tension off diarrhea hemorrhage groups like diuretics and base of dilators can cause, um, off starting apple tension. A treatment like second major dream or fludrocortisone um, investigation again, lying, standing BP. And again, do any see GI? Look at the medications around some of the medications. My problem, Q TC. You want to look at the Q T and then against seizures last longer than syncope. Patients come become cyanosis might be warts, which is deja vu. Tongue biting, urine incontinence again postictal. You don't feel tired and confused. Investigations for seizure would be the EKG and MRI and epilepsy is when they have two or more unprovoked seizures. So causes of epilepsy or seizures will be clean vascular cause. So I always look like looking surgical save so vascular so it could be in a little bean. A small formacion intracranial bleeds infections. That's a meningitis. Encephalitis or abscesses can cause seizures. Truma Walter mean so to Munich, a flight just metabolic. So hypoglycemia or the electrolyte abnormalities know sold the end. New plastics or tumors brooks. So alcohol withdraw or elicit drugs and functional as well. So non athletic attacked his oldest. The things that can people replica three things can lower the seizure threshold. This could be alcohol illness, sleep deprivation, flashing light. Draw things that can lower the seizure threshold the classifications. So conceptual League of Epilepsy. Highly Casca seizures. So you know, I have a partial generalized or left apostles. Focal be a simple focal complex complex is when they have loss of consciousness and then you can have a general secondary. Generalized. So the simple partial will congest resent room some other sensory symptoms. Motor symptoms, autonomic symptoms or psychic symptoms. So focal a simple seizure. You have no loss of awareness, um, complexes, loss of awareness so or a sore subject of sensation and simple for seizure. Um sonorous, a subjective sensation on. They have complete full awareness. You can have multiple symptoms on isolated limb jerking movement, which we call a Jacksonian march had turning. And then, since we things, which is deja vu jam a food visual or auditory or factory epigastric or, uh, and complex ones when you have loss of awareness. And they can present with automatisms, which is a non purposeful stereotypes. Repetitive movement. Um, these can happen in things that temporal lobe seizures, where we get chewing lips smacking, swallowing and then frontal lobe seizures could be more complex. Limb movements generalized so it could be secondary. Generalized. Usually, uh, for a focal seizure, you could have absence seizures, so usually just school child goes pale and just as, um, can later on, uh, present. We have 20 minutes easily when I a tonic clonic seizure atonic myoclonic. But these words we're going out of fashion nowadays, it's just call it a generalized seizure was investigations, seizures, MRI, E G and also the Bloods. So management use long term management could be carbamazepine for focal seizures. 11 to rest. Tonal was nose keppra for generalized seizures in terms of driving. If you've had a seizure, the car drive for six months after a single seizure has to be seizure free for 12 months if the about diagnosis epilepsy to two or more seizures. Then again, the can't drive for six months. If any of the medications have changed, so you might come across states is epileptic because in your practice, the status epilepticus seizures can happen if there levels of the athletic medication isn't quite right in the lower levels, they've had a brain injury. Congenital malformation, the brain. How do you vascular high pokes here? Jokes or alcohol? Would pro brain infections or medical problems. So initially, when you see someone have a seizure? The main part A B C D airway protection point, where we actually see whether it's a nasal pharyngeal on warfarin jewel away and then treat the hypoc CIA. So 15 liters of oxygen and then protect their service around. It's make sure they're not going to get hurt from things around them when they're having that seizure, when it's like safe to put him in a recovery position. So recovery position. Move any furniture, nothing. Make sure there's nothing that can aspirate on in their mouth oxygen and then keep them safe. Don't pony. So you've done. These things are trained intravenous access. So a large ball Can you learn the a CF? Take some bloods VBG Check my blood sugar levels. Most important thing. Um, and again, long term cardio risk patients could get cutting spiritually collapsed electrolyte imbalances from seizures. We can get rubbed on my license from muscle breakdown, lead into a Kaiser hypothermia organ failure and again scribble a demon. So these are sort things you think in plates want to do about the seizure. So treat the seizure benzodiazepine. Consider the possibility is, is this a non athletic attack? Functional cause a seizure could be pregnancy, but they haven't clamps here emergency on separate drugs, which is Benzo's investigation. So your blood, your VBG ABG think about hypoglycemia is, of course, again proper. Next, if you think it's alcohol of drawer, a low nutrition and then if the seizures not resolving the thing, is there another course? The seizure? Well, we're not treating the cough here. Is there something else? Keep maintaining that seizures that is a cancer. Uh huh. In that brain that's causing this seizure, in which case you might want to give them something that money tall, which will reduce the Subaru Dema Um And then again, the most important part in seizure is Thea Airway breathing and cardiovascular instability. So make sure you give him fluids with florist a shin. And then, if it's in refractory status, then you won't you soon, as when I see it, even for the crash, Call it. Get any stress there and where the good think I would want any stars that patients have a seizure to control their seizure. So the reason you can't keep giving benzodiazepine is that some of the seizure it is because benzodiazepine is a GABA rockin ist. Now what what happens is we got these gather receptors and therefore we give in patients benzodiazepine, having a seizure, to try and and it's named gobbles, being a bit glutamate. It's the excited You want to try and increase the inhibitory pathway, but given got badness. But as the seizure goes on or not, your urine's internalized these garbage receptors, therefore gather stops working and there. So, yeah, the gather receptors stop working because obviously they've been internalized. You don't look to make sure you further benzodiazepine doesn't work, and therefore you won't be thinking of anesthetizing the patient or the drugs and that's that's status and epilepsies. Then you know. So So we've covered moguls. Grossly. Is pockets disease on? Uh, let's see. Okay. Next time will be covering. Had injuries, strokes on dementia next week. So that's the end. Like you're almost like you're cold feet back. Any questions or any particular things were going to cover again. Thank you very much. Still in that was read out for From ever. Find helpful is all. Okay. Yeah. There's any questions. You guys got a new You're Mike's. Now tow us a spouse, or you can bring in chart. Sure. He'd be more than happy to answer any questions. Pull a mail address on the case. You have a question you guys are on if you ask. Think of any questions during the week or anything. I'm sure he'll be happy to go over next week. Can explain the last slide. Last light. So? So basically, we've got the two receptors in our central nervous system gabber, which is inhibitory in your glutamate, which is exciting. Now when someone has a seizure, you give them benzodiazepine going benzodiazepine because benzodiazepine is a gathering goodness. Now we give them, like, three doses of benzoyl that doesn't terminate the seizure. We don't want, you know, keep getting, um, Benzo's. We think of alternatives such as any citizen, the patient. The reason we do that is because a lot of time during the seizure you knew your port sites in your own will internalize the's GABA receptors. Therefore, there's normal government steps is left in the poor. Sign up on your own. Therefore, giving him extra keep giving him get benzos isn't no longer gonna work. And therefore, we need to think about alternatives such as anesthetics for to determine firmly about seizure. Does that make sense? Anything else? The auto link for the feedback from his Also for those are using that. For instance, you're actually just quit. Yes, there's no further questions. Uh, we will see you guys next tree, but there are any questions any time you can email. Oh, that's yeah. So you can give us Said you couldn't afford the mail question. You ever next week know if there's anything else, we will see you guys in three. Well, thank you all for attended the government. All right, All right,