One in 26 people will develop epilepsy in their lifetime, but many conditions – in addition to epilepsy – can trigger or look like a seizure. To help PCPs make efficient initial evaluations, neurologist Manu Hegde, MD, PhD, breaks seizures into basic classes and puts the numerous epilepsy syndromes into three useful categories. He discusses how to take better histories; what to check for during physical exams; and what to know about antiseizure drugs, including specific side effects.
well, thank you very much. I really appreciate the invitation and uh it's an honor to speak with primary care colleagues who are, you know, really the backbone of medicine. So thank you for your time. Um I want to try and make this talk as useful for you as possible. Um We'll talk a little bit about what a seizure is and how it relates to the diagnosis of epilepsy, the differential diagnosis and approach to a first time seizure um identifying the most common epilepsy syndromes. Just so you, you know what the terminology means and what those diagnoses are like. We'll talk a little bit about the risks and benefits of the most common anti seizure medications. There's a myriad of medications so we won't go through all of them, just just the ones that I think might be most relevant to you and talk a little bit about when to refer to specialty care and what we offer. So first of all definitions, a seizure is a paroxysmal stereotyped event that can include altered movement, sensation, experience, or consciousness, and it results from excessive brain electrical activity. We usually say that the hallmarks of that are hyper hyper synchronous brain activity. Um it arises from the cerebral cortex. You do not get seizures coming from deeper structures like the basil, ganglia of the cerebellum or spinal cord. Um and epilepsy is just defined as a disorder in which someone has recurrent unprovoked seizures. Usually we diagnosed epilepsy after someone has had two unprovoked seizures, although you can be diagnosed with epilepsy after a single seizure if you have characteristic risk factors on your work up that are identified. Um Epilepsy is the fourth most common neurological disorder. Um and it affects approximately 1% of the population. One in 26 people will develop epilepsy in their lifetime. Um And the ideologies uh you know we could go on and on with with the list but all sorts of insults to the brain um or developmental problems with the brain can result in epilepsy and those can sometimes cause other disabilities. Um But often times seizures are really the only manifestation of whatever that underlying causes epilepsy causes significant mortality and I think this is not well appreciated. More people die from seizure related incidents than uh died from breast cancer. Um and those with uncontrolled seizure 7 8 times greater risk of premature death. So it is something to be taken seriously and to be aware of. Um One problem with our field is that every five years or so a group of epilepsy specialists which sadly never includes me has some conference in the mediterranean and they changed the names of all the seizures. Um And uh so what used to be petite mall became complex, partial became focal. Um And so now the terminology that we're using is um is listed here by the International league Against epilepsy, latest classification. Um the things that you really need to know that I think are in yellow here seizures can be either focal onset or generalized onset, meaning how they appear to arise within the brain on an E. E. G. And within focal onset seizures. They can be with preserved awareness or impaired awareness. We used to call this simple and complex, partial but focal aware or focal unaware seizures and then the process of a seizure spreading and causing a tonic clonic seizure or convulsion, or a generalized seizure. We call those focal to bilateral tonic clonic seizures. And then the other type of seizure or type of epilepsy really are generalized epilepsy is in which the seizure seems to start all over the brain at once when you look at it. So these are the two major categories focal or generalized. Um and it's important to know the difference because the medications and the treatments that we use are different. How do we make a diagnosis? Well, we take a good history as we do with it with any condition. We try to identify risk factors and get more information about the seizure. Simi ology, meaning what did the seizure look like? What were the behaviors involved in the seizure? Um We usually try to get an M. R. I. Which is a structural test and an E. E. G. Which is a functional test. And so what's the differential diagnosis when someone has a seizure? Well, as you can imagine, and as you probably know, that's a huge list of paroxysmal events, right? And it will differ based on the characteristic of the event itself and the nature of the patient, the demographic that they're in. Um, and I think going through this entire differential is probably beyond our scope. But there are a few diagnoses that I think we should focus on because they are often confused with seizures and these are often relevant to folks in primary care. Um We should also talk about medications because there are medications that can provoke seizures or trigger seizures, seizure medications that can lower the seizure threshold. Um This is not an exhaustive list by any means, the actual um exhaustive list is huge. But um if you look at some of the most common medicines and and those that are most strongly associated with seizures, this would be a analgesics, mainly traMADol is the medication that we watch out for. There are a number of antimicrobials, antibiotics um that can potentially cause seizures as you've probably run into in your own practice. Problemas is an immunosuppressant that can often result in neuro toxicity manifesting as seizures. Their psychiatric medications, the most uh concerning of which are claws real and buPROPion, which can both provoke seizures and people who've never had them before, interfere on alpha can do this and then illicit drugs, um cocaine, methamphetamine alcohol withdrawal. These are all um uh drugs of abuse that can cause seizures and in some cases in someone with underlying epilepsy or at least a tendency towards epilepsy alcohol itself rather than the withdrawal can sometimes cause seizures. So let's talk about that differential diagnosis and and we'll do it with a case. I've got a few cases to talk about with you today. First case 21 year old previously healthy man goes to donate blood. He enters the facility, sees other people with I. V. lines and reports seeing black spots and feeling nauseous. He appears kind of sweaty and pale to those in the room. You lose consciousness. He slumps to the floor while on the ground though. He's noted to exhibit jerking movements of all extremities For less than 10 seconds. But then he recovers the baseline immediately after and is fully oriented with no neurological deficits. What's the likely diagnosis? And I'll let you think about that for a moment. Um And I'll tell you that this is a good case of syncope. Eva's a vagal syncope which I'm sure all of you have encountered. The the the one feature of this case that I think draws it into question is that that report of shaking or jerks. Um And I think it's important to realize that sync api can oftentimes be associated with some maya chronic jerks or even tonic clonic appearing movements. Um But they usually only last a few seconds. Um But we do see it in you know 10 12% of patients who have syncope. So this is something that's been studied and reported and just because someone has some jerking um due to a very transient period of cerebral hypoxia. That doesn't mean it's not sinking. It usually is still sinking. The other characteristics that help us um distinguish between the two are the pro dome. Um Those with seizures will often have an aura that consists of a smell, a taste and epic gastric sensation, deja vu, visual symptoms etcetera. For cinco P. I think the program is much more classic and stereotyped. It usually involves the person feeling lightheaded. They may have palpitations, they'll feel hot and clammy and they can report tunneling a vision, seeing dark spots, a graying out of vision. Uh Sync api is much more likely to be positional. It often is associated with a low blood pressure and a low heart rate, whereas we often see the exact opposite in people who are having seizures. Um Asymmetric posturing and tongue lacerations are rare with sync api versus seizures. Um And as we know, you can lose consciousness and in both conditions, but typically those with syncope e will have a much more rapid return to full awareness without any deficits. So the second case, this time we have a 28 year old woman, she presents to the er with recurrent episodes of violent whole body shaking and in the er she's witnessed to have side to side thrashing movements of her head and her arms with forced eye closure. She frequently arches her back and has some pelvic thrusting quality to her movements and the episodes last 5-10 minutes and have a waxing and waning quality after the episode, the patient reports that she was fully aware throughout and she remembers a memory prompt that was presented by caregivers at the bedside during the episode. Our neurological exam after the episode is normal. So what's her likely diagnosis? Well, a lot of the features here are very classic for what we call psychogenic non epileptic spells. This condition has a number of different names. Some people call them pseudo seizures, some people call them non epileptic seizures. In any case this is a psychological condition in which if you were to do an E E. G, the brain's electrical activity is completely normal. Um It's not something that people are doing intentionally, it's something people are doing unconsciously. Um And it bears a close relation to Samantha form or conversion disorder as defined by psychiatry. So how do we tell the difference between these? Obviously the gold standard for diagnosis would be E. G. During the event, but if you're just hearing the story or seeing someone in the er some of the features that will distinguish them are the duration, seizures usually have a beginning a middle and an end a crescendo and a. D. Crescendo that lasts usually two minutes or less. Um Non epileptic seizures can have a waxing and waning quality where people start having movements and stop and then start again. Um Those having seizures usually have their eyes open, whereas those with non epileptic seizures have forced eye closure as we talked about in the case, side to side, head shaking or up and down, head shaking um is much more common in non epileptic seizures. We really just see no head movement or unilateral deviation of the head during an epileptic seizure, um back arching, pelvic thrusting. Those are common movements, crying is much more common during a non epileptic seizure. Um and maybe the biggest giveaway in this case, uh and in most cases that you'll hear about is if you have whole body shaking and the person is retaining their awareness, it is much, much, much more likely to be a non epileptic spell than an epileptic seizure. There are very rare epileptic seizures where people can have bilateral movements and still have retained awareness, but you know, the vast majority of the time, you should be more suspicious of the non epileptic event. Um one other thing that people often tend to cling to is whether there's a history of abuse or trauma, we definitely think of these things as risk factors for psychogenic non epileptic spells. However, unfortunately, people with epilepsy are often the victims of abuse or trauma, sadly and so therefore that history can be common in both populations and doesn't really distinguish as well as you might like and I don't have a case for this, but seizure versus TIA is another question that comes up frequently. Transient ischemic attacks. Um the differences between them I think are good to know, You know, with seizures, we are much more likely to see positive symptoms, meaning the presence of a sensation or a movement rather than the absence of a movement or sensation. And with T. I. A, you're generally losing a function, so you'll have more negative symptoms and fewer positive symptoms. Maybe the most important thing distinguishing these two is the fact that seizures should be stereotyped, meaning that they're more or less the same experience for the patient each time. They may end differently, depending on whether the seizure spreads to a larger part of the brain or not. But the beginning should be the same with T. I. A. What we're postulating is that a thrombosis is traveling to some vessel in the brain, temporarily, including it and then uh dissolving. And if that's the case, you know, it would take quite a unique mechanism for the same vessel to get repeatedly um blocked off and then recant allies naturally um producing the same symptoms each time. So what I'm saying is that with T. I. A. You don't get stereotyped events. If someone's having multiple T. I. S, they're usually going to be different events each time. Um Loss of awareness is much more common with seizures than with T. I. A. Um and the duration is often much shorter with seizures vs. T. I. A. So what are some of the key things that we need to think about or ask about when we're evaluating someone with first time seizure? Well I think that the points of emphasis in the history, our recent history of trauma infection or exposures to drugs or alcohol. Um You want to know what the first behavioral change was because that helps us localize in the brain. The first symptom that patients experience in a seizure will often tell us where in the brain it started. Um It's good to know if there's loss of awareness that's important not just for understanding what happened to the patient but figuring out whether it's safe for them to drive, which we'll talk about. Um You want to know if there are any asymmetric features because that can sometimes help us lateral eyes where the seizures are coming from. Obviously the duration any post title meaning after the seizure deficits like a todd's paralysis where one side is weak, contra lateral to the side, where the seizures started. Um And you want to know if they're back to their baseline. Um The key components of the exam I think um you know a detailed neurological exam is always helpful but not really necessary or realistic. I think. Um For non neurologist, the main things you want to know about our, does the patient have sustained nystagmus do that eyes keep beating in one direction only. Um Do they have pro NATO drift? Does one side tend to you know pro Nate or or the fingers curl suggesting weakness on that side? Or do they have slower finger taps on one side and fast finger taps on the other? Um You can test this in kids with posting where you ask them to spin their arms and you'll find that one arm, it's just not moving as much as the other suggesting weakness in that arm and if they're a tactic, you know if they're off balance and and not walking properly. Um There are a number of labs that we typically get. I think you you know, all of these labs, I think a lumbar puncture is a good idea if you're suspicious for a C. N. S. Infection and there's no mass on imaging with a C. T. Or M. R. I. And as far as imaging itself a non con head C. T. Is fine for screening but ultimately you need an M. R. I. And we'll talk about that in a moment. It's important to file a confidential morbidity report. If the patient lost awareness, we'll talk about that in a second and I think a referral to a neurologist is very reasonable after a first time seizure. What about risk of recurrence? Well there are certain risk factors that suggest that the first seizure won't be the last. Um if they have a history of stroke or TBI i if the seizure happened out of sleep in the middle of the night? Um And then of course abnormal brain imaging or E. E. G. Um the odds of recurrence in the first two years range from 21 to 45% and that jumps 45-65%. If some element of the work up is abnormal. Um usually that that recurrence is going to be within two years and 50% of the time it happens in the first six months And the recurrence risk rises to 80% after someone has had two unprovoked seizures. So um that's why we you know very strongly recommend our patients start receiving treatment if they have a second seizure. All right. So one of the big questions that you're always gonna get asked about and we always get asked about from patients is can I drive? And um it's important to know the legal requirements. So um the California State law states that all physicians are legally required to file a confidential morbidity report which is this form that you can find online, you just google confidential morbidity report and the name of the city that you're in. Um And you're supposed to send this to the local department of Public Health if the patient has a condition that causes lapses of awareness, the same form oddly is used for S. T. D. S. Certain infectious diseases. So it's kind of a catch all form of things that the department of public health wants to know about. Um So if you think that there's any chance that this person it's going to have another loss of consciousness or you're not sure you should be filing this form. Oftentimes it's done in the er not always um and then patients come to see us and then um you know we're we're the bad guy because no one else told them that they have to stop driving but we do um so any time you can do that ahead of time that that helps us out. Um The Department of Public Health then forged the form to the D. M. V. And then the D. M. V. Sends the patient um The driver's medical evaluation which is like a 10 page or a page form where they have to fill out the first page and then a physician is supposed to fill out the rest really. You only have to fill out the section that's relevant for this patient. Um So if it's a seizure or something like a seizure there's just one small section you need to fill out and there's uh an area where you can write a paragraph explaining the circumstances. Generally then a patient will have their license suspended and they need to be seizure free for a minimum of three months according to California state law to be clear. Um And then for some patients you know the neurologists will want to observe them for longer before clearing them to dry. Um And we're happy to help with this process. We do this all the time. I would just say you know just be aware that legally anyone whether they're a neurologist or not. Um E. R. Doc's primary care doctor whoever are supposed to be filing these forms if you're patient lost consciousness and you think it could happen again. Now if it's something totally situational nova's a vagal syncope e at a blood draw or something like that I don't think it's necessary but if it's a condition where you think it's going to happen again um you should file the form. Okay so now turning to work up. So um we mentioned the E. G. And the electroencephalogram is you know an ancient test by modern medical standards but it's still super useful for us. It's good for for understanding superficial cortical electrical activity. It's not great for really deep structures. Um The electrodes are placed on the scalp. This is looking top down and these little circles represent where we put the electrodes across the head. Um And it records differences in electrical potential between electrodes or comparing the electrode to some reference electrode. The thing to know about it is that it has a lot of limitations. First of all it's very susceptible to artifacts. So any sort of movement of the muscles of the face causes you know things like this that look really impressive but are all just muscle artifact. We are trying to record something that is very low voltage um from the surface of the cortex and that signal has to travel through the meninges, the skull and the scalp to reach our electrodes. And so as you can imagine the muscles of the face, medical equipment around the patient, the movement of the heart and the chest or bad electric contacts or sweat. All of these things can cause artifacts that make the E. G. Very difficult to interpret. Secondly it's very reader dependent. So you may see different interpretations depending on where your patient is getting an E E. G. We have the benefit of you know doing EKGs all day every day. So we get a lot of practice and I think that that helps the quality of our reeds and then we've got you know a dozen other colleagues that we can turn to when we are stumped by an EEG. Um And then it's also important to know that it's just a snapshot in time so someone can have epilepsy and their E. G. Is totally normal on that day. Um There's a there's some luck involved. The yield is just under 30% Sometimes if you do multiple E. G. S. Or longer E. G. S. That yield improves. But epilepsy is really a clinical diagnosis and the EEG helps us but it doesn't make the diagnosis or if you rule it out um imaging. So the american Academy of neurology recommends either a brain C. T. Or an M. R. I. For any unprovoked seizure. A. C. T. Is what you know most patients are going to get in the emergency room and that's fine for gross structural lesions. So you know you can tell a patient look, I'm pretty sure you didn't have a giant stroke or a big tumor or a bleed. Um And that's you know that's going to be very reassuring. But there are a lot of smaller lesions that can only be picked up on M. R. I. You know very small masses, tiny strokes, vascular malformations um And early neurodegenerative process like alzheimer's disease or scarring in the brain called medial temporal sclerosis. That sets people up for epilepsy after usually after of febrile illness early in life. Um And these are some examples of M. R. I. Findings and patients that I take care of. This is a cavernous malformation. Um This is a patient here with toxoplasmosis secondary to HIV which then caused medial temporal sclerosis on the same side. This is where the hippocampus is. And you can see it's very shrunken when you compare it to the other side. Uh This is an example of a focal cortical dysplasia um abnormality of normal migration. Um That caused right frontal seizures for this patient. And then this is an example of a patient with a low grade tumor um that caused their seizures when in doubt. You know if you have a patient they need imaging, you want to sort of speed up the work up before they come and see a neurologist order of three Tesla epilepsy protocol M. R. I. If you use all of those words in the order radiology will nail it almost every time at at any hospital. Um Not every hospital has a three Tesla scanner I think, you know, we are very lucky to have really good scanners and more importantly, really good neuro radiologists who can help us sort these things out. Um at UCSF there are a number of different categories of seizures as we talked about before. You know, the primary categories are focal or generalized and then you combine those different types of seizures into um different types of epilepsy, whether it's focal, generalized, combined or unknown and then those can then be coalesced into epilepsy syndromes. And the ideologies as we said, can be, you know, um as broad of a differential as you can imagine for almost any complaint or any disease. And as far as the syndromes go, you know, there is a huge number of epilepsy syndromes, a real laundry list. But I think there's only a few that would be good for um those in um internal medicine or family practice or other types of primary care to to really keep in mind. Um really I think there are three that you should, you should be aware of. One is childhood at sans epilepsy which usually happens in early childhood um then there's juvenile maya chronic epilepsy which can start in adolescence or have on set up to someone's late teens or early twenties and then focal epilepsy which can really strike at almost any age. But in younger people might be due to uh problems with malformations of cortical development or traumatic brain injury. And then an older people, traumatic brain injury and neurodegenerative diseases, malignancy or stroke. So the ideologies may differ but the end result is the same and that's focal epilepsy. So we'll give you a couple of bullet points about each of these three syndromes very quickly childhood absence epilepsy. What's this stereotypical story or patient that you would hear about who has childhood absence. This would be a grade school child who has staring spells and inattention in school. And um when you uh analyze the story further you'll hear about 10 to 22nd episodes of unresponsive staring or blinking or eyelid fluttering. If it's an atypical absence seizure, they may go on to have a generalized tonic clonic seizure but that doesn't happen very often. Um They may have a partial lapse in awareness or a complete lapse of awareness. Oftentimes there's a genetic component, there may be a positive family history and the E. E. G. Shows three hertz, spike and wave if you're ever doing any sort of board exam or re certification exam it's highly unlikely anyone will show you an E E. G. But if they do it'll be three hertz spike and wave. An absent seizure um in which you know you see a spike followed by a wave. Um And it's three per second meaning three hertz. Um We can trigger this in the E. G. Lab with hyperventilation. So if you have a child blowing on a pinwheel continuously you can see this pattern and that makes the diagnosis. Um And it can be treated with a number of drugs, including ethicists might provoke acid and nitrogen, juvenile maya chronic epilepsy. The stereotypical story is the high school or college student who had this early morning jerks or twitches followed by a tonic clonic seizure. It usually happens during you know final exams week when they're sleep deprived or right after final exams when they've been drinking alcohol. And that's the sort of stereotypical story for a presentation of J. A. M. E. Maya, chronic jerks referred to lightning quick jerks involving one or more links. They're very very fast um And they may cause someone to drop an object or throw their phone across the room. Um And that may be unexplained until they have a bigger seizure. Um And those bigger seizures or tonic clonic seizures. This too has a genetic basis and has a similar appearance on E. G. Three but often times up to six hertz spike and wave. Um And the patients maybe photosensitive, so when you hear of someone having a seizure after strobe lights at a concert or a Pokemon video or something like that. That's this type of epilepsy in which we see it most commonly. It's very treatable. But unfortunately you have to take medicines usually for life and Valparaiso, casa, Loma trojan and Levitra system are the most common Case. three. So a 31 year old, previously healthy right handed man presents the clinic the day after a tonic clonic seizure. He doesn't remember anything about the seizure. He was just told that it happened. It's past medical history is known for a febrile seizure and early childhood. Um and no problems after that. on questioning who reports a 2-year history of monthly episodes of weird nostalgia in which everything around him seems familiar as if he's seen the scene before. He also reports significant life stress of late as he is going through a contentious divorce and his exam is notable for slowed finger taps and a flattened nasal labial fold on the right E. G, and MRI are pending. What's the likely diagnosis? Well, here, you know, we the, you know, the cliche for writing a normal neurological exam and a chart is to say it's non focal, right? Well here we've got uh an exam that's actually focal for a change and that's because this person has focal epilepsy. So focal epilepsy, there really is not a stereotypical story or patient. The one I just gave you is an example but not the example. Um there's a huge range of ages, ideologies and severity is for focal epilepsy basically it just means that the seizure starting in one part of the brain and spreading from there and the location of onset determines the symptoms. So for temporal lobe epilepsy people will often have behavioral arrest deja vu which was this the experience that the patient in our case was was describing and automate ISMs. Um For frontal lobe epilepsy they often have very violent movements, hyper mature IQ movements out of sleep. Um Occipital lobe epilepsy often starts with visual phenomena and parietal lobe can start with Samantha, sensory or mixed sensory modalities and all can secondarily generalize and become tonic clonic seizures but they don't have to. The treatment duration is variable but if there's a lesion on imaging, usually they're going to need longer treatment and there are a lot of different treatments. I think limo trojan, ox, carBAMazepine and carBAMazepine are the most common and kind of preferred drugs for this condition. Although we're getting newer drugs every you know every year. Um On the inpatient side we may use load herbal medications that you can really get a level quickly. Like or so the treatments I've already kind of alluded to medications are kind of the mainstay but behavioral modification is important like avoiding alcohol or sleep deprivation. Um surgery and neuromodulation. Torrey devices are sort of the cutting edge of the field and diets for epilepsy in particular, the ketogenic diet or modified atkins diet can often be helpful. Um We don't have time to talk about all of those but just to give you a sense of medications and how we use them. Um We have some drugs that are better for focal epilepsy, things like phenytoin, carBAMazepine and ox carBAMazepine. We have other drugs that are better for generalized epilepsy. For instance, for absence epilepsy. I mentioned foo SEK samide earlier as the drug of choice for infantile spasms, very rare type of epilepsy that affects small babies. We have a c th steroids and vigabatrin. But there are a lot of drugs and most of the drugs that come on the market nowadays are considered broad spectrum. They work for both types of Valparaiso, Kassid limo trojan Levitra system and two pyramids. These ones in purple here I think are the most popular drugs that you will see mentioned the most. But there's a long list of other drugs and that list is only growing. Most of the newer drugs have better side effect profiles. Most of them though are not that much better in terms of efficacy. Some of the principles of medical management that we use and that I think are worth knowing. Maybe if I if you only took one thing away from this pocket might be this treat the patient, not the drug level. So I think it's common that we get drug levels in the outpatient setting just to see you know where someone is at in terms of their Dilantin level orchestral level or what have you. Um And just because the level comes back high or super therapeutic doesn't mean that you need to change the dose. In fact, I would strongly encourage you to talk to a neurologist or epilepsy specialists before making any changes. Um and that's because patients outside of the normal range may not have any signs of toxicity at all and therefore you don't necessarily need to make a change unless the patient has a clinical syndrome suggesting anticonvulsant toxicity and that's usually going to be things like diplo pia, ataxia, extreme somnolence, dizziness, things of that nature. Um A lot of anti seizure medicines are enzyme inducers and therefore we'll have drug drug interactions. Um this is a chart that shows how certain anti seizure medicines are metabolized. And the take home here is that the pira mate, levitt, paracetamol, Capra and gabapentin are the three that are least hypothetically metabolized, most really metabolized and therefore least likely to have any drug drug interactions. So unless your patient is on one of these drugs, be careful about um the interactions between anti seizure medicines and other medicines you're prescribing. This is something we always check when we're meeting new patients um if someone has had a breakthrough seizure, the things that you want to ask about our infection. Non adherence or medication changes, you know, where they put on something else that interacted with the seizures growths and then these last two are more for neurologists, but I think we try to push anti seizure medicines to their highest tolerated dose before giving up on it and moving to another drug. So we don't like to have people on, you know, three low doses of medication of different medications. We'd rather have them on one at a higher dose. And when we're switching anti seizure medicines there's usually a ramping process where we're increasing the new one before we decrease the old ones, there is usually uh overlap there that can be several weeks or even a couple of months. And we're switching medicines. Okay? Case four. So a 23 year old previously healthy woman presents after a tonic clonic seizure at 5:30 a.m. She recalls having twitches in her shoulders on getting out of bed and then she lost consciousness and was found by her partner. This is our third such episode in the past two years previously. An E. E. G. Showed generalized spike and wave and an M. R. I. Was normal. So this is a pretty classic story for juvenile maya chronic epilepsy. Like we talked about, she's hoping to start a family in the next year and she's interested in starting an anti seizure medicine, which one of the following would be the worst choice, Valparaiso Kassid Levitra system remote region or to pyramid. And you know, again, I don't think it's necessary for you to know about a ton of drugs or a ton of facts about them. But I think it is important to know some of the adverse effects of the most popular ones. So in this case val provoke acid would be the worst choice. And the reason why is the side effect profile for Valparaiso kassid particularly for women of childbearing age is pretty scary. Can cause toronto genesis uh in their offspring pcos weight gain hair loss, osteopenia, pancreatitis and hyper um anemia, which are admittedly relatively rare. But a long list of side effects for feni tone, ginger will hyperplasia, peripheral neuropathy and osteopenia limo trojan rash, including stevens, johnson which we'll talk about Frocks, carBAMazepine. It's hyponatremia which can often be asymptomatic, but if it starts to get into the 120s it can be a problem. Levitra system, one of the most popular drugs causes a very high rate of irritability, anger and depression. Um And for two prior mate weight loss which some people are happy about um but also renal stones, cognitive slowing and can be bad for people at risk for glaucoma. So um those are unique side effects for some of our most popular medicines, but almost all of our side effects can cause dizziness, to propia, a taxi and fatigue. And a couple more words on toronto genesis for val protic acid. The risk is thought to be about 8% based on pregnancy registries of having a major congenital malformation. That's things like spina bifida or cleft palate. Um with most of our medicines. It's it's much lower than that and the malformations happened in the first four weeks of gestation. So before a woman even misses a period she um and knows she's pregnant. Um These things can happen. So therefore we often prescribed folic acid which mitigates this risk to any woman of childbearing age if there's any chance that they would become pregnant either intentionally or not and going back to rash. So um you know, there are a lot of benign drug eruptions that can happen with a lot of these medicines, but the ones who are most concerned about our dress which usually produces you know large areas of erythema that can be politic or stevens johnson syndrome, which can look similar but often is accompanied by blisters, joint pain and fever. So any of those things that's good to involve a neurologist and a dermatologist, a. S. A. And to wrap up, I'll talk about when patients are medically refractory. What happens if all of these drugs don't work? Well, we've got lots of data that suggests that about two thirds of patients will come will become seizure free on an anticonvulsant drug or some combination of anticonvulsant drugs once you get past the third drug, the odds of becoming seizure free are very very low. So if someone is on a second or third drug, they really should be seeing an epilepsy specialist to talk about what their options are and getting to a comprehensive epilepsy center, there is the key um there's a big treatment gap. Lots of patients are never referred. Unfortunately once they come and see us, we have the ability to localize seizures for those with focal epilepsy using a combination of E. G. High quality M. R. I. P. Pet scans, magneto encephalitis, graffiti, spect scans um and with invasive intracranial electrodes. Um These can be used to help us design a resection or implantation of a neuro modulator torrey device that can really be life changing for our patients and those surgical treatment, skin reception. We have laser ablation which is minimally invasive um and devices that are essentially neuro stimulation devices that can gradually reduce the number of seizures patients experience. We have a huge team. We're very fortunate in that regard. We have epilepsy epileptic ologists, both adult and pediatric. We have a number of outstanding nurses and nurse practitioners who have been with us for a long time. We have a fantastic surgeon, Edward chang on the adult side and Curtis august on the pediatric side who um I think do a phenomenal job and are really dedicated to their patients. And we have outstanding fellows. Um We're very lucky to have really great trainees coming through every year. Um and so with that I think I'll stop and see if we have any questions, mm hmm
