DIP Episode 39 - Neuro Pharmacology Part 2 (Seizure Meds)

Okay, welcome. My name is Divine. I am a PGOI one at this point. Residency has been a wonderful time. It's been quite busy. That's why I'm recording a podcast at 4 a.m. in the morning. But in today's episode of the Divine Intervention Podcast, I believe this is a 39th episode. We'll be continuing our discourse on neuroformal ecology. Today I'll primarily be talking about seizures. This is an area that's typically very frustrating for people. But there are a lot of high-yield things you need to know. I'll try to put it in a format that is a lot more digestible than the information you'll find in first step, for example. So let's begin. So for seizures, so start with a relatively simple kind of seizure. There's the February seizures. And the classic way it presents is in a child with high fever. And they tell you that the child has like one generalized seizure. Okay, generally for that you go ahead and use an inset. They usually don't do any kind of workup for those kids. If the kid has an atypical seizure, right, an atypical February seizure. So let's say instead of having a generalized seizure, they have like a focac seizure. Or they have more than one seizure in a 24-hour period. Or they have that seizure and they have some neurologic deficits under those circumstances. Even if it looks like a February seizure, you want to go ahead and do some kind of workup because those are not typical findings in a February seizure.

So atypical findings in a February seizure like a focac seizure or having more than one seizure in 24 hours or having a seizure with neurologic deficits, you probably want to go ahead and work that up. That's more for a third year. Now, right syndrome, right? Again, if you think about a child with like fever and let's say they have like an influenza infection and then they receive aspirin. Excuse me. And then they tell you that... Excuse me. And they tell you that the child is hypoglycemic and has a coma. Think about right syndrome whether that's the classic we present. So the associations with right syndrome right is if a child has the flu or gets like the flu vaccine or... Excuse me. Or has a very silent infection or gets the very silent vaccine and then they have like fever and then they give us a spray and then they get all these problems again. Essentially, the only time you give us a kid is if they have Kawasaki's disease. Remember Kawasaki's disease classically presents with a very high fever. Usually it's like greater than 105 on exams. They may have like a congenital injection. They may have a rash on their palms and so. Remember Kawasaki's disease is one of the causes of a rash on the palms and so. If you think back to your step one exam right, you probably remember the pneumonia about a person driving Kawasaki cars with their hands and feet. So I caught Kawasaki A virus. The causes hand foot mal disease, reketia, reketia, secondary syphilis.

Those things can all cause a rash on the palms and so. But Kawasaki's disease can as well. So think of a high fever, congenital injection, a rash on the palms and so strawberry, tongue and unilateral cervical infaninapathy. Those things are all pretty classic for Kawasaki's disease and under those circumstances you generally want to give IV, Asian, aspirate, high dose aspirate to those kids to prevent coronary problems. Now some other high-yout seizure associations. I'm just talking about seizure associations here. If they tell you about a kid having seizures and then they say they do a lumber puncture, they say a lot of red cells in the CSF where you want to think about some kind of herpes infection. Either like herpes meningitis or herpes in cephalitis which classically starts in the temporal lobes. And then don't forget your West syndrome. It's also known as an infantile spasms. Classic presentation is in a kid less than two years or usually less than a year old on exams. And they will tell you that the EEG shows something known as a hypsi-rhythmia. And these kids tend to have intellectual disability. If you see that, think about West syndrome. It's classically associated with tuberculosis. So in addition on an exam, they may tell you that the kid has like hypopecmented macules on the skin. Those are the ashtif spots. Or they may say, oh, they have like a cardiac tumor. Usually those are abdominal amazes. And don't forget that it's a horizontal dominant inheritance.

And in addition to the cardiac abdominal amazes, they can also have a kidney tumor known as an angio-myelipoma. So it contains blood vessels, contains muscle and it contains fat. Now for seizures, you can generally divide them as two types. There's vocal seizures and there's generalized seizures. And the thing is vocal seizures, there are seizures that are just localized to like one part of the body. And the most common location of vocal seizures is actually in the temporal lobe. And at least the most common location where it like originates. But the thing is a vocal seizure can then become generalized. And then the second kind of seizures are generalized seizures. And actually an absent seizure is a kind of generalized seizure. Remember on EEG, you'll classically find the three herds spike and slow with activity. You don't need to be able to recognize these, but you just need to remember the buzzword. For absent seizure, three herds spike and slow with activity. For West syndrome or infantile spasms, you want to remember the classic hips are with me. So now let's talk about the anti-seizure medications. So the first one is Fanny Toen. It's an anti-epileptic. The way it works is that it's a sodium channel blocker. So we're blocking those sodium channels effectively keep neurons in an inactivated state. So it prevents the neurons from firing. So really if you think about it, Fanny Toen essentially works very similar to your class one anti-rhythmics.

And remember those class one anti-rhythmics, because they work on myocardial, it should then make sense that Fanny Toen should potentially have cardiovascular side effects. And the thing is Fanny Toen, if you remember I've talked about this in the morning many times, you've probably learned it as you study for step one that Guinness, coronas and PB Rs induce chronic alcoholism. The P in the PBR stands for Fanny Toen. It's a Cp415 inducer. So it actually increases the metabolism of other drugs. So in general, you have to give higher doses of other drugs when a patient is on Fanny Toen. Classically, they describe it as a lady that has been taking those Cp's and then becomes pregnant. And she's recently studied a seizure medication. Think about Fanny Toen as the inciting med. Good also potentially think of a carburetor, that's another Cp450 inducer. Now what do we use Fanny Toen for? Fanny Toen, we classically use it to either chronically manage or cutely manage seizures. And actually let me just walk through the management pathway for seizures acutely. In general, if a patient has a seizure you start with a short active benzoyl pretty quickly. You give like diazopam or lorazopam. If that does not work, then you proceed to giving either Fanny Toen or Fos Fanny Toen. Fos Fanny Toen is just a water soluble form of Fanny Toen that can be used diving. If that doesn't work, may you proceed to a barbitrate.

So again, benzoyl first, Fanny Toen or Fos Fanny Toen second, and then a barbitrate. Now how is a Fanny Toen metabolize? This is another high yield thing to know. The thing is I'm not going to just give you extraneous detail on these drugs. I'll just give you the high yield ways they could potentially be tested. So the way Fanny Toen is metabolized is it's metabolized through a zero-order elimination. So basically, we've talked about this already. Remember the rate of elimination is basically constant regardless of the dose. So the plasma concentration decreases linearly with time. So you're essentially losing a fixed amount. Not a fixed percent, a fixed amount of drug with time. And there are other high yield drugs you want to know that are eliminated in a zero-order fashion. So the number of these P, like PAA, remember P is sort of shaped like a circle, which sort of looks like a zero, okay? To help you remember zero-order elimination. So the drugs that are metabolized that will include Fanny Toen. That's the P. Ethanol, that's the E, and then aspirin, which is the A. It so happens we've talked about aspirin with rising drug just there. And then again, constant amount of drug, zero-order elimination, constant percent of drug-illuminated per unit of time. That's first order elimination. Now, the thing is Fanny Toen. We can actually build, because it has zero-order elimination, it can build up in the bloodstream pretty quickly, and then you can get a lot of toxicity.

So you generally need to watch how you give a patient Fanny Toen. Now, one other high yield thing you need to know about Fanny Toen is that it depletes Fulit. So the thing is, in general, if Fulit wants to be absorbed in the GI tract, it needs to be married. Let's put it that way. It needs to be married to another amino acid to be absorbed. And the enzyme that makes that reaction happen is an enzyme known as conjugates. Okay, conjugates usually tags Fulit with an amino acid so that it can be absorbed in the GI tract. However, the thing is Fanny Toen actually inhibits conjugates. So when you inhibit conjugates with Fanny Toen, Fulit can no longer be reabsorbed, and then a megaloglastic anemia ensues. So, the key thing you want to remember there, though, is that if a patient has a Fulit deficiency, right, they will have increased levels of homocysteine. I believe I've talked about that homocysteine pathway if I have not. I'll try to talk about it in a different podcast. But basically, if a patient has a Fulit deficiency, don't forget that their levels of homocysteine will be high. But they do not have increased levels of methylmalonic acid. Contrast out a B12 deficiency where the homocysteine levels are increased because B12 is a cofactor for homocysteine methyl transferase, also known as methionin synthase. But in addition, you also have increased levels of methylmalonic acid because methylmalonic, methylmalonoque mutase uses vitamin B12 as a cofactor.

That's the second higher-year-old reaction that's done by vitamin B12. Now, what a higher-year-old phenetone is, it can cause a gingivol hyperplegia. Unfortunately, this is just a side effect you have to memorize. So, this is caused by phenetone, but it can also be caused by your calcium channel blockers and cyclosporin. And then, two other things with phenetone is, it can cause fetal hide and toeing syndrome. See how hide and toeing rhymes with phenetone. So, fetal hide and toeing syndrome classically presents as like spina bifida in a kid. Remember, if you have a fully deficiency, which is something that phenetone can cause, you can begin to have neuro tube defects like a spina bifida. So, spina bifida clef lip small head, so like microcephaly or like hypoplisio of the nails and cardiac problems. That's the cluster of findings you see with fetal hide and toeing syndrome. And then, phenetone and actually also cause hersotism. So, that's just something else you want to keep in mind. Now, let's talk about carbamazepine. So, carbamazepine is the next seizure I'll talk about. It also blocks sodium channels. The big thing you want to know about carbamazepine is that it's used to treat trigeminal neurasia. Another classic name for this is tigdolurus. So, basically, the way trigeminal neurasia shows up on the example is when a patient has like repetitive unilateral, like shooting pain in the distribution of cranial nerve 5. That's why it's called a trigeminal neurasia.

The first line of medication for this is carbamazepine, although you can do like some fancy kind of neurosurgery with that. Now, what are the side effects of carbamazepine you want to know? carbamazepine can cause a granuloseitis, just like the anti thyroid medications, PT and methamizole. It can also cause an SIDH, so the syndrome of inappropriate ADH secretion. If you have SIDH, you'll be absorbing more water at the level of the principal cell of the collecting duct. Because the ADH will act on visual pressing V2 receptors, so that aquaporin 2 receptors are inserted on the urine side of the principal cell and you begin to absorb water. So, obviously, if you're absorbing a total water, your serum or smolality would decrease. However, your urine or smolality would increase as well. If your urine is getting more concentrated, you should sort of be able to reason out that the urine-specific gravity also goes up as well. The classically show like, oh, SIDH has an arrow-like question on exam. So, those are some things you want to keep in mind. So, again, the ADH will act on the visual pressing V2 receptors on the blood side of principal cells. Remember, these V2 receptors are GS-copote. We've talked about these already. Contrast with the visual pressing V1 receptors that are GQ-copote. And, again, you cause the absorption of water because you're inserting aquaporin channels on the urine side of the principal cells in the collecting duct.

And then, the last high-o thing you need to know about carbon mesoping is that it actually induces cytochrome P450. So, again, don't forget the pneumonia. We've talked about this already. That Guinness, coronas, and PB Rs, the S is important there, induced chronic alcoholism. So, the G stands for Grecio-phobia. Remember, that's an antifongal that accumulates in keratin-rich tissue. The C is for carbon mesoping. The P is for phenetone. The B is for babbiturids. The R is for rifampine. Remember, that's used for TB. And then, the S is for St. John's Wart. That's a Habar supplement. That's classically used to treat depression. Remember, it's a serotonergic agent so you can actually trigger a serotonin syndrome. And then, the chronic alcoholism. That's just to tell you that chronic alcoholism can actually induce cytochrome P450. But, acute alcoholism does not. Acute alcoholism actually inhibits cytochrome P450. So, again, if your person takes a serotonin syndrome before 15-duser, it makes OCP less effective. Because OC Ps are substrates for the cytochrome P450 enzymes. Now, the next anti-seizure made I'll talk about is our pre-casset. The mechanism of acutero here is that it basically blocks T-type calcium channels. That's essentially the mechanism of acutero-soxamide as well. So, again, don't forget, it's not L-type calcium channels. It's T-type calcium channels. They want you to know that T-type on the exams.

And then, this drug also blocks sodium channels, so kind of like the wifin and it too, it works. And then, the final way it works is that it blocks an enzyme known as GABA Transamine. GABA Transamine is an enzyme that breaks down GABA. So, if you inhibit GABA Transamine, your levels of GABA increase. And if those levels of GABA increase, that's good for seizures. Because GABA is an inhibitor in your transmitter. So, it sort of comes down neurons if you may. Now, just another high-youth in a one-manager here though is that if you want to make GABA, right, you make it from glutamate. And the enzyme that does that is glutamate decarboxylase. And glutamate decarboxylase requires vitamin B6 as a cofactor. So, if a patient is taking isoniasid, for example, and the vitamin B6 is depleted, you have a net increasing glutamate and a net decreasing GABA. Because that glutamate decarboxylase doesn't work as well anymore. That's how isoniasid potentially causes seizures. Now, the next role I'll talk about is if those oxamides. The big mechanism of actually you won't remember is again, it blocks the thalamic T-type calcium channels. The big thing you want to know about if those oxamides are relatively clean drug is used to treat up sun seizures. So, again, if they give you a question about a kid less than 20 years old, they do not make this an adult question on NV Me's. They make it a pediatric question, because kids usually outgrow the seizure.

And they tell you that you see like a three herds or three per second spike and slow if pattern on EEG, again, think about absons seizures. Now, West Syndrome I've talked about this. It's basically a very severe epilepsy syndrome that's essentially composed of a triad, if you may. So, these kids tend to have an intellectual disability. They call it infantile spasms. That's the second part of the triad. And again, on EEG, you see a very chaotic pattern. If you look this up, you see why I'm just saying it's a chaotic pattern. But it's classically the buzzword you want to remember is a hypsin rhythmia. And then, vi-gaba-tree. Notice it has gab-a in the name. It's also an inhibitor of gab-a-transaminis. It's an irreversible inhibitor. So, the gab-a builds up. The reason I mentioned vi-gaba-tree right after West Syndrome is vi-gaba-tree is actually one of the drugs that can be used to treat West Syndrome. But here's the classic treatment for West Syndrome on exams, ACTH. The first line medication for the treatment of infantile spasms or West Syndrome on exams is ACTH. It doesn't make any sense, but they love to test it on NVM Es, so you definitely want to keep that in mind. You want to give ACTH. If ACTH is not an answer choice, then you can either choose steroids or vi-gaba-tree. Now, the next seizure drug I'll talk about is Lamotri-gene. Lamotri-gene, the big thing you want to know is it increases the risk of stiv-on-s-johns-in syndrome.

I won't worry about the mechanism of acutron of Lamotri-gene. Remember, stiv-on-johns-in syndrome is actually a pretty classic side-effect of most anti-epileptic drugs. Okay, but classic leads us to see that Lamotri-gene or carbamazepine or phenetolino-ythosoxamide. And then, to pyramid is the next seizure drug I'll talk about. The mechanism of acutron is essentially blocks our amper receptors. Remember, ampah is a kind of NMD receptor. NMD receptors are responsive to glutamate. Okay, so if you block glutamate-sensitive receptor, you have a reduction in excitatory activity in neurons. To pyramid also increases GABER action that's super low yield. It also blocks sodium channels, but again, that's also super low yield. The big thing I'll know is that it blocks amper receptors. Okay, so it decreases a neuron's responsivity to glutamate. Now, don't forget that ampah receptors. There are also some other receptors known as like kinetics receptors, like KAI and ATE. Okay, those play a role in a process known as a long-term potentiation. I'll probably describe that in a later podcast, but just remember that was word, long-term potentiation. Okay, and don't forget, right? While we're talking about things that block receptors that are responsive to glutamate. Remember, NMD receptors are one of those glutamate-responsive receptors. And we already talked about a couple of drugs that can be blocked by a couple of drugs that block those NMD receptors.

We already talked about Rai-Luzon that's used for new Gary's disease, right? So that's ALS or Mimantin, okay, for Alzheimer's, right? We've also talked about the Extramethorophane. I'll probably mention it in the Pomunary Pharmacology Podcast. And then, ketamine, right? It's a dissociative anesthetic. I'll probably discuss that in the next podcast. Those all work by blocking NMD receptors. Now, to pyramid, the big things you want to know is an actually increased risk of kidney stones, okay? And it can actually cause a mental slowing. There are some actually important clinical uses of to pyramid. So you can use it as a seizure control med, although that's really done. But another thing you can use to... Actually, that's not really done. It's actually done quite frequently. Sorry, I take that back. It can actually be used for weight loss, okay? So, a person has seizures and neurobeasts, right? To pyramid will be a great drug for them, okay? And it can actually be used as a chronic medication for the prevention of migrates, okay? Now, the last few drugs I'll probably talk about here before I quickly talk about the insomnia drugs are the benzoes, okay? And babiturids, okay? And I guess I can just throw in baclofen here for a good measure. So these drugs essentially all work on gabar receptors, okay? Remember, the gabar receptor is a chloride channel, okay? And chloride, it's primarily an extracellular ion.

So, when it flows into the cells down a chloride channel, it hyperpolarizes the cell and the cell does not fire. So, babiturids and benzoes, they work on gabar e-receptors, okay? And the big numaniq, you want to remember here, you've probably seen it in some step one study resource that ben likes to have it more frequently, but barb likes it to last longer, okay? So, benzoes, they increase the frequency of opening of chloride channels, but babiturids increase the duration, or you can install same babiturids, you can see babiturids, okay? Babiturids increase the duration of chloride channel opening, okay? Contrast that with baclofen, that actually works on gabar e-receptors, okay? So, remember the being baclofen for the being gabar bee, okay? Boyo benzoes and babiturids both work on gabar e-receptors. So, benzoes and babiturids, remember they can cause a severe respiratory depression, okay? And they actually have a pretty increased risk of dependence or addiction. That's why these drugs are not prescribed like willingly for like chronic management of stuff, okay? And actually, I want to compare and contrast something here, right? So, remember opioids are addictive, and they can also cause respiratory depression, but on an exam question, they will give you that the person has pinpoint opioids, okay? So, they have pupillary meiosis.

If a patient has like opioid intoxication, contrast that with benzoes and babiturids, they can cause respiratory depression, but the pupillary findings will be normal, okay? That's a classic way to differentiate those on exams. And the thing is, if a patient has like respiratory depression from a babiturid, is there anything you can do? Well, you can into be them and call your friendly anesthesiologist, but really there's no reversal agent for babiturid overdose. However, for benzo, you can actually reverse that with flomazineal, okay? Flomazineal is a competitive inhibitor that can displease benzoes from the the surface of the GABA receptor, the GABA-E receptor, okay? Now, let me end this by talking about some high-yield integrations. I also talk about baclofen for a short while. Well, let me talk about in some new drugs, okay? They're essentially all GABA receptor agonists, okay? You use them to treat insomnia, okay? And they're the Z drugs, okay? Like Zopidem, Zalaplan, and Zobiclo, okay? You can actually reverse these drugs with flomazineal. That's another pretty classic, but unusual example question. Now, one of the drugs that can be used for insomnia, right? So, let me, let's think about this disorder, narcolepsy, right? Narcolepsy is a classic condition where person feels sleepy during the day. So, think of narcolepsy as an excessive sleep disorder, right?

If you think back to this, in narcolepsy, patients tend to have a deficiency of something known as hypocritin or also known as orexin in their CSF, okay? So, they have low levels of orexin, also called hypocritin in the CSF. So, just put this chemical equation in your mind, that low levels of hypocritin or low levels of orexin can... So, put this equation in your mind that low levels of orexin, also called hypocritin, associated with excessive sleep, okay? So, what would you potentially want to do to orexin receptors if we were trying to treat insomnia? Well, hopefully, you are thinking that you want to block those things, because by blocking those things, you essentially induce, like, a narcoleptic state if you may, and you can cause the person to sleep really well, okay? So, that's how a drug known as orexin works. Orexin is an orexin receptor antagonist that's used for the treatment of insomnia. It's a relatively new drug, but it could shop on step one. Now, some other high-yield integrations here, right? So, let's assume you get an exam question about a patient that takes like a bit of it, and then they begin to have like skin problems and neurologic deficits, and they have like abdominal pain, and they have like vision problems, right? So, what are you thinking about here? I'll give you some time to think. Okay, well, I hope you're thinking about a AIP, acute intermithent pophyria, okay? The thing is, barbitra is contriger this, right?

So, those hym synthesis pathway problems are very high-o for step one and for step two, and I only imagine also for step three, okay? So, remember, in AIP, right, there is a deficiency of pophyobelinojin diaminase. I think about it as a peanut butter and jelly diaminase, like PBG diaminase. But basically, right? So, pophyobelinojin diaminase deficiency, basically you have a build-up of hym synthesis pathway intermediates, and those are bad for the skin, and in addition, they can cause neuro deficits, because those intermediates can deposit in the brain, although those neuro deficits are generally reversible. Barbitra is, again, a generally contraindicated in a patient that has any hym synthesis pathway defect, all right? Like AIP with PBG diaminase, or if a patient has like a pophyracutinia tarda, which I believe is a uro pophyrynojin, decarboxylase, or urod deficiency, okay? So, again, if you give up a bit of it, barbitra is induced the enzymes in the hym synthesis pathway, so you have increased flux through the pathway. Remember, you have like this build-up, right? So, it's just like saying that, oh, there is a road blockade, you're supposed to be removing cars from that road, so that you don't have like really bad traffic. But when you give up a bit rate, you are like sending more cars down that pathway, okay?

So, you have like a very, very bad traffic, and cars are beginning to build up behind that road blockade, and the road block, I guess, in this case, is the urod on the PBG diaminase deficiency, okay? So, barbitra is induced flux through the pathway, so you have an increase in those bad substrates that can then cause the skin and neuro problems and all the issues you get with hym synthesis pathway defects, okay? And in general, for these diseases, like AIP or pophyrynojinia tarda, you want to give him and glucose, okay? Because remember, those can inhibit the reclimitin enzyme of hym synthesis alas, eally synthase, okay? Remember, eally synthase uses vitamin B6 as a cofactor. That's one way that isonias it can cause a cyderoblastic anemia, right? Because by depleting B6, eally synthase doesn't work, okay? So, you have no ability to synthesize protoprofrate. Okay, now, another high-ealth and I want to talk about here is a regular heart syndrome, okay? Basically, this is a deficiency of UDPGT, okay? UDP glucoronocytransferase, it's the enzyme that converts indirect to direct bilirubin, okay? So, for patient has a heart syndrome, they have an indirect type of bilirubinemia, okay? So, the thing is, there are two types of cricklinal heart syndrome, there's a type one where you have like absolutely no UDPGT activity, that's fatal, kids are usually not born with that. And then there's a type two where they have less than, let's say like 10% activity, okay?

And basically, the way you treat that, or even confirm that diagnosis, is to give a bit of it. Okay, a bit of it again, the endocytocromp 450 enzyme, remember the B in that GNS coronas and PB Rs, no more an extensive of a bit of it. Okay, so you give a bit of it, the increase the endogenous activity of those UDPGT enzymes, okay? And that can be as a diagnostic test and as a treatment for cricklinal heart type two, because by giving barbitaries, you induce a grant P450 and enzymes of which UDPGT is one of them, okay? And that basically like increases the amount of those enzymes, or increases the activity, okay? And that can lower the indirect bilirubin levels in cricklinal heart syndrome type two, okay? So, because I've talked about barbitaries, I just decided to introduce this here, okay? And another quick thing here is if a patient has liver disease, okay? The only benzoes you can give them, benzoes you can remember the mnemonic lot, okay? So like lorazapam, oxazapam and temazapam. The reasoning here is that these benzoes is not that they are not metabolized by the liver, they are metabolized by the liver, okay? But they are metabolized by glucoronidation, which is a relatively minor pathway in the liver, if you may. Or let's think of it as a pathway that still exists when the liver is on its last legs. And then don't forget a clodarezapoxide, that's another benzo. If you've worked in the hospital for any period of time, you've probably heard of a lebrem.

A lebrem is clodarezapoxide, it's a long-dactin benzo, it's classically used for alcohol withdrawal. Okay, remember that if a patient withdraws from alcohol or benzoes or barbs, that withdrawal is actually fetal. Most of the withdrawal syndromes, the suck, boy, and they are not fetal. Well, these three benzoes, barbs, and alcohol, the withdrawal can be fetal. And then back to the thing, I already mentioned this already, it's a GABA B receptor agonist. It's used in like cerebral palsy, because it can relieve increased the muscle tone. And again, don't forget that it's a GABA B receptor agonist versus your benzoes and your barbs that are GABA A receptor agonist. So hopefully you've taken a lot from this seizure podcast. I will continue with neuropharmacology in our next podcast. I wish you a wonderful day ahead, and I guess it's time for me to be on service. Have a wonderful day, and God bless. Thank you.

Infantile spasms (seizures), intellectual disability, and characteristic findings like hypo-pigmented macules or abdominal/cardiac masses.

Barbiturates (e.g., phenobarbital). Phenytoin increases frequency; barbiturates increase duration.

It blocks T-type calcium channels, making it highly effective for absence seizures.

Elevated methylmalonic acid (MMA) and elevated homocysteine.

ACTH (Corticotropin). If ACTH is unavailable, steroids or vigabatrin are alternatives.

Carbamazepine.

3 Hz spike and slow wave complexes.

Phenytoin, Carbamazepine, Phenobarbital (The "GCPBRS" mnemonic helps recall these, plus Rifampin/St. John's Wort).

Phenytoin increases the frequency of chloride channel opening; Barbiturates increase the duration of chloride channel opening.

Barbiturates, because they induce heme synthesis enzymes and worsen the porphyric crisis.

Gingivolhyperplasia (gum overgrowth).

Topiramate.

3 Hz spike and slow wave complexes.

Phenytoin, Carbamazepine, Phenobarbital (The "GCPBRS" mnemonic helps recall these, plus Rifampin/St. John's Wort).

Phenytoin increases the frequency of chloride channel opening; Barbiturates increase the duration of chloride channel opening.

Barbiturates, because they induce heme synthesis enzymes and worsen the porphyric crisis.

Gingivolhyperplasia (gum overgrowth).

Topiramate.