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Like antidepressants anticonvulsants (ACs), or antiepileptic drugs (AEDs) - the terms are nearly interchangeable1 - are broken up into different classes based upon things like how your liver deals with them, chemical structure, and even how they work in your brain. Unlike antidepressants there is overlapping membership, classes that consist of a single drug, or a drug and subsequent drugs derived from it, and existing anticonvulsants will be added or removed from categories as the understanding of their pharmacodynamics and/or pharmacokinetics improved. Thus the taxonomy of AEDs is as complex and fungible as that of mushrooms.
The primary classifications of anticonvulsants are if they are benzodiazepines or non-benzodiazepine anticonvulsants. While some are used as AEDs, most benzos are prescribed only for anxiety and other conditions these days, so they get their own pages. Some, like Xanax (alprazolam), are not even approved by the FDA to treat epilepsy or any kind of seizure disorder. Unless otherwise specified the terms “antiepileptic drug” and “anticonvulsant” will refer to non-benzodiazepine anticonvulsants.
The next classifications are based on pharmacokinetics.
1. Enzyme-inducing AEDs
The first is which AEDs induce CYP450 and/or UGT enzymes. Enzyme-inducing AEDs (EIAEDs) can have numerous drug-drug interactions, as well as deplete your body of vitamin D3. EIAEDs include:
- Tegretol (carbamazapine)
- Dilantin (phenytoin)
- phenobarbital
- primidone
- Trileptal (oxacarbazepine)
- Topamax (topiramate)
- Sabril (vigabatrin)
Most of the time EIAEDs refers only to Tegretol, Dilantin, and phenobarbital, because:
- primidone is converted to phenobarbital.
- Trileptal’s induction of UGT enzymes is only moderate and it doesn’t do much in the way of CYP3A4/5 induction like Tegretol does.
- Topamax induces some enzymes, but only at higher dosages.
- Lamictal barely induces UGT enzymes, so it rarely makes a difference.
- Why Sabril speeds up the clearance of some meds hasn’t been identified. Enzyme induction is assumed.
- Anything else that may induce CYP or UGT enzymes is so rarely prescribed these days that any doctor who prescribes it had better know everything there is about that med.
Lots of other medications, both crazy and non-crazy meds, induce CYP450 and UGT enzymes. AEDs are singled out because epileptics have been given more than one med to control their seizures for over 150 years;2 so neurologists as a group are more aware of drug-drug interactions and how the slightest change in dosage can affect their patients’ symptoms than most other doctors.
2. Enzyme-inhibiting AEDs
Some doctors, researchers, et al. lump remaining AEDs into a category called non-EIAED, but the true flipside of enzyme induction is enzyme inhibition or suppression. There is only one group of commonly-prescribed AEDs that inhibits UGT (or any) enzymes involved in the metabolism of any medications to any meaningful extent, and that’s the valproates:
- Depakote (divalproex sodium)
- Depakene? (valproic acid)
- Depacon? (valproate sodium or sodium valproate)
3. Aromatic Anticonvulsants
The next group is the aromatic anticonvulsants. These meds don’t help you smell purty. Aromatic refers to aromatic hydroxylation, which is part of the process when these drugs are metabolized. With a very small percentage of people (somewhere between 1 in 1,500 to 1 in 10,000) the metabolism isn’t done correctly and a toxic substance (arene oxides) is left over instead of getting cleaned up. The leftover triggers anticonvulsant hypersensitivity syndrome, and that sucks donkey dong. Anticonvulsants with a particular chemical structure (similar to TCAs, and TCAs may trigger a similar reaction) are going to be converted into the problem toxin, but there’s no way (yet) of telling if someone won’t be able to properly metabolize the toxin once it is created. While the odds are a bad reaction of one of these drugs means a bad reaction to one or more, if not all of the others, someone may have a problem with just one of them.3 Or there may be one of them they can take.
- Lamictal (lamotrigine)
- Trileptal (oxcarbazepine)
- Zonegran (zonisamide)
- Tegretol (carbamazepine)
- Dilantin (phenytoin)
- phenobarbital (the data are mixed regarding primidone)
- Felbatol (felbamate)
Stevens-Johnson Syndrome (SJS), a.k.a. The Lamictal Rash, is thought to be a component of anticonvulsant hypersensitivity syndrome. So if you got SJS, or any rash scary enough that you and/or your doctor thought it best to discontinue one or more of the above meds, the odds are you’ll get a rash from one or more of the others.
4. All other AED classes
Finally we come to classifications of AEDs that are chemically related and/or work in similar ways. There may be only one drug per class because it is unique, or it is the only still on the market, or that ever made it to the market in the first place.
The classes Carbonic Anhydrase Inhibitors (CAI) and GABA Reuptake Inhibitors contain drugs that do only that, otherwise most AEDs would be classified as a GABA reuptake inhibitor, and Topamax and Zonegran would also be CAIs.
Barbiturates
- mephobarbital
- Nembutal (pentobarbital sodium)
- phenobarbital
Bromides
- potassium bromide
Carbamates
- Felbatol (felbamate)
Carbonic Anhydrase Inhibitors (CAIs)
- Diamox (acetazolamide)
- sultiame
Dibenzapine derivities (carboxamides)
Fatty acid derivities
- valproates:
- Gabatril (tiagabine)
- Gabrene (progabide)
- Sabril (vigabatrin)
GABA analogues
- Gabrene (progabide)
- Sabril (vigabatrin)
- Neurontin (gabapentin) and Lyrica (pregablain) were once considered GABA analogues.
GABA reuptake inhibitors
- Gabatril (tiagabine)
- Neurontin (gabapentin)
- Lyrica (pregablain) - although not everyone agrees on just how Neurontin and Lyrica work…
alpha 2 delta ligands
- Neurontin (gabapentin) - because they’re also categorized as this
- Lyrica (pregablain)
Hydantoins
- Peganone (ethotoin)
- Mesantoin (fosphentyoin)
- Dilantin (phenytoin)
Oxazolidinediones
- trimethadione
Phenyltriazines / Triazines
- Lamictal (lamotrigine)
Pyrrolidines
- Keppra (levetiracetam)
- Keppra derivatives (e.g. brivaracetam) that UCB is working on.
Succinimides
- ethosuximide
- methsuximide
- phensuximide
Sulfamate-substituted monosaccharides / Fructose derivatives
- Topamax (topiramate)
Sulfonamides
- Diamox (acetazolamide)
- sulthiame
- Zonegran (zonisamide)
5. AED equivalences
Given how there are so few AEDs in each class it’s little wonder few of them work the same way. Many people ask about AEDs/ACs that are equivalent, the way SSRIs are. Very few AEDs are:
- The valproates are essentially interchangeable, there are some dosage adjustments required, as well as getting used to different side effects.
- Trileptal is a derivative of Tegretol. They aren’t exactly alike, but they are close enough that switching from one to the other can be done without titration if absolutely necessary. 300mg of Trileptal (oxcarbazepine) = 200mg of Tegretol (carbamazepine USP). The US PI sheets (Trileptal’s prescribing information Tegretol’s prescribing information) are full of information about switching between the two.
- Lyrica isn’t derived from Neurontin, but they probably mechanisms of action, whatever they may be, that are similar.
- Diamox and sultiame
- Zonegran and Topamax have a vaguely similar chemical structure and a very similar mechanism of action.
1 Because some benzodiazepines aren't approved, and rarely, if ever prescribed off-label to treat epilepsy, not all anticonvulsants are AEDs. Similarly not all AEDs are in the anticonvulsant class of drugs, but only because they are being prescribed off-label. E.g. progesterone-based birth control.
2 Most modern AEDs are approved by the FDA to be used only with other AEDs. Topamax was the first AED in a long time to receive FDA approval to be used all by itself (monotherapy) to treat both partial and generalized seizures.
Potassium bromide is still in use after 150 years, although it is the final straw you'd ever want to grasp at. Phenobarbital is over 100 years old and may be in front of some newer meds to try if you're running out of options.
3 Cross-sensitivity, or in English, having the same sort of bad reaction to a similar substance, runs in the neighborhood of 40 to 80% when it comes to people who took one aromatic AC and had the same bad reaction to another one.
Page created by: Jerod Poore. Date created: 21 November 2010 Last edited by:
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