Class: Sodium-channel inhibitors

MAE: slows rate of channel recovery from inactivated to closed state

PharmKin: highly protein bound (90-95%), 7-24 hr half-life

A/E:CNS depression, n/v/c gingival hyperplasia, acne SJS alteration of vit d metab (osteopor)

Receptor: channels opened and closed high freq.

Therapeutic range:10-20 mcg/ free level 1-2 mcg

Metabolism: inducer of CYP3A4 1a2, 2c9/19, zero order kinetics

Class: Sodium-channel Inhibitor

MAE: same as dilantin, autoinducer (induces own metabolism and others metabolized b cyp3a4,1a2,2c9/19) 

A/E: CNS depression, hypnatremia, cholestatic jaundice, rash, leucopenia, aplastric anemia

C/I: causes low levels of cyp3a4 etc

Therapeutic: 6-12

Metabolized: Hepatic to active metabolite, first order kinetics

derivitive of carbamazepine with less interactions and A/E

Class: sodium-channel inhibitor

AE: Can cause benign/serious rash

Dosing: titrate up slowly

metabolized: liver

Class: Ca Channel inhibitors

MAE: not substantially protein bound

Dosing: Long-half life

A/E: GI CNS

Class: Ca channel inhibitor 

MAE: also slows rate of na+ channel recovery after inactivation and increases GABA, 80-90% protein bound

Metabolized: hepatically

A/E: CNS depression, tremor, GI upset, LFT elevation, thrombocytopenia, alopecia

Therapeutic levels: 50-120 mcg/ml

Class: Ca channel inhibitors

MAE: also enhances Gaba-mediated inhibition

Metabolized: RENALLY

A/E: CNS depression, weight gain

PK: negligible protein binding

Dosing: up to 3600 mg divided, short half-life needs multiple dosing

C/I: renal dysfunction

Enhancement of GABA-mediated inhibition

Used for acute treatment, or as needed

Class: Glutamate receptor inhibitor

MAE: also enhances Gaba transmission and limits Na+ firing

A/E: BLACK BOX WARNING acute hepatic failure and aplastic anemia

PK: 22-25% protein bound

Metabolism: RENAL (eliminated 50% as inactive metabl, 50% unchanged)

Receptors: inducer cyp3a4, inhibitor cyp2c19

MAE: inhibits GABA reuptake

PK: 96% protein bound

A/E: mild CNS Depression

MAE: blocks Na+ cahnnels, enhances Gaba NT, increases Gaba concentrations, inhibits gluatamate receptors

PK: minimal protein binding

A/E: mod- severe CNS depression, kidney stone, glaucoma, GI

MAE: unknown

Interactions: VERY FEW

Metabolized: RENALLY 66%

AE: mild cns, irritability

MAE: blocks Na+ and t-type Ca2+ channels

Metabolized: 60% hepatic

A/e: mild to mod CNS depression, kidney stone, SULFONAMID (**watch with sulfa allergy)

all seizure types-

felbamate, lamotrigine, keppra, rufinamid, topiramate, valproate, zonisamide

Simple, partial, complex partial, and secondarily generalized sz

Carbamazepine, neurontin, lacosamide, ox arbazeping, phenobarb, phenytoin, pregabalin, primidone, tiagabine, vigabatrn