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Epilepsy Drugs I by Mind Map: Epilepsy Drugs I
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Epilepsy Drugs I

Epilepsy in General


Partial (focal), Simple partial, Consciousness: preserved, EEG: localized spikes, Sx: Motor and sensory disturbance related to specific cortical area affected, Complex partial, Consciousness: disturbed, They just kinda check out for a while, EEG: focal spike originating in temporal lobe, Sx: confused behavior, automatisms, sensory/emotional distortions, Partial seizures secondarily generalized, Consciousness: lost, Origin: spread of epileptic activity from focal to both hemispheres, Sx: motor pattern similar to "generalized seizures, Commonly will start as a partial seizure w/ an aura or something

Generalized, Usually from a metabolic or idiopathic cause, Nonconvulsive type, Absence (Petit Mal), Consciousness: brief, abrupt loss, EEG: generalized 3/sec spike and wave, Sx: W/ or w/o clonic motor activity, Atypical absense, Similar to Petit mal, but w/ more motor activity, Convulsive type, Tonic-clonic (Grand Mal), Consciousness: lost, EEG: high voltage EEG spikes, followed by prolonged depression of activity, Sx: tonic contraction w/ clonic jerking, then prolonged postictal depression of CNS activity, Tonic, clonic, myoclonic (sudden, forceful contraction), atonic, Infantile spams ("jack knife" convulsion), can progress to Lenox-Gastou Syndrome, Status epilepticus, Can be fatal d/t prolonged anoxia

Can be either primary or secondary

M&M d/t anoxia during seizures

Also danger of excitotoxicity (repeated seizures lower the threshold)

General drug MOA

Antiepileptic drugs work by 3 mechanisms

Limiting firing of neurons by slowing rate of recovery in Na channels

Enhancing GABA-mediated synaptic inhibition, Note: GABA is the primary inhibitory NT in the brain

Limit activation of Ca++ channels, Slows synaptic transmission

Phenytoin (Dilantin)

Prevents seizures w/o producing general CNS depression


Reduces rate at which Na channels recover from inactivation, slows firing


All seizure types except absence

Tonic-clonic in adults and older children

Used in status epilepticus

Wound healing


Slow, variable oral absorption (3-12 hr to peak)

90% plasma protein bound, Therefore small changes in % free drug -> large changes in effective drug

98% metabolized by liver NZ, Metabolism can be saturated (loses linear increase), 1st order at sub-Tx doses, zero-order elimination at Tx doses

t1/2 = 6-24 hrs

Induces a lot of hepatic drug-metabolizing NZs, CYP3A4, along w/ several others, This is a big deal!


Acute toxicity after rapid IV admin, CV collapse, CNS depression, Use soluble prodrug fosphenytoin to decrease this effect, Don't use phenytoin for a fast effect

Acute tox after oral admin, ataxia, nystagmus, drowsiness, diplopia

Chronic tox, Epilepsy is a life-long Dz, Behavioral changes, gingival changes, peripheral neuropathy, hirsutism, GI disturbances and malabsorption, Osteomalacia d/t decreased Vit D, Also drug interferes w/ incorporation of Ca into bone, Decreased Vit B12 -> megaloblastic anemia, Depression of serum folate and Vit K levels

Drug allergies

Fetal hydantoin syndroms (Category D)

Avoid sudden withdrawal, Causes rapid increase in neuronal activity -> seizures (esp. status epilepticus)

DD interaxns

Drugs that inhibit metabolism, Chloramphenical, dicumerol, cimetidine, sulfonamides

Drugs that enhance metab, carbamazepine, decrease plasma levels

Phenobarbital and ethanol, Acutely: inhibit metab, Increase plasma levels, Chroincally: stimulate metab, Decrease plasma levels

Dicumerol, salicylates, BZDs, Displace phenytoin from binding sites, Rapid increase in plasma levels!

Phenytoin decreases effectiveness of OC!



Potentiates GABA inhibitory transmission, Both of these elevate seizure threshold and limit spread

Decreases glutamate excitation


Alternative to phenytoin, Stronger SE than DOC


Oral absorption slow, but complete

40-60% protein bound

Chronic use may induce hepatic NZ, but much less so than phenytoin


Sedation, ataxin, skin rash, megaloblastic anemia

Decreased cognitive ability, hyperactivity (kids), confusion (elderly), Most SE worse in young and old pts

acute intermittent porphyria

Causes tolerance and dependence, Sudden withdrawal -> status ep.

Potentailly teratogenic

DD interaxns

Variable results when in combo w/ phenytoin

Decreases plasma level of anticoagulants

Additive effect w/ CNS depressants



Structurally similar to phenobarbital, similar pharmacology, but less potent


Alternative Tx

Useful in Tx of myoclonic seizures in young children


Metabolized to phenobarbital and PEMA


similar to PBB

Greater incidence of drowsiness, dizziness, megaloblastic anemia

Pregnancy Cat. D



Structurally similar to tricyclic antidepressants

Slows recovery of Na channels, Like phenytoin


Tonic-clonic and partial seizures

Neuropathic pain

bipolar disorder


rapid oral absorp

70% protein bound

t1/2 = 13-17 hrs, Available in extended release forms, Carbatrol, tegretol-XR


Diplopia, blurred vision, drowsiness, dizziness, NV, ataxia, liver tox, wt gain

Blood dyscracias, Aplastic anemai, agranulocytosis

Skin rxns, Steven-Johnson Syndrome

Hypersensitivity rxns in Asians w/ HLA-B1502, Do genetic testing on Asian pts prior to starting Tx


Metab increased by phenytoin and phenobarbital

It increases metab of phenytoin, primidone, valproic acid


New drug same as carbamazepine, w/ fewer skin rxns and hematologic toxicity



Absence seizure


Decreases conductance in Ca channels in T current, Increases neuronal refractory peroid, T currents important in generation of absence seizures


long 1/2 life


NV and drowsiness - both dose-related

Parkinsonism, blood dyscrasias, utricaria, S-J syndrome


Metab delayed by valproic acid

Valproic Acid


absence and complex partial seizures

Maybe also grand mal, myoclonic, and febrile seizures

If pt doesn't respond to any drug, use this one


Block recovery of Na channels

Uses K channels to hyperpolarize

Some action on GABA-mediated inhibition, Wide variety of mechanisms -> why it works on so many diff kinds of seizure


Rapid and complete absorption, Slower w/ enteric coated prep (Depakote)

80-95% protein bound - high!

Inhibits CYP2C9

Oral or IV form


Low degree of tox

GI, sedation, ataxia, wt gain, prolonged bleeding, alopecia

Rare: pancreatitis in kids

Rare: hepatotox, Most common in kids < 2 yo or those on multiple drugs, Risk greatest early in 1st 4 months of Tx


It displaces phenytoin from protein binding sites

Inhibits metab of PBB, carbamazepine, phenytoin, ethosuximide



IV used for status ep.

Can -> CV & resp depression


status ep.


akinetic, myoclonic, & absence

Unusual seizures


Adjunct Tx for CPS


Relatively safe, but transient effect d/t quick tolerance, Rarely used for chronic Tx

New node


Suppresses seizure spread in the cortex, thalamus, and limbic structures

Facilitates GABA-mediated pre- and post-synaptic inhibition


IV diazepam, CV & resp depression

Clonazepam, Drowsiness, ataxia, paradoxical agression behavior, hyperkinesia, Most likely in kids and pts that are very emotionally controlled (the drug lowers inhibitions!)

Abrupt withdrawal -> Status ep.


Potentiates CNS depressant effects of antipyschotics, TC antidepressants, sedative hypnotics, and alcohol