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Developed for the treatment of partial and generalized seizure disorders, these second- and third-generation anticonvulsants are finding wider use in the treatment of chronic and neuropathic pain syndromes; mood disorders, including bipolar and generalized anxiety disorders; and migraine headache prophylaxis. Serious adverse effects with the therapeutic use of ezogabine (retinal pigment abnormalities, blue skin discoloration), felbamate (aplastic anemia, hepatic failure) and vigabatrin (permanent visual field deficits) have led to restrictions in their use.

Characteristics of several of these drugs are listed in Table II–7.



Anticonvulsants suppress neuronal excitation by one of four major mechanisms.

  1. Blockade of voltage-gated sodium channels by lamotrigine, topiramate, zonisamide, and felbamate. Lacosamide selectively enhances slow inactivation of these channels.

  2. Blockade of voltage-gated calcium channels by gabapentin, levetiracetam, and zonisamide. Pregabalin binds to the alpha-2 delta subunit of L-type calcium channels.

  3. Inhibition of excitatory amines. Lamotrigine inhibits glutamate release via sodium channel effects on presynaptic membranes. Felbamate is a competitive glutamate antagonist at the N-methyl-D-aspartate (NMDA) receptor. Perampanel is a selective noncompetitive antagonist at postsynaptic amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamate receptors.

  4. Gamma-aminobutyric acid (GABA) enhancement. Tiagabine inhibits GABA transporter GAT-1, preventing reuptake into presynaptic neurons. Vigabatrin inhibits GABA transaminase, blocking GABA metabolism. Gabapentin and pregabalin are GABA analogs that have no known activity at GABA receptors.

  5. Pharmacokinetics (see Tables II–7 and II–66)


with each medication. A 4-year-old boy had a 10-minute tonic–clonic seizure after the ingestion of 52 mg (3 mg/kg) of ...

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