Anticonvulsants Overview

Anticonvulsants: Bromides

• Mechanism of Action (MOA): Uncertain, decreases neuronal discharge and interferes with chloride transport. Sodium and potassium bromide are involved.
• Pharmacokinetics: Long half-life.
• Toxicity: Blindness, coma, dysphoria, stupor, ataxia, and paresis.
• Potassium Bromide: Typically compounded and taken with food. Serum levels must be monitored. Can be used with phenobarbital.
• Disadvantages: Respiratory dysfunction, nausea, vomiting, polyuria, polyphagia, sedation, and ataxia. Narrow therapeutic index.

Anticonvulsants: Dopamine, Phenobarbital, Primidone

• Phenobarbital: An alternative/option when other medications are not well-tolerated. Has multiple metabolites that produce an effect.
• Primidone: Another option with 3 metabolites, which results in an effect.
• Disadvantage: Hepatotoxicity (liver damage) and hepatic necrosis (cell death). Potentially no advantage over phenobarbital; good option if phenobarbital is not well-tolerated.
• Comparison: No clear advantage to using only primidone.

Anticonvulsants: Gabapentin

• Mechanism of Action (MOA): Alpha 2 delta ligands.

Anticonvulsants: Gamma Amino Acid Derivatives

• Glutamate blockers: Given orally. Reduce the release of excitatory neurotransmitter Glutamate, aiding with neuropathic pain and potentially used with phenobarbital or potassium bromide. May induce sedation.

Anticonvulsants: Zonisamide

• Mechanism of Action (MOA): Sodium and calcium channel blocker. Given by mouth (oral).
• Advantages: Alternative for animals reactive to phenobarbital and also can be used in conjunction with it. Minimal side effects. Wide therapeutic margin.
• Disadvantages: Limited understanding of full effects, expensive, and short half-life.