Levitiracetam has been shown to have a unique intracellular binding site, a synaptic vesicle protein (SV2A), the affinity
of binding to which appears to be correlated with the drug’s anticonvulsant potency. Binding to SV2A affects neurotransmission
via interactions between synaptotagmin and calcium ions, but the precise biochemical pathways remain undetermined.
Levitiracetam is an attractive anticonvulsant option due to its lack of side effects and favorable pharmacokinetic profile
(e.g., no hepatic metabolism, 100 percent oral bioavailability, no drug-drug interactions). There is limited published information
regarding its efficacy as an add-on anticonvulsant in dogs, but so far it is favorable. The dose usually used is 20 mg/kg
orally every eight hours. A lower-cost, generic form of oral levitiracetam is available.
Zonisamide has proven to be an effective add-on anticonvulsant drug in dogs, with few side effects. There are multiple proposed
mechanisms of action for zonisamide, including blockage of T-type calcium and voltage-gated sodium channels in the brain,
facilitating dopaminergic and serotonergic neurotransmission, free-radical scavenging, enhancing GABA activity and decreasing
Dogs concurrently receiving pheno-
barbital therapy tend to require a higher zonisamide dose (10 mg/kg, q 12 hours) than dogs not receiving phenobarbital (5
mg/kg, q 12 hours). The BID dosing schedule for zonisamide is an advantage over the other new anti-epileptic drugs for many
dog owners. It is available in the generic form.