The problem o€ recurrent seizures is a common and challenging one in veterinary medical practice. The pathophysiology and pharmacologic suppression of focal seizure activity have been studied extensively in basic research settings, yet little is known of the genesis, modulation, and termination of generalized seizures, the most common form of seizures noted to occur in companion animals. Knowledge concerning the pharmacokinetic fate of anticonvulsant drugs currently used in veterinary medicine is adequate, though prospective clinical studies of the efficacy of these drugs in the treatment of various types of seizures are lacking. This study will review the available literature regarding the pharmacology, use, and side effects of anticonvulsant drugs currently available for control of recurrent seizures in companion animals. Alternative anticonvulsant drugs will also be described. (Journal of Veterinary Internal Medicine 1990; 4:26-39) Pathophysiology of Seizure Generation SEIZURES are the clinical manifestation of rapid, excessive electrical discharge of neurons in the brain. Seizures may be classified by site of origin as primary (idiopathic, genetic) or secondary (acquired, symptomatic). The term epilepsy refers to recurrent seizures of intracranial origin. How seizure activity is expressed clinically, whether as localized or geneFalized motor or nonmotor (psychic, autonomic) activity, may determine the group of anticonvulsant drugs that would be appropriate for therapy, especially in human patients.In the normal resting state, the electrical difference across neuronal cell membranes is maintained by an active sodium-potassium pump, the net effect of which results in a resting membrane potential ( R M P ) of -70mV.' Transmission of changes in the RMP along axons ultimately causes release of a neurotransmitter with either excitatory or inhibitory effects on a network of postsynaptic neurons that includes adjacent and distant cells. A collateral feedback system allows each neuron to also influence its own excitability. Excitability is mediated by energy-dependent influx of sodium into