A 4-year-old, 6.5-kg, castrated male Boston Terrier was referred to the Cornell University Hospital for Animals for evaluation of seizures. Seizure activity was characterized by unconsciousness, tonic-clonic limb movements, and hypersalivation, with each seizure lasting approximately 1 minute. Three seizures had occurred during the 24 hours preceding presentation. Otherwise, the dog had been clinically healthy. No drugs were administered and toxin exposure was unlikely. Laboratory assessment completed by the referring veterinarian included CBC and serum biochemistry (sodium, potassium, chloride, total protein, albumin, globulin, BUN, creatinine, glucose, calcium, phosphorus, total bilirubin, and cholesterol concentrations; alkaline phosphatase [ALP], alanine aminotransferase [ALT], and amylase activities). Results disclosed eosinopenia (0.09 9 10 3 cells/lL; reference range 0.1-1.49 9 10 3 /lL) and mildly increased ALT activity (124 U/L; reference range, 10-100 U/L).On presentation, the dog was bright and alert with modest upper airway stridor attributable to brachycephalic conformation. Neurologic examination demonstrated decreased menace OD and equivocal cervical pain. h revealed multifocal, asymmetrical ill-defined intra-axial hyperintense areas in the cerebral cortex; these regions were slightly hyperintense to brain on T2-weighted images and fluid attenuated inversion recovery, but lacked contrast enhancement. A linear intra-axial lesion with the same signal intensity as cerebrospinal fluid (CSF) that did not contrast enhance was noted within spinal cord parenchyma at C1 and C2, consistent with mild syringohydromyelia.The CSF collected from the lumbosacral subarachnoid space was colorless and clear with normal nucleated cell count (3/lL; reference range, <5/lL) and total protein concentration (21 mg/dL; reference range, <45 mg/dL); cytologic examination disclosed 63% small lymphocytes and 37% macrophages. Collective findings were interpreted as changes secondary to the recent seizure activity and mild syringohydromyelia. The dog was prescribed the anticonvulsant zonisamide i (7.7 mg/kg PO q12h) for presumed idiopathic epilepsy.After 10 days of zonisamide administration, the dog was presented again for inappetence and vomiting. No seizure activity had occurred since instituting zonisamide. Results of CBC and serum biochemistry disclosed lymphopenia (0.5 9 10 3 /lL; reference range, 0.9-4.7 9 10 3 /lL), eosinopenia (0.0 9 10 3 /lL), mild thrombocytopenia (176 9 10 3 /lL; reference range, 186-545 9 10 3 /lL) with platelet clumps, few acanthocytes and keratocytes, marked increases in activities of ALT (16328 U/L) and aspartate aminotransferase (AST; 5908 U/L; reference range, 16-50 U/L), modest increases in activities of ALP (354 U/L; reference range, 12-122 U/L) and gamma-glutamyl transferase (GGT, 61 U/L; reference range, 0-10 U/L), and hyperbilirubinemia (2.3 mg/dL; reference range, 0-0.3 mg/ dL). Urine was concentrated (specific gravity 1.050) with bilirubinuria, 2+ proteinuria, pH 7.5, and sediment demonst...