An 11-month-old female neutered domestic shorthair cat presented to the referring veterinary surgery for seizures. Generalised tonic–clonic seizures began 1 month prior to presentation. Initially, the seizures occurred once weekly, increasing in frequency to every 5–6 h. Each seizure lasted approximately 30 s, with a postictal period lasting several hours. Partial seizures involving solely the head were also reported approximately 4 months prior to presentation. There were no interictal abnormalities reported apart from a mild right thoracic limb paresis. The cat was obtained at 5 months of age and housed both indoors and outdoors. Commercial supermarket wet and dry food was fed. Vaccination and worming status were current. Routine biochemistry, including resting bile acids, performed at the referring veterinary surgery was within normal limits. Haematology revealed mild lymphopenia (1.4 × 109/l; reference interval [RI] 1.60–7.0 × 109/l) and monocytosis (0.7 × 109/l; RI <0.6 × 109/l). Toxoplasma gondii and Cyptococcus gattii antibody titres were negative. The cat’s feline immunodeficiency virus/feline leukaemia virus status was also negative. The cat was referred for further management and diagnostics. On referral, physical examination revealed non-visual microphthalmia of the left eye () and right-sided hemiparesis. A full neurological examination, including cranial nerve assessment, revealed proprioceptive deficits present in both the right forelimb and right hindlimb. No other neurological abnormalities were identified. A generalised tonic–clonic seizure occurred during the examination, lasting 30 s and requiring no intervention. Seizures are generally indicative of a forebrain disorder. Causes can be either intracranial or extracranial in origin. In this case, given the concurrent micropthalmia, a congenital intracranial forebrain lesion was suspected. This was further localised to the left given the contralateral hemiparesis and proprioceptive deficits. The cat was commenced on phenobarbitone intravenously (IV) loaded at 15 mg/kg over a 24 h period. There were no further seizures noted during this period. The cat was discharged the following day on 2.15 mg/kg phenobarbitone PO q12h and returned 1 week later for advanced imaging. The cat was sedated with 0.2 mg/kg butorphanol IV and anaesthesia was induced with 1 mg/kg alfaxalone (Alfaxan; Jurox) IV. MRI of the brain and cranial neck was performed using a 1.5-Tesla MRI system (Siemens Avanto). T2-weighted Turbo Spin Echo, fluid-attenuation inversion recovery and short T1 inversion recovery sequences were performed with 3 mm slice thickness. Pre- and post-intravenous gadolinium contrast (Magnevist 0.2 ml/kg) T1-weighted sequences were performed with 3 mm and 1.6 mm slice thickness. MRI revealed protrusion of the left rostral rhinencephalon through the left cribriform plate into the left caudal nasal cavity consistent with a left frontoethmoidal encephalocele (). Increased T2-weighted signal was present around the protruding rostral brain tissue, ventral nasal meatus and left caudal nasal cavity consistent with inflammatory exudate or cerebrospinal fluid. The left globe was reduced in size, elliptical in shape and the lens was absent. This was consistent with congenital microphthalmia with aphakia (). The cat recovered uneventfully from anaesthesia. Conservative therapy with antiepileptic medication was elected and surgical correction was not performed. The cat was discharged the following day on the previously prescribed phenobarbitone. Leviteracetam (Keppra; UCB Pharma) was additionally commenced 4 weeks later at 22 mg/kg PO q8h as the cat presented to the clinic following two generalised tonic–clonic seizures in close succession. Seizures recurred again 3 months later and the phenobarbitone dose was subsequently increased to 4 mg/kg PO q12h. The cat responded to the increased phenobarbitone dose and seizures have been well controlled 12 months post-diagnosis of the encephalocele.