A 57-year-old woman had development of acute-onset, right-sided weakness and sensory change (face, arm, and leg) when at a casino. She was brought to the emergency department, and her symptoms had essentially resolved upon her arrival. Brain magnetic resonance imaging showed no acute stroke, and a transient ischemic attack was diagnosed. She was transferred to an academic medical center. Investigations showed high-grade left internal carotid artery stenosis; the same day, a stent was placed via endovascular procedure by an interventional neuroradiologist. Magnetic resonance imaging of the head showed an enhancing lesion with surrounding edema in the left frontal and parietal lobes at the cortex, also involving the nearby leptomeninges. Electroencephalography showed potentially epileptogenic discharges over the left central head region. Brain biopsy was performed, which showed abundant CD68+ macrophages, granulomatous inflammation, and necrosis associated with foreign material. The associated lymphocytic infiltrates were predominantly composed of CD3+ T cells and only sparse CD20+ B cells. The foreign material seen was lamellated, amorphous, nonpolarizable, and nonrefractile, typical of hydrophilic polymers commonly used in intravascular medical devices. The patient was diagnosed with seizures caused by multifocal, intracranial, foreign-body, granulomatous reaction to polymers that had embolized to brain parenchyma during the prior endovascular procedure. To suppress this inflammatory reaction, corticosteroids were initiated—intravenous methylprednisolone, followed by an oral prednisone course, with a plan to gradually taper. Antiseizure medication was continued at the same doses. The patient’s seizures remitted initially but relapsed upon corticosteroid dose reduction despite a very slow prednisone taper. At that point, 18 months after the initial onset of seizures, the patient had cushingoid features, depression, and chronic insomnia. During the next year, 2 steroid-sparing strategies were employed sequentially. In patients who have received neurovascular medical device therapy and have subsequent development of seizures, focal neurologic deficit, headache, or encephalopathy, central nervous system inflammation triggered by retained foreign-body material should be considered as a potential cause.