Case Presentation: A 23 year-old Central American male with a past medical history significant for an isolated seizure one year prior to present admission presents with seizure and headache. Vital signs, examination and laboratory studies at time of admission were unremarkable. CT head revealed a small eccentric nodule within a 1.0 x 0.8 x 1.1 cm cystic lesion within the right parietal lobe and a punctate parenchymal calcification within the right temporal lobe. MRI brain revealed a boomerang-shaped enhancing structure within the previously demonstrated right parietal cystic lesion. Lesion was without surrounding edema. Ventricular involvement was not observed. Radiologic findings were pathognomonic for viable neurocysticercosis. Ophthalmologic examination was within normal limits. Quantiferon Gold assay and strongyloides antibodies were negative. Decadron and levetiracetam therapies were initiated and followed by albendazole and praziquantel treatment. Patient was discharged to home with plan for repeat MRI brain in two months following hospitalization.

Discussion: Neurocysticercosis is a neuroparasitic pathology caused by ingestion of eggs of the tapeworm Taenia solium. Neurocysticercosis is the most common parasitic disease of the nervous system in developing countries. In the United States, neurocysticercosis is almost exclusively observed in immigrant populations. Seizure and headache are common presenting symptoms of parenchymal neurocysticercosis while encephalopathy and loss of consciousness are associated with ventricular disease. Radiographic progression of neurocysticercosis involves a viable cyst with indwelling scolex followed by cyst inflammation and subsequent residual calcification. Identification of a scolex within a cystic lesion is rarely seen and is the only pathognomonic radiographic finding for neurocysticercosis. Seizure commonly occurs during the inflammatory phase but may affect all stages. Tenets of therapy include antiepileptic, antiparasitic and anti-inflammatory modalities. Patient should be screened for tuberculosis (TB) and strongyloides prior to initiation of steroid therapy as patients with TB or strongyloides are at risk for dissemination of disease following immunosuppression with steroid therapy. All patients should additionally be evaluated for ocular of ventricular involvement as these disease subtypes require urgent evaluation.

Conclusions: Here we describe a case of neurocysticercosis in a Central American male presenting with seizure. Seizure one year prior to current evaluation was likely due to evolving neuroparasitic disease as evidenced by a punctate calcification within the temporal lobe. Progression from a viable to an inflammatory cyst likely resulted in recurrence of seizure in this patient. Though a rare etiology of seizure in the United States, neurocysticercosis is the primary cause of acquired epilepsy worldwide. A diagnosis of neurocysticercosis should be considered in patients from endemic regions who present with seizure.