Abstract
Introduction
Neurocysticercosis (NCC), caused by the larval form of Taenia solium, is a leading infectious cause of acquired seizures worldwide but may be overlooked in non-endemic regions. Diagnosis can be challenging when neuroimaging findings mimic malignancy and serologic testing is negative. We present a young man with recurrent seizures and enhancing intracranial lesions initially concerning for malignancy, in whom epidemiologic history and subsequent radiographic response supported a clinical diagnosis of NCC despite negative serology.
Case Info
A 22-year-old man who emigrated from Guatemala with a history of a seizure two years earlier presented after a witnessed seizure at home followed by confusion. In the emergency department, he developed a focal seizure progressing to a generalized tonic-clonic seizure. Initial metabolic evaluation, urine drug screening, and computed tomography of the head were unrevealing. Seizure activity was controlled with lorazepam and levetiracetam.
Brain MRI demonstrated an 8 × 7 × 7 mm rim-enhancing cortical lesion in the left frontoparietal region with approximately 2.4 × 1 cm of adjacent subcortical edema. There was no associated hemorrhage or diffusion restriction. Additional imaging review identified a rim-enhancing left occipital lesion without surrounding edema and a 3-mm solid-appearing enhancing right frontal nodule without associated reactive signal. The dominant lesion and surrounding edema initially raised concern for malignancy; however, the patient lacked constitutional symptoms, and systemic imaging failed to identify a primary malignancy.
Given his prior residence in Guatemala, a region endemic for Taenia solium, previous seizure history, and compatible intracranial lesions, NCC was considered. Taenia solium IgG antibody testing by ELISA was negative. Despite negative serology, clinical suspicion remained high, and he was treated with albendazole and dexamethasone while levetiracetam was continued.
The patient experienced no further seizures or focal neurologic deficits. Follow-up MRI demonstrated complete interval resolution of the previously enhancing posterior left frontal lesion and associated edema, with no residual pathologic enhancement or intracranial mass. At outpatient neurology follow-up, he remained asymptomatic and seizure-free.
Disc Clinical
This case highlights the diagnostic challenge of NCC when serologic testing is negative and neuroimaging initially suggests malignancy. Enhancing intracranial lesions with surrounding edema have a broad differential, including neoplastic and infectious etiologies. In this patient, the radiographic appearance initially favored malignancy; however, the absence of an identified primary malignancy and his epidemiologic history prompted reconsideration of NCC.
Negative serologic testing should not be interpreted in isolation to exclude NCC when clinical suspicion remains high. Prior residence in an endemic region, recurrent seizures, compatible neuroimaging, and complete resolution of the enhancing lesion and associated edema following antiparasitic and corticosteroid therapy supported NCC as the clinical diagnosis despite negative serology.
Conclusion
For patients presenting with seizures with unexplained enhancing intracranial lesions, a detailed country-of-origin and exposure history can provide a critical diagnostic clue even years after immigration from an endemic region. This case emphasizes the importance of integrating epidemiologic history, neuroimaging, serologic testing, and longitudinal radiographic response when individual diagnostic studies are inconclusive.