2310. Clinical Characteristics of Patients with Calcified Parenchymal Neurocysticercosis and Perilesional Edema in a large non-endemic cohort


 
 
 Perilesional edema (PLE) around calcified parenchymal neurocysticercosis (NCC) lesions is a transient inflammatory event that accounts for recurrent symptoms in NCC. Previous reports in endemic regions suggest that 50% of seizures in NCC are due to PLE. Its occurrence in non-endemic regions is largely unexplored.
 
 
 
 A retrospective review of medical records of patients with confirmed NCC followed at Jacobi Medical Center (Bronx, NY) from 1993 to 2021 was performed. Epidemiological, clinical and radiological data were obtained.
 
 
 
 180 patients were identified with calcified parenchymal NCC at any time during their course. PLE was documented in 37/180 patients (20.5%). Of these, 27 patients (72.9%) had PLE on presentation; ten patients presented with PLE after a median follow-up of 16.5 (9–36) months. 28 patients (75.6%) with PLE had only calcified parenchymal disease; the remaining 9 patients had mixed forms of NCC concurrently (viable parenchymal, subarachnoid or intraventricular NCC). 8 patients (21.6%) had more than 1 PLE episode with a median number of 3 (2–4) episodes; interval to recurrence was 9 (3.5–11) months. In 6 patients, the recurrence occurred in a calcification different to that of the first PLE episode. 2 patients had multiple calcifications simultaneously displaying PLE. 86.5% of PLE episodes were symptomatic; seizures were the most common symptom (70.3%). Clinical manifestations of PLE often varied during recurrent episodes, with only 2 patients displaying the same symptoms. 10 patients were treated with steroids, and 6 recurrent episodes of PLE occurred during a taper of steroids started for a prior PLE occurrence.
 
 
 
 PLE was a frequent phenomenon among NCC patients in our non-endemic cohort. Its clinical course is variable, occurring as a presenting feature in calcified disease. Treatment with steroids may not always be warranted given recurrence during taper periods. Many experts think this may be due to antigens "leaking" from the calcified lesion leading to inflammation, but the true pathophysiology is not known. Further studies are needed to elucidate the etiology and natural history of PLE in NCC patients.
 
 
 
 All Authors: No reported disclosures.
