1028. Clinical and radiologic characteristics of calcified parenchymal neurocysticercosis: A large series of a non-endemic region


 
 
 Neurocysticercosis (NCC) is the most common helminthic infection of the central nervous system and a common cause of seizures. Approximately, one-third of patients with epilepsy in endemic regions have NCC. Calcified parenchymal cysticercosis (CaNCC) was previously referred to as an inactive form of NCC, however, recent data suggests that the antigenic parasitic material within this lesion can intermittently elicit a host inflammatory response. The clinical and radiologic characteristics associated with calcified lesions have not yet been well characterized.
 
 
 
 We describe the clinical, radiologic, and serologic characteristics of a large series of patients with calcified parenchymal NCC who presented to Jacobi Medical Center, New York.
 
 
 
 Of 302 cases of NCC, 87 patients (32.5%) had exclusively CaNCC. Most individuals were female (50.7%) and born in Mexico (32.2%); the mean age was 38.4 ± 15.3 years and the median time from migration was 12 years [IQR 4-20 years]. The most common presentation was seizures (52.9%); among these patients, 23 individuals (53.5%) had perilesional edema on imaging which was always associated with enhancement on MR T1 image after gadolinium injection. Thirty-seven patients (42.5%) presented with headaches; among these, only 6 patients (16.2%) had perilesional edema at presentation. Nine patients (10.3%) were diagnosed incidentally. The Western blot was positive in 19 patients (21.8%) and the cysticercosis antigen in serum was negative in all cases.
 
 
 
 This large series of patients with CaNCC in a non-endemic area highlights the clinical spectrum of this form of NCC. Seizures were the most common symptom. Perilesional edema around calcified lesions was seen in 50% of individuals presenting with seizures, similar to findings in endemic regions. Headaches also were frequent; the pathophysiology is yet not well understood. Unlike extraparenchymal disease, serum antigen is not positive in CaNCC. Enhancement of the corresponding calcifications after gadolinium was frequently seen on MRI. More research on individuals with CaNCC is needed to better understand why certain calcified lesions develop perilesional edema. It is clear that CaNCC is not inactive and the etiology of both headaches and seizures is probably multifactorial.
 
 
 
 All Authors: No reported disclosures.
