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fn1Financial support: The study was partly supported by Universidad Espíritu Santo–Ecuador, Guayaquil–Ecuador. Dr. Román Research is supported by the Jack S. Blanton Presidential Distinguished Chair, the Fondren Fund, and the Wareing Family Fund at Houston Methodist Hospital.
fn2Authors’ addresses: Oscar H. Del Brutto and Aldo F. Costa, School of Medicine, Universidad Espíritu Santo—Ecuador, Guayaquil, Ecuador, E-mails: oscardelbrutto@hotmail.com and aldocosva_01@hotmail.com. Robertino M. Mera, Department of Epidemiology, Gilead Sciences, Inc., Foster City, CA, E-mail: rmm17189@gmail.com. Mauricio Zambrano, Community Center of the Atahualpa Project, Atahualpa, Ecuador, E-mail: zamaleon@hotmail.com. Gustavo C. Román, Department of Neurology, Houston Methodist Hospital, Houston, TX, E-mail: gcroman@houstonmethodist.org.
Abstract.
Mechanisms implicated in the association between neurocysticercosis (NCC) and cognitive impairment remain unknown. Atahualpa residents aged ≥ 40 years with calcified NCC were identified as case patients and paired 1:1 to age- and gender-matched controls. The selection process generated 79 pairs. Cognitive performance was measured by the Montreal Cognitive Assessment (MoCA). A conditional logistic regression model revealed no differences in MoCA scores across case patients and controls, after adjusting for education, epilepsy, depression, and hippocampal atrophy. The single covariate remaining significant was hippocampal atrophy. When participants were stratified according to this covariate, linear models showed lower MoCA scores among case patients (but not controls) with hippocampal atrophy. In a fully adjusted linear regression model, age remained as the single covariate explaining cognitive impairment among NCC patients. This study demonstrates an association between hippocampal atrophy and poor cognitive performance among patients with calcified NCC, most likely attributable to the effect of age.