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ORIGINAL ARTICLE
Year : 2016  |  Volume : 6  |  Issue : 1  |  Page : 51-55

Topographic congruence of calcified parenchymal neurocysticercosis and other structural brain lesions with epileptiform activity


1 Department of Neurology, Division of Neurology, Los Angeles Biomedical Research Institute, Torrance, CA 90502, USA
2 Department of Neurology, Division of Neurology, Los Angeles Biomedical Research Institute, Torrance, CA 90502; W. M. Keck Science Center, Pitzer College, Claremont, CA 91711, USA
3 Department of Neurology, Division of Neurology, Los Angeles Biomedical Research Institute, Torrance, CA 90502; Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095; Department of Neurology, Harbor UCLA Medical Center, Torrance, CA 90509, USA
4 Department of Neurology, Division of Neurology, Los Angeles Biomedical Research Institute, Torrance, CA 90502; Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095; Department of Neurology, Harbor-UCLA Medical Center, Torrance, CA 90509, USA

Correspondence Address:
Aaron Matthew McMurtray
Department of Neurology, Harbor-UCLA Medical Center, 1000 West Carson Street, Torrance, CA 90509
USA
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DOI: 10.4103/2229-5070.175093

PMID: 26998434

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Introduction: Calcified parenchymal neurocysticercosis (NCC) lesions are commonly detected in many individuals with refractory epilepsy. However, the relationship between these lesions and epilepsy is not fully determined. We sought to determine if calcified parenchymal NCC demonstrated topographic congruence with epileptiform activity in refractory epilepsy patients. Additional patients with other structural brain lesions were included for comparison. Subjects and Methods: Retrospective cross-sectional analysis of all patients treated at a community-based neurology clinic for refractory epilepsy during a 3-month period and with structural brain lesions detected by neuroimaging studies. Results: A total of 105 patients were included in the study, including 63 with calcified parenchymal NCC lesions and 42 with other structural brain lesions. No significant relationship was detected between hemispheric localization of calcified parenchymal NCC lesions and epileptiform activity. For those with other structural brain lesions, the hemispheric localization was significantly related to the side of epileptiform activity (Chi-square = 11.13, P = 0.025). In addition, logistic regression models showed that those with right-sided non-NCC lesions were more likely to have right-sided epileptiform activity (odds ratio = 4.36, 95% confidence interval [CI] =1.16-16.31, P = 0.029), and those with left-sided non-NCC lesions were more likely to have left-sided epileptiform activity (odds ratio = 7.60, 95% CI = 1.89-30.49, P = 0.004). Conclusion: The lack of correlation between the side of calcified parenchymal NCC lesions and the side of the epileptiform activity suggests that these lesions may be incidental findings in many patients.


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