John Libbey Eurotext

Neurocysticercosis and pharmacoresistant epilepsy: possible role of calcified lesions in epileptogenesis Volume 22, numéro 4, August 2020

Illustrations

  • Figure 1
  • Figure 2
Auteurs
1 Department of Neurology and Neurosurgery, Universidade Federal de São Paulo (UNIFESP), São Paulo/SP, Brazil
2 Department of Morphological Sciences, Medical Sciences Faculty, National Autonomous University of Honduras, Honduras
3 Department of Radiology, Universidade Federal de São Paulo (UNIFESP), São Paulo/SP, Brazil
* Correspondence: Mirian S. Bittar Guaranha Rua Pedro de Toledo, 650, 1° andar. CEP: 04039-002 - Vila Clementino, São Paulo/SP, Brazil

Neurocysticercosis is a neglected and usually poverty-related disease of high public importance. The mechanisms by which the calcified lesions cause epilepsy are not known, but have been attributed to residual perilesional gliosis or an inflammatory process. This case shows that an inflammatory response to a calcified granuloma may be associated with the development of epilepsy. The increase in glutamate and kinin B1 (pro-epileptogenic) receptors added by reduced expression of kinin B2 (anti-epileptogenic) receptors may explain the chronic epileptogenesis associated with the lesion, corroborating the hypothesis of inflammatory mechanisms involved in the pathophysiology of epilepsy in these patients.