“…Inflammation is thought to lead to epileptogenesis either by causing gliosis and/or by causing persistent areas of bloodbrain barrier dysfunction. 39 As evidence to support an association between the inflammatory response and epileptogenesis, subjects with active epilepsy due to NCC, compared with infected subjects without epilepsy, have 1) higher serum levels of blood-brain barrier breakdown molecules (MMP-9) and increase in proinflammatory cytokines (tumor necrosis factor [TNF]-α, interferon-γ, and interleukin [IL] 1-β), 2) increased expression of lymphocyte adhesion molecules, and 3) increased likelihood of mutations in the Toll-like receptor 4 that lead to an increased Th1 (pro-inflammatory) response (Figure 1). 19,20,57,58 Finally, a strong serologic response (³ 4 bands) 8,59 to parasite antigen on NCC EITB was associated with both epilepsy development and with a more severe course once epilepsy was established.…”