An Atypical Presentation of Pediatric Acute Neuropsychiatric Syndrome Responding to Plasmapheresis Treatment

Figure 1

Hypothetical mechanism of postinfectious autoimmune neuropsychiatric syndromes. (1) Causative organism must contain M-protein epitopes that are capable of evoking antibody production that react with human neurons in the basal ganglia. They must also produce super-antigens (SAGs) that activate T-cell releasing cytokines (Interferon γ, Interleukin 2, and Tumor Necrosis Factor β) and proliferate T-cell (V subsets) resulting in anamnestic cell response. (2) T-cells bind to cross-reactive M-protein epitopes when displayed on surface MHC Class II molecules of B-cells. (3) B-cells are activated and (4) produce antibodies to M-proteins that cross-react with neuronal antigens in basal ganglia through the mechanism of molecular mimicry resulting in clinical manifestations such as OCD / tics [10].