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Neuronal autoantibodies in patients with Rasmussen's encephalitis Volume 18, issue 2, June 2016

Figure 1

Axial T1-weighted (A) and coronal FLAIR (B) MR images of Patient 2, demonstrating typical atrophy on the right hemisphere.

Figure 2

Antibody assays performed using sera from patients with Rasmussen encephalitis (RE), autoimmune limbic encephalitis, multiple sclerosis (MS), and healthy controls. The cell-based assay (CBA) shows that serum antibodies from an autoimmune limbic encephalitis patient reacted (green) with HEK 293 cells expressing NR1/NR2 heteromers of the N-methyl-D-aspartate receptor (NMDAR). In contrast, serum IgGs of RE and MS patients and healthy controls did not show any immunoreactivity (upper row). Likewise, cultured hippocampal neurons incubated with serum from an NMDAR-antibody positive limbic encephalitis patient demonstrated intense immunolabelling (green) of neuronal membrane/synapse antigens, whereas serum antibodies from other patients and healthy controls did not show any reactivity to cultured hippocampal neurons (middle row). Immunoreactivity of serum IgG from a limbic encephalitis patient significantly co-localized with microtubule-associated protein-2 (MAP-2) antibody (Ab) (red) (lower row). Original magnification in upper panels (400x) and middle and lower panels (800x).