Table 3.
Histopathological studies in AIE.
| Histopathological seriesReferencesTissue(Number of patients) | NMDAR AIE | VGKC AIE | Seronegative AIE |
|---|---|---|---|
| Bien et al. (86)Brain biopsies(NMDAR = 3, VGKC = 4) | Complement deposition, minimal lymphocyte infiltrate | — | |
| Tuzun et al. (87)Autopsy(NMDAR = 2) | Perivascular lymphocyte infiltrate (plasma cells), IgG1 antibody deposition, microglial (CD68) proliferation, atrophy | — | — |
| Martinez-Hernandez et al. (88)Brain biopsies and Autopsy(NMDAR = 5) | Perivascular plasmablasts, no antibody deposition | — | — |
| Okamoto et al. (89)Autopsy(Seronegative = 3) | — | — | Microglial (CD68) proliferation, atrophy |
| Park et al. (90)Autopsy(VGKC = 1) | — | Microglial (CD68) proliferation | |
| Filatenkov et al. (91)Autopsy(NMDAR = 1, post-treatment) | Microglial activation and proliferation. CD3 lymphocyte parenchymal infiltration. Occasional CD20 lymphocyte. | — | — |
| Khan et al. (92)Autopsy(VGKC = 1) | — | Microglial activation. Perivascular CD20 lymphocyte infiltration. | — |
| Camdessanche et al. (93)Brain Biopsy(NMDA = 1) | Perivascular CD20 lymphocyte infiltration | — | — |
NMDAR, N-methyl-D-aspartate Receptor; AIE, Autoimmune Encephalitis; VGKC, Voltage-gated Potassium Channel.