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The hippocampi showed a significant decrease of NMDAR\u2010immunoreactivity that correlated with disease severity. The patient with NMDAR\u2010encephalitis and immunosuppression for kidney transplantation developed a brain monomorphic PTLD. Inflammatory changes were compatible with NMDAR\u2010encephalitis. Additionally, plasma cells accumulated in the vicinity of the necrotic tumor along with macrophages and activated microglia that strongly expressed pro\u2010inflammatory activation markers HLA\u2010DR, CD68, and IL18. The fourth patient developed demyelinating lesions in the setting of a relapse 4\u2009years after NMDAR\u2010encephalitis. These lesions exhibited the hallmarks of classic multiple sclerosis with radially expanding lesions and remyelinated shadow plaques without complement or immunoglobulin deposition, compatible with a pattern I demyelination.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Interpretation<\/jats:title>\n                    <jats:p>The topographic distribution of inflammation in patients with NMDAR\u2010encephalitis reflects the clinical symptoms of movement disorders, abnormal behavior, and memory dysfunction with inflammation dominantly observed in basal ganglia, amygdala, and hippocampus, and loss of NMDAR\u2010immunoreactivity correlates with disease severity. Co\u2010occurring pathologies influence the spatial distribution, composition, and intensity of inflammation, which may modify patients\u2019 clinical presentation and outcome. 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