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Figure 2: (a-e) Imaging of patients with anti-N-methyl-D-aspartate encephalitis: (a) Patient 5 shows fluid-attenuated inversion recovery hyperintensities (b) in bilateral basal ganglia and medial temporal lobe;(c) Patient 7 shows fluid-attenuated inversion recovery hyperintensities in bilateral medial temporal lobes; (d and e) Patient 9 shows fluid-attenuated inversion recovery hyperintensities in bilateral (left more than right) temporal lobes, insula, anterior cingulate, pulvinar regions; (f and g) Patient 5 with anti-voltage-gated potassium channel encephalitis shows fluid-attenuated inversion recovery hyperintensities in bilateral medial temporal lobes; (h-j) Patient 1 with anti-voltage-gated potassium channel encephalitis shows T1 fluid-attenuated inversion recovery hyperintensity in bilateral (right more than left) basal ganglia; (k) Patient 2 with anti-thyroid peroxidase antibody – diffuse cerebral atrophy; (l) Patient 8 with Hashimoto encephalitis showing a normal fluid-attenuated inversion recovery MRI.; (m-o) After 1-year of illness, the MRI shows disappearance of the basal ganglia signal changes along with diffuse cerebral atrophy and left frontotemporal chronic subdural hematoma

Figure 2: (a-e) Imaging of patients with anti-N-methyl-D-aspartate encephalitis: (a) Patient 5 shows fluid-attenuated inversion recovery hyperintensities (b) in bilateral basal ganglia and medial temporal lobe;(c) Patient 7 shows fluid-attenuated inversion recovery hyperintensities in bilateral medial temporal lobes; (d and e) Patient 9 shows fluid-attenuated inversion recovery hyperintensities in bilateral (left more than right) temporal lobes, insula, anterior cingulate, pulvinar regions; (f and g) Patient 5 with anti-voltage-gated potassium channel encephalitis shows fluid-attenuated inversion recovery hyperintensities in bilateral medial temporal lobes; (h-j) Patient 1 with anti-voltage-gated potassium channel encephalitis shows T1 fluid-attenuated inversion recovery hyperintensity in bilateral (right more than left) basal ganglia; (k) Patient 2 with anti-thyroid peroxidase antibody – diffuse cerebral atrophy; (l) Patient 8 with Hashimoto encephalitis showing a normal fluid-attenuated inversion recovery MRI.; (m-o) After 1-year of illness, the MRI shows disappearance of the basal ganglia signal changes along with diffuse cerebral atrophy and left frontotemporal chronic subdural hematoma