Article Figures & Data
Figures
- Figure 1 Clinical details and brain MRI from patient 1 with autoimmune encephalitis and serum myelin oligodendrocyte glycoprotein (MOG) antibodies
Cerebral MRI of a 14-year-old girl (Pat 1) who presented to the emergency department with severe headache, mental status changes, and seizures. Fluid-attenuated inversion recovery image shows pronounced signal alterations and effacement of the cortical gray matter, particularly in the right temporal-parietal lobe (A). In addition, increased signal intensity was noted on signal diffusion weighted-imaging, but no corresponding hypointense apparent diffusion coefficient areas reflecting vasogenic edema rather than cytotoxic injury (B and C). Contrast enhancement of the right temporal-parietal lobe was not seen (D). Four months later, she developed a third episode with sudden onset of memory problems, aggression, sleeping problems, and social withdrawal. Autoantibody studies in CSF and serum revealed NMDA receptor antibodies (abs) in addition to serum MOG abs. MRI of the brain showed a new and large T2 signal alteration in the pons with contrast enhancement (E and F). She was treated with steroids and rituximab. A fourth episode occurred 2 years and 10 months after the initial onset with dizziness and ataxia. Cerebral MRI showed a new patchy T2-hyperintense signal in the right pons and in the left cerebellar white matter (G and H). All lesions resolved completely without residuals. Since the third relapse, she was treated with subcutaneous immunoglobulins.
- Figure 2 Clinical details and brain MRI from patient 2 with autoimmune encephalitis and serum myelin oligodendrocyte glycoprotein antibodies
First cerebral MRI of a 12-year-old boy (Pat 2) with encephalopathy, fever, and ataxia reveals generalized edema of the cerebral cortex and the basal ganglia including the caudate nucleus, putamen, and globus pallidum. The initial examination was superimposed with strong movement artifacts, despite which the cortical edema can still be noted in the shown fluid-attenuated inversion recovery images (A and B). The second MRI of the brain performed 7 days later after treatment with high-dose cortisone and immunoglobulins still showed cortical involvement of the right fronto-temporal lobe (C). In the diffusion-weighted images, “T2-shine-through” (D) but no apparent diffusion coefficient (ADC) signal depression was found. In addition, a single new central pontine lesion was noted in the sagittal T2 images with increased signal intensity in diffusion-weighted imaging and ADC signal depression this time as a sign of cytotoxic injury (E and F) but still without contrast enhancement. In the third MRI of the brain performed 18 days after admission, the central pontine lesion was still present (G and H) associated with ADC depression (not shown).
- Figure 3 Clinical details and brain MRI from patient 3 with autoimmune encephalitis and serum myelin oligodendrocyte glycoprotein (MOG) antibodies
MRI of the brain of a previously healthy 16-year-old boy (Pat 3) who presented to the emergency department with a 6-day history of severe right-sided headache shows bilateral signal alterations in both hippocampi, particularly in the coronal fluid-attenuated inversion recovery sequences more pronounced on the right than left side (A). In the T2-weighted images, the alterations are less pronounced (C). Diffusion restriction or contrast medium enhancement was not noted in this patient (B and D). Follow-up MRI of the brain 3 months later did not reveal any abnormalities (not shown).
- Figure 4 Clinical details and brain MRI from patient 4 with autoimmune encephalitis and serum myelin oligodendrocyte glycoprotein antibodies
Brain MRI of a 10-year-old boy (Pat 4) with focal seizures, encephalopathy, and fever revealed a large hyperintense lesion of the right insular cortex and the adjacent juxtacortical white matter (A, fluid-attenuated inversion recovery). In the diffusion-weighted images, there is “T2-shine-through” but no apparent diffusion coefficient signal depression and therefore no diffusion restriction (B and C). This was the only patient in whom after administration of contrast agent, a streaky, garland-like contrast enhancement in the area of the insular cortex and the juxtacortical white matter on the right was noted (D). We assume that vascular leakage resulted in contrast medium accumulation with no lesion-specific pattern. In this patient, no other areas of the brain were affected.
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