case_images: PMC8072212_01
case_images: Brain magnetic resonance imaging findings of three patients with anti-glutamic acid decarboxylase 65 (GAD65) antibody-associated neurological syndromes. Patient 1: (A) An axial fluid-attenuated inversion recovery (FLAIR) sequence and (B) a coronal T2 sequence show increased signals in the bilateral hippocampus. Patient 2: (C,D) Axial FLAIR sequences demonstrate hyperintensity in a focal area of the right cingulate cortex and the bilateral hippocampus upon initial presentation, (E,F) new cortical/subcortical lesions at 15 months, and (G,H) progressive atrophy and temporal sclerosis at the 5-year follow-up. Patient 3: (I-K) Axial FLAIR sequences demonstrate diffuse abnormalities in the brainstem, thalamus, basal ganglia, and bilateral cerebral hemispheres; (L) Enhanced MRI shows no enhancement.
case_images: fneur-12-641024-g0001.jpg
case_images: PMC8072212_02_fneur-12-641024-g0001.jpg
case_images: F1
case_images: Initial brain MRI revealed bilateral hippocampal hyperintensity in T2-weighted sequences and FLAIR sequences (Figures 1C,D). Repeat brain MRI showed abnormalities in the bilateral frontal lobe, left parietal lobe, right temporal lobe, and insular cortex as well as the subcortical white matter and bilateral hippocampus (Figures 1E,F). Repeat brain MRI showed parenchymal atrophy (Figures 1G,H). Babinski sign. Brain MRI showed multiple diffuse abnormalities in the brainstem, thalamus, basal ganglia, and bilateral cerebral and cerebellar hemispheres on T2-weighted FLAIR imaging without enhancement (Figures 1I-L).
case_images: PMC8072212_02
case_images: Brain magnetic resonance imaging findings of three patients with anti-glutamic acid decarboxylase 65 (GAD65) antibody-associated neurological syndromes. Patient 1: (A) An axial fluid-attenuated inversion recovery (FLAIR) sequence and (B) a coronal T2 sequence show increased signals in the bilateral hippocampus. Patient 2: (C,D) Axial FLAIR sequences demonstrate hyperintensity in a focal area of the right cingulate cortex and the bilateral hippocampus upon initial presentation, (E,F) new cortical/subcortical lesions at 15 months, and (G,H) progressive atrophy and temporal sclerosis at the 5-year follow-up. Patient 3: (I-K) Axial FLAIR sequences demonstrate diffuse abnormalities in the brainstem, thalamus, basal ganglia, and bilateral cerebral hemispheres; (L) Enhanced MRI shows no enhancement.
case_images: fneur-12-641024-g0001.jpg
case_images: PMC8072212_02_fneur-12-641024-g0001.jpg
case_images: F1
case_images: Initial brain MRI revealed bilateral hippocampal hyperintensity in T2-weighted sequences and FLAIR sequences (Figures 1C,D). Repeat brain MRI showed abnormalities in the bilateral frontal lobe, left parietal lobe, right temporal lobe, and insular cortex as well as the subcortical white matter and bilateral hippocampus (Figures 1E,F). Repeat brain MRI showed parenchymal atrophy (Figures 1G,H). Babinski sign. Brain MRI showed multiple diffuse abnormalities in the brainstem, thalamus, basal ganglia, and bilateral cerebral and cerebellar hemispheres on T2-weighted FLAIR imaging without enhancement (Figures 1I-L).
case_images: Indirect immunofluorescence assays of serum and cerebrospinal fluid (CSF) in patient 3. Cell-based assays of serum (A) and CSF (B) were both positive. Tissue-based assays of serum (C) and CSF (D) were both positive.
case_images: fneur-12-641024-g0002.jpg
case_images: PMC8072212_02_fneur-12-641024-g0002.jpg
case_images: F2
case_images: Both serum and CSF were positive for GAD65-Abs, with titers of 1:100 and 1:320, respectively (Figure 2).