case_images: PMC8414607_01
case_images: Initial MRI of the brain from outside hospital. It showed T2-weighted fluid-attenuated
  inversion recovery (FLAIR) sequence hyperintensities in the bilateral basal ganglia and
  diffuse increased signal in the white matter in the bilateral cerebral hemispheres (c),
  with no structural abnormality, mass effect, hemorrhage, restricted diffusion, or
  enhancement. (a) T1-weighted, (b) T1-weighted post-contrast, (d) diffusion-weighted
  imaging, and (e) apparent diffusion coefficient.
case_images: 10.1177_2050313X211042984-fig1.jpg
case_images: PMC8414607_01_10.1177_2050313X211042984-fig1.jpg
case_images: fig1-2050313X211042984
case_images: IgG, proteinase 3 AB IgG, amphiphysin AB, Purkinje cell cytoplasmic AB type 1, 2, Tr, antiglial AB type 1, collapsin response-mediator protein-5 (CRMP-5):immunoglobulin G (IgG), P/Q type and N type calcium channel AB, antineuronal Nu type 1, 2, 3 AB, and neuronal (V-G) K channel AB), and lumbar puncture with normal opening pressure (OP) and cerebrospinal fluid (CSF) analyses (i.e. glucose, encephalitis panel, VDRL, cytology, West Nile virus, and protein 14-3-3), except for elevated protein at 86 mg/dL. A computed tomography (CT) of the head, magnetic resonance imaging (MRI) of the brain with and without gadolinium, magnetic resonance angiogram (MRA) of the head and neck, and cerebral angiogram were also performed and were negative, except for T2-weighted image hyperintensities in the bilateral basal ganglia and increased T2-weighted image signal of the white matter in the bilateral cerebral hemispheres (Figure 1). Initial electroencephalogram (EEG) showed intermittent left-sided frontotemporal slowing and sharp waves, and a subsequent one a week later showed diffuse slowing.
case_images: Temporal sequence MR imaging of the brain comparing initial MRI from outside hospital
  to those obtained at our institution. (a)-(c) Initial MRI from the outside hospital
  obtained on 9 July 2018. Serial MRIs are shown from our institution obtained on 18 July
  2018 (d)-(f) and 2 August 2018 (g)-(i). (a), (d), and (g) show temporal T2-weighted
  FLAIR sequences at the different dates above. (b), (e), and (h) show T1-weighted
  post-contrast images. (c) shows apparent diffusion coefficient image. (f) and (i) show
  diffusion-weighted imaging. Images again demonstrate the temporal history of the
  T2-weighted FLAIR sequence hyperintensities in the white matter in the bilateral
  cerebral hemispheres ((a), (d), and (g)).
case_images: 10.1177_2050313X211042984-fig2.jpg
case_images: PMC8414607_01_10.1177_2050313X211042984-fig2.jpg
case_images: fig2-2050313X211042984
case_images: MRI brain with and without contrast again demonstrated extensive white matter changes without abnormal enhancement (Figure 2).
case_images: Pathology of frozen sections from brain biopsy. (a) Low power demonstrating white
  matter spongiform changes (40x, H&E). (b) High power demonstrating white matter
  spongiform changes in a background of gliosis (400x, H&E). (c) CD68 IHC stain
  highlighting macrophages (200x, CD68). (d) GFAP IHC stain highlighting reactive gliosis
  (200x, GFAP).
case_images: 10.1177_2050313X211042984-fig3.jpg
case_images: PMC8414607_01_10.1177_2050313X211042984-fig3.jpg
case_images: fig3-2050313X211042984
case_images: A right frontal brain biopsy was performed and pathology revealed white matter spongiform changes, with reactive gliosis, and absence of any signs of inflammation (Figure 3), suggestive of toxin exposure.