PMC5797606_01
Clinical, therapeutic, and radiological course. Abbreviations: CSF cerebrospinal fluid; d, days; EEG, electroencephalography; GE, gadolinium-enhancement; IVIG, intravenous immunoglobulin; JCV-PCR John Cunningham virus-polymerase chain reaction; MP, methylprednisolone; MRI, magnetic resonance imaging; NCSE, non-convulsive status epilepticus.
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F1
A 67-year-old woman was diagnosed with squamous NSCLC 1 year before the current admission, details of the subsequent clinical course are outlined in Figure 1. Second-line treatment with nivolumab in the standard dosage of 3 mg/kg was subsequently initiated and details of the course are shown in Figure 1.
Neuroimaging. Brain CT in the postoperative course after the patient developed nausea, vomiting, and generalized weakness. The red arrows point at revealing wide-spread bilateral hypodensities in the subcortical white matter of the frontal, parietal, and occipital lobe (A,B). Brain MRI findings on day 14 of month 1 of the first nivolimab course. Fluid-attenuated inversion recovery (FLAIR) magnetic resonance imaging (MRI) showing multiple bilateral hyperintensities in gray cerebellar matter [(C), red arrows]. (D) T1-contrast enhanced images on the same level as image [(A) (red arrow)]. (D) MRI FLAIR images showing bilateral thalamic hyperintensities with corresponding T1-contrast enhancement left [(F), red arrow]. FLAIR MRI images showing confluent cortical hyperintensities (G) T1 contrast-enhancement showing pial gyriform pattern of enhancement [(H), red arrows].
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F2
Brain CT revealed wide-spread bilateral hypodense lesion in the subcortical white matter of the frontal, parietal, and occipital lobe (Figures 2A,B), which had vanished on follow-up 8 days later. Brain MRI 44 days showed multiple and confluent cortical and subcortical FLAIR hyperintensities within both cerebral hemispheres, as shown in Figures 2C,E,G. A pial and gyriform contrast enhancement was observed in some lesion (Figures 2D,F,H).
Histological examination of the brain. Microscopic examination disclosed necrotic tissue damage in the right thalamus [(A), H&E], and reactive astrogliosis in the cortex [(B), H&E]. Normal appearing white matter [(C), H&E]. Further stainings of the thalamus included LFB (D), MBP (E), and PLP (F). Additional findings were vascular wall hyalinosis (G) with presence of CD3-positive T-cells in the perivascular space (H), reactive astro and microgliosis [(I,J), respectively]. Abbreviations: GFAP Glial fibrillary acid protein, LFB Luxol fast blue, MBP Myelin basic protein, PLP Proteolipid protein.
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F3
Microscopic analysis revealed generalized mild edematous changes as well as hypoxic neuronal changes (Figure 3).