Milky Way sign (of PML)

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immune reconstitution inflammatory syndrome in Fingolimod-associated PML: a case report with 7 Tesla MRI data. Overview on paraclinical findings and treatment decisions. The figure chronologically displays treatment decisions (first row), lymphocyte counts (second row), laboratory (third row), and MRI findings (fourth and fifth row). At baseline, only very few punctate milky way-like lesions were detectable (circle). After recovery of lymphocytes, new punctate milky way-like lesions developed (circle), and again ceased after corticosteroid pulse therapy (circle). The initial PML lesion in the left hemisphere was stable over time (see Fig. 2). Unfortunately, new MS-like lesions developed after discontinuation of fingolimod (white arrows). Anti-JCV antibody detection and quantification was performed at Unilabs Copenhagen, Denmark. JCV-DNA-PCR from CSF was performed at Institute of Virology, University Clinic of Duesseldorf.

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immune reconstitution inflammatory syndrome in Fingolimod-associated PML: a case report with 7 Tesla MRI data. 3 T and 7 T MR imaging findings in early fingolimod-associated PML. The first row displays MRI images at baseline (a-c) and last follow up (d). At baseline, T2 weighted imaging (a) revealed a new C-shaped lesion with near microcystic appearance (zoom) that clearly infiltrates the short association fibres (“U fibres”). The lesion exhibited a patchy, irregular contrast enhancement (white arrow) on contrast enhanced T1 weighted images (b). The lesion was hyperintense on FLAIR (c, black arrow). The imaging pattern was strongly suggestive for PML. Thus, fingolimod was stopped immediately. Half year later, the size of the PML lesion remained unchanged (d, black arrow). The second and third row shows highly resolving 7 T MRI images. T2*w imaging with a resolution of 0.25 × 0.25mm2 delineates a small PML lesion (e). The PML lesion is T2*w hyperintense (black arrows), infiltrates the short association fibres (“U fibres”), and appears diffusely delineated against the white matter. Moreover, T2*w hypointense areas are visible within the surrounding cortex (black arrowhead). This finding is more pronounced on susceptibility weighted imaging (SWI, f, black arrowheads, “dark” signal). Unwrapped phase maps (g) showed positive phase changes (white arrowheads, “bright” signal) indicating paramagnetic effects. A minimal intensity projection map (MIP, h) of SWI illustrates SWI hypointense signal along white matter fibre tracts. Moreover, 7 T MRI differentiated between MS- and PML- associated lesions. On the one hand, 7 T T2* weighted MRI visualized a distinct central vein within MS-like lesions (J, white arrows). On top of that, numerous punctate contrast enhancing milky way-like lesions (I-L) were visible. Much of contrast enhancing lesions did not show a central vessel on T2*w images (i and j, black arrows). A very small vessel was faintly visible in other punctate lesions (j and k, black arrowheads). l demonstrates contrast-enhancement of the lesion displayed in K