перевел бы как "поражения (очаги) с (в форме) парамагнитным(ого) ободком(а) \ с парамагнитным контуром "
или
"парамагнитные ободковые (кольцевидные) поражения (очаги)"

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Note added at 13 час (2021-09-21 08:14:13 GMT)
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Касательно природы парамагнитных контуров (ободков) - это не результат накопления контраста (никакого МРТ с контрастным усилением не проводится), а результат накопления железа в определенных клетках и тканях. Достаточно посмотреть на определение PRL и прочитать несколько соответствующих статей. Другой момент, что эти парамагнитные контуры не являются признаком исключительно рассеянного склероза.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5209400/
Our study shows that iron in the brains of patients with relapsing or progressive MS accumulates at the edge of slowly expanding lesions in microglia/macrophages. There it persists for months to years when lesions are slowly expanding or when demyelinating activity has ceased. This iron deposition is visible by susceptibility-based MRI and indicates chronic lesions with pro-inflammatory microglia/macrophages, complete myelin loss within the rim and absence of remyelination.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3235560/
In multiple sclerosis, iron accumulation may reflect a multiplicity of pathological and physiological processes (Craelius et al., 1982; Connor et al., 1995; Levine and Chakrabarty, 2004). Hence, iron has the unique potential to serve as an in vivo tracer of disease pathology. At the inflammatory site, iron may be present during both the acute and chronic phase. Free iron may be released from non-haem proteins whose degradation is induced by respiratory burst molecules produced by microglia and macrophages during acute inflammation phases. In chronic inflammation, protein–iron deposits may be contained in macrophages indicating microglia activation and chronic inflammation at the site of white matter lesions, areas adjacent to white matter lesions and the inner cortex adjacent to the white matter (Craelius et al., 1982). At the demyelination site, iron is released from degrading oligodendrocytes (after myelin is destroyed). Independently of its source, free iron can partake in reactions leading to toxic-free radical formation, oxidative damage and mitochondrial injury. Iron accumulation, however, may also reflect active processes of physiological myelination or reparative remyelination through its essential role as co-factor for numerous enzymes involved in lipid biosynthesis associated to myelin formation (Connor et al., 1996).

http://www.ajnr.org/content/ajnr/39/7/1233.full.pdf
Chronic active lesions are pathologically characterized by a
hypocellular demyelinated core and a hypercellular edge of activated microglia/macrophages related to smoldering inflammation and axonal degeneration.1,2 On MR imaging, these lesions
have a characteristic paramagnetic rim on 7T susceptibility-based
MR imaging sequences; the paramagnetic shift is due to the stable
presence of iron-laden activated microglia/macrophages3-11 and,
potentially, reactive astrocytes12 at the lesion edge. Usually, paramagnetic rims are seen on 7T phase images, but a proportion can
also be detected on 7T T2* magnitude images, mostly when iron
content is higher.