The Great Pretender—How Sarcoidosis Gained Its Reputation as the Mimic of Other Pathology

In this lecture we will use advanced MR imaging techniques, perfusion (both contrast enhanced and arterial spin labelled), permeability, diffusion, and spectroscopy to understand the biological behavior of astrocytomas. Low grade astrocytomas may not show high choline on MRS but show high myoinositol which correlates with low perfusion values. Anaplastic astrocytomas produce metalloproteases and thus VEGF and PDGF can stimulate angiogenesis resulting in high perfusion with gadolium and ASL. Lastly, hypoxia induces formation of permeability factors leading to edema and contrast enhancement in glioblastomas. Necrosis, seen as lipids on MRS is a marker of glioblastoma. Presence of MGMT promoter and alterations in the IDH1 gene (present in most secondary glioblastomas) confer a better survival pattern to glioblastoma patients and these findings are seen predominantly in temporal and deep tumors and in those with little contrast enhancement and high signal on T2 and DWI images. Thus, the intial transformation in all low grade astrocytomas is ischemia that can be seen as the presence of lactate on MRS, while markers of higher grades such as angiogenesis, permeability, and necrosis can be identified with perfusion, K-trans maps, and MR spectroscopy. Lack of myoinositol on MRS indicates its consumption for production of metalloproteases and thus it is also an early marker of angiogenesis. Many of these changes occur before anatomical images may suggest them.