What are the causes of T1 hyperintensity?
Melanin, fat, proteinaceous fluid, blood in a methemoglobin state, paramagnetic substances (manganese, copper, extracellular calcium...), slow flow, posterior pituitary gland, and contrast (i.e. gadolinium).
The heterogeneous left frontobasal lesion displays both cystic and solid intralesional components with hyperintense elements on T1, T2, and fat-saturated sequences, resulting from subacute blood components or dense proteinaceous fluid. Some blooming artifacts on the GRE sequence probably correspond to calcifications without ruling out the possibility of intralesional hemorrhages. The contrast enhancement is vivid and heterogeneous, with some nodular enhancement along the lesion's inner border.