The initial T2-weighted images demonstrate a typically minimally T2 hyperintense abnormality demonstrating a slightly higher T2 central focus. Correspondingly this abnormality is largely isointense on T1 with a T1 hypointense central focus. Following contrast administration the lesion demonstrates diffuse heterogeneous enhancement with appearances that sometimes I think are somewhat comparable to a cut fruit, cauliflower or brain! This condition sometimes demonstrates a large artery extending to the central core, however, this is not present on the current examination. The equilibrium phase imaging demonstrates persistent mild hyperintensity that extends into the equilibrium phase. Notably the central region demonstrates progressive enhancement. These appearances are entirely specific for focal nodular hyperplasia, the diagnosis in this case.
Although occasionally it is stated that fibrolamellar carcinoma can appear similar with a central scar, in practise fibrolamellar carcinoma is exotically rare and more typically presents with heterogeneous lesion, with areas of more prominent cystic liquefactive change and/or calcification. The enhancement of central scars in focal nodular hyperplasia typically in my experience is progressive from the outer rim of the scar to the central portion which may sometimes not completely enhance. The lesion typically demonstrates diffuse complete arterial enhancement of the non scar portion of the lesion with persistent mild enhancement in more delayed phases. This is the so called "mother in law phenomenon" (comes early,stays late). Minimal T2 hyperintensity of a subcapsular lesion is typical as this lesion is a hamartoma of normal hepatic parenchyma. The lesion if necessary can be confirmed by demonstrating uptake on 25-minute liver specific contrast agent MRI studies (gadoxetic acid). This is more typically required for lesions without an overt scar to differentiate then from adenomas or hypervascular malignant neoplasms (e.g. neuroendocrine).