On unenhanced CT, FNH is seen as solitary lesion with central focal low attenuation scar surrounded by well defined homogenous area showing mass effect; the attenuation of which is similar to that of surrounding liver parenchyma. This typical feature of FNH is found in approximately 20% of patients [10] .

During the arterial phase of hepatic enhancement, FNH is homogenously enhanced (96%) with the exception of the central scar. In portal phase of hepatic enhancement, the lesion becomes iso-attenuating to the surrounding liver parenchyma but the central scar remains as low attenuated spot. Unexpectedly the central scar show enhancement in delayed phase which is due to the presence of abubdant myxomatous stroma [11] .

On T1WI, the FNH shows iso- or hypointensity (94% - 100%) and on T2WI the lesion shows hyper or isointensity (94% - 100%) and homogeneity (96%). At the same time the central scar is of decreased signal on T1WI and of increased signal (84%) on T2WI because of the bile ductules, edematous myxomatous tissue and its vascular supply [1] [12] .

Following intravenous gadolinium chelates, the whole lesion enhances expect the central scar in arterial phase but the central scar shows enhancement on delayed phase [11] .

Hepatic adenoma, which is a differential diagnosis of FNH, is distinguished from FNH by the presence of heterogenous MR SI due to intralesional hemorrhage or fat component [13] .

Also for central scar of fibrolamellar HCC is distinguished from FNH by presence of hypointense on T1WI and T2WI without definite enhancement [14] .

Atypical presentation may be showed by the size of the tumor if the size exceeds 5 cm in diameter although majority possess the size less than 5 cm. In study by Ishak and Rabin of the 130 patients with FNH, 85% of patients was found to have a single nodule less than 5 cm in diameter, 12% had a FNH which measured between 5 and 10 cm and only 3% had the lesion greater than 10 cm. Larger tumors if measure greater than 5 cm may cause symptoms because the lesions may expand the Glisson’s capsule or cause focal mass effect on surrounding structures [15] . Large tumors may cause abdominal pain or awareness of the presence of an abdominal mass. Abdominal pain is usually caused by the expansion of the Glisson’s capsule or focal mass effect on surrounding organs or vascular structures (Figure 3).

Another parameter of FNH showing atypical presentation is multiplicity of lesions. Although mostly FNH is solitary, 22% (8 patients out of 37 patients) of FNH were found to have multiple lesions in study of Vilgrain et al. [12] . Two lesions in each of six patients, three in one patient and four in another patient were found (Figure 4 and Figure 5).

Some of FNH is found having hemorrhage and necrosis which are unusual findings [1] . Ischemic necrosis of FNH occurs more rarely which has been reported in 3 women who have history of oral contraceptive use [16] . Estrogens may cause vascular changes in FNH (Figure 6 and Figure 7).

On Gd-EOB-DTPA-enhanced MRI, T1WI of FNH may show homogenously intense enhancement in early phase, subtle washout during the delayed phase and a low signal perfusion defect in the hepatobiliary phase

which is similar to the findings of an expanding nodular HCC. Some atypical findings of FNH of patients of he patitis B may include hepatic nodule taking complete enhancement during the early arterial phase of MDCT, the delayed phase without definite washout of the contrast enhancement although the portal venous phase shows iso-attenuation with T2WI showing a high SI and mild diffusion restriction on DWI (b-factor 800) apparent different coefficient imaging with Gadoxetic acid enhanced MRI showing early intense homogenous enhancement and subtle peripheral washout during portal phase and ring like peripheral enhancement with central washout during equilibrium phase and hepatobiliary phase; which gives vague differential diagnosis like well-dif- ferentiated HCC, a high grade dysplastic nodule and hepatic adenoma. In this situation, we need to go for USG guided biopsy for confirm diagnosis [6] [17] [18] .

Intralesional steatosis in FNH is thought to have association with several hepatic injury like alcoholic toxicity, obesity and protein malabsorbtion. But fatty infiltration in FNH without underlying cause has been found very rarely and has been documented only twice in the literature [19] . In earlier reports, hepatic steatosis was thought to be result of the patient’s underlying disease while describing the presence of fat in FNH (Figure 8 and Figure 9).

It is found that the central scar of FNH is undetectable on CT (16% - 40%) and on MRI (22%) due to its extremely tiny size [1] [2] [10] [12] . This non-visualized scar only can be noticed when there is deformity of liver configuration or presence of mass effects like displacement of adjacent hepatic vessels (Figure 10 and Figure 11).

Fibrous thick hyaline pseudocapsule surrounding FNH can be seen enhanced which is very rare [20] . The presence of pseudocapsule in FNH may suggest that underlying lesion is growing slowly, the capsule in this cases is fibrous, thick and hyaline (Figure 12 and Figure 13); however in some cases it may be confused with the eccentric compression of the lesion on hypertrophied feeding vessels.

In delayed phase on contrast-enhanced CT and on T1W MR, the central scar of FNH may still appear hypodense and hypointense respectively while may mimick the collagenous scar in hepatic adenoma, HCC, fibrolamellar carcinoma or intrahepatic cholagiocarcinoma [20] . After administration of constrast material, appearance of the nonenhanced central scar may be due to obliterative vascular hyperplasia of the central arteries [1] (Figure 14 and Figure 15).