crucial findings.
Fig. 6. Intestinal-type adenocarcinoma. MR in three coronal planes obtained with a TSE T2 (a) and TSE T1 sequences before (b) and after (c) contrast agent administration. The tumor (T) fills the left nasal fossa and extends along the septum to reach the olfactory fissure, where it displaces the left superior turbinate (dotted arrow). The neoplasm shows high and non-homogeneous signal intensity on T2 (a), due to large mucinous components. These parts appear hypointense on plain T1 (b), while the postcontrast enhancement is rather heterogeneous (c). The tumor reaches the nasal floor (black arrows). A mucocele (m) arises from an ethmoid cell. It is characterized by a typical pattern of signals: hypointensity on T2, mild hyperintensity on T1 – indicating the presence of dehydrated impacted mucus – and no enhancement. The mucocele remodels the lamina papyracea and the fovea ethmoidalis (white arrow). st, right superior turbinate; ob, olfactory bulbs; ms, blocked left maxillary sinus.
The first step consists of separating the tumor from the signal of the retained mucus or the inflamed thickened mucosa in a blocked sinus. On plain CT the discrimination is less clear than on T2W MRI sequences, where the mucus shows a greater signal than most tumors. However, if large mucinous components characterize the tumor, as in intestinal-type adenocarcinoma, the differentiation from retained secretions or mucoceles may be difficult. Enhancement of solid parts of the tumor after contrast agent administration improves discrimination on CT and MRI. An additional advantage of MRI is that long-standing blocked secretion, as well as many mucoceles, exhibit a recognizable increased signal on T1W sequences, due to the increase in protein content (Fig. 6).
The second step is mapping tumor spread to investigate either the accessibility for TES, or the need for an open access. Depending on the extent of the tumor, TES can be exclusively endonasal or combined with a transcranial approach (CER) [5, 30]. Purely endonasal approaches are graded into unilateral (i.e., the resection extends sagittally from the posterior wall of the frontal sinus to the planum sphenoidale and coronally from the nasal septum to the lamina papyracea) or bilateral (i.e. the resection extends from one lamina papyracea to the opposite one). TES may be extended to include the dura of the ASB from the posterior wall of the frontal sinus back to the planum sphenoidale (endoscopic resection with transnasal craniectomy).
Epicenter of Tumor Located in the Nasal Cavity or Ethmoid
When the epicenter of the tumor is located in the nasal cavity or the ethmoid, the checklist for assessing the 3D extent should include six “vectors of growth” to be scrutinized and reported.
1. The anterior vector of spread. The infiltration of nasal bones or invasion of the anterior wall of the frontal sinuses are contraindications to a pure TES. These bone structures cannot be properly reached by endoscopes due to the unfavorable angulation. Since a reconstruction could not be performed after resection of the bones, a deformity of the face would result. To properly assess this path of growth, the axial plane should be integrated by at least one sagittal plane (CT or MRI). Primary malignant neoplasms of the frontal sinus are very rare, with a reported incidence less than 2% [28].
2. The posterior vector of spread. A growth along this direction leads the tumor into the sphenoid sinus (above), choana, and nasopharynx (below). Primary malignant neoplasms arising from the sphenoid sinus are infrequently found, with an incidence of approximately 4% [31]. As for the anterior pattern of spread, the acquisition of sagittal planes is suggested.
When the tumor extends toward the sphenoid sinus, the checklist has to report whether the neoplasm simply obstructs the mucus drainage by blocking the sphenoethmoidal recess or if it grows into the sinus cavity. If the cavity is partially or completely occupied by tumor tissue, detailed analysis of the bone walls is mandatory. Tumor spread through the lateral wall eventually implies the invasion of the foramen rotundum, superior orbital fissure (below), Meckel’s cave (more posteriorly), and the cavernous sinus (above; Fig. 2). To properly evaluate this area, the anterior clinoid process (ACP) may be used as a landmark, particularly on high-resolution coronal CT and MR sections. In this plane of section, below and lateral to the ACP the posterior portion of the superior orbital fissure (fat tissue and nerves) is detectable. Medial to the ACP runs the optic nerve (surrounded by CSF) and the anterior genu of the intracavernous ICA. The morphology of the ACP itself needs to be evaluated to identify variants such as pneumatization (in this case, mucus retention is possible) or neoplastic involvement replacing the cancellous signal and eroding its cortical rim. More posteriorly (and below) is Meckel’s cave, filled with CSF.
Overall, the anatomical arrangement in this area is quite unique: it includes CSF-surrounded structures, cortical-cancellous bone boxes, venous-filled containers, and fat tissue-stripes. A combination of high-resolution T2W and postcontrast T1W, preferably volumetric sequences, is recommended. A postcontrast CISS sequence offers the simultaneous depiction of CSF and contrast-enhancing structures such as the venous network of the cavernous sinus (Fig. 3). The analysis should extend to the sphenoid sinus roof (sellar floor) and the posterior wall, where – beyond the cortical rim – a variable amount of cancellous bone is present. The medial wall is the least resistant, and is frequently transgressed. When the floor of the sphenoid sinus is invaded, the tumor accesses the roof of the nasopharynx – a sagittal plane, combined with a coronal one, is very useful to precisely delineate tumor spread.
In nasoethmoidal tumors that extend posteriorly, but mostly below the sphenoid sinus, a lateral spread at the level of the choana assumes great relevance for treatment planning. In fact, lateral to the choanae lies a crucial crossroads, the pterygopalatine fossa (PPF), which contains nerves (and vessels) and is in strict relationship with the inferior and superior orbital fissures. Imaging findings indicating tumor invasion of the PPF include destruction of the pterygoid laminae, with possible involvement of the pterygoid process, and obliteration of the fat tissue within the PPF, replaced by tumor signal. While CT easily shows the erosion of laminae and cortical rims, MRI has a greater sensitivity for bone marrow invasion, the submucosal extent of a tumor into fissures, and perineural spread (PNS) [32, 33] (Fig. 7). Even if CT can reveal cancellous bone sclerosis, its intrinsic contrast resolution is insufficient to detect bone marrow enhancement. A combination of pre- and postcontrast T1W sequences is the proper strategy to demonstrate the replacement of the hyperintense signal of fat (present both in fissures and bone marrow) by the low signal of the tumor (on plain T1W) and its enhancement after contrast administration. A significant thickening of the cancellous framework of the pterygoid process can be frequently observed in adenoid cystic carcinoma and lymphoma. It translates into marked hypointensity on plain T1W sequences [34]. A further lateral extent of the tumor into the infratemporal fossa has to be reported. Such a situation usually requires additional surgical approaches [35]. Indeed, invasion of the superior orbital fissure and apex cannot be approached by TES alone.
Fig. 7. Adenoid cystic carcinoma. a 3D isotropic GE sequence
