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 after contrast administration, axial plane. The neoplasm (T) occupies the posterior nasal cavities. Invasion of both sphenopalatine foramina and pterygopalatine fossae (black curved arrows) with bilateral PNS along the vidian canals. On the right side the linear enhancement reaches the petrous apex (possible PNS along the greater petrosal nerve, white arrow). The middle meningeal artery (ma) at the foramen spinosum, foramen ovale, and mandibular nerve (V3) are indicated, as is the horizontal segment of the left internal carotid artery (ica). b In the sagittal plane (TSE T1 after contrast administration) a thickened and enhancing vidian nerve (vn) runs across the vidian canal. Extensive sclerosis of the walls of the canal and of the clivus (black arrows) suggests the presence of permeative bone invasion.
Even if the patient does not show any neurological abnormalities, meticulous imaging is recommended to assess or rule out PNS along nerves, the distribution of which corresponds to the innervation of the sinonasal tract. This is a crucial point, since extracranial segments (and intraforaminal portions) of the maxillary and mandibular nerves and the vidian nerve can be resected by expanded TES. Conversely, intracranial segment involvement is a contraindication both for the difficulty to be reached and for the absence of improved survival of the patient. A key technical strategy to improve PNS detection by imaging consists in selecting technical parameters that maximize both spatial and contrast resolution. On CT and MRI, PNS may appear both as segmental thickening and asymmetric enhancement. Advanced involvement may result in significant nerve enlargement, leading to remodeling/erosion of fissures or foramina. In addition, the enlarged nerve causes obliteration of the fat planes or of the venous “coating” that accompanies the cranial nerves along skull base foramina. High spatial and contrast resolution are strongly recommended. High-resolution 3D gradient echo T1W sequences (VIBE, THRIVE, LAVA) provide an excellent solution. On these sequences, the normal nerve is hypointense, clearly detectable where it is surrounded by the enhanced venous plexus, for example along bony grooves and canals – like the vidian, maxillary, and mandibular nerves through their respective foramina. Muscular denervation is also a sign of PNS. Changes in the acute and late phase include edema and enhancement of the muscle(s) involved, and atrophy and fatty replacement, respectively.
Fig. 8. Adenocarcinoma. MRI in coronal planes obtained with a TSE T2 (a) and TSE T1 (b) sequence after contrast agent administration. The large tumor (T) is centered in the midline and grows toward the ACF floor (white arrows) without contacting the planum sphenoidale, above which are shown the olfactory tracts (ot), surrounded by normal CSF signal. The lesion, with a non-characteristic very low signal intensity on T2, shows exceptional postcontrast enhancement on the TSE T1 plane (b). Enhancement of a short segment of the dura (white arrows) lining the left portion of the planum sphenoidale is demonstrated. The enhancing dura is uniformly thin, without any nodular thickening. The absence of any “interruption” of the planum on the TSE T2 sequence (where the planum appears as a continuous regular black line) and the pattern of enhancement of the dura on the TSE T1 sequence are more consistent with an inflammatory reaction than with neoplastic invasion. The “short enhancing segment” is confined to the planum sphenoidale: its extent, therefore, does not contraindicate a TES approach. aea indicates the anterior ethmoidal artery canal leaving the left orbit.
Fig. 9. Adenocarcinoma. MRI in coronal planes obtained with a TSE T2 (a) and a TSE T1 sequence (b) after contrast agent administration. The neoplasm (T) reaches the sphenoid sinus roof where a segment of the bone is invaded (the black arrows indicate the invaded bone tract). Above the invaded segment the intracranial extent is limited by a thin continuous black line that, after contrast administration, shows a linear enhancement on the TSE T1 plane, indicating a reaction of the dura (a, b). A thin film of fluid, hyperintense on T2, hypointense on T1, corresponds to the CSF (csf, a, b). The overall pattern of signals indicates the intracranial extent without imaging findings of dura invasion.
Fig. 10. Intestinal-type adenocarcinoma. TSE T1 (a, b) in the coronal plane with fat saturation and after contrast agent administration. a The ethmoidal neoplasm (T) blocks the drainage from the maxillary (ms) and frontal (fs) sinuses where a thickened and enhancing mucosa outlines the walls of the sinuses, filled by mucus. The neoplasm invades the left ACF floor (arrows). On a more posterior plane (b), the enhancement of the dura (arrows) extends far over the left orbit roof, well beyond the midline, a contraindication for a TES approach. ss, sphenoid sinus.
3. The cranial vector of spread. Focal contact, infiltration of the ASB floor (cribriform plate or roof of the ethmoid), or of the overlying dural layer are not considered contraindications to TES [5] (Fig. 8,