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, 9). However, if the infiltration of the dura extends over the orbit beyond the mid-orbital line (Fig. 10) or a massive infiltration of the brain is detected, the endoscopic approach must be combined with an open access technique. Therefore, intracranial invasion requires thorough evaluation and to be graded via a proper imaging technique.
The intracranial extradural tumor extent is defined as a tumor growing through the bone but confined to the dural layer, which is raised and enhanced, but without a significant thickening. In fact, in the absence of thickening, dural enhancement alone has high sensitivity (88%) but poor specificity (50%) for transdural invasion [33]. The specificity reaches 100% if changes like nodularity or thickening greater than 5 mm are observed [36]. High-resolution 3D gradient echo T1W sequences (VIBE, THRIVE, LAVA) are indicated. Images reconstructed along planes perpendicular to the ASB floor (coronal, sagittal) are very useful [7]. Pial enhancement, when observed, has a very high predictive value for malignant invasion [33]. Unfortunately, the sensitivity is poor (50%). Therefore, preoperative MRI cannot rule out pial involvement. Further intracranial tumor progression can lead to brain parenchyma compression or invasion. Because brain compression by the tumor can cause edema, only the detection of intraparenchymal enhancement continuous with the tumor is a reliable sign of brain invasion. Hence, a combination of T2W, FLAIR, and postcontrast T1W sequences should be obtained (Fig. 11).
Fig. 11. Two patients, both affected by a nasoethmoidal squamous cell carcinoma with intracranial invasion. a In the sagittal TSE T2 plane, the neoplasm (T) “permeates” the black line of the ACF floor (curved white arrows), growing intracranially displacing the brain (white arrows), which appears mostly separated from the neoplasm by the CSF signal. The tumor invades the frontal sinus: anterior vector of spread (black arrow). b In the second patient, the sagittal TSE T2 plane shows a more extended permeation of the ACF floor (curved white arrows) and a larger intracranial invasion (white arrowheads). Apart from a short area of contact, sited posteriorly (black arrowheads), no CSF interface separates the tumor signal from the brain. An extensive area of brain edema (e) at the interface with the tumor indicates extensive cerebral invasion.
When substantial intracranial intradural neoplastic extent is detected by imaging, its relationships with the proximal branches of the anterior cerebral artery should be reported. CTA and
