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 MR angiography are used.
4. The lateral vector of spread. “High-risk” areas in this direction of growth are the medial wall of the orbit and lacrimal pathway. Most ethmoid and nasal neoplasms contact and displace the medial orbital wall, as soon as they reach an intermediate size. Because focal contact or focal infiltration does not contraindicate TES, the challenge for imaging is to grade the degree of orbital involvement, particularly when early invasion is suspected [3, 5, 30]. Bone erosion alone does not equal invasion. It is the periorbita, the fibrous capsule investing the whole orbital content, that is crucial, being more resistant to infiltration. The periorbita is not detectable by CT, but it can be identified by MRI as a thin regular stripe with low intensity on both T2W and T1W sequences (Fig. 12). Linear enhancement of the periorbita can also be observed, on the condition that fat saturation is used (Fig. 13). Focal interruption of the line by tumor indicates the presence of limited invasion. In this setting, MRI has been reported to be more sensitive and specific than CT in grading the tumor-orbit relationship, particularly in predicting early orbital invasion [37]. Special attention has to be paid to the orbital adipose tissue. Advanced orbital invasion should be reported when the tumor tissue replaces the extraconal fat, extends into the fat space between the extraocular muscles, and causes enlargement or abnormal signal intensity of the muscles. Tumor invading the extraocular muscles will require orbital clearance and thus an open approach [38, 39]. When focal or limited invasion involves the medial wall close to the orbital apex, the analysis of the fat planes surrounding the annulus of Zinn becomes more troublesome. High-resolution imaging in axial and coronal planes is recommended.
Fig. 12. Intestinal-type adenocarcinoma. Both the axial CT (a, postcontrast) and TSE T2 MR sequence (b) detect the invasion of the left medial orbital wall (white arrows). The intraorbital nodule is characterized by a regular outline (though lobulated), suggesting that the periorbita may still contain the neoplasm, a finding more clearly shown by a continuous “black line interface” on the MRI sequence. A compression on the medial rectus (mr) is present. acp, anterior clinoid process; sof, superior orbital fissure; oa, ophthalmic artery; im, impacted mucus.
The checklist should include assessment of the lacrimal pathways. Epiphora, or the presence of dilation of the lacrimal sac, requires a meticulous evaluation. The bony walls of the lacrimal canal are well imaged by CT, while the lining mucosa of the lacrimal duct is better analyzed by MRI. Limited involvement of the canal, especially the medial wall, does not contraindicate TES [5, 30]. Lacrimal drainage can be re-established via endoscopic dacryocystorhinostomy. On the contrary, an extensive invasion of the canal and the duct requires open access.
5. The medial vector of spread. Neoplastic invasion through the septum has to be reported, along with a detailed description of the tumor extent into the contralateral nasal cavity and ethmoid labyrinth. Special attention has to be paid to the involvement of the contralateral medial orbital wall.
6. The inferior vector of spread. When the tumor reaches or invades the hard palate, TES is contraindicated, since both the resection and reconstruction of the defect are very difficult to achieve via this approach alone [5].
Fig. 13. Sinonasal neuroendocrine carcinoma. Five MRI sequences in the coronal plane are obtained to analyze the relationship of the neoplasm with the orbital walls: two TSE T2 sequences without (a) and with (b) fat saturation, two TSE T1 sequences before (c) and after (d) contrast agent administration, and one VIBE sequence after contrast administration (e). The right nasoethmoidal neoplasm (T) grows into the maxillary sinus, blocking the drainage. The dehydrated impacted mucus (deh) has a signal lower than CSF on the T2W sequences (a, b) and higher on the T1W sequences (c–e). Non-dehydrated blocked mucus fills the right frontal sinus (white arrow): hyperintense on T2W sequences (a, b), and hypointense on T1W sequences (c–e). A mucocele arises from an anterior ethmoid cell (asterisk) blocked by tumor. The mucocele remodels the medial orbital wall (black curved arrow). Below the mucocele, it is the tumor itself that contacts the orbital wall, which is thickened (white arrows). The interface between the mucocele (above) and the tumor (below) with the displaced orbital wall is better appreciated on fat-saturated sequences (compare