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 a to b). Although the administration of contrast agent improves the differentiation between mucus and tumor (compare c to d) and improves the detection of the mucosa (white dotted arrows in d, e), the association of T1W “coupled” to fat saturation (e) amplifies enhancement of the periorbita (black curved arrows in e). ion, infraorbital nerve.
Malignant Tumors Arising in the Maxillary Sinus
Malignant tumors that arise within the maxillary sinus and grow toward the nasal cavity to eventually reach the ASB are, in most cases, very advanced and rare (Fig. 14). If surgery is considered in these patients, craniofacial resection is indicated, usually with adjuvant radiotherapy (± chemotherapy) [40]. The checklist for assessing the 3D extent should include, once more, six “vectors of growth.” They will comprise the potential invasion of the anterior wall and premaxillary soft tissues (anterior vector), the orbital floor and PNS along the infraorbital nerve (cranial vector), and the extension through the floor of the maxillary sinus, alveolar process, and hard palate (inferior and medial vectors). When a maxillary malignancy invades the posterolateral maxillary sinus wall (posterior and lateral vectors) it results in a deep pattern of growth, which leads to destruction of the pterygoid laminae, invasion of the PPF, and spread into the infratemporal fossa/masticator space. Further extent leads the tumor to infiltrate the middle skull base structures via involvement of the greater wing of the sphenoid, and its foramina, or the superior orbital fissure. Once the neoplasm grows inside these spaces and structures, there is a good chance of PNS along the branches of the trigeminal nerve into Meckel’s cave or into the cavernous sinus.
Olfactory Neuroblastoma
ONB can be regarded as the prototype of a neoplasm arising from the skull base itself. In most cases, the site of origin of the neoplasm is the cribriform plate or the adjacent superior turbinate and the superior half of the nasal septum. From this restricted area, the neoplasm permeates the ASB floor, extends intracranially, and also grows in the nasoethmoidal cavity. The result of these two vectors is an “hourglass” pattern: a solid intracranial and intranasal mass with a “waist” at the ASB floor (Fig. 15). In the checklist, it is important not to overlook the findings contraindicating TES. These include: a large invasion of the frontal sinus, a massive extension to the cerebral parenchyma, spread of the tumor above the orbits, or erosion of the anterior facial skeleton [41]. Among the ONB imaging findings described, intratumoral necrosis and significant postcontrast enhancement should be considered [42].
