Info

Imaging Findings

Imaging findings of adenoid cystic carcinoma depend on its particular pattern of growth which is characterized by early submucosal spread eventually leading to subperiosteal bone invasion, permeative invasion of adjacent connective spaces containing fat tissue and muscles, and by perineural spread. In addition, adenoid cystic carcinoma has a peculiar natural history, consisting of a protracted clinical course with a slow but relentless rate of growth, the occurrence of multiple recurrences, and late distant metastases (Kim et al. 1994; Fordice et al. 1999).

The sinonasal tract may be either the site of origin of the neoplasm or it may be invaded by a lesion arising from adjacent sites, more often the hard palate

(Kühel et al. 1992; Beckhardt et al. 1995; Ginsberg and DeMonte 1998). MR is the imaging technique of choice, as its superior contrast resolution enables to early detect signal changes due to the peculiar patterns of growth of this histotype.

However, both the CT density and the signal intensity on MR studies are non-specific and do not permit to differentiate adenoid cystic carcinoma from other malignancies (Fig. 9.18). Not even the signal intensity of adenoid cystic carcinoma on T2 sequences ensures to distinguish the solid subtype from the cribriform one (Yoüsem et al. 2000), although initial reports suggested (Sigal et al. 1992).

Nevertheless, adenoid cystic carcinoma may be suspected on imaging studies when a submucosal lesion is associated with findings indicating perineural spread, particularly if the neoplasm is located in the postero-inferior aspect of maxillary sinus and close to the hard palate (Maroldi et al. 1999).

Though perineural spread along named nerves may be thoroughly delineated by MR, there are two less evident patterns of spread that require dedicated techniques of study and meticulous images analysis: subperiosteal bone invasion and extent into fat spaces. Both patterns arise from the tendency of adenoid cystic carcinoma to invade fat and bone similarly to lymphomas (i.e., with permeative rather than

Maxillary Sinus Carcinoma

Fig. 9.18 Adenoid cystic carcinoma of left maxillary sinus. Post-contrast CT shows a mass with a pattern of growth similar to an antrochoanal polyp: the tumor extends from maxillary sinus into the nasopharynx. Nonhomogeneous enhancement and the association of erosion and sclerosis of the residual maxillary sinus wall suggest a tumor

Fig. 9.18 Adenoid cystic carcinoma of left maxillary sinus. Post-contrast CT shows a mass with a pattern of growth similar to an antrochoanal polyp: the tumor extends from maxillary sinus into the nasopharynx. Nonhomogeneous enhancement and the association of erosion and sclerosis of the residual maxillary sinus wall suggest a tumor

Treatment For Nasopharyngeal Cyst

Fig. 9.19a,b. Recurrent adenoid cystic carcinoma primary arising from left maxillary sinus, treated by surgery and radiation therapy 6 years before. The patient complained of periorbital pain for two months on left side, and had left exophthalmos. a Coronal plain T1 shows replacement of fat tissue within the masticator space (asterisk) without displacement of adjacent pterygoid muscles. In addition, nonhomogeneous hypointensity replaces the bone marrow signal of left sphenoid bone (arrows) (pterygoid process, greater wing, anterior clinoid, and sphenoid sinus floor). The cortical lining of these bony structures is not detectable. b Administration of contrast agent causes enhancement of neoplastic tissue permeating the masticator space, of pterygoid muscles - which maintain their organization in bundles. Enhancement of the diploic bone of the sphenoid (up to the left clinoid) is consistent with extensive lymphomatous-like invasion. Perineural spread is demonstrated by nodular thickening and enhancement of the third nerve (thick white arrow) and maxillary nerve (arrowhead). Irregular meningeal thickening is present along middle cranial fossa floor (thin white arrows)

Fig. 9.19a,b. Recurrent adenoid cystic carcinoma primary arising from left maxillary sinus, treated by surgery and radiation therapy 6 years before. The patient complained of periorbital pain for two months on left side, and had left exophthalmos. a Coronal plain T1 shows replacement of fat tissue within the masticator space (asterisk) without displacement of adjacent pterygoid muscles. In addition, nonhomogeneous hypointensity replaces the bone marrow signal of left sphenoid bone (arrows) (pterygoid process, greater wing, anterior clinoid, and sphenoid sinus floor). The cortical lining of these bony structures is not detectable. b Administration of contrast agent causes enhancement of neoplastic tissue permeating the masticator space, of pterygoid muscles - which maintain their organization in bundles. Enhancement of the diploic bone of the sphenoid (up to the left clinoid) is consistent with extensive lymphomatous-like invasion. Perineural spread is demonstrated by nodular thickening and enhancement of the third nerve (thick white arrow) and maxillary nerve (arrowhead). Irregular meningeal thickening is present along middle cranial fossa floor (thin white arrows)

expansive growth. As a result, even extensive replacement of fat by the hypointense tumor may be associated with few mass-effect signs on plain SE T1. In fact, muscles and vessels appear encased by tumor, which shows bright enhancement after contrast agent administration (Fig. 9.19).

Moreover, plain SE T1 are particularly useful to detect bone marrow replacement by tumor. One should carefully search for focal/diffuse hypointense areas within medullary/diploic bone of the maxillae - particularly the alveolar process - and sphenoid - mostly the pterygoid root, the greater and lesser wings -. If these abnormal areas are hypointense also on TSE T2 and enhance on fat-sat T1 sequences, permeative invasion associated with sclerotic changes is suggested. Though CT may reveal medullary bone sclerosis, its intrinsic contrast resolution is insufficient to detect bone marrow enhancement. Nevertheless, subperi-osteal bone invasion and fat tissue infiltration by adenoid cystic carcinoma may be suspected on high resolution CT whenever the technique shows subtle areas of cortical bone erosion, particularly if associated with sclerosis and fat tissue effacement.

Although imaging may reveal the occurrence of these two patterns of growth and detail the gross, macroscopic, extent of neoplasm, very often adenoid cystic carcinoma is characterized by extensive and unexpected submucosal microscopic spread that either imaging techniques or careful surgical examination fail to detect, being demonstrated only by random biopsies.

Was this article helpful?

0 0
Drug Addiction Report

Drug Addiction Report

You're going to discover so many things on addiction with little effort Not only will you discover the thrill of breaking free from your addiction, but you'll also learn extra bonus tips to actually help other people This new breakthrough book is a guide, really. A guide as a result of years of searching, studying, and scouring hundreds of websites, stores, and magazines.

Get My Free Ebook


Post a comment