Sinonasal lymphomas are almost exclusively non-Hodgkin lymphomas (Gufler et al. 1997), their imaging appearance is rather nonspecific. CT and MR findings consist of a diffusely infiltrating soft tissue mass with ill-defined borders (Gufler et al. 1997) (Fig. 9.37). On MR, slightly non-homogeneous signal may be observed, hyperintense on T2 and intermediate on T1 sequences (Han et al. 1993; Gufler et al. 1997; Ooi et al. 2000). Variable degrees of enhancement can be observed both on CT and MR after contrast administration (NaKAMura et al. 1997) (Fig. 9.38). Calcifications are not present, whereas tumor necrosis has been reported in T-cell natural killer lymphoma (jAFfl et al. 1996), more commonly in lesions with volume greater than 15mm3 (King et al. 2000).
Fig. 9.37a,b. Sinonasal non-Hodgkin lymphoma. The patient complained of right side nasal obstruction associated with sixth left cranial nerve palsy. Axial enhanced CT (a) and T2 (b) images show a soft tissue mass occupying the right ethmoid sinus (T). Spread into both anterior sphenoid sinus walls is present, with a thicker plaque on left side (short white arrows). Via osseous spread, tumor invades the left posterior sphenoid sinus (arrowhead), and extends into posterior cranial fossa probably invading the foramen of Dorello (long white arrows on a, black arrowheads on b) where sixth nerve runs. Cavernous sinus invasion is also present with tumor surrounding left internal carotid artery (black arrows). Erosion of right nasolacrimal duct is demonstrated by CT (black arrowhead on a)
T-cell NK lymphoma accounts for approximately 45% of all sinonasal lymphomas. This variant more commonly arises from midfacial structures (septum, nasal cavity, and hard palate) and provokes bone destruction in up to 78% of cases, mainly at the level of septum, the medial maxillary sinus wall and the lamina papyracea (Ooi et al. 2000). Due to its natural history, T-cell NK lymphoma, before the advent of im-munophenotypic characterization, has been labeled with a variety of different names, such as midline lethal granuloma, polymorphic reticulosis, progressive lethal granulomatous ulceration. According to King et al. (2000), posterior extension to the nasopharynx is common, whereas encroachment of the cribriform plate is not to be expected.
An additional pattern of bone destruction is reported consisting of permeative infiltration, i.e. the presence of tumor tissue on both sides of a bone boundary in the absence of detectable cortical erosion (Fig. 9.39). This phenomenon, described on both CT and MR examinations, may occur in up to 60% of cases. The lack of histological sub-typing in the majority of published reports does not allow ascertaining whether permeative bone infiltration is more frequent in any of the subtypes of non-Hodgkin lymphoma.
The list of differential diagnosis for sinonasal lymphoma potentially includes any other malignant histotype. Permeative bone infiltration is uncommon in most neoplasms, nonetheless it found also in adenoid cystic carcinoma (see section 9.2.5). In addition, whenever midfacial destruction is detected, the list
Fig. 9.39. Non-Hodgkin lymphoma extending from nasopharynx into the sinonasal tract. On the enhanced T1 in the sagittal plane, permeative invasion of the clivus is demonstrated (long arrows). A localization in the calvaria is also present. It is characterized by minimal changes in the diploic signal. Intracranial extent of this lesion appears as an epidural soft tissue mass, which - combined with thickening and enhancement of the adjacent dura mater - gives rise to the lenticular-like pattern of epidural lesions (short arrows). Extracranial extent with displacement of galea capitis is also seen
Fig. 9.39. Non-Hodgkin lymphoma extending from nasopharynx into the sinonasal tract. On the enhanced T1 in the sagittal plane, permeative invasion of the clivus is demonstrated (long arrows). A localization in the calvaria is also present. It is characterized by minimal changes in the diploic signal. Intracranial extent of this lesion appears as an epidural soft tissue mass, which - combined with thickening and enhancement of the adjacent dura mater - gives rise to the lenticular-like pattern of epidural lesions (short arrows). Extracranial extent with displacement of galea capitis is also seen of differentials to be considered is even wider as such a pattern is shared also by infectious and non-infectious destructive diseases (such as fungal infections, Wegener's granulomatosis, sarcoidosis, and cocaine induced midline destructive lesions).
Granulocytic sarcoma (chloroma) is a rare complication of acute and chronic myeloid leukemia, which may easily be confused with lymphomas, particularly when extracranial sites are also involved. It is usually associated with a myeloproliferative disorder but may be seen preceding the onset of leukemia. Granulocytic sarcoma is formed of malignant myeloid precursor cells occurring at an extramedul-lary site. On CT, an enhancing soft tissue mass with slightly infiltrating appearance may be observed. On MR, variable signal intensity is shown on T2 and T1 sequences (Freedy and Miller 1991; Prades et al. 2002) (Fig. 9.40).
Extramedullary plasmacytoma of the sinona-sal tract does not have specific imaging features (Fig. 9.41). A soft tissue lesion with possible bone destruction has been reported (Kondo et al. 1986; Ching et al. 2002) (Fig. 9.42).
Fig. 9.42a,b. Extramedullary plasmacytoma arising from right maxillary sinus. a On unenhanced axial T1, the epicenter of the mass is located between anterior wall and zygomatic bone (T). Signal intensity of the lesion results slightly greater than retained mucus in the maxillary sinus. Extensive thinning with irregular remodeling of the anterior sinusal wall (white arrowheads) and also focal bone invasion (black arrowheads) are present. b Coronal enhanced T1 image demonstrates the submucosal location of the mass - as suggested by displacement of thickened mucosa by tumor (white arrows)
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