Mucocele Of Paranasal Sinuses

CT and MR Findings of Skull Base and Dura Mater Invasion

Assessment of the deep extent of sinonasal tumors toward the dural layer is one of the issues that significantly influence the treatment planning.

Like in the invasion of orbital walls, bone destruction of the skull base is better demonstrated by CT. However, here the imaging findings differ from those observed in the other bone interfaces of the sinonasal area because when the skull base is invaded, the dura mater usually shows abnormal thickening and enhancement that can be due either to neoplastic invasion or to inflammatory, non-neo-plastic reaction.

Since dural invasion implies both a worse prognosis and a surgical resection not limited to the eroded bone, the goals of imaging focus on establishing the depth of skull base invasion (Kraus et al. 1992b; Shah et al. 1997).

MR has been reported to be more precise than CT. Early observations emphasized the usefulness of T2 (and T1 sequences) in separating the low signal of bone from the high signal of CSF (Fig. 4.14). Thickening and enhancement of the dura mater invaded by tumor were mentioned by Weissman and CurTin (1994). Other investigators reported that enhanced MR sequences could demonstrate leptomeningeal invasion (Volle et al. 1989; Kraus et al. 1992a). Moreover, in the series by Ishida et

Mucocele Serie Tomografica

Fig. 4.14. Naso-ethmoidal adenocarcinoma, intestinal-type, TSE T2. Upward displacement of the right fovea ethmoidalis (1) due to a small mucocele underneath (showing hyperin-tense signal) secondary to tumor (that shows homogeneous intermediate intensity). The tumor abuts the right medial orbital wall, remodeled, but not invaded (2). Because of fluid retention within the contralateral posterior ethmoid cells, the papyracea/periorbita is well demonstrated (3). Opposite arrows point to the right residual vertical lamella of the middle concha. Olfactory tract (4)

Fig. 4.14. Naso-ethmoidal adenocarcinoma, intestinal-type, TSE T2. Upward displacement of the right fovea ethmoidalis (1) due to a small mucocele underneath (showing hyperin-tense signal) secondary to tumor (that shows homogeneous intermediate intensity). The tumor abuts the right medial orbital wall, remodeled, but not invaded (2). Because of fluid retention within the contralateral posterior ethmoid cells, the papyracea/periorbita is well demonstrated (3). Opposite arrows point to the right residual vertical lamella of the middle concha. Olfactory tract (4)

al. (2002), as well as in our own, specific changes in the appearance of the hypointense/absent signal of bone and the overlying dura proved to correctly predict dural invasion.

A key diagnostic observation concerns the signal intensity of the three structures located at the interface between the ethmoid roof and brain at the anterior cranial fossa: cribriform plate and its double periosteal covering, dura mater, subarach-noid space.

On enhanced sagittal and coronal MR spin echo T1 or 3D GE fat sat T1 sequences the three layers give rise to a "sandwich" of different signals (bone-periosteum complex, dura, CSF) (Ishida et al. 2002).

If a malignant sinonasal neoplasm approaches the ACF floor, three different conditions may occur: (a) the neoplasm appears in close contact with an uninterrupted, hypointense cribriform plate or fovea ethmoidalis (Fig. 4.15); (b) the neoplasm erases the hypointensity of the cribriform plate, extends into the ACF and displaces an uninterrupted, hyperintense and thickened dura (Fig. 4.16); (c)

the neoplasm encroaches the dural hyperinten-sity without erasing the hypointense signal of CSF (Fig. 4.17, 4.18); (d) the neoplasm extends beyond the dura encroaching the hypointense CSF and invades brain tissue (Fig. 4.19).

This last sign is easier to detect if the signal intensity of the neoplasm is lower than the enhanced dura surrounding the invaded segment (Maroldi et al. 1997).

Resectability of tumors invading the brain does not stand only upon the assessment by imaging of the depth of tumor extent into the brain or on the detection of bilateral brain invasion. It requires a thorough evaluation of several other issues, the most important being the histotype and patient's performance status. Patients with limited brain invasion treated by craniofacial resection are reported to have non-significant decrease in survival compared to those with dural invasion only.

Contraindications to surgery other than brain invasion are considered to be the involvement of the internal carotid artery or of the cavernous sinus (Shah et al. 1997) (Fig. 4.20)

Sino Orbital Mucocele

Fig. 4.15a,b. Ethmoidal adenocarcinoma, intestinal-type, plain (a) and Gd-enhanced T1 (b). The black signal of the planum eth-moidalis/fovea is continuous and regular [opposite white arrows on (a)]. Mild and uniform enhancement of the dura is detected after Gd administration [white arrows on (b)]. Invasion of medial wall and part of the floor of the orbit (black arrows)

Fig. 4.15a,b. Ethmoidal adenocarcinoma, intestinal-type, plain (a) and Gd-enhanced T1 (b). The black signal of the planum eth-moidalis/fovea is continuous and regular [opposite white arrows on (a)]. Mild and uniform enhancement of the dura is detected after Gd administration [white arrows on (b)]. Invasion of medial wall and part of the floor of the orbit (black arrows)

Dural Invasion

Fig. 4.16a-e. Naso-ethmoidal SCC, T1 after Gd administration. Intracranial invasion with dural thickening and subtotal dural infiltration. a Minimal dural thickening at the periphery of the lesion (1), normal frontal bone appearance at the orbital roof (2). Focal thickening of the dura (3) more hyperintense than the tumor's signal (4). b No sign of dural layer trespassing at this level, bone has been eroded (black arrows). Mild dural thickening (1). c-e On the sagittal planes, bone erosion and subtotal replacement of the hyperintense signal of the focally thickened dura suggest intracranial extradural invasion. Posterior sphenoid sinus wall destruction with hypophysis invasion is present. Blockage of frontal sinus drainage is associated with mucous retention and mucosal thickening

Fig. 4.16a-e. Naso-ethmoidal SCC, T1 after Gd administration. Intracranial invasion with dural thickening and subtotal dural infiltration. a Minimal dural thickening at the periphery of the lesion (1), normal frontal bone appearance at the orbital roof (2). Focal thickening of the dura (3) more hyperintense than the tumor's signal (4). b No sign of dural layer trespassing at this level, bone has been eroded (black arrows). Mild dural thickening (1). c-e On the sagittal planes, bone erosion and subtotal replacement of the hyperintense signal of the focally thickened dura suggest intracranial extradural invasion. Posterior sphenoid sinus wall destruction with hypophysis invasion is present. Blockage of frontal sinus drainage is associated with mucous retention and mucosal thickening

Fig. 4.17. Sinonasal undifferentiated carcinoma, Gd-enhanced T1. Midline invasion of the anterior cranial fossa floor (white arrows) without dural thickening (intracranial intradural spread). No sign of brain edema. Lamino papyraces (opposite arrrows)

Fracture Anterior Cranial Fossa AcfMild Ethmoid Disease
Fig. 4.18a,b. Adenocarcinoma of the ethmoid sinus, Gd-enhanced T1. a Tumor and the enhanced dura have similar signal intensity. The thickened dura is seen investing the planum ethmoidalis posteriorly to neoplastic invasion (arrow). b Intracranial intradural spread without brain invasion (arrows)
Sinonasal Undifferentiated Carcinoma

Fig. 4.19a,b. Recurrent adenoid cystic carcinoma, left maxillary sinus was the primary site, Gd-enhanced GE-T1 sequences. Galea capitis (1) and temporal muscle (2) invasion. The intracranial mass arises from spread through the greater wing of the left sphenoid [black arrows in (a)]. Intracranial intradural spread exhibits a mushroom-like appearance. Double layer enhancement along the inner surface of the temporal and parietal bones (3) may be correlated to dural spread (it does not extend into the sulci), the more hyperin-tense layer abutting brain tissue, and to sub-periosteal spread, the less hyperintense layer closer to the bone. Intra-diploic enhancement is present: compare abnormal (4) to normal (5) diploic signal. Bone is clearly invaded at the temporal fossa (6). A cyst-like mass is demonstrated on the posterior aspect of the intracranial tumor (7)

Fig. 4.20. Recurrent SCC of the posterior ethmoid, Gd-enhanced GE coronal plane. Encasement of right internal carotid artery (arrows) with cavernous sinus invasion

Retention Cyst Cavernous Sinus Mri

References

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  • folco
    What mucocele of paranasal sinuses?
    7 years ago

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