Head and Neck ImagingSinonasal cavities, cancer
Malignant tumours arising from the sinonasal mucosal lining constitute less than 1% of all
malignant neoplasms. The risk of developing certain types of sinonasal
carcinoma is associated with exposure to certain exogenous factors (
adenocarcinoma head and neck in woodworkers;
squamous cell carcinoma head and neck with exposure to nickel). Tumours arising in the
paranasal sinuses have abundant room to grow, and associated inflammatory disease may overshadow the
tumour. For these reasons, sinonasal cancers are usually diagnosed in an advanced stage. Palatal deformation, pain or malfitting of a denture may be the first signs. Facial deformation or trismus originate from extrasinusal
tumour spread. Orbital symptoms and a variety of neurological symptoms may be encountered when the orbit or skull base is invaded. Nasal vestibule cancers have a natural history resembling that of skin cancer; tumours at this site may have spread more extensively than first suspected on clinical evaluation.
Squamous cell carcinoma is the most common sinonasal cancer, usually arising in the nose or the maxillary sinus, but at first presentation the tumour will usually have begun to spread into the ethmoidal cells and maxillary antrum. Adenocarcinoma more frequently arises in the ethmoid. Adenoid cystic carcinoma more commonly originates in the nose and maxillary sinus. Primary frontal or sphenoidal cancers are rare.
Sinonasal cancer appears as a solid, moderately enhancing mass lesion on CT studies. Local bone destruction is characteristic of malignant tumours, as opposed to the expansion of the sinus cavity seen with a benign tumour and mucocele.
On MRI sinonasal cancer usually shows an intermediate signal intensity, on both T2- and T1-weighted sequences. The intermediate T2 signal intensity allows separation of the tumour mass from high intensity inflammatory changes (Fig.1). Only a few sinonasal tumours show a high T2 signal intensity: this is mainly seen with tumours from salivary gland origin or neuromas, and in these cases differentiation from surrounding inflammatory changes may be more difficult on T2-weighted images. In such cases the gadolinium-enhanced T1-weighted images will help to differentiate the enhancing mass lesion from nonenhanced oedema or fluid within the sinonasal cavities.
Extension towards neighbouring structures
Anterior cranial fossaThe first sign of intracranial spread is erosion of the delicate bone interface between the sinonasal cavity and the anterior cranial fossa, best detected on coronal CT images. Tumour spread beyond the bony nasoethmoidal roof is best seen using MRI. Linear dural enhancement as seen on coronal or sagittal T1-weighted images often represents reactive (inflammatory) changes. Dural enhancement and focal nodularity, dural thickening of more than 5 mm, and pial enhancement are highly suggestive of neoplastic dural invasion. Brain invasion is seen as enhancement of the brain parenchyma, often with surrounding brain oedema (Fig.2).
OrbitThe earliest sign of orbital involvement is erosion of the delicate bony orbital borders (usually lamina papyracea and/or floor of the orbit). With further tumour growth, the extraconal fat will often be displaced laterally without direct invasion; the strong periorbita (the orbital 'periosteum') acts as a barrier to tumour spread, walling off the tumour from the orbital fat. Displacement of the periorbita cannot be distinguished from neoplastic invasion by imaging. When the tumour has crossed the periorbita, direct tumoral invasion of the various intraorbital structures becomes possible.
Infratemporal fossa and middle cranial fossaExtension towards the infratemporal fossa occurs through the posterolateral wall of the maxillary sinus (Fig. 3). After infiltration of the retromaxillary fat, the tumour will reach the masticatory muscles.The pterygopalatine fossa may become involved by tumour growth through the posterior wall of the maxillary sinus, or via perineural tumour spread, head and neckalong the infraorbital nerve, the posterior superior alveolar neurovascular bundle in the posterolateral wall of the maxillary sinus, or the neurovascular bundle in the greater and lesser palatine foramina. From the pterygopalatine fossa, the tumour may extend to the cavernous sinus, through the orbital apex or via the maxillary nerve (Fig. 3).
Therapeutic relevance of imaging findings
Many patients with sinonasal cancer are managed surgically. Most cancers will require some form of transfacial surgical approach, with more or less extensive resection of sinonasal structures. See craniofacial resection.
Surgery can be the sole treatment modality or part of a multimodality treatment plan, depending on tumour extent; often a combined treatment will be necessary. In advanced sinonasal cancer, surgery is often combined with radiation therapy to improve the outcome. The radiation fields are individualized based on disease extent; CT and/or MRI findings play an important role in this regard.
RH
RH
To view high resolution images,
please register first.
Click
here
to register.
Already registered? Enter your e-mail in the window below.Re-registerFig.2
Squamous cell carcinoma.
a. Coronal unenhanced CT image (bone window), in a patient complaining of frontal headache and a single episode of epistaxis. A large right-sided nasoethmoidal mass is seen, growing through the superior part of the nasal septum and destructing the bony ethmoidal walls and middle turbinate. Erosions in the roof of the nasal cavity and ethmoidal cells are noted (arrowheads).
b. Coronal T2-weighted spin-echo image. The tumour mass appears with intermediate signal intensity, and is clearly growing through the nasal septum. Subtle brain hyperintensity is seen in the anterior cranial fossa (arrowheads). At this stage, the patient has retro-obstructive inflammation in the right maxillary sinus.
c. Coronal gadolinium-enhanced T1-weighted spin-echo image. The enhancing tumour mass is seen to extend into the anterior cranial fossa (white arrowheads), and cannot be delineated from the overlying brain parenchyma. Neighbouring enhancing dural thickening (arrows), probably due to reactive inflammation; some extradural tumour extension is suspected at the right side. Note the subtle enhancement against the orbital side of the lamina papyracea (black arrowhead), representing early orbital invasion. The brain invasion, the reactive dural changes and the intraorbital extension were pathologically proven in this patient.
 | |  | |  |
Sinonasal cavities, cancer, Fig.1 (a) | | Sinonasal cavities, cancer, Fig.1 (b) | | Sinonasal cavities, cancer, Fig.2 (a) |
 | |  | |  |
Sinonasal cavities, cancer, Fig.2 (b) | | Sinonasal cavities, cancer, Fig.2 (c) | | Sinonasal cavities, cancer, Fig.3 (a) |
 | |  | |  |
Sinonasal cavities, cancer, Fig.3 (b) | | Sinonasal cavities, cancer, Fig.3 (c) | | Sinonasal cavities, cancer, Fig.3 (d) |