Presentation
Acute right facial weakness and pain
Patient Data
CT angiography of the head and neck was obtained for suspicion of stroke. No territorial infarction, hemorrhage, or intracranial mass effect are evident. The major intracranial and cervical arteries are widely patent (only 3 mm thick images are shown). A mass infiltrates the right parotid gland and contains calcifications.
Targeted ultrasound of the right parotid gland shows diffuse heterogeneity and a central nodular lesion with calcifications measuring 1.5 cm.
MRI of the neck shows enhancing soft tissue replaces nearly the entire right parotid gland parenchyma. This tissue has low apparent diffusion coefficients (in the range 700-950 x 10-6 mm2/s depending on the region of interest selection). The infiltrative tissue surrounds a nodule that has a thick low-intensity rim and internal component that has mixed high and low signal intensity on T2WI, which has been termed the black ring sign.
Case Discussion
Acute facial weakness often prompts stroke imaging when bedside clinicians are unsure of whether the etiology is central (forehead-sparing) or peripheral (forehead-involving) based on their physical exam. Radiologists routinely evaluate these exams for central etiologies such as a middle cerebral artery territory infarct or intracerebral hemorrhage but should also examine the parotid gland for malignancy, which uncommonly presents with an acute facial weakness. On the neurologist's examination following CT, the facial weakness was determined to be peripheral in etiology. The development of peripheral facial paralysis with pain prompted dedicated imaging of the parotid, first with ultrasound and then MRI.
The imaging findings were concerning for carcinoma, specifically invasive carcinoma ex pleomorphic adenoma owing to a recently described imaging finding termed the black ring sign 1. The patient reported a remote history (15 years ago) of being told he had a calcified preauricular nodule that was presumed to be a lymph node and was not further evaluated until the current presentation. Fine needle aspirate was inconclusive and biopsy was repeated with a core needle due to the high level of clinicoradiologic concern. The biopsy showed salivary duct carcinoma ex pleomorphic adenoma.
Parotidectomy and neck dissection was performed. Final surgical pathology confirmed the diagnosis of invasive carcinoma ex pleomorphic adenoma, with salivary duct carcinoma histology. There was extensive lymphovascular invasion, perineural invasion, and multiple nodal metastases with extranodal extension. The pathologic stage (AJCC 8th edition) was pT4bN3b and adjuvant therapy was instituted. The patient had no evidence of disease at 1 year follow-up.
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