PMC6195916_01
(a) Ultrasound image (longitudinal) demonstrating a poorly defined, irregular, hypoechoic lesion that corresponds to the primary parotid tumour, within the superficial parotid gland extending towards the deeper lobe. (b) Coronal T
2 weighted craniofacial MRI image demonstrating a low signal lesion within the left parotid gland, adjacent to the mandible (black arrow), which corresponds to the primary parotid tumour.
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fig1
The patient originally presented with a 1-year history of a left parotid region mass and co-existing ipsilateral facial nerve palsy, with the diagnosis confirmed using ultrasound, MRI (Figure 1a,b) and core biopsy of the lesion (Figure 2a,c).
(a) H and E-labelled section (10x magnification) of the parotid tumour demonstrating tumour invasion of the normal serous acini of the parotid gland. The tumour cells have eccentrically-placed nuclei consistent with plasmacytoid morphology seen frequently in PAs. (b) H and E-labelled section (10x magnification) of the parotid tumour demonstrates an area of myxoid stroma (black arrow), which is further evidence that the tumour arose from a pre-existing PA. (c) H and E-labelled section (10x magnification) of the parotid tumour showing hyalinization (black arrow), which occurs more frequently in PAs that undergo malignant transformation. Extensive perineural invasion (black arrowhead) is also shown, highlighting the aggressiveness of the tumour. (All histological images were provided courtesy of Dr Reshma Agrawal, Specialist Registrar in Oral Pathology, Division of Cellular Pathology at The Royal London Hospital, London, UK.) H and E, haematoxylin and eosin; PA, pleomorphic adenoma.
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fig2
The patient originally presented with a 1-year history of a left parotid region mass and co-existing ipsilateral facial nerve palsy, with the diagnosis confirmed using ultrasound, MRI (Figure 1a,b) and core biopsy of the lesion (Figure 2a,c).
(a) Axial gadolinium-enhanced T
1 weighted MRI demonstrating the large pineal region tumour obstructing the cerebral aqueduct and giving rise to acute hydrocephalus. (b) Sagittal gadolinium-enhanced T
1 weighted MRI demonstrating the pineal region tumour as well as contrast enhancement along the folia of the superior cerebellar parenchyma (black arrow) in keeping with leptomeningeal spread of the tumour. (c) Axial gadolinium-enhanced T
1 weighted MRI of the posterior fossa demonstrating the left cerebellopontine angle deposit (black arrow) that extends into the left internal auditory meatus. (d) Whole body 18F-FDG positron emission tomography scan (posterior view) demonstrating the FDG-avid left supraclavicular fossa lymph nodes, as well as metabolically active bilateral hilar lymph nodes and widespread metastatic bony infiltration. FDG, 2-deoxy-2-[18F]-fluoro-D-glucose.
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fig3
A subsequent urgent MRI demonstrated an avidly enhancing, large pineal region tumour with resulting obstructive hydrocephalus (Figure 3a). Additionally, abnormal leptomeningeal enhancement was shown extending from the mass over the folia of the superior cerebellar parenchyma (Figure 3b). A small, discrete, enhancing lesion was also present in the left cerebellopontine angle (Figure 3c). This was confirmed on subsequent whole body 2-deoxy-2-[18F]-fluoro-D-glucose (18F-FDG) positron emission tomography/CT (PET/CT) imaging, which also revealed multiple bone metastases and bilateral metabolically active hilar lymph nodes, also suspicious for metastases (Figure 3d).
(a) H and E-labelled section (20x magnification) of the primary parotid tumour demonstrating cells with eccentrically placed nuclei consistent with plasmacytoid morphology (black arrows). (b) Magnified H and E-labelled section (10x magnification) from the pineal tumour biopsy demonstrating cells with a plasmacytoid morphology (black arrows) that are analogous to those demonstrated within the parotid gland tumour. H and E, haematoxylin and eosin.
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fig4
In this case, when the histology from the pineal gland was compared with the original histology, the intracranial lesion was consistent with a metastatic adenocarcinoma from the parotid gland (Figure 4a,b).
(a) Coronal gadolinium-enhanced T
1 weighted MRI demonstrating progression of the leptomeningeal disease along the superior cerebellar folia. The pineal region tumour is also demonstrated but the hydrocephalus has resolved after ventriculostomy. The shallow right subdural and subgaleal collections are post-procedural. (b) Sagittal gadolinium-enhanced T
1 weighted MRI demonstrating the posterior fossa leptomeningeal enhancement as well as the meningeal enhancement along the anterior cervical spinal cord (black arrow). Also the widespread abnormal bone marrow signal within the vertebral bodies in keeping with metastatic deposits is noteworthy.
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fig5
Although the patient was neurologically intact at her next follow-up appointment, and the ventricular system had been successfully decompressed, the contrast-enhanced MRI demonstrated that the leptomeningeal enhancement had progressed dramatically and now extended throughout the neuraxis (Figure 5a,b).