Seizure disorder since age 14, recently had an episode in which she had some carpopedal spasm associated with hyperventilation. Evaluation in the emergency room revealed a very high prolactin of 66. She denies any visual field cuts. No causes were identified on physical exam for the hyperprolactinemia.
The right common carotid is visible on the most inferior slices of the scan and is diminutive. The left common carotid is 2 to 3 times the size of the right. The right external carotid artery is patent and normal size however the right internal carotid artery is absent and there is no carotid canal at the skull base suggesting congenital absence. The left internal carotid has a normal course through the carotid canal and cavernous sinus and appears normal at the circle of Willis. There are also large posterior communicating arteries that reconstitute the circle of Willis. The right middle cerebral artery is hypoplastic but opacifies normally. Both anterior cerebral arteries are fed from the left carotid system. Vertebral arteries and basilar artery appear normal.
This is a great “blink and you will miss it” case on the brain MRI. The findings on the MRI are subtle but if you are looking for them, you would find it. These are evident on the CUBE images which are smack you in the face obvious. I had the benefit of reading follow-up postgadolinium study which does not show any intracranial meningioma that would lead down the path of neurofibromatosis. The initial diagnosis was on CT which is also in the gallery showing calcified mass. The differential considerations are fairly narrow and as this was a woman, calcified metastatic breast cancer is a consideration.
As far as nerve sheath tumors (schwannoma or neurofibroma), this is unlikely to represent either given its position in the posterior lateral thecal sac with an intra-dural but extra medullary location.
I initially thought this was another case of silent sinus syndrome but after looking at it more the differential broadened and I do not think I could drop the hammer on any particular diagnosis. It has some features of fibrous dysplasia and there is always overlap between fibrous dysplasia and chronic sinus disease. The destructive bony defect in the anterior maxillary wall is more unusual and this makes me lean more towards chronic sinus disease with silent sinus and an old operative intervention. Obviously, these differential considerations can be distinguished easily with appropriately obtained clinical information which is never supplied in my reading context.