Metastatic renal cell carcinoma metastasising into a cerebral cavernous malformation
A 71‐year‐old man presented acutely to his local hospital with left hand weakness and numbness. He had no past medical history of note and was otherwise well. On examination, he was alert and fully orientated, but he had some mild weakness of his left hand and impairment of fine movements. His hand was also numb and he had a mild gait disturbance. A computerized tomography (CT) CT SOMATOM Definition AS scanner, Siemens Healthcare, GmbH, Erlangen, Germany brain scan was performed to investigate for a possible stroke and this demonstrated the presence of an enhancing lesion within the right frontal lobe with an associated haemorrhagic component and surrounding perilesional oedema. He was prescribed dexamethasone and his left hand weakness subsequently improved. A metastasis was considered the most likely diagnosis, so the patient underwent a CT scan of his body. This demonstrated a 6.4 cm peripherally enhancing soft tissue mass with central necrosis arising from the lower pole of the right kidney.
A magnetic resonance imaging (MRI) scan of his brain demonstrated that the lesion was centred deep within the right inferior frontal gyrus. It had heterogeneous signal intensity but little peripheral post‐contrast enhancement and a significant amount of adjacent vasogenic oedema was associated with the abnormality. No other intracranial lesions were identified. His case was reviewed at the neuro‐oncology multidisciplinary meeting and surgery was recommended to resect the lesion and confirm a histological diagnosis.
The patient underwent an uneventful neurosurgical procedure and a small curious lesion was identified and completely resected. At surgery, the lesion appeared most like a cavernoma with a surrounding gliotic, haemosiderin‐stained plane and an outer layer of small friable vessels; however, within this, a small solid lesion was found intertwined with more blood vessels. The patient recovered well following his surgery and was discharged home a few days later. His post‐operative MRI demonstrated complete resection of the tumour with no pathological enhancement seen at the site of surgical resection. No adjuvant treatment was recommended and he is currently under clinical and radiological surveillance.
Neuropathological examination (Figure 1) demonstrated nodules of a tumour enclosed within and adhering to the walls of a closely packed leash of cavernous vascular spaces with inflamed fibrous walls containing abundant haemosiderin and demonstrating neovascularization. A Trichrome stain (Verhoeff–Van Gieson elastic) demonstrated the fibrotic walls of the vascular channels devoid of elastic fibres or smooth muscle. CD31 and CD34 highlighted small neovessels lining and growing into the walls of these channels. The tumour nodules comprised large, predominantly clear cells organized in nests and sheets, displaying large central nuclei with prominent nucleoli and separated by vascularised fibrous septa containing frequent collections of neutrophil polymorphs. There was marked pleomorphism, brisk mitiotic activity and extensive fresh haemorrhage. The tumour cells displayed uniform strong reactivity for pan‐CK (MNF116) and EMA (Epithelial Membrane Antigen) and crisp membranous labelling for CD10. Labelling for CK7, CK20 and TTF‐1 was negative. The histology was consistent with the intra‐operative impression of a renal cell carcinoma metastasizing within a cavernous haemangioma.
Metastatic spread of extracranial systemic cancer into intracranial lesions is well documented in the literature but spread to CCMs is extremely rare. Meningiomas are by far the most common intracranial host tumour with breast, lung and renal cancers metastasizing most frequently 1.