Neuroradiology

Metastasis

CNS metastatic disease from extracranial primary tumours may occur by direct spread or by haematogenous spread. Metastases by direct spread may occur from nasopharyngeal carcinoma and skull base malignancies and are discussed along with these tumours. Haematogenous metastases may affect the skull, the dura, the leptomeninges and the brain. Dural and leptomeningeal invasion may be seen secondary to skull and parenchymal metastases, respectively. Solitary dural metastases are uncommon: they may be focal or diffuse (pachymeningeal carcinomatosis). Focal lesions may resemble meningiomas. Leptomeningeal metastases are more common than dural metastases and are found associated with parenchymal metastases in 6-18% of cases. Leptomeningeal spread is usually diffuse and is the commonest type of lymphomatous CNS metastases. Prostate, lung and breast carcinomas are the commonest sources of skull metastases. Skull metastases appear most often as lytic lesions. Lytic involvement of cortical bone is a clue to the diagnosis along with the multiplicity of lesions seen in most cases. Prostate metastases may cause mixed hyperostosis and bone destruction with an associated soft-tissue mass that may resemble a meningioma. The lateral orbital wall is a favourite site for prostate metastases.

Intraparenchymal brain metastases are the most common type of CNS metastatic disease. Brain metastases are found in up to 24% of all patients that die from cancer and represent between 20-30% of all brain tumours in adults. The commonest sites of origin are lung, breast, skin (melanoma), gastrointestinal tract, and genitourinary tract. The probability of clinically silent lesions as an occasional finding at staging is maximum in patients with lung carcinoma [especially adenocarcinoma (40%) and oat cell carcinoma (11%)] and melanoma (11%). The brain is often the only site of metastases particularly in bronchogenic carcinoma and melanoma.

Metastases are most often multiple but the incidence of solitary lesions is estimated to be as high as 30% to 50% in some malignancies such as melanoma, lung and breast carcinoma. Metastases tend to be most commonly located in the supratentorial compartement with the exception of those from renal cell carcinoma that tend to be infratentorial. Early metastatic foci are commonly found at grey-white matter interfaces, a feature shared by all haematogenously disseminated embolic diseases. Macroscopically, intracerebral metastases are generally well circumscribed and round lesions most commonly surrounded by massive amounts of oedema. The nodules are usually distinguishable from their associated oedema on both CT and MRI on postcontrast scans (Fig.1). Factors such as cellularity, necrosis, haemorrhage, and (rarely) calcification are major determinants of precontrast density on CT and signal intensity on MR. Highly cellular lesions tend to be more dense on CT and to display hypointensity on both T1- and T2-weighted images (another determinant of low T2 signal is the mucinous component of some tumours such as gastrointestinal adenocarcinoma). Necrosis is responsible for cystic nonenhancing hypodense lesions on CT and T1 hypo/T2 hyperintense lesions on MR. Haemorrhagic degeneration determines relative hyperdensity on CT and hyperintensity on all sequences on MR. In metastases from melanoma MR T1 hyperintensity may also be the result of paramagnetic effects of melanin (melanotic melanoma). Contrast-enhanced MR is the most sensitive method of detecting metastatic foci.

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Fig.1

a, b. CT scan without contrast. The picture appears almost normal and only questionable punctate inhomogeneous abnormalities can be guessed in the white matter. c. MR, T2-weighted image. Multiple small nodules, iso-hyperintense, are seen deep in the basal ganglia and white matter. d, e. MR, T1-weighted axial images following gadolinium injection. A very high number of nodules of different sizes enhance, both homogeneously and with a ring-like appearance. The primary tumour was a breast carcinoma.
Metastasis, Fig.1 (a)
Metastasis, Fig.1 (b)
Metastasis, Fig.1 (c)
Metastasis, Fig.1 (d)
Metastasis, Fig.1 (e)