Cerebral metastases account for approximately 25-50 % of intracranial tumours in hospitalised patients. In many instances the brain is a reservoir of disease when systemic disease is under control, largely due to the blood brain barrier reducing the efficacy of many systemic chemotherapeutic agents.
The true incidence of brain metastases is unknown, but recent estimates are as high as 200,000 cases per year in the United States alone 1.
80% of brain metastases can be accounted for by five primary tumours 2 :
- lung cancer
- breast cancer
- renal cell carcinoma
- gastrointestinal tract adenocarcinomas (the majority colorectal carcinoma)
A population-based study of 169,444 cancer patients from 1973 to 2001 in Detroit revealed that overall, 10% of patients diagnosed with one of these five primaries went on to develop brain metastases. Specifically, 19.9% of lung cancers, 6.9% of melanomas, 6.5% of renal cancers, 5.1% of breast cancers and 1.8% of colorectal cancers metastasized to the brain 3.
Parenchymal blood flow is an important determinant of the distribution of metastases. 80% of metastases localize to the cerebral hemispheres, 15% localize to the cerebellum and 3% localize to the basal ganglia. Often these tumours can be found at the gray/white matter junction.
Clinical presentation and prognosis
These patients can commonly present with headaches, seizures, mental status alterations, ataxia, nausea and vomiting and visual disturbances. However, 10% of patients may be asymptomatic.
Typically metastases are relatively well demarcated from the surrounding parenchyma and usually there is a zone of peritumoural oedema out of proportion with the tumour size.
Typically well-demarcated with the exception of melanoma metastases. Their histological appearance will of course depend on the primary tumour.
There is a great deal of variability in the appearance of these tumours, however some generalizations can be made. It should also be noted that although we tend to think of cerebral metastases as being multiple, approximately 50% are seemingly solitary at diagnosis and in a minority of cases no known or identifiable malignancy is present 4.
On precontrast imaging the mass may be iso to hypodense, surrounded by variable amounts of vasogenic oedema.
Following administration of contrast, enhancement is also variable and can be intense, punctate, nodular or ring-enhancing if the tumour has out grown it's blood supply.
- typically iso to hypointense
- if haemorrhagic may have intrinsic high signal
- melanoma metastases also hyperintense due to the paramagnetic properties of melanin
- enhancement pattern can be uniform, punctate, or ring-enhancing, but it is usually intense. Delayed sequences may show additional lesions, therefore contrast-enchance MR is the current standard for small metastases detection.
- typically hyperintense
- haemorrhage may alter this
- FLAIR - typically hyperintense with hyperintense peri-tumoural oedema
MR spectroscopy :
- intratumoural choline peak with no choline elevation in the peritumoural oedema
- any tumour necrosis results in a lipid peak.
- NAA depleted
- DWI - oedema is out of proportion with tumour size and appears dark on trace-weighted DWI.
FDG PET : Generally considered the best imaging tool for metastases. However it can only detect mets up to 1.5 cm in size, therefore contrast MRI remains the gold standard to rule out small mets. Lung, breast, colorectal, head and neck, melanoma and thyroid mets are usually hypermetabolic. Mucinous adenocarcinoma and RCC are typically hypometabolic and gliomas and lymphomas are variable. Any central hypometabolism indicates necrosis.
Treatment and prognosis
Symptomatic - Corticosteroids are given to limit the effects of peritumoural edema. Hyperosmolar agents (eg mannitol) can be given to decrease ICP and anticonvulsants are given to prevent seizures. Recently, methylphenidate and donepezil have been used to improve cognition, mood and quality of life.
Therapeutic : Radiation (whole brain external beam or stereotactic for smaller masses), chemotherapy and surgical resection are done to prolong survival and palliate symptoms. Other than germ cell tumours, leukemias and lymphomas, palliation is the rule and curative therapy is the subject of case reports.
Overall patients with brain metastases typically have a mean survival of one month without treatment. With treatment, survival improves, but it is still dismal. The mean age of survival is still less than one year, although in some patients with solitary metastases longer survival is encountered.
General imaging differential considerations include
- 1. Eichler AF, Loeffler JS. Multidisciplinary management of brain metastases. Oncologist. 2007;12 (7): 884-98. doi:10.1634/theoncologist.12-7-884 - Pubmed citation
- 2. Kumar V, Abbas AK, Fausto N et-al. Robbins and Cotran pathologic basis of disease. W B Saunders Co. (2005) ISBN:0721601871. Read it at Google Books - Find it at Amazon
- 3. Barnholtz-Sloan JS, Sloan AE, Davis FG et-al. Incidence proportions of brain metastases in patients diagnosed (1973 to 2001) in the Metropolitan Detroit Cancer Surveillance System. J. Clin. Oncol. 2004;22 (14): 2865-72. doi:10.1200/JCO.2004.12.149 - Pubmed citation
- 4. Greenberg MS. Handbook of Neurosurgery. Thieme Medical Pub. (2010) ISBN:1604063262. Read it at Google Books - Find it at Amazon
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