Brain metastasis from prostate carcinoma

Abstract

We read with interest the article on brain metastasis from prostate carcinoma (CaP) by McCutcheon et al.1 published in Cancer. For the benefit of the readers, we would like to update and refine the data regarding solitary brain metastasis from CaP. Using the MEDLINE database, we reviewed the data concerning brain metastasis and prostate carcinoma in living patients from 1960 to 1999. We excluded patients who lacked a negative metastatic survey and a brain biopsy consistent with CaP. We found a total of eight patients who met our criteria. Sites of single metastasis included pons alone (one patient), pons at the cerebellar-pontine angle (one patient), pons and cerebral peduncle (one patient), pons and cerebellar peduncle (one patient), pons and midbrain (one patient), the parietal lobe (one patient), the temporal lobe (one patient), and the frontoparietal lobe (one patient). Brain biopsy yielded seven patients with CaP and one patient with papillary adenocarcinoma. Brain histology included poorly differentiated (two patients), moderately differentiated (one patient), and well differentiated (four patients) CaP. The rate of incidence of brain metastasis from CaP in the recent study by McCutcheon et al. was 0.7%.1 One study proposes four reasons for the low incidence rate of clinically suspect solitary brain metastasis from CaP: 1) lower detection rate of tumor spread to brain (even in autopsy data), 2) late occurrence of brain involvement in the course of the disease, 3) clinically silent growth related to the most common site of tumor involvement, and 4) rare and nonspecific symptoms due to brain metastasis from CaP.2, 3 Another hypothesis for the rarity of solitary brain metastases in patients with CaP is that the brain parenchyma does not represent “fertile soil” for CaP cells, just as, conversely, the skeleton provides a preferential milieu for these cells.4 We believe our review shows the highest percentage of prostate metastasis to the pons ± cerebrum, cerebellum, and midbrain reported to date. McCutcheon et al.'s large series included only three patients who had metastatic disease solely to the brain. One patient had metastases specifically to the hypothalamus and the right temporal lobe. The other two patients had multiple frontal metastases. Their review also included seven additional patients who presented with a solitary brain metastasis. To our knowledge the study by Gupta et al. was the only analysis that met the criteria for our study.5 The number of solitary brain metastasis from CaP may indeed be higher than previously thought. McCutcheon et al. were correct to speculate that given the obscuring effect of bone artifact in the posterior fossa on computed tomography (CT) scans of the brain, tumor in this location actually may be underreported when CT is the primary method used. The fact that magnetic resonance imaging diagnosed all the patients with a solitary brain metastasis to the pons lends support to their theory. In addition, recent improvement in treatments allows patients to live longer. Given these facts, we predict that the incidence rate of brain metastases and solitary brain metastasis in patients with CaP will begin to increase. The possibility of solitary intraparenchymal metastases always should be considered in patients who develop neurologic symptoms. The authors thank M. R. Shetty, M.D. Neetha S. Alva M.D.*, Suraj Alva M.D. , * Department of Internal Medicine, Roger Williams Medical Center, Boston University, School of Medicine, Providence, Rhode Island, Division of Urology, Boston VA Healthcare System, West Roxbury, Massachusetts