1. may also reach the CNS by permeating the calvaria or samples (Balhuizen et al., 1978; Bigner, 1992). A common complication of leptomeningeal dissemination is infiltra- compared with those from other primary sites (Delattre et tion of the segments of cranial or spinal nerves that traverse al., 1988; Engelhoff et al., 1992). Prostatic adenocarcinothe subarachnoid space, resulting in specific clinical deficits mas also exhibit a predilection for the posterior fossa, that depend on the particular nerves infiltrated. In the vast although their deposits are more typically dura-based than majority of cases of leptomeningeal dissemination, the pri- intraparenchymatous (Kleinschmidt-DeMasters, 2001). mary site is well established prior to the time of presenta- The neurohypophysis, choroid plexus, and pineal gland tion. Leptomeningeal dissemination can also occur in (Ortega et al., 1951; Henson and Urich, 1982) represent association with primary brain tumors, such as is com- rarer but well-documented sites of metastasis. Pre-existing monly seen with primitive neuroectodermal tumors and intracranial lesions such as tumors (tumor-to-tumor occasionally gliomas (leptomeningeal gliomatosis) (Erlich metastasis) (Schmitt, 1984; Mørk and Rubinstein, 1988; and Davis, 1978; Bigner and Johnston, 1984). Muller and Schroder, 1999; Brown et al.2003), infarcts, and vascular malformations (Nielsen andPosner, 1983) are rare targets for metastatic tumors. Conversely, brain