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32 1 89 94 10.3171/jns.1970.32.1.0089 An Unusual Metallic Foreign Body Within the Brain Rabindranath G. S. Azariah January 1970 32 1 95 99 10.3171/jns.1970.32.1.0095 Unusual Pneumoencephalogram Following Fragment Wound of the Brain Lewis J. Brown January 1970 32 1 100 102 10.3171/jns.1970.32.1.0100 Bilateral Carotid Ligation Sun Wuk Kim Kee Chan Lee January 1970 32 1 103 107 10.3171/jns.1970.32.1.0103 Painless Intraspinal Leptomeningeal Carcinomatosis: A Myelographic Demonstration J. Grafton Love Chun C. Kao Hillier L. Baker Jr. January 1970

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J. Grafton Love, Chun C. Kao and Hillier L. Baker Jr.

C arcinomatosis of the leptomeninges in the absence of any associated gross focal metastasis within the central nervous system has been known since Siefert's description 10 in 1902. An excellent review by Jacobs and Richland 3 in 1951 concluded that dissemination was via the hematogenous route and discarded the theory of spreading through the “perineural lymph spaces.” Intraspinal leptomeningeal carcinomatosis certainly is not uncommon, 2 and cases of lymphosarcoma, 12 melanoma, 11 sarcoma, 4 and Hodgkin's disease 7 have been reported. Preoperative

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Dispersion of central nervous system tumors

Correlation between clinical aspects and tissue culture studies

Ulrich Batzdorf and Vivian Gold

pseudocapsule (attenuated diaphragma sellae) presumably precedes the infrequent subarachnoid spillage and implantation of this tumor. 24, 33 Meningiomas are in contact with the subarachnoid space over much of their surface area and occasionally occur as masses lying almost free within the ventricle, as in the instance cited above. Metastatic cancers not infrequently invade the leptomeninges, shed cells into the CSF, and, in other instances, produce diffuse leptomeningeal carcinomatosis. A discrepancy exists, however, between the occurrence of cancer cells in the choroid

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J. Chris Balhuizen, Gerard Th. A. M. Bots, Aart Schaberg and Fré T. Bosman

astrocytoma Grades I, II 27 66 4 70 astrocytoma Grades III, IV 83 104 28 132 ependymoma Grades I, II 13 28 2 30 ependymoma Grades III, IV 15 44 4 48 oligodendroglioma 17 23 3 26 medulloblastoma 17 89 1 90 sarcoma 8 15 0 15 choriocarcinoma 1 4 0 4 malignant teratoma 1 9 0 9 metastatic tumors 41 64 12 76 leptomeningeal carcinomatosis  and sarcomatosis 6 37 0 37 vertebral and peridural metastases 33 51 0 51

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Yasuo Suzuki and Ryuichi Tanaka

tumor patients and 38 control patients. The clinical summary of the nine positive patients is shown in Table 3 . Among the eight metastatic brain tumors with elevated CEA levels in CSF, six were leptomeningeal carcinomatosis and two were parenchymal metastasis. All six cases of leptomeningeal carcinomatosis assayed for CEA in CSF in this study showed elevated CEA levels. In this study, CSF cytology was performed in 12 patients with metastatic brain tumors. All five patients with positive tumor cells (Cases 1, 3, 4, 5, and 6; Table 3 ) showed positive CEA

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Hydrocephalus and infratentorial tumors

Incidence, clinical picture, and treatment

Anthony J. Raimondi and Tadanori Tomita

distinctly different diseases which complicate one another and contribute to the complex clinical picture of increasing ICP: 1) a tumor, and 2) hydrocephalus. Changes in cerebral blood flow that result from an increase in ICP and ventricular dilatation must be considered in the pathogenetic cycle of events. Hydrocephalus associated with a brain tumor may be communicating, as one finds in choroid plexus papilloma or leptomeningeal carcinomatosis. Parasellar, third ventricle, brain-stem, and posterior fossa tumors may block the third ventricle, the fourth ventricle, or its

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Intramedullary spinal cord metastasis

A clinicopathological study of 13 cases

Donal A. Costigan and Marc D. Winkelman

matter of the posterior horn ( Fig. 3 ), and the fourth in the nearby deep white matter of the lateral column. No clinical features of spinal cord disease were present. Fig. 3. Case 6. Photomicrograph of the thoracic cord with several clusters of metastatic tumor cells (arrow) in the posterior horn. H & E, × 260. Parenchymal Invasion Secondary to Leptomeningeal Involvement Four of the 40 cases of leptomeningeal carcinomatosis in our series were associated with invasion of the parenchyma of the cord ( Table 3 , Group II). The avenue of entry

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Virginia G. Johnson, Charles Wrobel, Debra Wilson, John Zovickian, Larry Greenfield, Edward H. Oldfield and Richard Youle

TfR should provide an effective target for immunotoxin therapy. It has previously been shown that TfR's are expressed on human medulloblastoma and glioblastoma cells. 33 This report demonstrates that transferrin (Tf) or an anti-TfR monoclonal antibody conjugated to CRM 107 has potential for effective treatment of medulloblastoma and breast leptomeningeal carcinomatosis. Materials and Methods Established Cell Lines The SNB75 cell line was established by primary explants from a tumor removed from a 72-year-old woman with a bifrontal glioblastoma multiforme

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Richard A. Bronen and Gordon Sze

were sometimes nodular and more peripheral (that is, away from the parasagittal region). Abnormal enhancement was seen in up to two-thirds of patients with proven leptomeningeal carcinomatosis. When dura adjacent to the skull was involved, contrast-enhanced MR imaging demonstrated abnormal meningeal enhancement better than postcontrast CT because bone obscures adjacent contrast enhancement on CT. Contrast-enhanced CT was equal to contrast-enhanced MR imaging in detection of meningeal nodules. Postoperative Lesions Residual or recurrent tumor in patients who

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Fotios D. Vrionis, Julian K. Wu, Peimin Qi, William G. Cano and Van Cherington

continuously for 6 weeks instead of 2 weeks in animals treated with Walker-tk+ cells (data not shown). In Situ Treatment of Established Walker Leptomeningeal Carcinomatosis In the previous experiments, Walker cells were premixed in different ratios with HSV-tk+ effector cells to determine the maximum therapeutic effect of those cells under ideal conditions. To assess the efficacy of Walker-tk+ cells in in situ treatment of Walker leptomeningeal neoplasia, we treated 3-day-old Walker tumors with either a single or multiple (that is, × 3) injections of Walker