Leptomeningeal dissemination of primary central nervous system tumors of childhood

Packer, Roger J.; Siegel, Kathy R.; Sutton, Leslie N.; Litmann, Phillip; Bruce, Derek A.; Schut, Luis

doi:10.1002/ana.410180209

Cited by 122 publications

(66 citation statements)

References 20 publications

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“…Others also found that medulloblastomas and malignant gliomas were more commonly encountered in positive CSF samples. [8][9][10][11][15][16][17] However, in the majority of these series, the ependymoma patients with positive CSF samples constituted only a very small fraction (1 to 5 cases) of cases. In a relatively larger series reported by Balhuizen et al, 17 positive CSF samples were detected in 5 of 28 (17.8%) patients with ependymoma.…”

Section: Discussionmentioning

confidence: 99%

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Cerebrospinal fluid cytology in patients with ependymoma

Qian

Goumnerova

Girolami

et al. 2008

Cancer

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Section: Discussionmentioning

confidence: 99%

“…15,20,24 In a patient with an ependymoma, leptomeningeal spread usually occurs at the time of disease recurrence. However, the value of CSF cytology in the evaluation of patients with ependymoma and suspected recurrent disease and/or leptomeningeal disease in the modern era of routine MRI imaging may be limited.…”

Section: Discussionmentioning

confidence: 99%

Cerebrospinal fluid cytology in patients with ependymoma

Qian

Goumnerova

Girolami

et al. 2008

Cancer

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“…One of 2 chemotherapy regimens was used to treat all patients as follows: (1) weekly VCR (1.5 mg/m 2 ) during craniospinal radiation therapy and for 6 weeks thereafter; then 8 cycles (1 cycle every 6 to 8 weeks) of CDP (75 mg/m 2 ) and CCNU (50 mg/m 2 ) on day 1 and VCR (1.5 mg/m 2 ) given 3 times per cycle. Ten patients were treated with this regimen based on a protocol designed by Packer et al (1985Packer et al ( , 1991. (2) Preradiation chemotherapy with cycles of CDP (20 mg/m 2 on days 1-5 or 90 mg/m 2 on day 1) and etoposide (75-100 mg/m 2 for 3 to 5 days) alternating with CTX (450-1580 mg/m 2 on days 1 and 2) and VCR (1.5 mg/m 2 on day 1) (Duffner et al, 1993).…”

Section: Methodsmentioning

confidence: 99%

“…Therefore, we decided to treat both good-and poor-risk adult patients with craniospinal radiation and multiagent therapy (Le et al, 1997;Prados et al, 1995). Relapse occurs predominately at the original site, but also in the leptomeninges and extraneurally in bone (Packer et al, 1985;Prados et al, 1995).…”

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confidence: 99%

Adult medulloblastoma: Multiagent chemotherapy

Greenberg¹

2001

Neuro-Oncology

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In this study, the records of 17 adult patients with medulloblastoma treated with craniospinal radiation and 1 of 2 multiagent chemotherapy protocols were reviewed for progression-free survival, overall survival, and toxicity, and the patients were compared with each other and with similarly treated children and adults. Records of patients treated at 3 institutions were reviewed. Seventeen medulloblastoma patients (11 female, 6 male) with a median age of 23 years (range, 18-47 years) were treated with surgery, craniospinal radiation (CSRT) plus local boost, and 1 of 2 adjuvant chemotherapy regimens. All tumors were infratentorial (10 in 4th ventricle and 7 in left or right hemisphere). Ten patients presented with hydrocephalus, and 7 of them were shunted. Eight patients had gross total resection, 7 had subtotal resection (>50% removed), and 2 had partial resection (<50% removed). Postoperatively, 3 patients had positive cytology and 3 had positive spinal MRI. Five patients were classi ed as good risk and 12 were classi ed as poor risk (Chang staging system). Ten patients were treated with the "Packer protocol," consisting of CSRT plus weekly vincristine followed by 8 cycles of cisplatin, lomustine, and vincristine. Seven patients were treated with the Pediatric Oncology Group (POG) protocol, consisting of alternating courses of cisplatin/etoposide and cyclophosphamide/vincristine, followed by CSRT. Eight of 17 patients relapsed, with all 8 relapsing at the primary site. Other relapse sites included the leptomeninges (5), bone (1), and brain (1). The estimated median relapse-free survival (Kaplan-Meier) for all patients was 48 months (95% con dence interval, >26 months to ¥). Median relapse-free survival for patients on the Packer protocol was 26 months, and for those on the POG regimen was 48 months (P = 0.410). Five of 10 on the Packer protocol were relapse-free, while 4 of 7 were relapse-free on the POG regimen. Two patients relapsed during chemotherapy and 6 relapsed after completing all therapy at 18, 18, 26, 30, 40, and 48 months. The estimated median survival of all patients was 56 months (95% con dence interval, 27 to ¥) with 11 patients alive; for the Packer protocol, median survival was 36 months, and for the POG protocol, it was 57 months (P = 0.058). The hazard ratio was 0 (95% con dence interval, 0 to ¥). Toxicity during the Packer protocol was moderately severe, with only 1 of 10 patients able to complete all therapy. Two patients had severe abdominal pain during CSRT + vincristine, and 5 had peripheral neuropathy during vincristine therapy. Hearing loss (>20 dB) occurred in 7, neutropenia (<500 µl) in 6, thrombocytopenia (<50,000 µl) in 6, nephrotoxicity (>25% ¯by creatinine clearance) in 2, and decreased pulmonary function (diffusing capacity for carbon monoxide ¯>40%) in 1. On the POG protocol, only 1 patient had persistent nausea and vomiting, 2 had peripheral neuropathy, and 3 had hearing de cit (>20 dB) or tinnitus. The POG and Packer protocols did not have a statistically signi cant differenc...

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“…Most reports on tumour dissemination of HGG and DIPG after diagnosis, so called secondary dissemination of disease (SDD), are case reports or small series; few reports include large numbers of patients (Packer et al, 1985(Packer et al, , 1990(Packer et al, , 1993Dropcho et al, 1987;Vertosick and Selker, 1990;Grabb et al, 1992;Arita et al, 1994;Heideman et al, 1997;Donahue et al 1998;Allen et al, 1999;Endo et al, 2003;Saito et al, 2003). These series mostly come from the late 1980s and early 1990s, when MRI was not routinely available for follow-up investigations (Awad et al, 1986;Vertosick and Selker, 1990;Arita et al, 1994).…”

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confidence: 99%

Secondary dissemination in children with high-grade malignant gliomas and diffuse intrinsic pontine gliomas

et al. 2006

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In children, treatment regimen for high-grade gliomas (HGG) and diffuse intrinsic pontine gliomas (DIPG) are generally not stratified according to disease stage. The hypothesis was that secondary disseminating disease (SDD) in children with HGG is related to an even worse outcome. Description of SDD pattern was performed. In total, 270 children with newly diagnosed HGG or DIPG were eligible for retrospective analysis of SDD. Medical and computer records of these patients were reviewed for demographic characteristics, sites of dissemination, prognostic variables. Forty-six (17%) of the 270 patients had developed SDD. The median time to SDD was 8.2 months. The median overall survival (OS) after dissemination was 3.2 months. The SDD was located parenchymal in the supratentorial (34.8%), infratentorial (6.5%), supratentorial and infratentorial (19.6%), spinal (10.9%), spinal and cerebral (6.5%) regions of the CNS, or leptomeningeal (21.7%). For HGG patients, the median OS was shorter among patients with SDD than among patients without SDD (1.02 vs 1.41 years, P ¼ 0.0495). In the group of patients with SDD, patients with cerebrospinal fluid dissemination had a worse outcome compared with patients with parenchymal metastases. Summarising, SDD is a negative prognostic factor for patients with HGG outside the pons. Treatment stratification should be considered.

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Leptomeningeal dissemination of primary central nervous system tumors of childhood

Cited by 122 publications

References 20 publications

Cerebrospinal fluid cytology in patients with ependymoma

Cerebrospinal fluid cytology in patients with ependymoma

Adult medulloblastoma: Multiagent chemotherapy

Secondary dissemination in children with high-grade malignant gliomas and diffuse intrinsic pontine gliomas

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