Effektivität und Toxizität einer Re-Bestrahlung (Re-RT) bei metastatisch bedingter Rückenmarkkompression (MBRK)

Rades, Dirk; Stalpers, Lukas J.A.; Veninga, Theo; Schulte, Rainer; Hoskin, Peter; Alberti, Winfried

doi:10.1007/s00066-005-1406-7

Cited by 18 publications

(8 citation statements)

References 23 publications

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“…In our previous studies of spinal Re-RT, we found a cumulative BED 100 Gy 2 to be the safe limit because of the smaller number of patients who received a cumulative BED >100 Gy 2 in those series. 13,14 The safety of a cumulative BED 120 Gy 2 is in accord with the review by Nieder et al, who presented 78 patients who had received spinal Re-RT for different reasons (not MSCC alone). 5 Nieder and colleagues found no case of radiation myelopathy when the cumulative BED did not exceed 120 Gy 2 , the BED of each RT (first course of RT plus Re-RT) did not exceed 98 Gy 2 , and when the interval between first course of RT and Re-RT was at least 6 months.…”

Section: Discussionsupporting

confidence: 60%

“…The Re-RT schedule had no significant impact on motor function, which has been previously reported for both first course of RT and Re-RT of MSCC. [12][13][14][27][28][29] Therefore, in accord with data for the first course of RT, one may consider single-fraction RT or multifraction short-course RT for patients with a poor estimated survival, who will probably not benefit from longer-course RT in terms of better recalcification and local control. 1,30 Survival after Re-RT may be predicted with the help of the prognostic factors identified in this series.…”

Section: Discussionmentioning

confidence: 99%

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Prognostic factors for functional outcome and survival after reirradiation for in‐field recurrences of metastatic spinal cord compression

Rades

Rudat

Veninga

et al. 2008

Cancer

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Objective: We examined whether glucose transporter 1 (GLUT1) deficiency causes common idiopathic generalized epilepsies (IGEs). Methods: The IGEs are common, heritable epilepsies that usually follow complex inheritance; currently little is known about their genetic architecture. Previously considered rare, GLUT1 deficiency, due to mutations in SLC2A1, leads to failure of glucose transport across the blood–brain barrier and inadequate glucose for brain metabolism. GLUT1 deficiency was first associated with an encephalopathy and more recently found in rare dominant families with epilepsy and paroxysmal exertional dyskinesia (PED). Five hundred four probands with IGEs and 470 controls underwent SLC2A1 sequencing. Glucose transport was assayed following expression of SLC2A1 variants in Xenopus oocytes. All available relatives were phenotyped, and SLC2A1 was sequenced. Results: Functionally validated mutations in SLC2A1 were present in 7 of 504 (1.4%) probands and 0 of 470 controls. PED, undiagnosed prior to study, occurred in 1 proband and 3 of 13 relatives with mutations. The IGEs in probands and relatives were indistinguishable from typical IGE. Three cases (0.6%) had mutations of large functional effect and showed autosomal dominant inheritance or were de novo. Four (0.8%) cases had a subtle functional effect; 2 showed possible dominant inheritance, and 2 did not. These alleles leading to subtle functional impairment may contribute to complex, polygenic inheritance of IGE. Interpretation: SLC2A1 mutations contribute to approximately 1% of IGE both as a dominant gene and as a susceptibility allele in complex inheritance. Diagnosis of GLUT1 deficiency has important treatment (ketogenic diet) and genetic counseling implications. The mechanism of restricted glucose delivery differs from the current focus on IGEs as ion channel disorders. ANN NEUROL 2012;72:807–815

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Section: Discussionsupporting

confidence: 60%

Section: Discussionmentioning

confidence: 99%

Prognostic factors for functional outcome and survival after reirradiation for in‐field recurrences of metastatic spinal cord compression

Rades

Rudat

Veninga

et al. 2008

Cancer

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“…Various neuro-oncologic diseases such as metastatic spinal cord compression (MSCC), cerebral metastases, and brain tumors may lead to neurologic deficits [5,14,18,19]. Twenty to 40% of cancer patients develop metastases within the brain.…”

Section: Introductionmentioning

confidence: 99%

Whole-Brain Radiotherapy with 20 Gy in 5 Fractions for Brain Metastases in Patients with Cancer of Unknown Primary (CUP)

et al. 2007

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“…Local radiotherapy is indicated postoperatively to achieve local tumor control [21,36,46,47,50] and should be initiated as soon as possible (LoE IIa, grade of recommendation A).…”

Section: Radiotherapymentioning

confidence: 99%

DEGRO Practice Guidelines for Palliative Radiotherapy of Metastatic Breast Cancer

et al. 2009

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Bone metastases as well as MSCC should be managed in an interdisciplinary approach mostly as combined-modality treatment according to the specific clinical situation. The present practice guidelines offer criteria and recommendations for different radiooncologic treatment schedules based on the best available levels of evidence. Preferred technique, targeting and different dose schedules are described in detail.

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Effektivität und Toxizität einer Re-Bestrahlung (Re-RT) bei metastatisch bedingter Rückenmarkkompression (MBRK)

Abstract: Re-RT is an effective treatment for an in-field recurrence of MSCC. After a cumulative EQD2 < or = 50 Gy, radiation myelopathy appears unlikely.

Cited by 18 publications

References 23 publications

Prognostic factors for functional outcome and survival after reirradiation for in‐field recurrences of metastatic spinal cord compression

Prognostic factors for functional outcome and survival after reirradiation for in‐field recurrences of metastatic spinal cord compression

Whole-Brain Radiotherapy with 20 Gy in 5 Fractions for Brain Metastases in Patients with Cancer of Unknown Primary (CUP)

DEGRO Practice Guidelines for Palliative Radiotherapy of Metastatic Breast Cancer

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