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Somatostatin receptor subtype 2 upregulation is very common in meningiomas, and the use of peptide receptor radionuclide therapy (PRRT) is recognized in recent European guidelines, with long-term stable disease and a long overall survival. Treatment efficacy of radionuclide treatments is correlated with tumour radiation absorbed dose. Meningioma patients with low tumour uptake might benefit less from treatment. Thus, a method to increase tumour uptake in these patients is needed. We describe a case treated with both intravenous and intra-arterial PRRT. Tumour uptake after intravenous PRRT was disappointing, and after intra-arterial administration significantly increased tumour uptake was seen. Patient had a partial response on imaging and reduction in tumour-related complaints. Potentially, intra-arterial administration of PRRT could increase treatment efficacy in meningioma patients.Level of Evidence 5 (case report). [ABSTRACT FROM AUTHOR]

Background and Purpose: T2-FLAIR mismatch is a highly specific imaging biomarker of IDH -mutant diffuse astrocytoma in adults. It has however also been described in MYB/MYBL1 -altered low grade tumors. Our aim was to assess the diagnostic power of the T2-FLAIR mismatch in IDH -mutant astrocytoma and MYB/MYBL1 -altered low-grade tumors in children and correlate this mismatch with histology., Materials and Methods: We evaluated MR imaging examinations of all pediatric patients, performed at the Princess Máxima Center for Pediatric Oncology and the University Medical Center Utrecht between January 2012 and January 2023, with the histomolecular diagnosis of IDH -mutant astrocytoma, diffuse astrocytoma MYB/MYBL1 -altered, or angiocentric glioma, and the presence of T2-FLAIR mismatch was assessed. Histologically, the presence of microcysts in the tumor (a phenomenon suggested to be correlated with T2-FLAIR mismatch in IDH -mutant astrocytomas in adults) was evaluated., Results: Nineteen pediatric patients were diagnosed with either IDH -mutant astrocytoma ( n  = 8) or MYB/MYBL1 -altered tumor ( n  = 11: diffuse astrocytoma , MYB- or MYBL1 -altered n  = 8; or angiocentric glioma n  = 3). T2-FLAIR mismatch was present in 11 patients, 3 (38%) in the IDH -mutant group and 8 (73%) in the MYB/MYBL1 group. No correlation was found between T2-FLAIR mismatch and the presence of microcysts or an enlarged intercellular space in either IDH -mutant astrocytoma ( P  = .38 and P  = .56, respectively) or MYB/MYBL1 -altered tumors ( P  = .36 and P  = .90, respectively)., Conclusions: In our pediatric population, T2-FLAIR mismatch was more often found in MYB/MYBL1 -altered tumors than in IDH -mutant astrocytomas. In contrast to what has been reported for IDH -mutant astrocytomas in adults, no correlation was found with microcystic changes in the tumor tissue. This finding challenges the hypothesis that such microcystic changes and/or enlarged intercellular spaces in the tissue of these tumors are an important part of explaining the occurrence of the T2-FLAIR mismatch., (© 2024 by American Journal of Neuroradiology.)

Introduction: Lesion-symptom mapping is a key tool in understanding the relationship between brain structures and behavior. However, the behavioral consequences of lesions from different etiologies may vary because of how they affect brain tissue and how they are distributed. The inclusion of different etiologies would increase the statistical power but has been critically debated. Meanwhile, findings from lesion studies are a valuable resource for clinicians and used across different etiologies. Therefore, the main objective of the present study was to directly compare lesion-symptom maps for memory and language functions from two populations, a tumor versus a stroke population., Methods: Data from two different studies were combined. Both the brain tumor (N = 196) and stroke (N = 147) patient populations underwent neuropsychological testing and an MRI, pre-operatively for the tumor population and within three months after stroke. For this study, we selected two internationally widely used standardized cognitive tasks, the Rey Auditory Verbal Learning Test and the Verbal Fluency Test. We used a state-of-the-art machine learning-based, multivariate voxel-wise approach to produce lesion-symptom maps for these cognitive tasks for both populations separately and combined., Results: Our lesion-symptom mapping results for the separate patient populations largely followed the expected neuroanatomical pattern based on previous literature. Substantial differences in lesion distribution hindered direct comparison. Still, in brain areas with adequate coverage in both groups, considerable LSM differences between the two populations were present for both memory and fluency tasks. Post-hoc analyses of these locations confirmed that the cognitive consequences of focal brain damage varied between etiologies., Conclusion: The differences in the lesion-symptom maps between the stroke and tumor population could partly be explained by differences in lesion volume and topography. Despite these methodological limitations, both the lesion-symptom mapping results and the post-hoc analyses confirmed that etiology matters when investigating the cognitive consequences of lesions with lesion-symptom mapping. Therefore, caution is advised with generalizing lesion-symptom results across etiologies., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 The Author(s). Published by Elsevier Inc. All rights reserved.)

Purpose: Numerous brain MR imaging studies have been performed to understand radiation-induced cognitive decline. However, many of them focus on a single region of interest, e.g. cerebral cortex or hippocampus. In this study, we use deformation-based morphometry (DBM) and voxel-based morphometry (VBM) to measure the morphological changes in patients receiving fractionated photon RT, and relate these to the dose. Additionally, we study tissue specific volume changes in white matter (WM), grey matter (GM), cerebrospinal fluid and total intracranial volume (TIV)., Methods and Materials: From our database, we selected 28 patients with MRI of high quality available at baseline and 1 year after RT. Scans were rigidly registered to each other, and to the planning CT and dose file. We used DBM to study non-tissue-specific volumetric changes, and VBM to study volume loss in grey matter. Observed changes were then related to the applied radiation dose (in EQD2). Additionally, brain tissue was segmented into WM, GM and cerebrospinal fluid, and changes in these volumes and TIV were tested., Results: Performing DBM resulted in clusters of dose-dependent volume loss 1 year after RT seen throughout the brain. Both WM and GM were affected; within the latter both cerebral cortex and subcortical nuclei show volume loss. Volume loss rates ranging from 5.3 to 15.3%/30 Gy were seen in the cerebral cortical regions in which more than 40% of voxels were affected. In VBM, similar loss rates were seen in the cortex and nuclei. The total volume of WM and GM significantly decreased with rates of 5.8% and 2.1%, while TIV remained unchanged as expected., Conclusions: Radiotherapy is associated with dose-dependent intracranial morphological changes throughout the entire brain. Therefore, we will consider to revise sparing of organs at risk based on future cognitive and neurofunctional data., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2021 The Author(s).)

A 69-year-old man presented with leptomeningeally metastasised pituitary carcinoma, rapidly progressing despite previous treatment with resection, radiotherapy and cabergoline. The patient received temozolomide chemotherapy, resulting in a complete clinical, radiological and biochemical response after 14 cycles, which has been maintained since then. This case lends further support to the role of temozolomide in refractory pituitary tumours.