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The 2021 World Health Organization Classification of Tumors of the Central Nervous System (CNS5), introduced significant changes, impacting tumors ranging from glial to ependymal neoplasms. Ependymal tumors were previously classified and graded based on histopathology, which had limited clinical and prognostic utility. The updated CNS5 classification now divides ependymomas into 10 subgroups based on anatomic location (supratentorial, posterior fossa, and spinal compartment) and genomic markers. Supratentorial tumors are defined by zinc finger translocation associated (ZFTA) (formerly v-rel avian reticuloendotheliosis viral oncogene [RELA]), or yes-associated protein 1 (YAP1) fusion; posterior fossa tumors are classified into groups A (PFA) and B (PFB), spinal ependymomas are defined by MYCN amplification. Subependymomas are present across all these anatomic compartments. The new classification kept an open category of "not elsewhere classified" or "not otherwise specified" if no pathogenic gene fusion is identified or if the molecular diagnosis is not feasible. Although there is significant overlap in the imaging findings of these tumors, a neuroradiologist needs to be familiar with updated CNS5 classification to understand tumor behavior, for example, the higher tendency for tumor recurrence along the dural flap for ZFTA fusion-positive ependymomas. On imaging, supratentorial ZFTA-fused ependymomas are preferentially located in the cerebral cortex, carrying predominant cystic components. YAP1-MAMLD1-fused ependymomas are intra- or periventricular with prominent multinodular solid components and have significantly better prognosis than ZFTA-fused counterparts. PFA ependymomas are aggressive paramedian masses with frequent calcification, seen in young children, originating from the lateral part of the fourth ventricular roof. PFB ependymomas are usually midline, noncalcified solid-cystic masses seen in adolescents and young adults arising from the fourth ventricular floor. PFA has a poorer prognosis, higher recurrence, and higher metastatic rate than PFB. Myxopapillary spinal ependymomas are now considered grade II due to high recurrence rates. Spinal-MYCN ependymomas are aggressive tumors with frequent leptomeningeal spread, relapse, and poor prognosis. Subependymomas are noninvasive, intraventricular, slow-growing benign tumors with an excellent prognosis. Currently, the molecular classification does not enhance the clinicopathologic understanding of subependymoma and myxopapillary categories. However, given the molecular advancements, this will likely change in the future. This review provides an updated molecular classification of ependymoma, discusses the individual imaging characteristics, and briefly outlines the latest targeted molecular therapies.
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Meningiomas, the most common primary intracranial neoplasms, account for over a third of primary CNS tumors. While traditionally viewed as benign, meningiomas can be associated with considerable morbidity, and specific meningioma subgroups display more aggressive behavior with higher recurrence rates. The risk stratification for recurrence has been primarily associated with the World Health Organization (WHO) histopathological grade and extent of resection. However, a growing body of literature has highlighted the value of molecular characteristics in assessing recurrence risk. While maintaining the previous classification system, the 5th edition of the 2021 WHO CNS tumor (CNS5) book expands upon the molecular information in meningiomas to help guide management. The WHO CNS5 stratifies meningioma into three grades (1-3) based on histopathology criteria and molecular profile. pTERT mutations and CDKN2A/B deletions now signify a grade 3 meningioma with increased recurrence risk. Tumor location also correlates with underlying mutations. Convexity and most spinal meningiomas carry 22q deletion and/or NF2 mutations, while skull base meningiomas have AKT1, TRAF7, SMO, and/or PIK3CA mutations. MRI is the primary imaging modality for diagnosing and treatment planning of meningiomas, while DOTATATE-PET imaging offers supplementary information beyond anatomical imaging. Herein, we review the evolving molecular landscape of meningiomas, emphasizing imaging/genetic biomarkers, and treatment strategies relevant to neuroradiologists.ABBREVIATIONS: AKT1=AKT serine/threonine kinase 1; BAP1=BRCA1-associated protein 1; CDK4/6=Cyclin-dependent kinases 4 and 6; KLF4=Krüppel-like factor 4; NF2=Neurofibromatosis type 2; PIK3CA=Phosphatidylinositol-4,5-Bisphosphate 3-Kinase catalytic subunit alpha; POLR2A=RNA polymerase II subunit A; SMO: Smoothened, frizzled class receptor; SMARCB1=SWItch/sucrose non-fermentable related, matrix associated, actin dependent regulator of chromatin, subfamily b, member 1; TERT=Telomerase reverse transcriptase; TRAF7=TNF receptor-associated factor 7.
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Glial fibrillary acidic protein (GFAP) astrocytopathy is a recently described autoimmune inflammatory disorder of the CNS characterized by the presence of specific antibodies targeting the intracellular filament protein in mature astrocytes. The pathogenesis is heterogeneous and poorly understood, with around 20%-34% of cases occurring as a paraneoplastic syndrome, most frequently associated with ovarian teratomas. It presents clinically as acute or subacute encephalomyelitis, and the diagnosis relies on imaging and detection of GFAP-Immunoglobulin (GFAP-IgG) in the CSF. Characteristic imaging findings include linear perivascular enhancement in the white matter extending in a radial pattern. Other imaging findings include periependymal enhancement, longitudinally extensive cord signal changes, intramedullary enhancement, optic neuritis, and papillitis. There is significant imaging overlap with other neuroinflammatory diseases like neuromyelitis optica spectrum disorder and lymphoproliferative conditions. GFAP astrocytopathy is characteristically responsive to steroids with, however, a significant rate of relapse. Currently, literature on this novel entity is limited with no established diagnostic criteria or standard treatment regimen. This comprehensive review explores the clinical, radiographic, and histopathologic aspects of GFAP astrocytopathy, shedding light on its complex nature and potential diagnostic challenges. The paper highlights the neuroimaging findings with a focus on differentiating GFAP astrocytopathy from other neuroinflammatory disorders.
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Light-chain deposition disease (LCDD) is a rare CNS disorder characterized by the extracellular accumulation of monoclonal immunoglobulin light chains in various organs. LCDD typically arises secondary to an underlying plasma cell dyscrasia, such as monoclonal gammopathy of undetermined significance (MGUS) or multiple myeloma. However, rare cases can occur in the absence of a demonstrable plasma cell disorder. The kidneys, liver, lungs, and heart are the most affected organs. Intracerebral LCDD, particularly without an underlying plasma cell neoplasm, represents an exceedingly uncommon entity with limited documented cases in literature. This review article explores the pathogenesis, histopathological features, and characteristic neuroimaging findings of intracerebral LCDD. We emphasize the diverse imaging presentations of this disease, which can closely resemble other neurological pathologies. Recognizing these potential mimics is crucial for avoiding misdiagnosis, especially in the absence of a known underlying plasma cell disorder. This article aims to provide a comprehensive overview from a neuroradiological perspective, facilitating the recognition and differentiation of this challenging entity.ABBREVIATIONS: LCDD, light chain deposition disease; ALD, amyloidoma.
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The International League Against Epilepsy (ILAE) is an organization of 120 national chapters providing the most widely accepted and updated guidelines on epilepsy. In 2022, the ILAE Task Force revised the prior (2011) classification of focal cortical dysplasias to incorporate and update clinicopathologic and genetic information, with the aim to provide an objective classification scheme. New molecular-genetic information has led to the concept of "integrated diagnosis" on the same lines as brain tumors, with a multilayered diagnostic model providing a phenotype-genotype integration. Major changes in the new update were made to type II focal cortical dysplasias, apart from identification of new entities, such as mild malformations of cortical development and cortical malformation with oligodendroglial hyperplasia. No major changes were made to type I and III focal cortical dysplasias, given the lack of significant new genetic information. This review provides the latest update on changes to the classification of focal cortical dysplasias with discussion about the new entities. The ILAE in 2017 updated the classification of seizure and epilepsy with 3 levels of diagnosis, including seizure type, epilepsy type, and epilepsy syndrome, which are also briefly discussed here.
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Epilepsia , Malformações do Desenvolvimento Cortical , Fenótipo , Humanos , Malformações do Desenvolvimento Cortical/diagnóstico por imagem , Malformações do Desenvolvimento Cortical/genética , Malformações do Desenvolvimento Cortical/classificação , Epilepsia/diagnóstico por imagem , Epilepsia/genética , Epilepsia/classificação , Neuroimagem/métodos , Displasia Cortical FocalRESUMO
BACKGROUND AND PURPOSE: Feature variability in radiomics studies due to technical and magnet strength parameters is well-known and may be addressed through various preprocessing methods. However, very few studies have evaluated the downstream impact of variable preprocessing on model classification performance in a multiclass setting. We sought to evaluate the impact of Smallest Univalue Segment Assimilating Nucleus (SUSAN) denoising and Combining Batches harmonization on model classification performance. MATERIALS AND METHODS: A total of 493 cases (410 internal and 83 external data sets) of glioblastoma, intracranial metastatic disease, and primary CNS lymphoma underwent semiautomated 3D-segmentation post-baseline image processing (BIP) consisting of resampling, realignment, coregistration, skull-stripping, and image normalization. Post-BIP, 2 sets were generated, one with and another without SUSAN denoising. Radiomics features were extracted from both data sets and batch-corrected to produce 4 data sets: (a) BIP, (b) BIP with SUSAN denoising, (c) BIP with Combining Batches, and (d) BIP with both SUSAN denoising and Combining Batches harmonization. Performance was then summarized for models using a combination of 6 feature-selection techniques and 6 machine learning models across 4 mask-sequence combinations with features derived from 1 to 3 (multiparametric) MRI sequences. RESULTS: Most top-performing models on the external test set used BIP+SUSAN denoising-derived features. Overall, the use of SUSAN denoising and Combining Batches harmonization led to a slight but generally consistent improvement in model performance on the external test set. CONCLUSIONS: The use of image-preprocessing steps such as SUSAN denoising and Combining Batches harmonization may be more useful in a multi-institutional setting to improve model generalizability. Models derived from only T1 contrast-enhanced images showed comparable performance to models derived from multiparametric MRI.
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Noninvasive tumor control of vestibular schwannomas through stereotactic radiosurgery allows high rates of long-term tumor control and has been used primarily for small- and medium-sized vestibular schwannomas. The posttreatment imaging appearance of the tumor, temporal patterns of growth and treatment response, as well as extratumoral complications can often be both subtle or confusing and should be appropriately recognized. Herein, the authors present an imaging-based review of expected changes as well as associated complications related to radiosurgery for vestibular schwannomas.
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High-grade astrocytoma with piloid features (HGAP) is a recently identified brain tumor characterized by a distinct DNA methylation profile. Predominantly located in the posterior fossa of adults, HGAP is notably prevalent in individuals with neurofibromatosis type 1. We present an image-centric review of HGAP and explore the association between HGAP and neurofibromatosis type 1. Data were collected from 8 HGAP patients treated at two tertiary care institutions between January 2020 and October 2023. Demographic details, clinical records, management, and tumor molecular profiles were analyzed. Tumor characteristics, including location and imaging features on MR imaging, were reviewed. Clinical or imaging features suggestive of neurofibromatosis 1 or the presence of NF1 gene alteration were documented. The mean age at presentation was 45.5 years (male/female = 5:3). Tumors were midline, localized in the posterior fossa (n = 4), diencephalic/thalamic (n = 2), and spinal cord (n = 2). HGAP lesions were T1 hypointense, T2-hyperintense, mostly without diffusion restriction, predominantly peripheral irregular enhancement with central necrosis (n = 3) followed by mixed heterogeneous enhancement (n = 2). Two NF1 mutation carriers showed signs of neurofibromatosis type 1 before HGAP diagnosis, with one diagnosed during HGAP evaluation, strengthening the HGAP-NF1 link, particularly in patients with posterior fossa masses. All tumors were IDH1 wild-type, often with ATRX, CDKN2A/B, and NF1 gene alteration. Six patients underwent surgical resection followed by adjuvant chemoradiation. Six patients were alive, and two died during the last follow-up. Histone H3 mutations were not detected in our cohort, such as the common H3K27M typically seen in diffuse midline gliomas, linked to aggressive clinical behavior and poor prognosis. HGAP lesions may involve the brain or spine and tend to be midline or paramedian in location. Underlying neurofibromatosis type 1 diagnosis or imaging findings are important diagnostic cues.
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Astrocitoma , Neoplasias Encefálicas , Neurofibromatose 1 , Adulto , Humanos , Masculino , Feminino , Pessoa de Meia-Idade , Neurofibromatose 1/diagnóstico por imagem , Neurofibromatose 1/patologia , Astrocitoma/diagnóstico por imagem , Astrocitoma/genética , Astrocitoma/patologia , Neoplasias Encefálicas/diagnóstico por imagem , Neoplasias Encefálicas/genética , Neoplasias Encefálicas/patologia , Histonas/genética , Encéfalo/patologia , MutaçãoRESUMO
Given the recent advances in molecular pathogenesis of tumors, with better correlation with tumor behavior and prognosis, major changes were made to the new 2021 World Health Organization (WHO) classification of CNS tumors, including updated criteria for diagnosis of glioblastoma (GBM). Diagnosis of GBM now requires absence of isocitrate dehydrogenase and histone 3 mutations (IDH-wild-type and H3-wild-type) as the basic cornerstone, with elimination of the IDH-mutant category. The requirements for diagnosis were conventionally histopathological, based on the presence of pathognomonic features such as microvascular proliferation and necrosis. However, even if these histologic features are absent, many lower-grade (WHO grade 2/3) diffuse astrocytic gliomas behave clinically similar to GBM (grade 4). The 2021 WHO classification introduced new molecular criteria that can be used to upgrade the diagnosis of such histologically lower-grade, IDH-wild-type, astrocytomas to GBM. The 3 molecular criteria include: concurrent gain of whole chromosome 7 and loss of whole chromosome 10 (+7/-10); telomerase reverse transcriptase promoter mutation; and epidermal growth factor receptor amplification. Given these changes, it is now strongly recommended to have molecular analysis of WHO grade 2/3 diffuse astrocytic, IDH-wild-type, gliomas in adult patients, as identification of any of the above mutations allows for upgrading the tumor to WHO grade 4 ("molecular GBM") with important prognostic implications. Despite an early stage, there is active ongoing research on the unique MR imaging features of molecular GBM. This paper highlights the differences between "molecular" and "histopathological" GBM, with the aim of providing a basic understanding about these changes.
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Neoplasias Encefálicas , Glioblastoma , Organização Mundial da Saúde , Humanos , Glioblastoma/genética , Glioblastoma/diagnóstico por imagem , Glioblastoma/patologia , Neoplasias Encefálicas/genética , Neoplasias Encefálicas/diagnóstico por imagem , Neoplasias Encefálicas/patologia , Isocitrato Desidrogenase/genética , Mutação , Gradação de TumoresRESUMO
Cauda Equina Neuroendocrine Tumors (CE-NET), previously referred to as paragangliomas are a rare subset of spinal tumors, with limited data on imaging. Herein, we present a retrospective review of clinical and imaging findings of CE-NETs in ten patients who were evaluated at our institution over the past two decades. All patients had well-defined intradural lesions in the lumbar spine which demonstrated slow growth. A review of imaging findings revealed the presence of an eccentric vascular pedicle along the dorsal aspect of the tumor in 8 of the 10 patients (eccentric vessel sign), a distinctive finding that has not previously been reported with this tumor and may help improve the accuracy of imaging-based diagnosis. In all cases, a gross-total resection was performed, with resolution of symptoms in most of the cases.
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Cauda Equina , Neoplasias do Sistema Nervoso Central , Tumores Neuroendócrinos , Paraganglioma , Neoplasias da Coluna Vertebral , Humanos , Neoplasias da Coluna Vertebral/patologia , Tumores Neuroendócrinos/diagnóstico por imagem , Tumores Neuroendócrinos/cirurgia , Tumores Neuroendócrinos/patologia , Cauda Equina/diagnóstico por imagem , Cauda Equina/cirurgia , Paraganglioma/diagnóstico por imagem , Paraganglioma/cirurgia , Neoplasias do Sistema Nervoso Central/patologia , Imageamento por Ressonância MagnéticaRESUMO
The nervous system is commonly involved in a wide range of genetic tumor-predisposition syndromes. The classification of genetic tumor syndromes has evolved during the past years; however, it has now become clear that these syndromes can be categorized into a relatively small number of major mechanisms, which form the basis of the new 5th edition of the World Health Organization book (beta online version) on genetic tumor syndromes. For the first time, the World Health Organization has also included a separate chapter on genetic tumor syndromes in the latest edition of all the multisystem tumor series, including the 5th edition of CNS tumors. Our understanding of these syndromes has evolved rapidly since the previous edition (4th edition, 2016) with recognition of 8 new syndromes, including the following: Elongator protein complex-medulloblastoma syndrome, BRCA1-associated protein 1 tumor-predisposition syndrome, DICER1 syndrome, familial paraganglioma syndrome, melanoma-astrocytoma syndrome, Carney complex, Fanconi anemia, and familial retinoblastoma. This review provides a description of these new CNS tumor syndromes with a focus on imaging and genetic characteristics.
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Neoplasias do Sistema Nervoso Central , Neoplasias Cerebelares , Síndromes Neoplásicas Hereditárias , Neoplasias do Sistema Nervoso , Neoplasias da Retina , Humanos , Neoplasias do Sistema Nervoso Central/diagnóstico por imagem , Neoplasias do Sistema Nervoso Central/genética , Neoplasias do Sistema Nervoso/genética , Síndromes Neoplásicas Hereditárias/diagnóstico por imagem , Síndromes Neoplásicas Hereditárias/genética , Predisposição Genética para Doença , Organização Mundial da Saúde , Ribonuclease III/genética , RNA Helicases DEAD-box/genéticaRESUMO
INTRODUCTION: Survival prediction in glioblastoma remains challenging, and identification of robust imaging markers could help with this relevant clinical problem. We evaluated multiparametric magnetic resonance imaging-derived radiomics to assess prediction of overall survival (OS) and progression-free survival (PFS). METHODOLOGY: A retrospective, institutional review board-approved study was performed. There were 93 eligible patients, of which 55 underwent gross tumor resection and chemoradiation (GTR-CR). Overall survival and PFS were assessed in the entire cohort and the GTR-CR cohort using multiple machine learning pipelines. A model based on multiple clinical variables was also developed. Survival prediction was assessed using the radiomics-only, clinical-only, and the radiomics and clinical combined models. RESULTS: For all patients combined, the clinical feature-derived model outperformed the best radiomics model for both OS (C-index, 0.706 vs 0.597; P < 0.0001) and PFS prediction (C-index, 0.675 vs 0.588; P < 0.001). Within the GTR-CR cohort, the radiomics model showed nonstatistically improved performance over the clinical model for predicting OS (C-index, 0.638 vs 0.588; P = 0.4). However, the radiomics model outperformed the clinical feature model for predicting PFS in GTR-CR cohort (C-index, 0.641 vs 0.550; P = 0.004). Combined clinical and radiomics model did not yield superior prediction when compared with the best model in each case. CONCLUSIONS: When considering all patients, regardless of therapy, the radiomics-derived prediction of OS and PFS is inferior to that from a model derived from clinical features alone. However, in patients with GTR-CR, radiomics-only model outperforms clinical feature-derived model for predicting PFS.
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Neoplasias Encefálicas , Glioblastoma , Imageamento por Ressonância Magnética Multiparamétrica , Humanos , Glioblastoma/diagnóstico por imagem , Glioblastoma/terapia , Estudos Retrospectivos , Neoplasias Encefálicas/diagnóstico por imagem , Neoplasias Encefálicas/terapia , Neoplasias Encefálicas/patologia , Imageamento por Ressonância Magnética/métodosRESUMO
RATIONALE AND OBJECTIVES: Imaging-based differentiation between glioblastoma (GB) and brain metastases (BM) remains challenging. Our aim was to evaluate the performance of 3D-convolutional neural networks (CNN) to address this binary classification problem. MATERIALS AND METHODS: T1-CE, T2WI, and FLAIR 3D-segmented masks of 307 patients (157 GB and 150 BM) were generated post resampling, co-registration normalization and semi-automated 3D-segmentation and used for internal model development. Subsequent external validation was performed on 59 cases (27 GB and 32 BM) from another institution. Four different mask-sequence combinations were evaluated using area under the curve (AUC), precision, recall and F1-scores. Diagnostic performance of a neuroradiologist and a general radiologist, both without and with the model output available, was also assessed. RESULTS: 3D-model using the T1-CE tumor mask (TM) showed the highest performance [AUC 0.93 (95% CI 0.858-0.995)] on the external test set, followed closely by the model using T1-CE TM and FLAIR mask of peri-tumoral region (PTR) [AUC of 0.91 (95% CI 0.834-0.986)]. Models using T2WI masks showed robust performance on the internal dataset but lower performance on the external set. Both neuroradiologist and general radiologist showed improved performance with model output provided [AUC increased from 0.89 to 0.968 (p = 0.06) and from 0.78 to 0.965 (p = 0.007) respectively], the latter being statistically significant. CONCLUSION: 3D-CNNs showed robust performance for differentiating GB from BMs, with T1-CE TM, either alone or combined with FLAIR-PTR masks. Availability of model output significantly improved the accuracy of the general radiologist.
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PURPOSE: To determine if machine learning (ML) or deep learning (DL) pipelines perform better in AI-based three-class classification of glioblastoma (GBM), intracranial metastatic disease (IMD) and primary CNS lymphoma (PCNSL). METHODOLOGY: Retrospective analysis included 502 cases for training (208 GBM, 67 PCNSL and 227 IMD), with external validation on 86 cases (27:27:32). Multiparametric MRI images (T1W, T2W, FLAIR, DWI and T1-CE) were co-registered, resampled, denoised and intensity normalized, followed by semiautomatic 3D segmentation of the enhancing tumor (ET) and peritumoral region (PTR). Model performance was assessed using several ML pipelines and 3D-convolutional neural networks (3D-CNN) using sequence specific masks, as well as combination of masks. All pipelines were trained and evaluated with 5-fold nested cross-validation on internal data followed by external validation using multi-class AUC. RESULTS: Two ML models achieved similar performance on test set, one using T2-ET and T2-PTR masks (AUC: 0.885, 95% CI: [0.816, 0.935] and another using T1-CE-ET and FLAIR-PTR mask (AUC: 0.878, CI: [0.804, 0.930]). The best performing DL models achieved an AUC of 0.854, (CI [0.774, 0.914]) on external data using T1-CE-ET and T2-PTR masks, followed by model derived from T1-CE-ET, ADC-ET and FLAIR-PTR masks (AUC: 0.851, CI [0.772, 0.909]). CONCLUSION: Both ML and DL derived pipelines achieved similar performance. T1-CE mask was used in three of the top four overall models. Additionally, all four models had some mask derived from PTR, either T2WI or FLAIR.
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Progressive multifocal leukoencephalopathy (PML) is a rare viral central nervous system (CNS) demyelinating disease primarily associated with a compromised immune system. PML is seen mainly in individuals with human immunodeficiency virus, lymphoproliferative disease, and multiple sclerosis. Patients on immunomodulators, chemotherapy, and solid organ or bone marrow transplants are predisposed to PML. Recognition of various PML-associated typical and atypical imaging abnormalities is critical for early diagnosis and differentiating it from other conditions, especially in high-risk populations. Early PML recognition should expedite efforts at immune-system restoration, allowing for a favorable outcome. This review aims to provide a practical overview of radiological abnormalities in PML patients and address differential considerations.
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Síndrome Inflamatória da Reconstituição Imune , Vírus JC , Leucoencefalopatia Multifocal Progressiva , Esclerose Múltipla , Humanos , Leucoencefalopatia Multifocal Progressiva/diagnóstico por imagem , Natalizumab/uso terapêutico , Esclerose Múltipla/tratamento farmacológico , Diagnóstico PrecoceRESUMO
Metastatic malignancies have limited management strategies and variable treatment responses. Cancer cells develop beside and depend on the complex tumor microenvironment. Cancer-associated fibroblasts, with their complex interaction with tumor and immune cells, are involved in various steps of tumorigenesis, such as growth, invasion, metastasis, and treatment resistance. Prooncogenic cancer-associated fibroblasts emerged as attractive therapeutic targets. However, clinical trials have achieved suboptimal success. Fibroblast activation protein (FAP) inhibitor-based molecular imaging has shown encouraging results in cancer diagnosis, making them innovative targets for FAP inhibitor-based radionuclide therapies. This review summarizes the results of preclinical and clinical FAP-based radionuclide therapies. We will describe advances and FAP molecule modification in this novel therapy, as well as its dosimetry, safety profile, and efficacy. This summary may guide future research directions and optimize clinical decision-making in this emerging field.
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Fibroblastos Associados a Câncer , Neoplasias , Humanos , Serina Endopeptidases/metabolismo , Proteínas de Membrana/metabolismo , Neoplasias/diagnóstico por imagem , Neoplasias/radioterapia , Neoplasias/metabolismo , Fibroblastos Associados a Câncer/metabolismo , Radioisótopos/uso terapêutico , Radioisótopos/metabolismo , Tomografia por Emissão de Pósitrons combinada à Tomografia Computadorizada , Fibroblastos/patologia , Radioisótopos de Gálio , Microambiente TumoralRESUMO
Malignant brain tumors including parenchymal metastatic (MET) lesions, glioblastomas (GBM), and lymphomas (LYM) account for 29.7% of brain cancers. However, the characterization of these tumors from MRI imaging is difficult due to the similarity of their radiologically observed image features. Radiomics is the extraction of quantitative imaging features to characterize tumor intensity, shape, and texture. Applying machine learning over radiomic features could aid diagnostics by improving the classification of these common brain tumors. However, since the number of radiomic features is typically larger than the number of patients in the study, dimensionality reduction is needed to balance feature dimensionality and model complexity. Autoencoders are a form of unsupervised representation learning that can be used for dimensionality reduction. It is similar to PCA but uses a more complex and non-linear model to learn a compact latent space. In this work, we examine the effectiveness of autoencoders for dimensionality reduction on the radiomic feature space of multiparametric MRI images and the classification of malignant brain tumors: GBM, LYM, and MET. We further aim to address the class imbalances imposed by the rarity of lymphomas by examining different approaches to increase overall predictive performance through multiclass decomposition strategies.
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A 44-year-old male was referred to our clinic (2015) to evaluate multiple lung nodules with increasing fatigue, dyspnea, and weight loss. He was being assessed to an outside hospital for the same since 2010. The X-ray and computed-tomography (CT)-chest showed numerous pulmonary nodules and bilateral hilar adenopathy. Imaging workup at our institute (2015) redemonstrated extensive calcified pulmonary nodules. 18fluoro-2-deoxy-d-glucose positron emission tomographyCT showed widespread pulmonary nodules with low-grade uptake. Video-assisted thoracic surgery lung biopsy revealed pulmonary hyalinizing granuloma (PHG). Recently because of increasing symptoms, he is being evaluated for a lung transplant. This case represents a rare diagnosis of PHG with a decade follow-up.
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BACKGROUND AND OBJECTIVES: Cerebrovascular manifestations in neurosarcoidosis (NS) were previously considered rare but are being increasingly recognized. We report our preliminary experience in patients with NS who underwent high-resolution vessel wall imaging (VWI). METHODS: A total of 13 consecutive patients with NS underwent VWI. Images were analyzed by 2 neuroradiologists in consensus. The assessment included segment-wise evaluation of larger- and medium-sized vessels (internal carotid artery, M1-M3 middle cerebral artery; A1-A3 anterior cerebral artery; V4 segments of vertebral arteries; basilar artery; and P1-P3 posterior cerebral artery), lenticulostriate perforator vessels, and medullary and deep cerebral veins. Cortical veins were not assessed due to flow-related artifacts. Brain biopsy findings were available in 6 cases and were also reviewed. RESULTS: Mean patient age was 54.9 years (33-71 years) with an M:F of 8:5. Mean duration between initial diagnosis and VWI study was 18 months. Overall, 9/13 (69%) patients had vascular abnormalities. Circumferential large vessel enhancement was seen in 3/13 (23%) patients, whereas perforator vessel involvement was seen in 6/13 (46%) patients. Medullary and deep vein involvement was also seen in 6/13 patients. In addition, 7/13 (54%) patients had microhemorrhages in susceptibility-weighted imaging, and 4/13 (31%) had chronic infarcts. On biopsy, 5/6 cases showed perivascular granulomas with vessel wall involvement in all 5 cases. DISCUSSION: Our preliminary findings suggest that involvement of intracranial vascular structures may be a common finding in patients with NS and should be routinely looked for. These findings appear concordant with previously reported autopsy literature and need to be validated on a larger scale.