Symptom resolution in infiltrating WHO grade II-IV glioma patients undergoing surgical resection

Burks, Joshua D.; Bonney, Phillip A.; Glenn, Chad A.; Conner, Andrew K.; Briggs, Robert G.; Ebeling, Peter A.; Toho, Lucas C.; Sughrue, Michael E.

doi:10.1016/j.jocn.2016.03.006

Cited by 6 publications

(2 citation statements)

References 24 publications

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“…In addition to the typical symptoms, the rst symptoms of 27 patients were poor temper and personality changes such as crying, laughing, or somniloquy. In recent years, many studies have focused on patients' atypical symptoms [19], their chief complaint is muscle weakness, which is di cult to distinguish from other patients [20]. The Chinese Neurosurgery Society published the Expert Consensus on Comprehensive Treatment of Brainstem Glioma, which also noted that pBSGs often present atypical symptoms such as emotional and behavioral abnormalities [21].…”

Section: Clinical Manifestation and Imaging Ndingmentioning

confidence: 99%

Survival and prognostic factors of pediatric brainstem gliomas: a single institution experience of 96 cases

Wang

et al. 2023

Preprint

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Purpose Brainstem gliomas (BSGs) have a poor prognosis, especially in children. The clinical manifestations of pediatric brainstem gliomas (pBSGs) are atypical, and systematic studies in this population are scarce. This study aimed to investigate the comprehensive features of pBSGs and prognostic factors associated with survival. Methods Data from primarily diagnosed BSGs were collected, including clinical, radiological, treatment, and molecular characteristics. Survival analysis was performed by the Kaplan-Meier method and the Cox regression method. Results 96 BSG patients were included, and the median overall survival (OS) was 11.23 months. Primary symptoms included gait instability in 73 cases, choking on water in 49 cases, limb weakness in 48 cases, and personality changes in 27 cases. Univariate regression analysis showed that ring enhancement, Lansky score, H3K27M, TP53, and EZH2 protein expression might affect the survival of patients with BSG (P < 0.05). Multifactorial Cox regression analysis showed that the patients with H3K27M wild-type, Lansky score ≥ 60, and MRI without noticeable ring enhancement had a more extended survival period (P < 0.05). In patients with H3K27M mutation, the median OS of the EZH2 mutant patients was shorter (P = 0.025). Conclusion PBSGs have a poor prognosis and should be considered in the differential diagnosis of children who present clinically with unexplained behavioral changes. An accurate pathological biopsy is essential for prognosis.

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Section: Clinical Manifestation and Imaging Ndingmentioning

confidence: 99%

Survival and prognostic factors of pediatric brainstem gliomas: a single institution experience of 96 cases

Wang

et al. 2023

Preprint

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“…Glioblastoma (GBM), used to refer to Grade-IV astrocytoma, is the most common, aggressive, and malignant form of primary brain tumors in adults. GBM patients typically present a spectrum of generalized or focal neurologic symptoms including headaches, partial or generalized seizures, unilateral or bilateral paresis, hemiplegia, ataxia, visual defects, cognitive impairment, and personality changes (Iacob and Dinca, 2009; Burks et al, 2016; Georgakis et al, 2018). These symptoms persist throughout the course of the disease and worsen following surgical resection, severely limiting day-to-day functions, impacting patients’ quality of life, and even influencing survival outcomes (Martinez et al, 2008; Iacob and Dinca, 2009; Georgakis et al, 2018; Lee et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

An Inflammatory Landscape for Preoperative Neurologic Deficits in Glioblastoma

et al. 2019

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Introduction: Patients with glioblastoma (GBM), one of the most aggressive forms of primary brain tumors, exhibit a wide range of neurologic signs, ranging from headaches to neurologic deficits and cognitive impairment, at first clinical presentation. While such variability is attributed to inter-individual differences in increased intracranial pressure, tumor infiltration, and vascular compromise, a direct association with disease stage, tumor size and location, edema, and necrotic cell death has yet to be established. The lack of specificity of neurologic symptoms often confounds the diagnosis of GBM. It also limits clinicians’ ability to elect treatment regimens that not only prolong survival but also promote symptom management and high quality of life. Methods: To decipher the heterogeneous presentation of neurologic symptoms in GBM, we investigated differences in the molecular makeup of tumors from patients with and without preoperative neurologic deficits. We used the Ivy GAP (Ivy Glioblastoma Atlas Project) database to integrate RNA sequencing data from histologically defined GBM tumor compartments and neurologic examination records for 41 patients. We investigated the association of neurologic deficits with various tumor and patient attributes. We then performed differential gene expression and co-expression network analysis to identify a transcriptional signature specific to neurologic deficits in GBM. Using functional enrichment analysis, we finally provided a comprehensive and detailed characterization of involved pathways and gene interactions. Results: An exploratory investigation of the association of tumor and patient variables with the early development of neurologic deficits in GBM revealed a lack of robust and consistent clinicopathologic prognostic factors. We detected significant differences in the expression of 728 genes (FDR-adjusted p -value ≤ 0.05 and relative fold-change ≥ 1.5), unique to the cellular tumor (CT) anatomical compartment, between neurologic deficit groups. Upregulated differentially expressed genes in CT were enriched for mesenchymal subtype-predictive genes. Applying a systems approach, we then identified co-expressed gene sets that correlated with neurological deficit manifestation (FDR-adjusted p -value < 0.1). Collectively, these findings uncovered significantly enriched immune activation, oxidative stress response, and cytokine-mediated proinflammatory processes. Conclusion: Our study posits that inflammatory processes, as well as a mesenchymal tumor subtype, are implicated in the pathophysiology of preoperative neurologic deficits in GBM.

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