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The oncological and functional outcomes in glioblastoma (GBM) patients following supratotal resection (SupTR), involving complete resection of contrast-enhancing enhanced (CE) tumors and areas of methionine (Met) uptake on 11C-met positron emission tomography (Met-PET), are unknown. We conducted a retrospective review in newly diagnosed, IDH1 wild-type GBM patients, comparing SupTR with gross total resection (GTR), in which only CE tumor tissue was resected. All patients underwent standard radiotherapy and temozolomide treatment, and were followed for tumor recurrence and overall survival (OS). Among the 30 patients included in this study, 7 underwent SupTR and 23 underwent GTR. Awake craniotomy with cortical and subcortical mapping was more frequently performed in the SupTR group than in the GTR group. During the follow-up period, significantly different patterns of disease progression were observed between groups. Although more than 80% of recurrences were local in the GTR group, all recurrences in the SupTR group were distant. Median OS in the GTR and SupTR groups was 18.5 months (95% confidence interval [CI] 14.2–35.1) and not reached (95% CI 30.5-not estimable), respectively; this difference was statistically significant (p = 0.03 by log-rank test). No postoperative neurocognitive decline was evident in patients who underwent SupTR. Compared to GTR alone, aggressive resection of both CE tumors and areas with Met uptake (SupTR) under awake craniotomy with functional mapping results in a survival benefit associated with better local control and neurocognitive preservation. [ABSTRACT FROM AUTHOR]

In the management of patients with newly diagnosed glioblastoma, there is no standard duration for adjuvant temozolomide treatment. This study aimed to assess the feasibility of finalizing adjuvant temozolomide treatment on the basis of methionine uptake in methionine positron emission tomography (Met-PET). We conducted a retrospective review of glioblastoma patients who underwent more than twelve cycles of temozolomide (extended temozolomide) treatment after resection and concomitant chemoradiotherapy with no evidence of recurrence on MRI. In addition to the methionine uptake value at the completion of extended temozolomide, local and distant recurrence and progression-free survival were also analyzed. Forty-four patients completed the extended temozolomide treatment. Among these, 18 experienced some type of tumor recurrence within one year. A Tmax/Nave value of 2.0 was the optimal cut-off value indicating progression. More than 80% of the patients with low methionine uptake completed the temozolomide treatment, and subsequent basic MRI observations showed no recurrence within one year after Met-PET. Subgroups with high uptake (≥2.0), even with continuation of temozolomide treatment, showed more frequent tumor progression than patients with low uptake (<2.0) who completed the extended temozolomide treatment (p < 0.001, odds ratio 14.7, 95% CI 3.46–62.3). The tumor recurrence rate increased in stepwise manner according to methionine uptake. Finalization of the extended temozolomide treatment on the basis of low uptake value was feasible with a low recurrence rate. Compared to MRI, Met-PET shows better ability to predict tumor progression in long-term glioblastoma survivors with extended temozolomide use. [ABSTRACT FROM AUTHOR]

Corpus callosum (CC) infarction has been reported to be rare because of the rich blood supply in the CC. The pathophysiology of CC infarction associated with acute hydrocephalus is unknown. The aim of the present study was to clarify the characteristics and mechanism of CC infarction associated with acute noncommunicating hydrocephalus (ANCH). We reviewed clinical the data from all patients who had undergone surgical intervention for ANCH at Chiba University Hospital from January 2008 to March 2018. Patients with vascular lesions, a history of hydrocephalus, and lacking magnetic resonance imaging studies were excluded. The clinical, surgical, and radiological parameters were obtained retrospectively for pathophysiological analysis. A total of 23 patients with ANCH who had undergone surgical intervention and had met the inclusion criteria were included in the present study. Of the 23 patients, 6 (23%) had developed CC infarction. All CC infarctions were located in the splenium. Although no clinical or surgical features were associated with splenial infarction, the radiological parameters of lateral ventricle enlargement and a narrower callosal angle at the posterior commissure and the foramen of Monro were significantly associated with splenial infarction. The present study has presented evidence that increased intraventricular pressure by ANCH applied transversely in the splenium will directly induce compression of the superior branch of the posterior callosal artery and pericallosal pial plexus, resulting in splenium-specific infarction in patients with ANCH. [ABSTRACT FROM AUTHOR]

Background Delayed infarction in the lenticulostriate artery (LSA) area after insular glioma resection is not common, and its pathophysiology remains unknown. Case Description A 32-year-old right-handed man with a giant insular low-grade glioma with frontal and temporal extension underwent awake craniotomy with an intentional staged surgery strategy. Preoperative radiologic images demonstrated a diagonally elevated middle cerebral artery (MCA) by the temporal tumor and a significantly compressed striatum. With intraoperative subcortical direct electrical stimulation, the resection was finalized in the temporal part of the tumor due to the semantic paraphasia induced in the temporal stem, fatigue, and loss of concentration. The immediate postoperative clinical course was uneventful. However, on postoperative day 20, he suddenly experienced right hemiparesis. Repeated images revealed infarction in the LSA area. The previously compressed striatum was then relieved and relocated to its original position in just 20 days, and the M1 segment of the MCA was remarkably downward, in which the MCA resembled a hammock. Angiography confirmed the hammock-shaped MCA and significantly stretched LSA, suggesting the combination of freed striatum from the compression and loss of temporal structure by the tumor resection as the key mechanism of severe dislocation of the MCA and delayed ischemia. Conclusions In a staged resection of giant insular glioma, attention should be paid to a possible severe dislocation of the MCA in a delayed postoperative period, which may lead to LSA stretching and delayed infarction. [ABSTRACT FROM AUTHOR]

Blake's pouch cyst (BPC), a rare cystic malformation in the posterior fossa, is believed to be caused by the congenital expansion of the posterior membranous area that normally regresses during embryogenesis. However, due to the wide spectrum of the onset pattern and age of patients, the natural history and the pathogenesis are poorly understood. The authors describe the case of a girl who admitted with headache and right abducens nerve paresis at the age of 3 years and 10 months. Magnetic resonance (MR) imaging demonstrated a tetraventricular hydrocephalus, an open aqueduct, and a posterior fossa cyst compatible with BPC. Multiple tumors were also noticed in the ventricular wall. Tumor biopsy and an endoscopic third ventriculostomy were performed. Intraoperative observation confirmed the BPC, and pathological diagnosis was pilomyxoid astrocytoma. In retrospect, MR imaging was performed twice in the past, at the age of 8 months and again at 22 months, and no anomaly was detected, suggesting that Blake's pouch was once regressed. Therefore, a BPC in this patient was certainly developed after her second or third year of life. The ventricular tumors may influence the cerebrospinal fluid (CSF) absorption, which triggered the re-expansion of BPC from the possible remnant of Blake's pouch. This is a rare but important report providing evidence that in addition to the classic congenital BPC in which the remnant of Blake's pouch remains persistent, there could be postnatal or secondary BPC, which develops after birth. Possible mechanisms include that the remnant of Blake's pouch, which originally disappears, may re-expand postnatally in association with unknown trigger or a change in CSF dynamics or absorption. [ABSTRACT FROM AUTHOR]

Intermittent monitoring of abnormal muscle response (iAMR) has been reported to be useful for improving the surgical outcome of microvascular decompression (MVD) for hemifacial spasm (HFS). However, iAMR has not elucidated the relationship between AMR change and the corresponding surgical procedure, or the pathogenesis of AMR and HFS. The purpose of this study is to clarify the usefulness of continuous AMR monitoring (cAMR) for improving the surgical results of MVD and for understanding the relationship between AMR change and corresponding surgical procedure, and the pathogenesis of AMR and HFS. Fifty consecutive patients with HFS treated by MVD under cAMR monitoring, which continuously records AMR every minute throughout the surgical period, were retrospectively analyzed. The patients were assessed for the presence of HFS 1 week after the surgery and at final follow-up. Forty-six patients showed the complete disappearance of HFS. In 32, AMR disappeared abruptly and simultaneously with decompression of an offending vessel. AMR showed dynamic and various changes including temporary disappearance, or sudden, gradual, or componential disappearance before and during the decompression procedure, and even during the dural and skin closure after the initial decompression procedure. Facial spasm remained in four patients despite permanent AMR disappearance. cAMR monitoring improves the outcome of MVD. Although the main cause of HFS and AMR is vascular compression at the facial nerve, hyperexcitability of the facial nucleus is also involved in the pathogenesis of HFS and AMR. The proportional involvement of these causes differs between patients. [ABSTRACT FROM AUTHOR]

Amino acid positron emission tomography (PET) may provide additional information to computed tomography and magnetic resonance imaging for detecting the pretreatment diagnosis of intracranial lesions. The purpose of this study was to investigate the role of cutoff values of 11C-METPET, an amino acid PET tracer, in the differentiation of pretreatment brain tumors from non-neoplastic lesions. This retrospective cohort study analyzed 101 pretreatment patients with a definitive diagnosis out of a total of 425 consecutive 11C-METPET imaging studies. The standardized uptake values (SUV) and the ratios of lesion to contralateral normal frontal-lobe gray matter uptake (L/N ratios) were measured. Cutoff values for the differential diagnosis of brain tumors from non-neoplastic lesions were determined using receiver operating characteristics curve (ROC) analysis. Based on the ROC analyses, the cutoffs were 3.33 for maximum SUV, 2.54 for mean SUV, 2.33 for peak SUV, 2.04 for Lmax/Nmean, and 2.23 for Lmax/Nmax. The sensitivity and specificity of these cutoffs were 69.2% and 82.6%, respectively, for maximum SUV, 64.1% and 91.3% for mean SUV, 69.2% and 91.3% for peak SUV, 70.5% and 91.3% for Lmax/Nmax and 75.6% and 82.6% for Lmax/Nmean. In differentiating intracranial brain tumor from non-neoplastic lesion with 11C-METPET, the use of optimal cutoff values indicates the high specificity, which means that positive result indicates the high likelihood of brain tumor. Considering the high specificity of 11C-METPET, more invasive examinations such as biopsy may be considered in positive cases. • The role of optimal cutoff for pretreatment 11C-METPET differentiation of intracranial brain tumors from non-neoplastic lesions is debatable. • Considering the high specificity using optimal cutoffs, 11C-METPET is useful for definitive diagnosis. • In positive cases, additional intrusive procedures such as biopsy may be undertaken based on 11C-METPET imaging. [ABSTRACT FROM AUTHOR]

Glioblastoma is the most common and aggressive type of brain tumor with high recurrence and fatality rates. Although various therapeutic strategies have been explored, there is currently no effective treatment for glioblastoma. Recently, the number of immunotherapeutic strategies has been tested for malignant brain tumors. Invariant natural killer T (iNKT) cells play an important role in anti-tumor immunity. To address if iNKT cells can target glioblastoma to exert anti-tumor activity, we assessed the expression of CD1d, an antigen-presenting molecule for iNKT cells, on glioblastoma cells. Glioblastoma cells from 10 of 15 patients expressed CD1d, and CD1d-positive glioblastoma cells pulsed with glycolipid ligand induced iNKT cell-mediated cytotoxicity in vitro. Although CD1d expression was low on glioblastoma stem-like cells, retinoic acid, which is the most common differentiating agent, upregulated CD1d expression in these cells and induced iNKT cell-mediated cytotoxicity. Moreover, intracranial administration of human iNKT cells induced tumor regression of CD1d-positive glioblastoma in orthotopic xenografts in NOD/Shi-scid IL-2RγKO (NOG) mice. Thus, CD1d expression represents a novel target for NKT cell-based immunotherapy for glioblastoma patients. [ABSTRACT FROM AUTHOR]