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Yutaka Hayashi, Mitsutoshi Nakada, Shingo Tanaka, Naoyuki Uchiyama, Yasuhiko Hayashi, Daisuke Kita and Jun-ichiro Hamada


Fluorescence-guided surgery using 5-aminolevulinic acid (5-ALA) has been broadly recognized as a beneficial tool for the resection of glioblastoma multiforme (GBM). Fluorescence in the ventricular walls, which were apparently free of macroscopic tumor or MR imaging enhancement indicative of CSF dissemination, was detected during surgery for GBM. To evaluate the clinical significance of the 5-ALA fluorescence, the authors resected ventricle wall tissue together with the adjacent tumors for pathological examination and then followed up the clinical courses of the patients.


Seven consecutive GBMs located near the lateral ventricle were surgically treated using a fluorescence-guided technique with 5-ALA at the authors' hospital since acquiring instrumentation for the detection of 5-ALA fluorescence in 2007. All of the procedures were performed using a ventricular entry, and 5-ALA fluorescence of the ventricular wall was detected despite the absence of macroscopic tumor invasion of the wall.


A pathological examination of the resected ventricular wall tissues revealed tumor cells in 6 of the 7 cases and disruption of the ependymal cell layer in all 7 cases. Delayed communicating hydrocephalus followed surgery in all 7 patients, and ventricular wall enhancements on MR imaging were demonstrated after hydrocephalus in 2 of the patients.


Data in this study suggest that 5-ALA fluorescence of the ventricular wall may be predictive of postoperative hydrocephalus associated with CSF dissemination even in cases without evidence of CSF dissemination on MR imaging studies before surgery. The authors also speculate that postoperative radiotherapy covering the whole ventricular system may be a better therapeutic option for these patients.

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Masashi Kinoshita, Riho Nakajima, Harumichi Shinohara, Katsuyoshi Miyashita, Shingo Tanaka, Hirokazu Okita, Mitsutoshi Nakada and Yutaka Hayashi


Although the right prefrontal region is regarded as a silent area, chronic deficits of the executive function, including working memory (WM), could occur after resection of a right prefrontal glioma. This may be overlooked by postoperative standard examinations, and the disabilities could affect the patient's professional life. The right prefrontal region is a part of the frontoparietal network and is subserved by the superior longitudinal fasciculus (SLF); however, the role of the SLF in spatial WM is unclear. This study investigated a persistent spatial WM deficit in patients who underwent right prefrontal glioma resection, and evaluated the relationship between the spatial WM deficit and the SLF.


Spatial WM was examined in 24 patients who underwent prefrontal glioma resection (right, n = 14; left, n = 10) and in 14 healthy volunteers using a spatial 2-back task during the long-term postoperative period. The neural correlates of spatial WM were evaluated using lesion mapping and voxel-based lesion-symptom mapping. In addition, the spatial 2-back task was performed during surgery under direct subcortical electrical stimulation in 2 patients with right prefrontal gliomas.


Patients with a right prefrontal lesion had a significant chronic spatial WM deficit. Voxel-based lesion-symptom mapping analysis revealed a significant correlation between spatial WM deficit and the region that overlapped the first and second segments of the SLF (SLF I and SLF II). Two patients underwent awake surgery and had difficulties providing the correct responses in the spatial 2-back task with direct subcortical electrical stimulation on the SLF I, which was preserved and confirmed by postoperative diffusion tensor imaging tractography. These patients exhibited no spatial WM deficits during the postoperative immediate and long-term periods.


Spatial WM deficits may persist in patients who undergo resection of the tumor located in the right prefrontal brain parenchyma. Injury to the dorsal frontoparietal subcortical white matter pathway, i.e., the SLF I or SLF I and II, could play a causal role in this chronic deficit. A persistent spatial WM deficit, without motor and language deficits, could affect the professional life of the patient. In such cases, awake surgery would be useful to detect the spatial WM network with appropriate task during tumor exploration.

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Ko Ikuta, Junichi Arima, Takayuki Tanaka, Masayoshi Oga, Soichiro Nakano, Kosuke Sasaki, Kohei Goshi, Masaki Yo and Shingo Fukagawa

Object. The authors applied the technique of microendoscopic discectomy to posterior decompression procedures for lumbar spinal stenosis. The purpose of this study was to determine the feasibility of using an endoscopic technique to treat lumbar spinal stenosis and to evaluate the clinical and radiographic results of microendoscopic posterior decompression (MEPD).

Methods. Microendoscopic posterior decompression, which involves a unilateral endoscopic approach for bilateral decompression, was performed in 47 patients. Clinical and radiographic/neuroimaging results were evaluated during the follow-up period (minimum duration 1 year). The clinical results were compared with those of the conventional laminotomy. Radiographic instability and the degree of surgical invasion of the facet joints were evaluated. In a control a group of 29 patients open laminotomy was performed.

The clinical outcome was evaluated in 44 patients. The mean follow-up duration was 22 months. The mean rate of improvement was 72% based on the Japanese Orthopaedic Association score, and good results were obtained in 38 patients. Although the rate of morbidity decreased in the MEPD group, the incidence of complication was slightly higher. Effective decompression was demonstrated in the majority of the patients by using magnetic resonance imaging. Radiographic instability appeared in one patient postoperatively, and based on computerized tomography scanning, a tendency toward invasion of the facet joint on the approach side was noted.

Conclusions. Microendoscopic posterior decompression is a minimally invasive procedure and is as useful as other conventional procedures in treating lumbar spinal stenosis; however, a few technical problems remain to be solved.

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Takuma Hara, Hiroyoshi Akutsu, Shingo Takano, Hiroyoshi Kino, Eiichi Ishikawa, Shuho Tanaka, Hidetaka Miyamoto, Noriaki Sakamoto, Keiichiro Hattori, Mamiko Sakata-Yanagimoto, Shigeru Chiba, Takashi Hiyama, Tomohiko Masumoto and Akira Matsumura


The Wnt/β-catenin signaling pathway is strongly implicated in the pathogenesis of adamantinomatous craniopharyngioma (adaCP). However, there is no evidence that the CTNNB1 mutation activates the target gene of Wnt/β-catenin signaling, and it is unknown whether it affects the tumorigenesis of adaCP. To assess the effect of the CTNNB1 mutation of adaCP, the authors analyzed the correlation between the mutation and clinical, radiological, pathological, and biological findings.


Between 2003 and 2015, 42 patients (24 male and 18 female, median age 42 years) with either papillary craniopharyngioma (papCP) or adaCP underwent tumor resection at the authors’ institution. BRAF V600E and CTNNB1 in papCP and adaCP samples were sequenced by next-generation sequencing and the Sanger method, and mRNA expression levels of Axin2 and BMP4 were evaluated by RT-PCR. Axin2, BMP4, β-catenin, and BRAF expression were evaluated by immunohistochemistry. Other data were collected from clinical reports.


The BRAF V600E mutation was detected in all 10 cases of papCP (100%). CTNNB1 exon 3 mutations were detected in 21 of 31 (68%) cases of adaCP, excluding 1 case for which there were no available sequence data. The mRNA expression level of Axin2 was significantly higher in adaCPs with a CTNNB1 mutation than in those without (p < 0.05). The immunohistochemical findings of Axin2 and BMP4 did not correlate with CTNNB1 mutation positivity. When patients who received adjuvant radiation therapy were excluded, progression-free survival was shorter in the mutation-positive group than in the mutation-negative group (log-rank test, p = 0.031). Examination of clinical characteristics and immunohistochemical findings of adaCPs showed that there was no significant correlation between CTNNB1 mutation positivity and age, sex, tumor volume, gross-total resection, optic tract edema, calcification, or T1 signal intensity of cyst fluid on MRI, β-catenin, and MIB-1 index.


These results raise the possibility that the CTNNB1 mutation in adaCP may be associated with disease recurrence, and genes related to the Wnt/β-catenin signaling pathway might represent a therapeutic target.