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Purpose We report the treatment results of AVAgamma therapy combining gamma knife (GK) and bevacizumab (Bev) for recurrent glioblastoma. Subjects From August 2013 to July 2022, 56 patients with recurrent glioblastoma treated with AVAgamma therapy as salvage therapy at the time of relapse after initial treatment. When the irradiation volume of GK was 15 ml or less, a single irradiation with a marginal dose of 20 to 26 Gy was performed. More than that received a single marginal dose of 12-15 Gy in two fractions or 8 Gy in three fractions. The mean therapeutic marginal dose was 23.9 Gy. Bev was administered 10 mg / kg or 15 mg / kg 1 to 10 times after GK. Methods Median progression-free survival (mPFS) and median survival (mOS) from AVAgamma treatment, and mOS and 5-year survival rate from initial treatment were compared with historical controls (GK group: 30 patients) who received only GK at the time of recurrence. Results The mPFS from AVAgamma therapy was 6 months, PFS-6m was 39%, OS-6m was 76%, and mOS was 10 months. The mOS from initial treatment was 25 months, which was prolonged compared to 21 months in the GK group (p=0.05). The 5-year survival rate for recurrent glioblastoma was 5% in the GK group and 22% in the AVAgamma group (p=0.04). The 5-year survival rate for glioblastoma with KPS is 70% or more at recurrence was 0% in the GK group and 33% in the AVAgamma group (p=0.017). Discussion Combined use of Bev with GK was considered to provide local control of recurrent lesions and prolong life prognosis in patients with good KPS at the time of recurrence. Conclusion AVAgamma therapy is thought to prolong the survival of recurrent glioblastoma and play an important role as salvage treatment.

Purpose: We report the treatment results of AVAgamma therapy combining gamma knife (GK) and bevacizumab for recurrent malignant glioma. Subjects: From August 2013 to January 2021, 71 patients (Grade 2:8 patients, Grade3:16 patients, Grade 4:47 patients) with recurrent malignant glioma treated with AVAgamma therapy as salvage therapy at the time of relapse after initial treatment. The average age is 55.7 years, with 44 men and 27 women. The tumor volume is 150 ml or less, and KPS is 40% or more as the indication of AVAgamma therapy. When the irradiation volume of the gamma knife was 15 ml or less, the marginal dose was 20 to 26 Gy, and when the irradiation volume was 15 ml or more, the marginal dose was 12 to 15 Gy in two divided doses.The mean therapeutic borderline dose was 24 Gy. Bevacizumab was administered 10 mg / kg or 15 mg / kg 1 to 10 times after GK. Methods: Median progression-free survival (mPFS) from AVAgamma treatment, median survival (mOS), and mOS from initial treatment were examined and compared with mOS in the RPA classification of recurrent glioma. Results: In relapsing glioma RPA classification, NABTT CNC class 2 mOS is 17.2 months, class 3 mOS is 3.8 months, class 5 mOS is 5.6 months, class 6 mOS is 6.4 months, but mOS from AVAgamma therapy is 18 months in class 3, 11 months in class 5, 9 months in class 6. The survival time has been extended in class3, class5, class6. Discussion: By AVAgamma therapy, it was thought that recurrent lesions were locally controlled and life prognosis was prolonged. Conclusion: AVAgamma therapy is thought to prolong the survival of recurrent malignant glioma and play an important role as salvage treatment.

Purpose: We report the treatment results of AVAgamma therapy combining gamma knife (GK) and bevacizumab for recurrent glioblastoma. Subjects: From August 2013 to April 2020, 44 patients (88 lesions) with recurrent glioblastoma treated with AVAgamma therapy as salvage therapy at the time of relapse after initial treatment. The average age is 61.5 years, with 26 men and 18 women. The tumor volume is 150 ml or less, and KPS is 40% or more as the indication of AVAgamma therapy. When the irradiation volume of GK is 15 ml or less, a single irradiation with a boundary dose of 20 to 26 Gy was performed, and when the irradiation volume was 15 ml or more, a single irradiation boundary dose was divided into two divided irradiations of 12 to 15 Gy. The mean therapeutic borderline dose was 24 Gy. Bevacizumab was administered 10 mg / kg or 15 mg / kg 1 to 10 times after GK. Methods: Median progression-free survival (mPFS), 6-month progression-free survival (PFS-6m), 6-month survival (OS-6m), median survival (mOS) from treatment with AVAgamma Considered mOS from initial treatment. Results: The mPFS from AVAgamma therapy was 5 months, PFS-6m was 37%, OS-6m was 79%, and mOS was 9 months. The mOS from initial treatment were 25 months. In relapsing glioma RPA classification, NABTT CNC class 5 mOS is 5.6 months, class 6 mOS is 6.4 months, but mOS from AVAgamma therapy is 9 months in class 5, 9 months in class 6. The survival time has been extended. Discussion: By AVAgamma therapy, it was thought that recurrent lesions were locally controlled and life prognosis was prolonged. Conclusion: AVAgamma therapy is thought to prolong the survival of recurrent glioblastoma and play an important role as salvage treatment.

PURPOSE We report the treatment results of AVAgamma therapy combining gamma knife (GK) and bevacizumab for recurrent glioblastoma. SUBJECTS From August 2013 to April 2018, 42 patients (183 lesions) with recurrent glioblastoma treated with AVAgamma therapy as salvage therapy at the time of relapse after initial treatment. The average age is 61.1 years, with 25 men and 17 women. The tumor volume is 100 ml or less, and KPS is 40% or more as the indication of AVAgamma therapy. When the irradiation volume of GK is 15 ml or less, a single irradiation with a boundary dose of 20 Gy was performed, and when the irradiation volume was 15 ml or more, a single irradiation boundary dose was divided into two divided irradiations of 12 to 15 Gy. The mean therapeutic borderline dose was 24 Gy. Bevacizumab was administered 10 mg / kg or 15 mg / kg 1 to 10 times after GK. METHODS Median progression-free survival (mPFS), 6-month progression-free survival (PFS-6m), 6-month survival (OS-6m), median survival (mOS) from treatment with AVAgamma Considered mOS from initial treatment. [Results]: The mPFS from AVAgamma therapy was 5 months, PFS-6m was 37%, OS-6m was 84%, and mOS was 9 months. The mOS from initial treatment were 25 months. In relapsing glioma RPA classification, NABTT CNC class 5 mOS is 5.6 months, class 6 mOS is 6.4 months, but mOS from AVAgamma therapy is 9 months in class 5, 9 months in class 6. The survival time has been extended. DISCUSSION By AVAgamma therapy, it was thought that recurrent lesions were locally controlled and life prognosis was prolonged. CONCLUSION AVAgamma therapy is thought to prolong the survival of recurrent glioblastoma and play an important role as salvage treatment.

BACKGROUND For primary grade II/III glioma, we usually combine radiation therapy and chemotherapy after surgical resection. However, the treatment of recurrent grade II/III glioma is controversial. For lesions that can be safely resected, the second surgery may be optimal, but grade II/III glioma often occurs in or near the eloquent areas, so partial resection is often performed. In such cases, if a second surgery for the recurrent tumor is performed, total resection is often difficult. We have performed gamma knife radiosurgery with concurrent bevacizumab (GKRS with Bev) as salvage therapy for recurrent grade II/III gliomas, which were considered difficult to resect. OBJECTIVE To investigate the outcome of GKRS with Bev for recurrent grade II/III gliomas. We retrospectively reviewed initial pathological findings, PFS/OS from GKRS with Bev, and OS from initial treatment for 23 cases receiving GKRS with Bev for recurrent grade II/III gliomas at our institution between August 2013 and March 2019. RESULTS In the initial pathological findings, grade II were 8 cases (DA: 7, OD: 1), and grade III were 15 cases (AA: 14, AOA: 1). Regarding IDH mutations, in grade II, 3 cases were mutant type, 2 cases were wild type, and 3 cases were unknown. Similarly, in grade III, 5, 6, and 4 cases, respectively. From salvage therapy, PFS was median 6 months in grade II and 8 months in grade III, and OS was median 11 months in grade II and 16 months in grade III. From the initial treatment, OS was median 95 months in grade II, and 38 months in grade III. CONCLUSION Because most of our cases were astrocytic tumors, when they relapsed, it seemed that some of them progressed to glioblastoma. Even in these severe cases, GKRS with Bev can play an important role as salvage therapy.

The number of patients receiving chronic dialysis treatment in Japan currently exceeds 300,000 people. Few reports have described carotid endarterectomy(CEA)for chronic renal failure patients because of the unacceptable rate of perioperative stroke and other morbidities. A strategy for and treatment results of CEA for chronic renal failure patients in our hospital are described herein.The present study included 6 patients who underwent CEA while receiving dialysis treatment between April 2011 and November 2014.Dialysis treatment was initiated due to diabetes in 4 patients and renal sclerosis in 2 patients. All the patients were men, with a mean age of 74.0 years. Two patients were symptomatic, and four were asymptomatic. In all the patients, heart vascular lesions and arteriosclerosis risk factors were present. Postoperatively, pneumonia transient cranial neuropathy, heart failure, and pneumonia in 1 case required extensive treatment. However, by the time of discharge from hospital, no cases had deteriorated compared with their pre-CEA state. The modified Rankin scale score on discharge was 0-2 for all the patients.CEA can be performed safely in patients receiving dialysis, but further operative procedures and careful postoperative management are likely to be needed for patients with CEA who are receiving dialysis.

[123I]iomazenil (IMZ) is a specific radioligand for the central benzodiazepine (BZ) receptor that may be useful as a marker of cortical neuron loss after cerebral ischemia using single photon emission computed tomography (SPECT). This study used statistical imaging analysis for IMZ-SPECT to investigate the relationship between higher brain dysfunction and cortical neuron loss in the medial frontal lobes, to establish a confirmatory diagnosis of higher brain dysfunction in patients with adult moyamoya disease. IMZ-SPECT was estimated by three-dimensional stereotactic surface projections (3D-SSP). Cortical neuron loss was analyzed using the stereotactic extraction estimation (SEE) method (level 3: gyrus level) for 3D-SSP Z-score maps (Z-score >2). Extent of pixels with significant reduction of BZ receptor density within the target gyri (i.e. bilateral medial frontal gyri [MFGs] and anterior cingulate gyri [ACGs]) was calculated. In 6 patients with higher brain dysfunction, significant cortical neuron loss was observed in the bilateral MFGs in 4 patients, unilateral MFG in 1 patient, and bilateral ACGs in 2 patients. In 12 patients without higher brain dysfunction, no significant cortical neuron loss was observed in the bilateral MFGs or ACGs, and mild loss was observed in the bilateral MFGs in 2 patients, unilateral MFG in 4 patients, and unilateral ACG in 2 patients. Long-standing mild hemodynamic ischemia in the anterior circulation of patients with adult moyamoya disease could lead to incomplete brain infarction within the medial frontal lobes. Statistical imaging analysis using 3D-SSP and SEE methods for IMZ-SPECT could demonstrate significant cortical neuron loss in the bilateral frontal medial cortices involving MFG and/or ACG which correlate with higher brain dysfunction in patients with adult moyamoya disease.

We examined the operative findings of cerebral aneurysms that grew during follow-ups over the past 5 years. We defined aneurysmal growth as form change such as the bleb formation or more than 2-mm growth compared with past findings. In operation, we confirmed a very thin wall of cerebral aneurysm correspond to aneursymal growth during follow-up. Rupture rates appear to be high in aneurysms caused by a change such as the above. Clipping can prevent aneurysmal rupture in these cases.

In contrast to pilocytic astrocytomas(PAs), pilomyxoid astrocytomas(PMAs)demonstrate monophasic piloid cells with angiocentric distribution and a more aggressive clinical course. Recently, several reports have described combined histological features of both subtypes;accordingly, these were termed intermediate pilomyxoid tumors(IPTs). The KIAA1549-BRAF fusion gene has been found in approximately 70% of PAs, but is reportedly rare in PMAs. We describe a clinicopathological study of two patients with pilomyxoid-spectrum astrocytoma(PMSA). Case 1 was of a 29-year-old man who presented with a generalized seizure. Gadolinium-magnetic resonance imaging(Gd-MRI)demonstrated a less enhanced tumor in the left temporal lobe. Case 2 was of a 9-year-old boy who presented with headache. Gd-MRI revealed an irregularly enhanced tumor in the left cerebellum. In Case 1, the tumor showed monomorphous bipolar cells in a myxoid background and angiocentric arrangement;therefore, the diagnosis was PMA. In Case 2, part of the tumor had a myxoid, angiocentric pattern characteristic of PMA;the other part had a biphasic pattern characteristic of PA. PMA and PA were mixed in a 7:3 ratio;therefore, IPT was diagnosed. No BRAF V600E mutations were found by immunohistochemistry and sequencing in either case. Three major KIAA1549-BRAF fusion subtypes were analyzed by quantitative reverse transcription polymerase chain reaction(RT-PCR)and sequencing. No fusions were found in Case 1. However, K16-B9 fusion was identified in Case 2, and this fusion was more prevalent in the PA component than in the PMA component. In summary, no BRAF V600E mutations were found in PMSAs, but KIAA1549-BRAF fusion was identified in IPT, particularly in the PA component.

Pilocytic astrocytoma is the most common glioma in children, in whom the majority arise in the cerebellum. In contrast, pilocytic astrocytomas are less common in adults. The most frequent locations involved are the basal ganglia, cerebellum, optic chiasm, and hypothalamus. Overall survival rates are good. The case presented involved a pilocytic astrocytoma of the right parietal lobe in a 36-year-old man. Cranial magnetic resonance imaging (MRI) revealed a small mural nodule in the wall of the cyst, with no edema around the tumor. This nodule showed a hyperintense signal on gadolinium-enhanced MRI. Computed tomography (CT) scanning revealed a hypodense right parietal lobe mass with calcification. At surgery, the cyst contents were aspirated, and the mural nodule was excised. Postoperative radiotherapy was not given. Neuropathological examination revealed a pilocytic astrocytoma (Grade I). The MIB-index was 3.3%. There has been no recurrence after 1 year of postoperative follow-up.

We report a case of carotid endarterectomy preceding distal plaque-end dissection followed by internal shunt insertion. A 60-year-old man was admitted to hospital with right hemiparesis. Magnetic resonance imaging detected multiple fresh infarcts in the left hemisphere, and the patient was transferred to our hospital. Angiography revealed high-grade stenosis in the left internal carotid artery at the level of the second cervical vertebra. Computed tomography angiography showed calcification in the proximal and the distal side of the stenotic lesion in the left carotid artery. The lesion was thought to be high position though an accurate assessment of the distal tip was difficult. The patient also received a blood transfusion for advanced anemia due to gross hematuria associated with bladder cancer. Carotid endarterectomy was performed one month after onset. Because atheromatous plaque had progressed far from the incision, we considered that arterial shunt insertion would induce embolic complications. Thus, we proceeded with distal plaque-end dissection, and then inserted the internal shunt and removed the plaque. This procedure resulted in successful revascularization.