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The aim of this study was to evaluate the course of occluded distal vessels before mechanical thrombectomy (MT) for acute large vessel occlusion (LVO) with non-contrast magnetic resonance imaging (MRI). The variable flip-angle three-dimensional turbo spin-echo (VRFA-3D-TSE) method was used to evaluate the course of occluded distal vessels quickly and clearly in acute LVO cases before MT.Patients with acute LVO who were indicated for MT between April 2021 and March 2022 were examined by the VRFA-3D-TSE method to evaluate the distal course of occluded vessels. We included internal carotid artery (ICA) occlusion, M1 occlusion of the middle cerebral artery, and basilar artery (BA) occlusion. Preoperative images were compared to the angiographic findings after recanalization or with follow-up magnetic resonance angiography, and the results were assessed by 2 endovascular treatment specialists as excellent, good, or poor imaging.MT was performed in a total of 27 patients. There were 17 patients with intracranial occlusion of the ICA, M1, and BA. Occlusion was found in the intracranial ICA in 6 patients, the M1 in 7, and the BA in 4. VRFA-3D-TSE MRI was performed in all patients, and the imaging was rated (by the 2assessors) as excellent in 12 of 17 and 14 of 17 cases, good in 5 of 17 and 3 of 17 cases, and poor in 0 of 17 cases.In patients with acute LVO, VRFA-3D-TSE MRI enabled rapid and good depiction of the course of occluded distal vessels before MT without the use of contrast medium.

Summary Ferroptosis, a type of oxidative stress cell death, has been implicated in cell injury in several diseases, and treatments with specific inhibitors have been shown to protect cells and tissues. Here we demonstrated that a treatment with the nitroxide radical, 2,2,6,6-tetramethylpiperidine-N-oxyl (TEMPO), prevented the ferroptotic cell death in an airborne manner. Other TEMPO derivatives and lipophilic antioxidants, such as Trolox and ferrostatin-1, also prevented cell death induced by erastin and RSL3; however, only TEMPO exhibited inhibitory activity from a physically distant location. TEMPO vaporized without decomposing and then dissolved again into a nearby water solution. Volatilized TEMPO inhibited glutamate-induced cell death in mouse hippocampal cell lines and also reduced neuronal cell death in a mouse ischemia model. These results suggest that TEMPO is a unique cell protective agent that acts in a volatility-mediated manner.

Objective It is challenging to safely treat blood blister–like aneurysms (BBAs) of the internal carotid artery. Endovascular surgery has been reported, but the optimal strategy is yet to be established. We report our endovascular treatment strategy using the Low-profile Visualized Intraluminal Support (LVIS) stent. Methods Twelve patients with ruptured BBAs including 1 patient with 2 separate aneurysmal bulges were treated from December 2017 to January 2020. Single LVIS stent-assisted coil embolization was performed as the initial treatment. If the coil could not be placed in the aneurysm, or follow-up angiography showed persistent filling or regrowth of the aneurysm, a second LVIS stent was deployed as an overlapping stent. Clinical characteristics, treatment details, and clinical outcomes were retrospectively examined. Results Single stent-assisted coiling was performed in 8 patients (69%), 2 overlapping stents with coiling in 1 (8%), a single stent in 2 (15%), and 2 overlapping stents in 2 (15%). Three patients with persistent filling or regrowth of the aneurysm were re-treated with overlapping stents. Follow-up angiography confirmed complete occlusion in 12 aneurysms (92%). No re-rupture occurred. Postoperative symptomatic ischemia was confirmed in 4 patients (33%), and all 4 patients suffered severe subarachnoid hemorrhage. Modified Rankin scale was 0–2 in 8 patients (67%). Conclusions LVIS stent-assisted coil embolization is effective in preventing re-rupture of BBAs. However, the morphology of the aneurysm may change within a short period, so careful angiographic follow-up is needed. Appropriate preoperative antiplatelet administration and optimal timing of the treatment may reduce the risk of postoperative ischemic complication.

Background: When severe aortic stenosis (AS) is concomitant with carotid stenosis, carotid artery stenting (CAS) will become a high-risk procedure because baroreceptor reflex-induced bradycardia and hypotension may cause irreversible circulatory collapse. When carotid stenosis-related misery perfusion is present, the risk of cerebral hyperperfusion syndrome increases after carotid revascularization. We report a case of severe carotid disease concomitant with severe AS successfully treated by a combination of staged angioplasty (SAP) and transcatheter aortic valve implantation (TAVI). Case Description: An 86-year-old man presented with transient deterioration of mental status and sluggish responsiveness continuous from the previous day. Magnetic resonance imaging of the brain revealed a right putaminal infarction, occlusion of the right internal carotid artery (ICA), and severe stenosis of the left ICA. Severe AS was diagnosed and single-photon emission computed tomography showed misery perfusion at the bilateral ICA territories. We performed a staged treatment consisting of SAP for the left carotid stenosis and TAVI. A first-stage carotid angioplasty was performed, followed by TAVI 2 weeks later and second-stage CAS 1 week after that. There were no apparent periprocedural complications throughout the clinical course. Conclusion: Combining SAP and TAVI may be an effective treatment option for severe carotid stenosis with misery perfusion concomitant with severe AS.

A 40-year-old man was admitted to our hospital because of disorientation and mild left-sided weakness. Radiological examination revealed a solid and cystic tumor in the right temporal lobe, and total resection was performed. Histologically, the tumor was composed mainly of low-grade gangiloglioma and had some high-grade glial components with focal necrosis and microvascular proliferations. In the high-grade component, there were epithelioid cells with round cytoplasm and eccentric nuclei. The high-grade area with epithelioid cells was intermingled within the low-grade area, which suggests that epithelioid cells were an anaplastic transformation of ganglioglioma. The epithelioid cells were histologically similar to neoplastic cells of epithelioid glioblastoma (E-GBM), a rare aggressive variant of isocitric dehydrogenase wild-type glioblastoma. A BRAF V600E mutation, frequently observed in E-GBM, was detected in both the ganglioglioma and epithelioid cell components. The epithelioid cells were mitotically active, which suggests that if the surgery was delayed, the histological appearance might have eventually evolved into E-GBM. Indeed, a case of pleomorphic xanthoastrocytoma which transformed into E-GBM after a long latency was reported elsewhere. This is the first report to describe focal epithelioid cells in anaplastic ganglioglioma.

In cancer cells the small compounds erastin and RSL3 promote a novel type of cell death called ferroptosis, which requires iron‐dependent accumulation of lipid reactive oxygen species. Here we assessed the contribution of lipid peroxidation activity of lipoxygenases (LOX) to ferroptosis in oncogenic Ras‐expressing cancer cells. Several 12/15‐LOX inhibitors prevented cell death induced by erastin and RSL3. Furthermore, siRNA‐mediated silencing of ALOX15 significantly decreased both erastin‐induced and RSL3‐induced ferroptotic cell death, whereas exogenous overexpression of ALOX15 enhanced the effect of these compounds. Immunofluorescence analyses revealed that the ALOX15 protein consistently localizes to cell membrane during the course of ferroptosis. Importantly, treatments of cells with ALOX15‐activating compounds accelerated cell death at low, but not high doses of erastin and RSL3. These observations suggest that tumor ferroptosis is promoted by LOX‐catalyzed lipid hydroperoxide generation in cellular membranes.

We experienced a case of sphenoid sinus type meningoencephalocele manifesting as severe cerebrospinal fluid (CSF) rhinorrhea. A 35-year-old man became aware of serous nasal discharge 1 year previously, which had gradually worsened. The nasal discharge was diagnosed as CSF rhinorrhea. Head computed tomography (CT) showed several small depressions in the bone of the left middle cranial fossa, and the largest depression extended through the bone to the lateral sphenoid sinus. Head magnetic resonance imaging revealed that the meningoencephalocele projected to the lateral sphenoid sinus, through this small bone defect of the middle cranial fossa. We performed a combined craniotomy and epidural approach without intradural procedures using neuronavigation. Multiple meningoencephaloceles protruded into small depressions in the middle skull base. The small protrusions not passing through the sphenoid sinus were coagulated. The largest protrusion causing the CSF leakage was identified by neuronavigation. This meningoencephalocele was cut. Both the dural and bone sides were closed with double layers to prevent CSF leakage. The CSF rhinorrhea completely stopped after the surgery. In our case, identification of the leak site was easy with neuronavigation based on bone window CT. The epidural approach also has significant advantages with double layer closure, including both the dural and bone sides. If the site of CSF leakage is outside the foramen rotundum (as with the most common type of lateral sphenoid sinus meningoencephalocele), we recommend the epidural approach using neuronavigation for surgical treatment.

Pharmacological challenges to oncogenic Ras-expressing cancer cells have shown a novel type of cell death, ferroptosis, which requires intracellular iron. In the present study, we assessed ferroptosis following treatment of human fibrosarcoma HT1080 cells with several inhibitors of lysosomal activity and found that they prevented cell death induced by the ferroptosis-inducing compounds erastin and RSL3. Fluorescent analyses with a reactive oxygen species (ROS) sensor revealed constitutive generation of ROS in lysosomes, and treatment with lysosome inhibitors decreased both lysosomal ROS and a ferroptotic cell-death-associated ROS burst. These inhibitors partially prevented intracellular iron provision by attenuating intracellular transport of transferrin or autophagic degradation of ferritin. Furthermore, analyses with a fluorescent sensor that detects oxidative changes in cell membranes revealed that formation of lipid ROS in perinuclear compartments probably represented an early event in ferroptosis. These results suggest that lysosomal activity is involved in lipid ROS-mediated ferroptotic cell death through regulation of cellular iron equilibria and ROS generation.

Background: Patients with intracerebral hemorrhage taking anticoagulants are increasingly common in Japan due to the aging population. The clinical benefit of restarting anticoagulants is established, but the optimal timing of resumption is controversial. Risk factors for hemorrhagic and cardioembolic events in the acute phase are also unknown. This study investigated hemorrhagic and cardioembolic events and risk factors in intracerebral hemorrhage patients taking anticoagulants. Methods: The clinical data of 65 consecutive intracerebral hemorrhage patients taking anticoagulants were retrospectively reviewed. Hemorrhagic and cardioembolic complications and risk factors were analyzed. Results: Lobar hemorrhage was the most frequent (21 of 65 cases, 32.3%). At discharge, 31 patients (47.7%) showed severe disability or had died. Eight (18.6%) of 43 patients who restarted anticoagulants after initial treatment developed hemorrhagic events, including recurrent intracerebral hemorrhage in 3. HAS-BLED score was 2-3 in these 3 patients. Six (15.8%) of 38 patients who took anticoagulants for cardiogenic factors suffered cardioembolism. Systemic inflammatory response syndrome was significantly more common in the cardioembolic group (66.7%) compared with the noncardioembolic group (21.9%, P

Superficial temporal artery-to-middle cerebral artery (STA-MCA) anastomosis is a common procedure for neurosurgeons. The surgery necessarily requires accurate and speedy manipulation of microscope, for which a specific training is needed. Unexpected bypass occlusion sometimes happen during surgery. Generally, conventional interrupted or continuous suture has been used for vascular anastomosis, despite various ideas have been attempted in the other surgery fields. We propose a horizontal mattress suture technique for intracranial microvascular bypass surgery. This is the first report ever published on intracranial vascular anastomosis. We had four patients of STA-MCA bypass surgery with “mattress anastomosis” from March to May of 2012. During the procedure, there was no bypass occlusion and good patency was confirmed in all cases. Intimae of the recipient and the donor blood vessel contact each other precisely with this technique. Although a long-term assessment of patency is needed, it is useful for the intracranial bypass surgery.