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Tomohito Hishikawa, Koji Tokunaga, Kenji Sugiu, and Isao Date

Object

There is no description of the change in the posterior cerebral artery (PCA) in the diagnostic criteria of moyamoya disease (MMD). However, PCAs are often involved in the clinical setting, and an understanding of the significance of PCA lesions is therefore of great importance when evaluating the disease progression and predicting prognosis. The aim of this study was to assess the difference in posterior circulation involvement in pediatric and adult patients with MMD.

Methods

The records of 120 consecutive patients with MMD were reviewed. The clinical manifestations at diagnosis were evaluated on the basis of symptoms and CT and MRI findings. The degree of steno-occlusive internal carotid artery (ICA) lesions and the existence of steno-occlusive PCA lesions were evaluated by observing a total of 240 ICAs and PCAs on angiography. Angiographic correlation between anterior and posterior circulation was assessed in pediatric and adult patients with MMD.

Results

Seventeen (26%) of 66 pediatric patients and 18 (33%) of 54 adult patients exhibited steno-occlusive PCA lesions. There was no significant difference in the prevalence of PCA lesions between pediatric and adult patients with MMD (p = 0.36). The prevalence of infarction in pediatric and adult patients with PCA involvement was significantly higher than that in pediatric and adult patients without PCA involvement (p = 0.0003 and p = 0.003, respectively). There was no significant difference in the distribution of infarction areas between pediatric and adult patients with PCA involvement (p = 0.62). On the basis of the staging system used, steno-occlusive lesions in ICAs ipsilateral to PCAs with lesions were in significantly advanced stages compared with lesions in ICAs ipsilateral to PCAs without lesions in both pediatric and adult cases (p < 0.0001 and p = 0.0008, respectively). Pediatric patients had less advanced steno-occlusive lesions in ICAs ipsilateral to PCAs with lesions compared with adults (p < 0.05).

Conclusions

The clinical significance of posterior circulation involvement in MMD was similar between pediatric and adult patients. The only significant difference was that less advanced ICA lesions could complicate posterior circulation involvement in pediatric patients.

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Shunji Mugikura and Shoki Takahashi

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Tomohito Hishikawa, Koji Iihara, Naoaki Yamada, Hatsue Ishibashi-Ueda, and Susumu Miyamoto

Object

The aim of this study was to assess the histopathological differences between advanced atherosclerotic carotid artery (CA) plaques with signal hyperintensity on T1-weighted MR images and those without, focusing on necrotic core size and intraplaque hemorrhage (IPH).

Methods

Thirty-five patients scheduled for carotid endarterectomy underwent preoperative CA MR imaging using 3D inversion-recovery-based T1-weighted imaging (magnetization-prepared rapid acquisition gradient-echo [MPRAGE]). The signal intensity of the CA plaque on MPRAGE sequences was classified as “high” when the intensity was more than 200% that of adjacent muscle. A total of 96 axial MR images obtained in 35 patients were compared with corresponding histological sections from 36 excised specimens. The area of the necrotic core in histological sections was compared between specimens with and without high signal intensity on MPRAGE sequences. The IPH was histopathologically graded according to the size of the area positive for glycophorin A as revealed by immunohistochemical staining. The difference between plaques with and without high signal intensity was investigated with respect to the degree of IPH. The relationship of the severity of IPH to size of the necrotic core was also evaluated.

Results

The area of the necrotic core in plaques with high signal intensity on MPRAGE sequences was significantly larger than that in plaques without high signal intensity (median 51.2% [interquartile range 43.3–66.8%] vs 49.0% [33.2–57.6%], p = 0.029). Carotid artery plaques with high signal intensity had significantly more severe IPH than plaques with lower signal intensity (p < 0.0001). The severity of IPH was significantly associated with the size of the necrotic core (p < 0.0001).

Conclusions

Atherosclerotic CA plaques with high signal intensity on MPRAGE sequences had large necrotic cores with IPH in patients with high-grade stenosis; MPRAGE is useful for the evaluation of CA plaque progression.

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Koji Iihara, Masakazu Okawa, Tomohito Hishikawa, Naoaki Yamada, Kazuhito Fukushima, Hidehiro Iida, and Susumu Miyamoto

The authors report a rare case of slowly progressive neuronal death associated with postischemic hyperperfusion in cortical laminar necrosis after radial artery/external carotid artery–middle cerebral artery bypass graft surgery for an intracavernous carotid artery aneurysm. Under barbiturate protection, a 69-year-old man underwent high-flow bypass surgery combined with carotid artery sacrifice for a symptomatic intracavernous aneurysm. The patient became restless postoperatively, and this restlessness peaked on postoperative Day (POD) 7. Diffusion-weighted and FLAIR MR images obtained on PODs 1 and 7 revealed subtle cortical hyperintensity in the temporal cortex subjected to temporary occlusion. On POD 13, 123I-iomazenil (123I-IMZ) SPECT clearly showed increased distribution on the early image and mildly decreased binding on the delayed image with count ratios of the affected–unaffected corresponding regions of interest of 1.23 and 0.84, respectively, suggesting postischemic hyperperfusion. This was consistent with the finding on 123I-iodoamphetamine SPECT. Of note, neuronal density in the affected cortex on the delayed 123I-IMZ image further decreased to the affected/unaffected ratio of 0.44 on POD 55 during the subacute stage when characteristic cortical hyperintensity on T1-weighted MR imaging, typical of cortical laminar necrosis, was emerging. The affected cortex showed marked atrophy 8 months after the operation despite complete neurological recovery. This report illustrates, for the first time, dynamic neuroradiological correlations between slowly progressive neuronal death shown by 123I-IMZ SPECT and cortical laminar necrosis on MR imaging in human stroke.

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Masafumi Hiramatsu, Kenji Sugiu, Tomohito Hishikawa, Shingo Nishihiro, Naoya Kidani, Yu Takahashi, Satoshi Murai, Isao Date, Naoya Kuwayama, Tetsu Satow, Koji Iihara, and Nobuyuki Sakai

OBJECTIVE

Embolization is the most common treatment for dural arteriovenous fistulas (dAVFs). A retrospective, multicenter observational study was conducted in Japan to clarify the nature, frequency, and risk factors for complications of dAVF embolization.

METHODS

Patient data were derived from the Japanese Registry of Neuroendovascular Therapy 3 (JR-NET3). A total of 40,169 procedures were registered in JR-NET3, including 2121 procedures (5.28%) in which dAVFs were treated with embolization. After data extraction, the authors analyzed complication details and risk factors in 1940 procedures performed in 1458 patients with cranial dAVFs treated with successful or attempted embolization.

RESULTS

Transarterial embolization (TAE) alone was performed in 858 cases (44%), and transvenous embolization (TVE) alone was performed in 910 cases (47%). Both TAE and TVE were performed in one session in 172 cases (9%). Complications occurred in 149 cases (7.7%). Thirty-day morbidity and mortality occurred in 55 cases (2.8%) and 16 cases (0.8%), respectively. Non–sinus-type locations, radical embolization as the strategy, procedure done at a hospital that performed dAVF embolization in fewer than 10 cases during the study period, and emergency procedures were independent risk factors for overall complications.

CONCLUSIONS

Complication rates of dAVF embolization in Japan were acceptable. For better results, the risk factors identified in this study should be considered in treatment decisions.

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Mikito Hayakawa, Kenji Sugiu, Shinichi Yoshimura, Tomohito Hishikawa, Hiroshi Yamagami, Mayumi Fukuda-Doi, Nobuyuki Sakai, Koji Iihara, Kuniaki Ogasawara, Hidenori Oishi, Yasushi Ito, and Yuji Matsumaru

OBJECTIVE

Cerebral hyperperfusion syndrome (CHS) is a serious complication after carotid artery stenting (CAS). Staged angioplasty (SAP)—i.e., angioplasty followed by delayed CAS—has been reported as a potential CHS-avoiding procedure. The purpose of this study was to clarify the effectiveness of SAP in avoiding CHS after carotid revascularization for patients at high risk for this complication.

METHODS

The authors retrospectively studied cases involving patients at high risk for CHS from 44 Japanese centers who were scheduled for SAP, regular CAS, angioplasty, or staged procedures other than SAP between October 2007 and March 2014. They investigated the rate of CHS in the population scheduled for SAP or regular CAS, and for safety analysis, the composite rate of transient ischemic attack (TIA) and ischemic stroke in the population eventually receiving SAP or regular CAS.

RESULTS

Data from a total of 525 patients (532 lesions, mean age 72.5 ± 7.5 years, 74 women ) were analyzed. Scheduled procedures included SAP for 113 lesions and regular CAS for 419 lesions. The rate of CHS was lower in the SAP group than in the regular CAS group (4.4% vs 10.5%, p = 0.047). Multivariate analysis showed that SAP was negatively related to CHS (OR 0.315; 95% CI 0.120–0.828). In the population eventually receiving SAP (102 lesions) or regular CAS (428 lesions), the composite rate of TIA and ischemic stroke was comparable between the SAP group and the regular CAS group (9.8% vs 9.3%).

CONCLUSIONS

SAP may be an effective and safe carotid revascularization procedure to avoid CHS.

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Yohei Mineharu, Yasushi Takagi, Akio Koizumi, Takaaki Morimoto, Takeshi Funaki, Tomohito Hishikawa, Yoshio Araki, Hitoshi Hasegawa, Jun C. Takahashi, Satoshi Kuroda, Kiyohiro Houkin, and Susumu Miyamoto

OBJECTIVE

Although many studies have analyzed risk factors for contralateral progression in unilateral moyamoya disease, they have not been fully elucidated. The aim of this study was to examine whether genetic factors as well as nongenetic factors are involved in the contralateral progression.

METHODS

The authors performed a multicenter cohort study in which 93 cases with unilateral moyamoya disease were retrospectively reviewed. The demographic features, RNF213 R4810K mutation, lifestyle factors such as smoking and drinking, past medical history, and angiographic findings were analyzed. A Cox proportional hazards model was used to find risk factors for contralateral progression.

RESULTS

Contralateral progression was observed in 24.7% of cases during a mean follow-up period of 72.2 months. Clinical characteristics were not significantly different between 67 patients with the R4810K mutation and those without it. Cox regression analysis showed that the R4810K mutation (hazard ratio [HR] 4.64, p = 0.044), childhood onset (HR 7.21, p < 0.001), male sex (HR 2.85, p = 0.023), and daily alcohol drinking (HR 4.25, p = 0.034) were independent risk factors for contralateral progression.

CONCLUSIONS

These results indicate that both genetic and nongenetic factors are associated with contralateral progression of unilateral moyamoya disease. The findings would serve to help us better understand the pathophysiology of moyamoya disease and to manage patients more appropriately.

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Masafumi Hiramatsu, Tomohito Hishikawa, Koji Tokunaga, Hiroyasu Kidoya, Shingo Nishihiro, Jun Haruma, Tomohisa Shimizu, Yuji Takasugi, Yukei Shinji, Kenji Sugiu, Nobuyuki Takakura, and Isao Date

OBJECTIVE

The aim of this study was to evaluate whether combined gene therapy with vascular endothelial growth factor (VEGF) plus apelin during indirect vasoreconstructive surgery enhances brain angiogenesis in a chronic cerebral hypoperfusion model in rats.

METHODS

A chronic cerebral hypoperfusion model induced by the permanent ligation of bilateral common carotid arteries (CCAs; a procedure herein referred to as “CCA occlusion” [CCAO]) in rats was employed in this study. Seven days after the CCAO procedure, the authors performed encephalo-myo-synangiosis (EMS) and injected plasmid(s) into each rat's temporal muscle. Rats were divided into 4 groups based on which plasmid was received (i.e., LacZ group, VEGF group, apelin group, and VEGF+apelin group). Protein levels in the cortex and attached muscle were assessed with enzyme-linked immunosorbent assay (ELISA) on Day 7 after EMS, while immunofluorescent analysis of cortical vessels was performed on Day 14 after EMS.

RESULTS

The total number of blood vessels in the cortex on Day 14 after EMS was significantly larger in the VEGF group and the VEGF+apelin group than in the LacZ group (p < 0.05, respectively). Larger vessels appeared in the VEGF+apelin group than in the other groups (p < 0.05, respectively). Apelin protein on Day 7 after EMS was not detected in the cortex for any of the groups. In the attached muscle, apelin protein was detected only in the apelin group and the VEGF+apelin group. Immunofluorescent analysis revealed that apelin and its receptor, APJ, were expressed on endothelial cells (ECs) 7 days after the CCAO.

CONCLUSIONS

Combined gene therapy (VEGF plus apelin) during EMS in a chronic cerebral hypoperfusion model can enhance angiogenesis in rats. This treatment has the potential to be a feasible option in a clinical setting for patients with moyamoya disease.

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Tomohisa Shimizu, Tomohito Hishikawa, Shingo Nishihiro, Yukei Shinji, Yuji Takasugi, Jun Haruma, Masafumi Hiramatsu, Hirokazu Kawase, Sachiko Sato, Ryoichi Mizoue, Yoshimasa Takeda, Kenji Sugiu, Hiroshi Morimatsu, and Isao Date

OBJECTIVE

Although cortical spreading depolarization (CSD) has been observed during the early phase of subarachnoid hemorrhage (SAH) in clinical settings, the pathogenicity of CSD is unclear. The aim of this study is to elucidate the effects of loss of membrane potential on neuronal damage during the acute phase of SAH.

METHODS

Twenty-four rats were subjected to SAH by the perforation method. The propagation of depolarization in the brain cortex was examined by using electrodes to monitor 2 direct-current (DC) potentials and obtaining NADH (reduced nicotinamide adenine dinucleotide) fluorescence images while exposing the parietal-temporal cortex to ultraviolet light. Cerebral blood flow (CBF) was monitored in the vicinity of the lateral electrode. Twenty-four hours after onset of SAH, histological damage was evaluated at the DC potential recording sites.

RESULTS

Changes in DC potentials (n = 48 in total) were sorted into 3 types according to the appearance of ischemic depolarization in the entire hemisphere following induction of SAH. In Type 1 changes (n = 21), ischemic depolarization was not observed during a 1-hour observation period. In Type 2 changes (n = 13), the DC potential demonstrated ischemic depolarization on initiation of SAH and recovered 80% from the maximal DC deflection during a 1-hour observation period (33.3 ± 15.8 minutes). In Type 3 changes (n = 14), the DC potential displayed ischemic depolarization and did not recover during a 1-hour observation period. Histological evaluations at DC potential recording sites showed intact tissue at all sites in the Type 1 group, whereas in the Type 2 and Type 3 groups neuronal damage of varying severity was observed depending on the duration of ischemic depolarization. The duration of depolarization that causes injury to 50% of neurons (P50) was estimated to be 22.4 minutes (95% confidence intervals 17.0–30.3 minutes). CSD was observed in 3 rats at 6 sites in the Type 1 group 5.1 ± 2.2 minutes after initiation of SAH. On NADH fluorescence images CSD was initially observed in the anterior cortex; it propagated through the entire hemisphere in the direction of the occipital cortex at a rate of 3 mm/minute, with repolarization in 2.3 ± 1.2 minutes. DC potential recording sites that had undergone CSD were found to have intact tissue 24 hours later. Compared with depolarization that caused 50% neuronal damage, the duration of CSD was too short to cause histological damage.

CONCLUSIONS

CSD was successfully visualized using NADH fluorescence. It propagated from the anterior to the posterior cortex along with an increase in CBF. The duration of depolarization in CSD (2.3 ± 1.2 minutes) was far shorter than that causing 50% neuronal damage (22.4 minutes) and was not associated with histological damage in the current experimental setting.

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Masafumi Hiramatsu, Ryota Ishibashi, Etsuji Suzuki, Yuko Miyazaki, Satoshi Murai, Hiroki Takai, Yuji Takasugi, Yoko Yamaoka, Kazuhiko Nishi, Yu Takahashi, Jun Haruma, Tomohito Hishikawa, Takao Yasuhara, Masaki Chin, Shunji Matsubara, Masaaki Uno, Koji Tokunaga, Kenji Sugiu, and Isao Date

OBJECTIVE

There have been no accurate surveillance data regarding the incidence rate of spinal arteriovenous shunts (SAVSs). Here, the authors investigate the epidemiology and clinical characteristics of SAVSs.

METHODS

The authors conducted multicenter hospital-based surveillance as an inventory survey at 8 core hospitals in Okayama Prefecture between April 1, 2009, and March 31, 2019. Consecutive patients who lived in Okayama and were diagnosed with SAVSs on angiographic studies were enrolled. The clinical characteristics and the incidence rates of each form of SAVS and the differences between SAVSs at different spinal levels were analyzed.

RESULTS

The authors identified a total of 45 patients with SAVSs, including 2 cases of spinal arteriovenous malformation, 5 cases of perimedullary arteriovenous fistula (AVF), 31 cases of spinal dural AVF (SDAVF), and 7 cases of spinal epidural AVF (SEAVF). The crude incidence rate was 0.234 per 100,000 person-years for all SAVSs including those at the craniocervical junction (CCJ) level. The incidence rate of SDAVF and SEAVF combined increased with advancing age in men only. In a comparative analysis between upper and lower spinal SDAVF/SEAVF, hemorrhage occurred in 7/14 cases (50%) at the CCJ/cervical level and in 0/24 cases (0%) at the thoracolumbar level (p = 0.0003). Venous congestion appeared in 1/14 cases (7%) at the CCJ/cervical level and in 23/24 cases (96%) at the thoracolumbar level (p < 0.0001).

CONCLUSIONS

The authors reported detailed incidence rates of SAVSs in Japan. There were some differences in clinical characteristics of SAVSs in the upper spinal levels and those in the lower spinal levels.