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Hitoshi Fukuda, Benjamin Lo, Yu Yamamoto, Akira Handa, Yoshiharu Yamamoto, Yoshitaka Kurosaki, and Sen Yamagata

OBJECTIVE

Plasma D-dimer levels elevate during acute stages of aneurysmal subarachnoid hemorrhage (SAH) and are associated with poor functional outcomes. However, the mechanism in which D-dimer elevation on admission affects functional outcomes remains unknown. The aim of this study is to clarify whether D-dimer levels on admission are correlated with systemic complications after aneurysmal SAH, and to investigate their additive predictive value on conventional risk factors for poor functional outcomes.

METHODS

A total of 187 patients with aneurysmal SAH were retrospectively analyzed from a single-center, observational cohort database. Correlations of plasma D-dimer levels on admission with patient characteristics, initial presentation, neurological complications, and systemic complications were identified. The authors also evaluated the additive value of D-dimer elevation on admission for poor functional outcomes by comparing predictive models with and without D-dimer.

RESULTS

D-dimer elevation on admission was associated with increasing age, female sex, and severity of SAH. Patients with higher D-dimer levels had increased likelihood of nosocomial infections (OR 1.22 [95% CI 1.07–1.39], p = 0.004), serum sodium disorders (OR 1.11 [95% CI 1.01–1.23], p = 0.033), and cardiopulmonary complications (OR 1.20 [95% CI 1.04–1.37], p = 0.01) on multivariable analysis. D-dimer elevation was an independent risk factor of poor functional outcome (modified Rankin Scale Score 3–6, OR 1.50 [95% CI 1.15–1.95], p = 0.003). A novel prediction model with D-dimer had significantly better discrimination ability for poor outcomes than conventional models without D-dimer.

CONCLUSIONS

Elevated D-dimer levels on admission were independently correlated with systemic complication, and had an additive value for outcome prediction on conventional risk factors after aneurysmal SAH.

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Kazumichi Yoshida, Tao Yang, Yu Yamamoto, Yoshitaka Kurosaki, Takeshi Funaki, Takayuki Kikuchi, Akira Ishii, Hiroharu Kataoka, and Susumu Miyamoto

OBJECTIVE

Accumulated findings in the pathophysiology of atherosclerosis have demonstrated that not only luminal narrowing but also plaque characteristics influence the risk of future ischemic events. The morphology of the carotid artery (CA) changes in response to atherosclerotic development by expansive remodeling (ER), the clinical significance of which remains unclear. This study aimed to define associations between ER and local risk factors, including CA geometry and traditional systemic risk factors for ischemic events, to determine whether ER could serve as a clinical marker of carotid vulnerable plaque.

METHODS

The authors retrospectively analyzed 66 patients with CA stenosis who were scheduled to undergo carotid endarterectomy or CA stenting. They calculated ER ratios in the internal CA (ICA) from long-axis MR images and as the maximal distance between the lumen and the outer borders of the plaque perpendicular to the axis of the ICA/the maximal luminal diameter of the distal ICA at a region unaffected by atherosclerosis. Relative overall signal intensity (roSI) was calculated to assess intraplaque hemorrhage and defined as the signal intensity of plaque on an axial T1-weighted image with maximal stenosis relative to that of the adjacent sternocleidomastoid muscle. The authors evaluated CA geometry by calculating the angles between the common CA (CCA) and ICA, and between the CCA and external CA (ECA) using digital subtraction angiography. The ER ratios, age, sex, percentage of stenosis, roSI, hypertension, hyperlipidemia, low-density lipoprotein, statin medication, diabetes, smoking habit, and ischemic heart disease were compared between 33 symptomatic and 33 asymptomatic patients. The authors also compared symptomatic status, age, sex, percentage of stenosis, ICA angle, ECA angle, roSI, and other traditional atherosclerotic risk factors between groups with extensive and slight ER.

RESULTS

The ER ratio was significantly greater in symptomatic than in asymptomatic patients (1.91 ± 0.46 vs 1.68 ± 0.40, p < 0.05). The ICA angle was significantly larger in the group with extensive ER than in those with slight ER (33.9° ± 20.2° vs 21.7° ± 13.8°, p < 0.01). The roSI, ECA angle, percentage stenosis, or any other traditional vascular risk factors were not associated with ER.

CONCLUSIONS

Carotid ER might be an independent indicator of carotid vulnerable plaque, which should be validated in a longitudinal study of patients with carotid atherosclerosis, including those with nonstenotic to moderate stenosis.

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Kosuke Hayashi, Hiroharu Kataoka, Manabu Minami, Taichi Ikedo, Takeshi Miyata, Kampei Shimizu, Manabu Nagata, Tao Yang, Yu Yamamoto, Masayuki Yokode, and Susumu Miyamoto

OBJECTIVE

Zinc is an essential micronutrient with multiple biological effects, including antiinflammation. Previously, the authors demonstrated that the pathogenesis of intracranial aneurysms (IAs) is strongly related to chronic inflammation. In this study, the authors investigated whether administration of zinc inhibits the growth of IAs in a rat model.

METHODS

The authors analyzed surgically induced IAs in Sprague-Dawley male rats, which were subsequently treated with intraperitoneal injections of zinc sulfate heptahydrate (ZnSO4; 3 mg/kg/day) or vehicle for 4 weeks.

RESULTS

Size and wall thickness ratios of experimentally induced IAs were assessed in both treatment groups after induction and in a control group. The effects of zinc administration in IAs were examined by immunohistochemistry and Western blotting. Zinc administration significantly suppressed aneurysm size and also preserved the internal elastic lumen. Administration of zinc significantly attenuated infiltration of macrophages into IAs.

CONCLUSIONS

Zinc treatment significantly increased expression of the antiinflammatory signaling protein A20, an inhibitor of the nuclear factor κB (NF-κB) pathway, in rat IAs. Zinc administration may prevent the growth of rat IAs by inducing A20-attributed inactivation of NF-κB signaling.

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Tao Yang, Kazumichi Yoshida, Takakuni Maki, Yasutaka Fushimi, Kiyofumi Yamada, Masakazu Okawa, Yu Yamamoto, Naoki Takayama, Keita Suzuki, and Susumu Miyamoto

OBJECTIVE

Carotid webs (CWs) have increasingly been recognized as a cause of recurrent ischemic stroke. However, the natural history and clinical course of CWs remain unclear. The authors aimed to clarify the prevalence, imaging features, and optimal treatment of CWs in a Japanese cohort study.

METHODS

A series of 444 consecutive Japanese patients who had undergone CTA of the head and neck between April 2011 and October 2016 was retrospectively reviewed. CW was diagnosed on CT angiograms as a membrane-like intraluminal filling defect along the posterior wall of the carotid bulb or the origin of the internal carotid artery (ICA) on oblique sagittal images and a corresponding thin septum on axial images.

RESULTS

Two patients with CWs were identified among 132 patients with suspected stroke. The prevalence of CWs among symptomatic patients with suspected stroke was 1.5%. The prevalence of asymptomatic CWs was 2.2% (7 of 312 cases). The CWs were located in the posterior wall of the carotid bulb in 7 patients and just distal to the ICA origin in 2 patients. There were no apparent differences in the location or lesion length between symptomatic and asymptomatic CWs. Four of the 7 asymptomatic CWs remained asymptomatic for at least 2 years of follow-up. Two patients with symptomatic CWs developed recurrent cerebral infarction and transient ischemic attack despite being on a regimen of oral antiplatelet agents, and carotid endarterectomy was performed as radical treatment. Patients with CWs were younger than controls (median age 55 vs 69 years, p = 0.003) and were less frequently male than controls (33% vs 72%, p = 0.025). CW cases showed significantly fewer common atherosclerosis risk factors than the control group (p < 0.05).

CONCLUSIONS

Although limited to CTA patients, this study reported on the prevalence and common site of CWs, focusing on symptomatic and asymptomatic Japanese patients. Extensive cross-sectional and prospective observational studies are warranted to elucidate the overall prevalence and natural history of CWs.

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Kosuke Hayashi, Hiroharu Kataoka, Manabu Minami, Taichi Ikedo, Takeshi Miyata, Kampei Shimizu, Manabu Nagata, Tao Yang, Yu Yamamoto, Masayuki Yokode, and Susumu Miyamoto

OBJECTIVE

Zinc is an essential micronutrient with multiple biological effects, including antiinflammation. Previously, the authors demonstrated that the pathogenesis of intracranial aneurysms (IAs) is strongly related to chronic inflammation. In this study, the authors investigated whether administration of zinc inhibits the growth of IAs in a rat model.

METHODS

The authors analyzed surgically induced IAs in Sprague-Dawley male rats, which were subsequently treated with intraperitoneal injections of zinc sulfate heptahydrate (ZnSO4; 3 mg/kg/day) or vehicle for 4 weeks.

RESULTS

Size and wall thickness ratios of experimentally induced IAs were assessed in both treatment groups after induction and in a control group. The effects of zinc administration in IAs were examined by immunohistochemistry and Western blotting. Zinc administration significantly suppressed aneurysm size and also preserved the internal elastic lumen. Administration of zinc significantly attenuated infiltration of macrophages into IAs.

CONCLUSIONS

Zinc treatment significantly increased expression of the antiinflammatory signaling protein A20, an inhibitor of the nuclear factor κB (NF-κB) pathway, in rat IAs. Zinc administration may prevent the growth of rat IAs by inducing A20-attributed inactivation of NF-κB signaling.

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Yuji Ito, Satoshi Maesawa, Epifanio Bagarinao, Yu Okai, Daisuke Nakatsubo, Hiroyuki Yamamoto, Hiroyuki Kidokoro, Naotaka Usui, Jun Natsume, Minoru Hoshiyama, Toshihiko Wakabayashi, Gen Sobue, and Norio Ozaki

OBJECTIVE

The authors recently reported a novel subsecond analysis method of analyzing EEG–functional MRI (fMRI) to improve the detection rate of epileptic focus. This study aims to validate the utility of this method for presurgical evaluation in pharmacoresistant focal epilepsy.

METHODS

Among 13 patients with focal epilepsy undergoing presurgical examinations including simultaneous EEG-fMRI at 3T, 11 patients had interictal epileptiform discharges (IEDs) during fMRI. The authors used the sequence of topographic maps during the IEDs as a reference to obtain subsecond fMRI activation maps with the same temporal resolution as the EEG data, and constructed “spike-and-slow-wave-activation-summary” (SSWAS) maps that showed the activation frequency of voxels during IEDs. Clusters were defined by thresholding the SSWAS maps (voxel value > 10), and those containing voxels with the top 3 highest activation frequencies were considered significant. Significant hemodynamic responses using conventional event-related (ER) analysis and SSWAS maps were compared with the resection areas and surgical outcomes at 1 year after surgery.

RESULTS

Using ER analysis, 4 (36%) of 11 patients had significant hemodynamic responses. One of 4 patients had significant hemodynamic responses in the resection area and good surgical outcome. Using SSWAS maps, 10 (91%) of 11 patients had significant hemodynamic responses. Six of 10 patients had significant hemodynamic responses in the resection area, and 5 of the 6 patients achieved good surgical outcomes. The remaining 4 patients had significant hemodynamic responses distant from the resection area, and only 1 of the 4 patients achieved good surgical outcomes. The sensitivity, specificity, positive predictive value, and negative predictive value of SSWAS maps were 83.3%, 75.0%, 83.3%, and 75.0%, respectively.

CONCLUSIONS

This study demonstrated the clinical utility of SSWAS maps for presurgical evaluation of pharmacoresistant focal epilepsy. The findings indicated that subsecond EEG-fMRI analysis may help surgeons choose the resection areas that could lead to good surgical outcomes.

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Oral Presentations

2010 AANS Annual Meeting Philadelphia, Pennsylvania May 1–5, 2010