We aimed to clarify the outcomes of carotid artery stenting (CAS) in the Japanese population. For this purpose, we reviewed data from the Japanese Registry of NeuroEndovascular Therapy 3 (JR-NET3), a retrospective, nation-wide, multi-center, observational study of neuroendovascular treatments in Japan. Of the 9207 patients who underwent CAS between January 2010 and December 2014, 8458 satisfied the inclusion criteria for our analysis. The outcome statistics of this JR-NET3 cohort were compared to those of JR-NET1 and 2 cohorts fitting the same inclusion criteria. Of the 8458 JR-NET3 patients analyzed, 8042 (95.1%) were treated by surgeons with board certification from the Japanese Society for NeuroEndovascular Therapy. Technical success was achieved in 8417 patients (99.5%), whereas 198 patients (2.3%) had clinically significant complications (CSCs). These findings mirrored those obtained for the JR-NET1 and 2 cohorts. On multivariate analysis, risk factors for CAS-associated CSC included symptomatic lesion [odds ratio (OR), 1.91; 95% confidence interval (CI), 1.23–3.00; P = 0.003] and hypoechoic lesion on carotid artery ultrasound (OR, 1.85; 95% CI, 1.21–2.84; P = 0.005), whereas use of closed-cell stents was a predictor of better outcome (OR, 0.53; 95% CI, 0.35–0.79; P = 0.002). The findings of JR-NET3 reflect good outcomes of CAS, but non-modifiable risk factors reflecting lesion characteristics remain of concern. Using closed-cell stents is advisable. Technological advances such as the introduction of new materials may help further improve CAS outcomes in Japanese patients.
Subarachnoid hemorrhage (SAH) is mainly attributable to the rupture of intracranial aneurysms (IAs). Although the outcome of SAH is considerably poor in spite of the recent intensive medical care, mechanisms regulating the progression of IAs or triggering rupture remain to be clarified, making the development of effective preemptive medicine to prevent SAH difficult. However, a series of recent studies have been expanding our understanding of the pathogenesis of IAs. These studies have suggested the crucial role of macrophage-mediated chronic inflammation in the pathogenesis of IAs. In histopathological analyses of IA lesions in humans and induced in animal models, the number of macrophages infiltrating in lesions is positively correlated with enlargement or rupture of IAs. In animal models, a genetic deletion or an inhibition of monocyte chemotactic protein-1, a major chemoattractant for macrophages, or a pharmacological depletion of macrophages consistently suppresses the development and progression of IAs. Furthermore, a macrophage-specific deletion of Ptger2 (gene for prostaglandin E receptor subtype 2) or a macrophage-specific expression of a mutated form of IκBα which inhibits nuclear translocation of nuclear factor κB significantly suppress the development of IAs, supporting the role of macrophages and the inflammatory signaling functioning there in the pathogenesis of IAs. The development of drug therapies suppressing macrophage-mediated inflammatory responses in situ can thus be a potential strategy in the pre-emptive medicine targeting SAH. In this manuscript, we summarize the experimental evidences about the pathogenesis of IAs focused on inflammatory responses and propose the definition of IAs as a macrophage-mediated inflammatory disease.
The “cerebrospinal fluid (CSF) circulation theory” of CSF flowing unidirectionally and circulating through the ventricles and subarachnoid space in a downward or upward fashion has been widely recognized. In this review, observations of CSF motion using different magnetic resonance imaging (MRI) techniques are described, findings that are shared among these techniques are extracted, and CSF motion, as we currently understand it based on the results from the quantitative analysis of CSF motion, is discussed, along with a discussion of slower water molecule motion in the perivascular, paravascular, and brain parenchyma. Today, a shared consensus regarding CSF motion is being formed, as follows: CSF motion is not a circulatory flow, but a combination of various directions of flow in the ventricles and subarachnoid space, and the acceleration of CSF motion differs depending on the CSF space. It is now necessary to revise the currently held concept that CSF flows unidirectionally. Currently, water molecule motion in the order of centimeters per second can be detected with various MRI techniques. Thus, we need new MRI techniques with high-velocity sensitivity, such as in the order of 10 μm/s, to determine water molecule movement in the vessel wall, paravascular space, and brain parenchyma. In this paper, the authors review the previous and current concepts of CSF motion in the central nervous system using various MRI techniques.
Local brain cooling of an epileptic focus at 15°C reduces the number of spikes on an electrocorticogram (ECoG), terminates seizures, and maintains neurological functions. In this study, we attempted to suppress generalized motor seizures (GMSs) by cooling a unilateral sensorimotor area. GMSs were induced in rats by intraperitoneal injection of bicuculline methiodide, an antagonist of gamma-aminobutyric acid. While monitoring the ECoG and behavior, the right sensorimotor cortex was cooled for 10 min using an implanted device. The number of spikes recorded from the cooled cortex significantly decreased to 71.2% and 62.5% compared with the control group at temperatures of 15 and 5°C (both P <0.01), respectively. The number of spikes recorded from the contralateral mirror cortex reduced to 61.7% and 62.7% (both P <0.05), respectively. The ECoG power also declined to 85% and 50% in the cooled cortex, and to 94% and 49% in the mirror cortex by the cooling at 15 and 5°C, respectively. The spikes regained in the middle of the cooling period at 15°C and in the late period at 5°C. Seizure-free durations during the 10-min periods of cooling at 15 and 5°C lasted for 4.1 ± 2.2 and 5.9 ± 1.1 min, respectively. Although temperature-dependent seizure alleviation was observed, the effect of local cortical cooling on GMSs was limited compared with the effect of local cooling of the epileptic focus on GSMs.
Multi-vessel cervical arterial injury after blunt trauma is rare, and its pathophysiology is unclear. Although blunt cerebrovascular injury is a common cause of cerebral ischemia, its management is still controversial. We describe a 23-year-old man in previously good health who developed three-vessel cervical arterial dissections due to blunt trauma. He was admitted to our emergency and critical care center after a motor vehicle crash. Computed tomography showed a thin, acute subdural hematoma in the right hemisphere and fractures of the odontoid process (Anderson type III), pelvis, and extremities. He was treated conservatively, and about 1 month later, he developed bleariness. Computed tomography angiography showed bilateral internal carotid and left vertebral artery dissection. Aspirin therapy was started immediately, and then clopidogrel was added to the regimen. Two weeks later, magnetic resonance angiography (MRA) showed improved blood flow of the vessels. Only aspirin therapy was continued. About 3 months after discharge, MRA demonstrated further improvement of the blood flow of both internal carotid arteries, but the dissection flap on the right side remained. Therefore, we extended the duration of antiplatelet therapy. On the basis of our experience with this case, we think that antithrombotic therapy is crucial for the management of multi-vessel cervical arterial injury, and agents should be used properly according to the injury grade and phase; however, further study is needed to confirm this recommendation.