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Interaction between the stent retriever and clot is a key factor for recanalization during mechanical thrombectomy. The aim of this study was to evaluate the association between radiographically apparent features during thrombectomy and angiographic outcomes using the Trevo stent retriever with a fully radiopaque strut.We retrospectively reviewed 50 patients with acute middle cerebral artery occlusion who were treated with the Trevo. Patients were divided into groups that achieved (first-pass recanalization group, n = 21) or did not achieve (non-first-pass recanalization group, n = 29) a modified Thrombolysis in Cerebral Ischemia score of 2b or 3 with the first-pass procedure. Patients were also divided into a thromboembolic (n = 39) and atherosclerotic (n = 11) group by occlusion etiology. We evaluated radiographic findings of the Trevo's strut (e.g., degree of stent expansion and filling defect of the thrombus in the strut [in-stent thrombus sign]) during the first-pass procedure.Median stent expansion was significantly greater in the first-pass recanalization group than in the non-first-pass recanalization group (60% vs. 34%; P0.01) and in the thromboembolic group than in the atherosclerotic group (45% vs. 31%; P0.01). The receiver operator characteristic curve showed moderate capacity for prediction of recanalization and etiology, with an area under the curve of 0.83 and 0.73, respectively. In-stent thrombus sign was significantly more common in the thromboembolic group than in the atherosclerotic group (86% vs. 10%; P0.01).Greater stent expansion was associated with recanalization after thrombectomy. The in-stent thrombus sign may be useful for etiology prediction. These radiographic findings could provide useful real-time feedback during procedures, reflecting clot-stent interaction.

Background and Purpose: High blood pressure increases bleeding risk during treatment with antithrombotic medication. The association between blood pressure levels and the risk of recurrent stroke during long-term secondary stroke prevention with thienopyridines (particularly prasugrel) has not been well studied. Methods: This was a post hoc analysis of the randomized, double-blind, multicenter PRASTRO-I trial (Comparison of Prasugrel and Clopidogrel in Japanese Patients With Ischemic Stroke-I). Patients with noncardioembolic stroke were randomly assigned (1:1) to receive prasugrel 3.75 mg/day or clopidogrel 75 mg/day for 96 to 104 weeks. Risks of any ischemic or hemorrhagic stroke, combined ischemic events, and combined bleeding events were determined based on the mean level and visit-to-visit variability, including successive variation, of systolic blood pressure (SBP) throughout the observational period. These risks were also compared between quartiles of mean SBP level and successive variation of SBP. Results: A total of 3747 patients (age 62.1±8.5 years, 797 women), with a median average SBP level during the observational period of 132.5 mm Hg, were studied. All the risks of any stroke (146 events; hazard ratio, 1.318 [95% CI, 1.094–1.583] per 10-mm Hg increase), ischemic stroke (133 events, 1.219 [1.010–1.466]), hemorrhagic stroke (13 events, 3.247 [1.660–6.296]), ischemic events (142 events, 1.219 [1.020–1.466]), and bleeding events (47 events, 1.629 [1.172–2.261]) correlated with increasing mean SBP overall. Similarly, an increased risk of these events correlated with increasing successive variation of SBP (hazard ratio, 3.078 [95% CI, 2.220–4.225] per 10-mm Hg increase; 3.051 [2.179–4.262]; 3.276 [1.172–9.092]; 2.865 [2.042–4.011]; 2.764 [1.524–5.016], respectively). Event rates did not differ between the clopidogrel and prasugrel groups within each quartile of SBP or successive variation of SBP. Conclusions: Both high mean SBP level and high visit-to-visit variability in SBP were significantly associated with the risk of recurrent stroke during long-term medication with either prasugrel or clopidogrel after stroke. Control of hypertension would be important regardless of the type of antiplatelet drugs. Registration: URL: https://www.clinicaltrials.jp ; Unique identifier: JapicCTI-111582.

Background Endovascular treatment (EVT) has increasingly become the standard treatment of acute cerebral large vessel occlusion (LVO). We evaluated the impact of introducing EVT on LVO therapy in a single center where intravenous thrombolysis (IVT) had been the only recanalization therapy. Materials and methods Between April 2013 and March 2017, 354 consecutive patients with LVO admitted to our institution were analyzed. We compared outcomes between two chronological groups before (Pre-EVT group) and after (Post-EVT group) introducing EVT in April 2015. We assessed prognostic factors for favorable outcomes (modified Rankin scale score ≤2 at 90 days). Results In the Pre-EVT group, all 140 patients were treated medically, including 30 patients (21%) undergoing IVT. In the Post-EVT group, 118 patients (55%) underwent EVT, and the remaining 96 patients treated medically, including six patients (3%) undergoing IVT. The proportion undergoing recanalization therapy with IVT or EVT significantly increased after introducing EVT (21% versus 58%, p < 0.001). The rate of patients achieving favorable outcomes also significantly increased (14% versus 31%, p < 0.001). In multivariate regression analysis, introducing EVT was an independent predictive factor after adjusting for age, stroke severity and extent, and time (p = 0.005). The arrival time in patients with helicopter transport was significantly shorter than that with ground ambulance for a distance of more than 10 km (p < 0.001). Conclusions This study demonstrated that the introduction of EVT improved outcomes of acute LVO patients, increasing the opportunity to receive recanalization therapy. Further efforts to establish medical systems to provide EVT are required throughout the country., Neurology; Neurosurgery; Emergency medicine; Internal medicine; Radiology; Clinical research; Acute ischemic stroke; Large vessel occlusion; Endovascular treatment; Mechanical thrombectomy; Intravenous thrombolysis; Helicopter transport.

There are limited data about the prognostic factors predicting outcomes after mechanical thrombectomy with stent retrievers for the elderly. Here, we evaluated outcomes in elderly patients in a real-world setting.Between April 2015 and January 2017, 80 patients with anterior intracranial acute large vessel occlusion, who had lived independently before ictus, were treated with mechanical thrombectomy using a stent retriever at our institute. We compared outcomes between patients ≥80 years old (n = 36) and those80 years old (n = 44), and assessed prognostic factors for favorable outcomes (modified Rankin Scale score 0-2) at 90 days in all patients.There was no significant difference in baseline National Institutes of Health Stroke Scale score and Alberta Stroke Program Early Computed Tomography Score between the 2 groups. Successful revascularization (modified Thrombolysis in Cerebral Infarction [mTICI] scores 2b/3) (83% versus 93%, P = .286), complete recanalization (mTICI 3) (47% versus 50%, P = .826), and favorable outcomes (42% versus 57%, P = .261) were achieved more often in those80 years old, but differences did not reach statistical significance. Multivariate regression analysis showed that baseline National Institutes of Health Stroke Scale (P = .013) and mTICI scores of 3 (P = .006) were significant predictive factors, but being ≥80 years old and baseline Alberta Stroke Program Early Computed Tomography Score were not. In those ≥80 years old, mTICI score of 3 was an influential factor for favorable outcome (P = .017).Being aged 80 years or older was not a significant predictor for outcomes after mechanical thrombectomy, whereas complete recanalization was an influential predictor of outcome in the elderly.

Mechanical thrombectomy using the stent retriever has been proven to be effective for select patients with acute ischemic stroke. We evaluated our early experience using the device after its approval in 2014 in Japan, with a special emphasis on the occlusion site. Fifty consecutive endovascular revascularization procedures for treating anterior acute large vessel occlusion were performed using the Trevo ProVue as the first-line device at our institute between April 2015 and March 2016. Focusing on the involvement of the M1-M2 bifurcation with deployment or retrieval of the stent retriever, we regarded the middle cerebral artery M1 mid-portion as the boundary and divided the cases into proximal (n = 26) and distal (n = 24) groups. We assessed the overall clinical outcome and compared the outcome between the two groups. Among 50 patients (median age, 80 years; National Institutes of Health Stroke Scale score (NIHSS) score, 20), successful (modified Thrombolysis in Cerebral Infarction score (TICI) 2b or 3) or complete revascularization (TICI 3) was achieved in 41 patients (82%; 88% in the proximal group vs 75% in the distal group, P = 0.28) and in 27 patients (54%; 73% vs 33%, P = 0.01), respectively. Symptomatic intracranial hemorrhage occurred in three patients (6%; 4% vs 8%, P = 0.60). A good outcome (mRS score 0 to 2) was obtained in 25 patients at 90 days (50%; 54% vs 46%, P = 0.78). Mechanical thrombectomy using the Trevo ProVue was safe and effective in patients with acute cerebral artery occlusion, especially for proximal occlusions. The efficacy of the procedure for distal occlusions was somewhat inferior to those for proximal occlusions, which might be resolved by next generation devices.

39歳男性.スノーボード外傷の約1カ月後に頭痛,嘔気,めまい,嚥下障害および構音障害が出現し,臨床的に左Wallenberg症候群と診断された.頭部MRIでは左延髄背外側と左小脳半球に梗塞巣が描出された.左椎骨動脈造影では,椎骨動脈の頭蓋内入口部から脳底動脈移行部におよぶ動脈閉塞を認め,MRIでは同部位に解離性動脈瘤が確認された.本例はスノーボード外傷による頭頸部の過伸展,回旋が原因で椎骨動脈障害を生じたものと考えられた.近年スノーボードが大流行し,種々のタイプの外傷が報告されているが,外傷性解離性椎骨動脈瘤を生じ,Wallenberg症候群を呈した報告の中でスノーボード外傷に起因した症例は,我々が調べ得た限りでは未だ報告されていない.しかし,今後もスノーボード外傷は増加すると考えられるので,スノーボード外傷性脳血管障害に対する諸家の注意を喚起する目的で報告した.

The vasodilatory action of potassium channel openers through a membrane hyperpolarizing action is well known, but little is known about the effect of these drugs on ischemia-induced glutamate release in the brain. We evaluated the effects of a potassium channel opener (Y-26763), given intravenously at 0.03 mg/kg/h from 50 min prior to occlusion until 3 h postocclusion, on cerebral blood flow, extracellular glutamate concentration, and infarct volume in rats with focal ischemia. Y-26763 significantly inhibited the increase in extracellular glutamate concentration at 50 and 60 min of ischemia with a significant reduction of mean arterial blood pressure. However, there was no significant difference in blood flow in the core of infarcted cortex or in infarct volume between Y-26763- and vehicle-treated groups. These results suggest that Y-26763 inhibited presynaptic glutamate release through hyperpolarizing the membrane, but infarct volume was not reduced because of insufficient perfusion owing to its hypotensive effect.

Research into the causes of ischemic damage has evolved into an exploration of the brain's molecular responses. In attempting to discover the specific mechanisms by which ischemic cells die, a number

This is the first report which demonstrates the presence of glutathione peroxidase in the autopsied brain of 5 patients without cerebral infarction and 21 patients with cerebral infarction by the indirect enzyme-labeled antibody technique with monoclonal antibody to human glutathione peroxidase. In 2 out of 5 patients without cerebral infarction, a weak reaction for glutathione peroxidase was demonstrated both in neurons and glia. In 6 patients who had died within 5 days after stroke, no staining was observed in infarcted brain tissue except in macrophages. In all 15 patients who had died more than 6 days after stroke, however, a reaction for glutathione peroxidase was demonstrated in the cytoplasm of glial cells in the marginal area around the infarction, and there was a patchy reaction in the cytoplasm of macrophages in the core lesion. These results suggest that glutathione peroxidase in glial cells of the marginal area around the infarction may play a protective role against lipid peroxidation after cerebral infarction, or alternatively, may be involved in the healing process after ischemia.

We present a case in which the clinical manifestations mimicked amyotrophic lateral sclerosis (ALS) and the pathological findings showed diffuse cerebrospinal gliomatosis. Diffuse cerebrospinal gliomatosis may be disguised as ALS when it predominantly involves the spinal cord and brain stem, and may not be easily differentiated from ALS. Therefore, diffuse cerebrospinal gliomatosis should be taken into consideration in the differential diagnosis of ALS.(Internal Medicine 32: 476-479, 1993)

患者は50歳, 男性.突然の複視で発症し, 左眼の下転障害と右眼の上転障害を主徴とし, MRIにて視床中脳境界部左側に限局した血腫が認められた.右Horner症候群, 輻輳障害を認めたが, 他の神経症候はみられなかった.垂直眼球運動の中枢として吻側内側縦束間質核 (riMLF) が人間に於いても注目され, その障害で発症したとする “vertical one-and-a-half” 症候群の例が報告されているが, 本例では視床中脳出血により一側のriMLFが障害され, 病巣側の下転障害と反対側の上転障害という特異な垂直眼球運動障害を呈したと考えられた.我々の知る限りでは今までにこの特異な眼球所見に関する報告はなく, riMLFの概念を支持するものと考え報告した.

Introduction: Nontraumatic coma in adults has a poor prognosis, and late recovery of consciousness is unlikely. Functional recovery is usually extremely poor. However, a few nontraumatic comatose patients have shown late recovery of both awareness and function. Methods: A retrospective survey was conducted by reviewing the medical records of all inpatients to our department during the 1990s. Patients with persistent but reversible nontraumatic coma were identified according to the following criteria: (a) deep coma with a Glasgow Coma Scale (GCS) score of 7 or less on admission; (b) nontraumatic cause; (c) persistence of unconsciousness for longer than 1 month; and (d) subsequent recovery of GCS (total) to normal. The clinical spectrum of patients meeting these criteria was evaluated. Results: Six patients (ages 16–75 years) met the criteria. Viral encephalitis was diagnosed in five (two with herpes simplex virus, two with cytomegalovirus, and one with Epstein-Barr virus or cytomegalovirus). Two young female patients with encephalitis manifested extremely protracted coma persisting for 3 and 18 months, respectively. Complications included nonconvulsive status epilepticus in two patients and relative overdose of clonazepam in one patient. Conclusion: Recognition of the clinical spectrum of persistent but reversible nontraumatic coma is important.

We recently reported that cortical spreading depression (CSD), used to precondition rat brain, reduced cortical infarction volume resulting from focal cerebral ischemia by middle cerebral artery occlusion (MCAO) 3 days later. The mechanisms underlying this protective effect by CSD remains to be explored. In this study, we confirm that CSD is neuroprotective when KCl is applied epidurally rather than intracortically. Neocortical infarct volume was 101.3+/-48.5 mm3 and 45.3+/-44.1 mm3 in the sham and CSD group, respectively (p0.05). Using image analysis, we identified the cortical region spared from infarction by the prior CSD. We then determined the distribution of brain-derived neurotrophic factor (BDNF) and basic fibroblast growth factor (bFGF) mRNA and the time course of their expression in groups of animals treated with CSD and their controls. We also examined the response of astrocytes to CSD using glial fibrillary acidic protein (GFAP) as a marker. In situ hybridization (done at 0, 3, 12, 24, 72 or 168 h after CSD) showed significant elevation of BDNF mRNA in the cortex immediately after CSD in a distribution surrounding the spared cortex, while bFGF mRNA rose 12 h after CSD and appeared more within the core of the ischemic region. Immunohistochemistry (done at 1, 3 or 7 days after CSD) demonstrated GFAP in the neocortex, with a peak at 3 days after CSD. Heat shock protein 72 (HSP72) expression was not affected by CSD. We concluded that upregulation of trophic factors and activation of glial cells may contribute to the neuroprotection induced by CSD.

The possibility that cortical spreading depression (CSD) may have neuroprotective action during subsequent focal cerebral ischemia was examined in rats. Three days before the imposition of focal cerebral ischemia CSDs were elicited by applying potassium chloride (KCl) for 2 h through a microdialysis probe implanted in the occipital cortex. Control animals were handled identically except that saline was infused instead of KCl. Focal ischemia was produced by the intraluminal suture method and cortical and subcortical infarct volumes were measured 7 days later. Neocortical infarct volume was reduced from 124.8 ± 49.5 mm3 in the controls to 62.9 ± 59.5 mm3 in the animals preconditioned with CSD (p = 0.012). There was no difference between the two groups in the subcortical infarct volume or in CBF, measured by the hydrogen clearance method, during or immediately after the ischemic interval. Our data indicate that preconditioning CSD applied 3 days before middle cerebral artery occlusion may increase the brain's resistance to focal ischemic damage and may be used as a model to explore the neuroprotective molecular responses of neuronal and glial cells.

Although a number of studies have demonstrated the neuroprotective effects of antagonists of postsynaptic N-methyl-d-aspartate (NMDA) and non-NMDA receptors in cerebral ischemia, little is known about the treatment of cerebral infarction through presynaptic blocking of extracellular glutamate release. We evaluated the effects of a presynaptic selective N-type calcium channel antagonist (SNX-111, given intravenously by continuous infusion at 5 mg/kg/h from 20 min prior to occlusion until 2 h postocclusion) on blood flow, extracellular glutamate, and infarct volume in rats with permanent occlusions of the right middle cerebral and right common carotid arteries plus 1-h transient occlusion of the left common carotid artery. There was no significant difference in CBF in the occluded cortex during the experiment between the treated and vehicle groups. SNX-111 significantly reduced total amount of extracellular glutamate during the experiment and the peak value of the glutamate after occlusion from 44.2 ± 15.8 μ M (mean ± SD) to 21.4 ± 11.4 μ M (p < 0.01). Infusion of SNX-111 also significantly reduced the cortical volume of infarction from 47.2 ± 5.8 to 19.9 ± 7.3% (p < 0.0001). These results suggest that SNX-111 has a protective effect against focal ischemia through the inhibition of glutamate release from presynaptic sites, although SNX-111 may also affect the release of other neurotransmitters.

Background and Purpose The possibility that the brain may be preconditioned to be more tolerant of ischemia is an important concept with important clinical implications. Exploring the concept offers the possibility of advancing our understanding of protective molecular responses in the brain. This article compares two preconditioning methods and explores the role that changes in regional cerebral blood flow (rCBF) may play in conferring ischemic protection. Methods Temporary occlusion of the middle cerebral artery (MCA) using the thread model was preceded 4 days earlier by short-lasting focal or global ischemia or by sham surgery. rCBF was measured in the frontoparietal region of the ischemic hemisphere during all focal ischemia episodes. Four days after the second ischemic exposure, animals were killed, and the size of infarction was determined. Results rCBF was significantly higher in the frontoparietal region during MCA occlusion when it was preceded by prior focal ischemia (36.8±7.6 mL · 100 g −1 · min −1 at 30 minutes) compared with controls (24.7±4.0 mL · 100 g −1 · min −1 , P =.0008). Despite this, there was no significant difference in the resulting infarct volume. In contrast, when MCA occlusion was preceded by global ischemia, infarct volume was significantly reduced (68.1±30.9 mm 3 in the controls versus 22.9±22.1 mm 3 in the preconditioned group, P =.002) without significant change in rCBF. Conclusions Protection from ischemic injury requires specific conditions of prior exposure to ischemia. Improved perfusion would not seem to be a sufficient or necessary accompaniment to providing neuroprotection.