Blog
About

4
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Common features in patients with intracerebral hemorrhage following superficial temporal artery-middle cerebral artery bypass in steno-occlusive cerebrovascular disease☆

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Five patients treated for intracranial cerebral hemorrhage after superficial temporal artery-middle cerebral artery bypass in Xuwu Hospital, Capital Medical University, Beijing, China, from 2005-2011 were included in this study. Prior to superficial temporal artery-middle cerebral artery bypass, all patients showed diminished cerebrovascular reactivity and an ipsilateral ischemic lesion. Intracranial cerebral hemorrhage developed within 1–4 days following superficial temporal artery-middle cerebral artery bypass. Transcranial Doppler showed increased middle cerebral artery velocity of 50–100% in the operated hemisphere. These findings suggested that focal hyperperfusion, an ipsilateral ischemic lesion and diminished cerebrovascular reactivity are the important characteristics of intracerebral hemorrhage following superficial temporal artery-middle cerebral artery bypass in patients with steno-occlusive cerebrovascular disease.

          Related collections

          Most cited references 33

          • Record: found
          • Abstract: found
          • Article: not found

          Failure of extracranial-intracranial arterial bypass to reduce the risk of ischemic stroke. Results of an international randomized trial. The EC/IC Bypass Study Group.

          (1985)
          To determine whether bypass surgery would benefit patients with symptomatic atherosclerotic disease of the internal carotid artery, we studied 1377 patients with recent hemisphere strokes, retinal infarction, or transient ischemic attacks who had atherosclerotic narrowing or occlusion of the ipsilateral internal carotid or middle cerebral artery. Of these, 714 were randomly assigned to the best medical care, and 663 to the same regimen with the addition of bypass surgery joining the superficial temporal artery and the middle cerebral artery. The patients were followed for an average of 55.8 months. Thirty-day surgical mortality and major stroke morbidity rates were 0.6 and 2.5 per cent, respectively. The postoperative bypass patency rate was 96 per cent. Nonfatal and fatal stroke occurred both more frequently and earlier in the patients operated on. Secondary survival analyses comparing the two groups for major strokes and all deaths, for all strokes and all deaths, and for ipsilateral ischemic strokes demonstrated a similar lack of benefit from surgery. Separate analyses in patients with different angiographic lesions did not identify a subgroup with any benefit from surgery. Two important subgroups of patients fared substantially worse in the surgical group: those with severe middle-cerebral-artery stenosis (n = 109, Mantel-Haenszel chi-square = 4.74), and those with persistence of ischemic symptoms after an internal-carotid-artery occlusion had been demonstrated (n = 287, chi-square = 4.04). This study thus failed to confirm the hypothesis that extracranial-intracranial anastomosis is effective in preventing cerebral ischemia in patients with atherosclerotic arterial disease in the carotid and middle cerebral arteries.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Effect of a novel free radical scavenger, edaravone (MCI-186), on acute brain infarction. Randomized, placebo-controlled, double-blind study at multicenters.

              (2002)
            Edaravone, a novel free radical scavenger, demonstrates neuroprotective effects by inhibiting vascular endothelial cell injury and ameliorating neuronal damage in ischemic brain models. The present study was undertaken to verify its therapeutic efficacy following acute ischemic stroke. We performed a multicenter, randomized, placebo-controlled, double-blind study on acute ischemic stroke patients commencing within 72 h of onset. Edaravone was infused at a dose of 30 mg, twice a day, for 14 days. At discharge within 3 months or at 3 months after onset, the functional outcome was evaluated using the modified Rankin Scale. Two hundred and fifty-two patients were initially enrolled. Of these, 125 were allocated to the edaravone group and 125 to the placebo group for analysis. Two patients were excluded because of subarachnoid hemorrhage and disseminated intravascular coagulation. A significant improvement in functional outcome was observed in the edaravone group as evaluated by the modified Rankin Scale (p = 0.0382). Edaravone represents a neuroprotective agent which is potentially useful for treating acute ischemic stroke, since it can exert significant effects on functional outcome as compared with placebo.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Reperfusion and neurovascular dysfunction in stroke: from basic mechanisms to potential strategies for neuroprotection.

              Effective stroke therapies require recanalization of occluded cerebral blood vessels. However, reperfusion can cause neurovascular injury, leading to cerebral edema, brain hemorrhage, and neuronal death by apoptosis/necrosis. These complications, which result from excess production of reactive oxygen species in mitochondria, significantly limit the benefits of stroke therapies. We have developed a focal stroke model using mice deficient in mitochondrial manganese-superoxide dismutase (SOD2-/+) to investigate neurovascular endothelial damage that occurs during reperfusion. Following focal stroke and reperfusion, SOD2-/+ mice had delayed blood-brain barrier breakdown, associated with activation of matrix metalloproteinase and high brain hemorrhage rates, whereas a decrease in apoptosis and hemorrhage was observed in SOD2 overexpressors. Thus, induction and activation of SOD2 is a novel strategy for neurovascular protection after ischemia/reperfusion. Our recent study identified the signal transducer and activator of transcription 3 (STAT3) as a transcription factor of the mouse SOD2 gene. During reperfusion, activation of STAT3 and its recruitment into the SOD2 gene were blocked, resulting in increased oxidative stress and neuronal apoptosis. In contrast, pharmacological activation of STAT3 induced SOD2 expression, which limits ischemic neuronal death. Our studies point to antioxidant-based neurovascular protective strategies as potential treatments to expand the therapeutic window of currently approved therapies.
                Bookmark

                Author and article information

                Affiliations
                Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing 100053, China
                Author notes
                [☆]

                Zhiqi Mao, Studying for doctorate, Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing 100053, China

                Corresponding author: Feng Ling, Professor, Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing 100053, China ling-feng@ 123456vip.163.com . (N20120524001/H)

                Author contributions: All authors were responsible for data collection and evaluation, study design and implementation.

                Journal
                Neural Regen Res
                Neural Regen Res
                NRR
                Neural Regeneration Research
                Medknow Publications & Media Pvt Ltd (India )
                1673-5374
                1876-7958
                15 July 2012
                : 7
                : 20
                : 1585-1590
                NRR-7-1585
                10.3969/j.issn.1673-5374.2012.20.009
                4308755
                Copyright: © Neural Regeneration Research

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Categories
                Clinical Practice

                Comments

                Comment on this article