Influence of Differences in Case Mix on the Better Outcome of Smokers after Intravenous Thrombolysis for Acute Cerebral Ischemia

2012 ◽  
Vol 67 (3) ◽  
pp. 178-183 ◽  
Author(s):  
Solène Moulin ◽  
Visnja Padjen-Bogosavljevic ◽  
Aurélie Marichal ◽  
Charlotte Cordonnier ◽  
Dejana R. Jovanovic ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Intravenous Thrombolysis ◽  
Case Mix ◽  
Acute Cerebral Ischemia

Abstract T P167: Emergent Identification of Type A Aortic Dissection as a Cause of Acute Ischemic Stroke

Stroke ◽  
2014 ◽  
Vol 45 (suppl_1) ◽  
Author(s):  
Tomoyuki Ohara ◽  
Kazunori Toyoda ◽  
Hiroyuki Yokoyama ◽  
Kenji Minatoya ◽  
Eijiro Tanaka ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Back Pain ◽  
Cerebral Ischemia ◽  
Aortic Dissection ◽  
Intravenous Thrombolysis ◽  
Type A ◽  
Neurological Deficits ◽  
Diagnostic Tools ◽  
Acute Cerebral Ischemia ◽  
D Dimer

Background: Acute aortic dissection (AAD) sometimes presents with predominant neurological symptoms of acute cerebral ischemia. Fatal AAD patients after thrombolysis for stroke without noticing AAD were reported. The purpose of this study was to clarify the characteristics of AAD patients with acute cerebral ischemia and develop a score to emergently identify AAD for such patients. Methods: From the database of Stanford type A-AAD patients admitted in our hospital between 2007 and 2012, we selected those presenting with acute focal neurological deficits due to ischemic stroke/TIA. Patients presenting with shock state or cardiopulmonary arrest were excluded. Physiological, radiological, and blood examinations were assessed for AAD identification. Results: Of 187 AAD patients, 19 patients (10%) with focal neurological deficits as an initial presentation were studied. Involvement of one or more main branches of the aortic arch was observed in all of 19 patients. Stroke experts, not cardiovascular experts, were primarily called to ER in 18 patients, and 12 were potential candidates for intravenous thrombolysis. Left hemiparesis (14 patients, 74%) was the most common neurological symptom. Nine patients (47%) complained of chest or back pain. As components of the score, (1) systolic BP differential >20mmHg between upper extremities was present in 11 of 17 patients (65%), (2) mediastinal widening on chest radiography in 13/16 (81%), (3) occlusion or the intimal flap of the proximal common carotid artery on carotid ultrasonography in 14/16 (88%), (4) pericardial effusion on echocardiography in 10/19 (47%), and (5) abnormal elevation of D-dimer levels in all 19 (median 24.8 [range 4.2-406.2] μg/ml). Two components were positive in 4 patients, three in 6, four in 5, and all the five in 4. Conclusions: Only half of AAD patients with stroke/TIA complained of chest or back pain. All the AAD patients with stroke/TIA showed high D-dimer levels and one or more additional abnormal findings in physiological and radiological examinations. Combination of such handy diagnostic tools is helpful to identify AAD without long time delay and to avoid unnecessary thrombolysis for AAD patients.

Abstract TMP61: Improved Routing of Comprehensive Stroke Center Appropriate Patients via Mobile Stroke Unit Conclusive Field Diagnosis

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Bryan Villareal ◽  
Kevin Brown ◽  
Kenny Harrell ◽  
Jeffrey L. Saver ◽  
Mersedeh Bahr Hosseini ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Los Angeles ◽  
Intracranial Hemorrhage ◽  
Intravenous Thrombolysis ◽  
Patient Disposition ◽  
Mobile Stroke Unit ◽  
Acute Cerebral Ischemia ◽  
Comprehensive Stroke Center ◽  
Stroke Center ◽  
Los Angeles Motor Scale

Background: Mobile Stroke Units (MSUs) are capable of rapid initiation of intravenous thrombolysis and have the potential to improve acute stroke patient routing by providing conclusive imaging diagnosis of LVO (arterial sequences) and intracranial hemorrhage (parenchymal/extraparenchymal sequences). However, the incremental increase in diagnostic accuracy and effect on patient disposition have not been well delineated. Methods: Consecutive transports in a regionally-deployed MSU from September 2017-August 2019) were analyzed, comparing patient routing that would have occurred under standard ambulance protocols to routing and process outcomes after CT/CTA MSU imaging. Standard ambulance regional routing policy was direct to nearest PSC if Los Angeles Motor Scale (LAMS) 0-3 and direct to nearest CSC within 30m if LAMS 4-5. Results: Among 83 MSU transports, final diagnosis was acute cerebral ischemia in 68% and intracranial hemorrhage in 10%. Among 57 acute cerebral ischemia patients, Los Angeles Motor Scale (LAMS) score was 0-3 in 65% and 4-5 in 35%. All (100%) of patients with ICA/M1 occlusions had LAMS score 4-5. However, among patients with expanded range endovascular target occlusions (M2, basilar), LAMS scores were 0-3 in 56%, and MSU imaging permitted improved routing. Among 8 intracranial hemorrhage patients (2 IPH, 5 SDH, 1 SAH), MSU imaging permitted improved direct-to-CSC routing in the 62% of patients with LAMS scores 0-3. Among all MSU admissions, 15% (13) were rerouted based solely upon in-vehicle imaging, including 7% for radiographically proven endovascularly treatable occlusion, 7% for neurosurgical/NICU intracranial hemorrhage care, and 1% for neurosurgical tumor care. Transport times for re-routed patients was median 12 minutes, compared to closest stroke center median 6 minutes. Conclusion: More than 1 in 7 MSU evaluations result in improved routing of comprehensive stroke center-appropriate patients directly to a CSC facility, including AIS patients potentially eligible for thrombectomy, intracranial hemorrhage patients, and acutely-presenting brain tumor patients. In addition to speeding start of intravenous thrombolysis, MSUs can substantially improve timely access to CSC care.

Intravenous Thrombolysis for Acute Cerebral Ischemia in Belgrade, Serbia: Comparison with Lille, France

2011 ◽  
Vol 66 (1) ◽  
pp. 30-36 ◽  
Author(s):  
Visnja Bogosavljevic ◽  
Marie Bodenant ◽  
Ljiljana Beslac-Bumbasirevic ◽  
Charlotte Cordonnier ◽  
Dejana R. Jovanovic ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Intravenous Thrombolysis ◽  
Acute Cerebral Ischemia

Effect of carvedilol on the redox-status of plasma low-molecular-weight aminothyols in rats with acute cerebral ischemia

2018 ◽  
pp. 12-18
Author(s):  
К.А. Никифорова ◽  
В.В. Александрин ◽  
П.О. Булгакова ◽  
А.В. Иванов ◽  
Э.Д. Вирюс ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Cerebral Ischemia ◽  
Carotid Arteries ◽  
Redox Status ◽  
Global Cerebral Ischemia ◽  
Low Molecular Weight ◽  
Adrenergic Antagonist ◽  
Acute Cerebral Ischemia ◽  
Common Carotid Arteries ◽  
Reduced Forms

Цель. Установить влияние неспецифического адреноблокатора карведилола на редокс-статус низкомолекулярных аминотиолов (цистеин, гомоцистеин, глутатион) в плазме крови при моделировании глобальной ишемии головного мозга у крыс. Методика. Нами была использована модель глобальной ишемии (пережатие общих сонных артерий с геморрагией длительностью 15 мин). Препарат вводили за 1 ч до операции. Уровни аминотиолов измеряли через 40 мин после начала реперфузии. Анализ уровня аминотиолов проводили методом жидкостной хроматографии. Результаты. Установлено, что у крыс, не подвергавшихся ишемии, карведилол в дозе 10 мг/кг вызывает рост редокс-статуса цистеина и глутатиона (в 3 и 3,5 раза соответственно по сравнению с контролем, p = 0,04 и p = 0,008) за счет увеличения их восстановленных форм. При ишемии данного эффекта не наблюдалось. Редокс-статус у крыс с ишемией на фоне карведилола (Цис = 0,85 ± 0,14%, Глн = 1,8 ± 0,7%, Гцис = 1,1 ± 0,8%) оставался таким же низким, как и у крыс с ишемией без введения карведилола (р > 0,8). Заключение. Полученный результат демонстрирует, что в условиях ишемии головного мозга карведилол не оказывает эффекта на гомеостаз аминотиолов плазмы крови, несмотря на выраженный антиоксидантный эффект в нормальных условиях. Aim. Effect of a nonspecific adrenergic antagonist carvedilol on the redox status of plasma low-molecular-weight aminothiols (cysteine, homocysteine, glutathione) was studied in rats with global cerebral ischemia (occlusion of common carotid arteries with hemorrhage). Methods. A model of global ischemia (occlusion of common carotid arteries with 15-min hemorrhage) was used. The drugs were administered one hour before the operation. Aminothiol levels were measured by HPLC with UV detection at 40 minutes after the onset of reperfusion. Results. Carvedilol 10 mg/kg increased the redox status of cysteine and glutathione in rats not exposed to ischemia (3 and 3.5 times, respectively, compared with the control, p = 0.04 and p = 0.008, respectively) but not of homocysteine, by increasing their reduced forms. However, this effect was not observed in ischemia. In rats with ischemia treated with carvedilol, the redox status (Cys = 0.85 ± 0.14%, GSH = 1.8 ± 0.7%, Hcys = 1.1 ± 0.8%) remained low similar to that in rats with ischemia not treated with carvedilol (p >0.8, 0.8, and 0.9, respectively). Conclusion. Carvedilol did not affect the homeostasis of blood plasma thiols in cerebral ischemia despite the pronounced antioxidant effect under the normal conditions.

scholarly journals A dose-escalation study of large doses of naloxone for treatment of patients with acute cerebral ischemia.

Stroke ◽  
1986 ◽  
Vol 17 (3) ◽  
pp. 404-409 ◽  
Author(s):  
H P Adams ◽  
C P Olinger ◽  
W G Barsan ◽  
M J Butler ◽  
N R Graff-Radford ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Dose Escalation ◽  
Dose Escalation Study ◽  
Acute Cerebral Ischemia

MRI of spontaneous fluctuations after acute cerebral ischemia in nonhuman primates

2007 ◽  
Vol 26 (4) ◽  
pp. 1112-1116 ◽  
Author(s):  
Yutong Liu ◽  
Helen D'Arceuil ◽  
Julian He ◽  
Mike Duggan ◽  
Gilberto Gonzalez ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Nonhuman Primates ◽  
Acute Cerebral Ischemia ◽  
Spontaneous Fluctuations

Activation of complement by tissue plasminogen activator, but not acute cerebral ischemia, in a rabbit model of thromboembolic stroke

1997 ◽  
Vol 86 (1) ◽  
pp. 139-142 ◽  
Author(s):  
Martin M. Bednar ◽  
Cordell E. Gross ◽  
Sheila R. Russell ◽  
David Short ◽  
Patricia C. Giclas
Keyword(s):  
Cerebral Ischemia ◽  
Plasminogen Activator ◽  
Complement Activation ◽  
Rabbit Model ◽  
Thromboembolic Stroke ◽  
Content Type ◽  
Acute Cerebral Ischemia ◽  
Tissue Plasminogen ◽  
Before And After ◽  
Fine Print

✓ Although complement activation is associated with tissue injury during inflammatory and ischemic states, complement activation in states of acute cerebral ischemia before and after administration of tissue plasminogen activator (TPA) has not yet been examined and is the focus of this investigation. Twenty-four New Zealand White rabbits weighing 3 to 3.5 kg were used for this study. Of these, 20 were subjected to intracranial autologous clot embolization via the internal carotid artery. Three hours postembolization, rabbits received an intravenous infusion of TPA (6.3 mg/kg, 20% bolus with the remainder infused over a 2-hour interval; 12 animals) or vehicle (eight animals). All animals were observed for a total of 7 or 8 hours postembolization. These two groups were compared to a cohort undergoing sham operation with subsequent TPA infusion (four animals). Plasma samples to quantify complement component C5 hemolytic activity (C5H5O) were obtained at the following time points: 30 minutes before and after clot embolization; 1 hour before and 1 hour after the initiation of therapy with TPA or vehicle and at the completion of the protocol; 7 to 8 hours after clot embolization. The C5 activation was not detected as the result of acute cerebral ischemia. However, animals receiving TPA with or without concomitant clot embolization exhibited C5 activation as assessed by a reduction in C5 hemolytic function, both 1 hour after initiation of TPA infusion (78.7 ± 10.3% and 77.5 ± 9.9% of baseline value, respectively; mean ± standard error of the mean [SEM]) and at the end of the protocol, 2 hours after the completion of the TPA infusion (72.5 ± 8.8% and 53.3 ± 8.1%, respectively; mean ± SEM, p < 0.05, each group). This study supports the conclusion that TPA, but not acute cerebral ischemia, may activate the complement cascade in this rabbit model of thromboembolic stroke.

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