Diagnosing cerebral ischemia with door-to-thrombolysis times below 20 minutes

Neurology ◽  
2018 ◽  
Vol 91 (6) ◽  
pp. e498-e508 ◽  
Author(s):  
Saana Pihlasviita ◽  
Olli S. Mattila ◽  
Juhani Ritvonen ◽  
Gerli Sibolt ◽  
Sami Curtze ◽  
...  
Keyword(s):  
Emergency Department ◽  
Cerebral Ischemia ◽  
Admission Diagnosis ◽  
Stroke Mimics ◽  
Antiplatelet Medication ◽  
Acute Cerebral Ischemia ◽  
Emergency Department Stay ◽  
Observational Cohort ◽  
Initial Imaging ◽  
Neurologic Emergency

ObjectivesTo clarify diagnostic accuracy and consequences of misdiagnosis in the admission evaluation of stroke-code patients in a neurologic emergency department with less than 20-minute door-to-thrombolysis times.MethodsAccuracy of admission diagnostics was studied in an observational cohort of 1,015 stroke-code patients arriving by ambulance as candidates for recanalization therapy between May 2013 and November 2015. Immediate admission evaluation was performed by a stroke neurologist or a neurology resident with dedicated stroke training, primarily utilizing CT-based imaging.ResultsThe rate of correct admission diagnosis was 91.1% (604/663) for acute cerebral ischemia (ischemic stroke/TIA), 99.2% (117/118) for hemorrhagic stroke, and 61.5% (144/234) for stroke mimics. Of the 150 (14.8%) misdiagnosed patients, 135 (90.0%) had no acute findings on initial imaging and 100 (67.6%) presented with NIH Stroke Scale score 0 to 2. Misdiagnosis altered medical management in 70 cases, including administration of unnecessary treatments (thrombolysis n = 13, other n = 24), omission of thrombolysis (n = 5), delays to specific treatments of stroke mimics (n = 13, median 56 [31–93] hours), and delays to antiplatelet medication (n = 14, median 1 [1–2] day). Misdiagnosis extended emergency department stay (median 6.6 [4.7–10.4] vs 5.8 [3.7–9.2] hours; p = 0.001) and led to unnecessary stroke unit stay (n = 10). Detailed review revealed 8 cases (0.8%) in which misdiagnosis was possible or likely to have worsened outcomes, but no death occurred as a result of misdiagnosis.ConclusionsOur findings support the safety of highly optimized door-to-needle times, built on thorough training in a large-volume, centralized stroke service with long-standing experience. Augmented imaging and front-loaded specialist engagement are warranted to further improve rapid stroke diagnostics.

Safety and predictors of stroke mimics in The Norwegian Tenecteplase Stroke Trial (NOR-TEST)

2018 ◽  
Vol 14 (5) ◽  
pp. 508-516 ◽  
Author(s):  
Christopher Elnan Kvistad ◽  
Vojtech Novotny ◽  
Halvor Næss ◽  
Guri Hagberg ◽  
Hege Ihle-Hansen ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Cerebral Ischemia ◽  
Transient Ischemic Attack ◽  
Sensory Loss ◽  
Stroke Mimics ◽  
Symptomatic Intracerebral Hemorrhage ◽  
Acute Cerebral Ischemia ◽  
Stroke Mimic ◽  
Ischemic Attack ◽  
Stroke Trial

Background Stroke mimics are frequently treated with thrombolysis in clinical practice and thrombolytic trials. Although alteplase in stroke mimics has proven to be safe, safety of tenecteplase in stroke mimics has not been assessed in an ischemic stroke study setting. We aimed to assess clinical characteristics and safety of stroke mimics treated with thrombolysis in the Norwegian Tenecteplase Stroke Trial. We also aimed to identify possible predictors of stroke mimics as compared to patients with acute cerebral ischemia. Methods Norwegian Tenecteplase Stroke Trial was a phase-3 trial investigating safety and efficacy of tenecteplase vs. alteplase in patients with suspected acute cerebral ischemia. Two groups were defined based on diagnose at discharge: patients with a different diagnose than ischemic stroke or transient ischemic attack (stroke mimics group) and patients diagnosed with ischemic stroke or transient ischemic attack (acute cerebral ischemia group). Logistic regression analyses were performed with stroke mimics vs. acute cerebral ischemia as dependent variable to identify predictors of stroke mimics. Results Of 1091 randomized patients, 181 (16.6%) were stroke mimics. Migraine (22.2%) and peripheral vertigo (11.4%) were the two most frequent stroke mimic-diagnoses. There was no symptomatic intracerebral hemorrhage in the stroke mimics group. Stroke mimics were independently associated with age ≤60 years (OR 2.75, p < 0.001), female sex (OR 1.48, p = 0.026), no history of myocardial infarction (OR 2.03, p = 0.045), systolic BP ≤ 150 mmHg (OR 2.33, p < 0.001), NIHSS ≤ 6 points (OR 1.83, p = 0.011), sensory loss (OR 1.55, p = 0.015), and no facial paresis (OR 2.41, p < 0.001) on admission. Conclusion Thrombolysis with tenecteplase seems to be as safe as with alteplase in stroke mimics. Predictors were identified for stroke mimics which may contribute to differentiate stroke mimics from acute cerebral ischemia in future stroke trials.

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

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

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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