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Background and Purpose: Retrospective studies have found that patients receiving general anesthesia for endovascular treatment in acute ischemic stroke have worse neurological outcome compared with patients receiving conscious sedation. In this prospective randomized single-center study, we investigated the impact of anesthesia technique on neurological outcome in acute ischemic stroke patients., Methods: Ninety patients receiving endovascular treatment for acute ischemic stroke in 2013 to 2016 were included and randomized to general anesthesia or conscious sedation. Difference in neurological outcome at 3 months, measured as modified Rankin Scale score, was analyzed (primary outcome) and early neurological improvement of National Institutes of Health Stroke Scale and cerebral infarction volume. Age, sex, comorbidities, admission National Institutes of Health Stroke Scale score, intraprocedural blood pressure, blood glucose, Paco 2 and Pco 2 modified Thrombolysis in Cerebral Ischemia score, and relevant time intervals were recorded., Results: In the general anesthesia group 19 of 45 patients (42.2%) and in the conscious sedation group 18 of 45 patients (40.0%) achieved a modified Rankin Scale score ≤2 ( P =1.00) at 3 months, with no differences in intraoperative blood pressure decline from baseline ( P =0.57); blood glucose ( P =0.94); PaCO2 ( P =0.68); time intervals ( P =0.78); degree of successful recanalization, 91.1% versus 88.9% ( P =1.00); National Institutes of Health Stroke Scale score at 24 hours 8 (3-5) versus 9 (2-15; P =0.60); infarction volume, 20 (10-100) versus 20(10-54) mL ( P =0.53); and hospital mortality (13.3% in both groups; P =1.00)., Conclusions: In endovascular treatment for acute ischemic stroke, no difference was found between general anesthesia and conscious sedation in neurological outcome 3 months after stroke., Clinical Trial Registration: URL: https://www.clinicaltrials.gov. Unique identifier: NCT01872884., (© 2017 American Heart Association, Inc.)

Background and Purpose: In retrospective studies, patients receiving general anesthesia for endovascular treatment for acute ischemic stroke have worse neurological outcome compared with patients receiving conscious sedation. It has been suggested that this is caused by general anesthesia-associated hypotension. We investigated the effect of intraprocedural hypotension on neurological outcome., Methods: One hundred eight patients with acute ischemic stroke, who underwent endovascular treatment in general anesthesia between 2007 and 2012, were included. Analyzed predictors of neurological outcome were age, sex, comorbidities, baseline National Institutes of Health Stroke Scale, intraprocedural relative changes in mean arterial blood pressure from baseline, blood glucose, modified Thrombolysis in Cerebral Infarction score, and elapsed time from stroke to computed tomography, groin puncture, and recanalization/end of procedure., Results: A fall in mean arterial blood pressure of >40% was an independent predictor for poor neurological outcome (P=0.032), as were higher admission National Institutes of Health Stroke Scale score (P=0.008) and lack of recanalization (P=0.003)., Conclusions: Profound intraprocedural hypotension is an independent predictor for poor neurological outcome in patients with acute ischemic stroke undergoing endovascular therapy in general anesthesia., (© 2015 American Heart Association, Inc.)

Background and Purpose: Aneurysmal subarachnoid hemorrhage (aSAH) stands out from other subtypes of stroke because of the high early mortality and the risk of complications. Serum glial fibrillary acidic protein (s-GFAP) concentrations are increased after stroke. The aim of this study was to investigate whether s-GFAP could be used as a marker of brain damage and outcome after aSAH., Methods: Serum samples were obtained on a regular basis from 116 adults during a 2-week period after aSAH and analyzed using an enzyme-linked immunosorbent assay. The World Federation of Neurological Surgeons scale was used for neurological evaluation. Outcome was assessed after 1 year and categorized according to the Extended Glasgow Outcome Scale., Results: Increased s-GFAP levels were seen in 81 of the 116 patients. Maximum s-GFAP correlated with World Federation of Neurological Surgeons scale on arrival and on days 10 to 15 (r=0.37, P<0.001 and r=0.47, P<0.001, respectively). Furthermore, maximum s-GFAP levels were increased in the patient group with radiological signs of focal lesions acute or at 1 year, compared with the group without focal lesions (P<0.001 in both comparisons). Patients with secondary events (re-bleeding or ischemia) reached maximum levels later in the series and both maximum and final s-GFAP levels increased compared with the levels in patients without secondary events (P<0.001 in all 3 comparisons). Finally, maximum s-GFAP correlated with outcome (r=-0.48, P<0.001) and s-GFAP was an independent predictor of dichotomized outcome., Conclusions: s-GFAP provides information about brain injury severity and outcome after aSAH, which can be useful as a complement to clinical data.

Background and Purpose: The neuronal death that accompanies an ischemic stroke has previously been attributed to a necrotic process. However, numerous studies in experimental models of ischemia have recently indicated that programmed cell death, also called apoptosis, may contribute to neuronal death. The aim of the present study was to investigate the intrathecal levels of proteins regulating apoptosis in acute stroke and to relate these levels to brain damage and to production of proinflammatory and anti-inflammatory cytokines., Methods: Thirty stroke patients were studied prospectively on days 0 to 4, 7 to 9, 21 to 26, and after day 90 with clinical evaluation, radiological assessment, and analysis of cerebrospinal fluid (CSF) levels of soluble (s) Fas/APO-1 and sbcl-2, 2 proteins that regulate apoptosis. In addition, analysis of the intrathecal levels of cytokines interleukin (IL)-1beta, IL-6, IL-8, IL-10, granulocyte-macrophage colony-stimulating factor (GM-CSF), and tumor necrosis factor-alpha was performed. Nineteen CSF samples from healthy subjects were used for control purposes. The patients were examined with MRI 1 to 3 months after stroke onset for measurement of infarct volume, Results: Significantly decreased CSF levels of sFas/APO-1 were observed during the entire observation period, with a maximal decrease on day 21 after the onset of stroke. The intrathecal levels of sFas/APO-1 were significantly negatively correlated with the volume of brain infarct and with the neurological deficit 3 weeks and 3 months after the onset of the stroke. In addition, the intrathecal levels of sFas/APO-1 were significantly correlated with the levels of IL-1beta, IL-6, IL-10, and GM-CSF 3 weeks after the onset of the disease. The intrathecal levels of sbcl-2 were significantly decreased during the first 3 days after stroke onset and at the same time were positively correlated with the levels of IL-6 and tumor necrosis factor-alpha., Conclusions: Our study demonstrates decreased intrathecal levels of proteins with antiapoptotic properties, suggesting that patients with acute stroke display a propensity toward apoptosis. Control of factors regulating apoptosis may lead to decreased delayed brain damage in stroke.

Background and Purpose: Patients resuscitated from cardiac arrest have a high early mortality rate. Prognostic evaluation based on clinical observations is uncertain and would benefit from the use of biochemical markers of hypoxic brain damage. The astroglial protein S-100 is an established biochemical marker of central nervous system injury. The purpose of the present study was to validate the use of serum determinations of S-100 with regard to outcome after cardiac arrest., Methods: Levels of serum S-100 were measured with a radioimmunoassay in 41 patients the first 3 days after out-of-hospital cardiac arrest. The main outcome variable was fatal outcome within 14 days., Results: S-100 levels were increased after cardiac arrest compared with controls with the highest levels observed the first day. S-100 levels day 1 and 2 correlated to the degree of coma as well as to the time of anoxia. Seventeen patients died within 14 days after the cardiac arrest. The deceased patients had increased S-100 levels on days 1 through 3 compared with survivors. All patients (100%) with an S-100 level of > or =0.2 on day 2 after the cardiac arrest died within 14 days, and 89% of the patients with levels below this limit value survived (positive and negative predictive values). The corresponding predictive values on day 1 were 71% and 85%, respectively., Conclusions: The present study shows that hypoxic brain damage after cardiac arrest can be estimated by measurement of serum S-100 concentrations. The method can be used in early prognostic evaluation of short-term outcome after cardiac arrest.

Background and Purpose: We have previously demonstrated that stroke influences systemic immune responses. The aim of the present study was to investigate patterns of local inflammatory response as a consequence of acute stroke., Methods: Thirty stroke patients were studied prospectively on days 0 to 3, 7 to 9, 21 to 26, and after day 90 with clinical evaluations, radiological assessments, and analysis of serum and cerebrospinal fluid cytokine levels., Results: Significantly increased levels of interleukin-6 (IL-6) in cerebrospinal fluid (P < .001) were observed in virtually all patients studied compared with healthy control subjects. This increase was observed during the whole observation period but was significantly more pronounced within the first days after stroke onset, with a peak level on days 2 and 3. This initial increase was significantly correlated (r = .65, P = .002) with the volume of infarct measured by MRI 2 to 3 months later. Serum levels of IL-6 in stroke patients were significantly lower than cerebrospinal fluid levels of IL-6 (P = .013) and did not display any significant correlation to the size of the brain lesion. Also, increase in intrathecal but not systemic production of IL-1 beta was observed early during the stroke. Only minor increases of cerebrospinal fluid interferon-gamma levels were observed in two patients., Conclusions: Our study demonstrates an intrathecal production of IL-6 and IL-1 beta in patients with stroke, supporting the notion of localized inflammatory response to acute brain lesion. In addition, the significant correlation between early intrathecal production of IL-6 and the subsequent size of the brain lesion can be used as a prognostic tool, predicting the size of the brain damage before it is possible to accurately visualize it with radiological methods.