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Search Results: 1 - 10 of 168667 matches for " Sander E Connolly "
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Hemorrhagic Transformation: A Review of the Rate of Hemorrhage in the Major Clinical Trials of Acute Ischemic Stroke
Eric S. Sussman,E. Sander Connolly Jr.
Frontiers in Neurology , 2013, DOI: 10.3389/fneur.2013.00069
Abstract: Acute ischemic stroke is a devastating disease that is often complicated by hemorrhagic transformation. While significant advances have been made over the past two decades with regard to emergent treatment of AIS, many of the therapeutic options are limited by an increased risk of hemorrhage. Here, we sought to review the rates of hemorrhagic transformation in the major clinical trials of AIS intervention. Since the reviewed clinical trials vary significantly in terms of study design, eligibility criteria, stroke severity, and baseline demographic data, direct comparisons between the various trials is not valid. Nevertheless, this review is intended to consolidate the pertinent data on hemorrhagic transformation in order to call attention to any patterns that may warrant further investigation.
Revisiting normal perfusion pressure breakthrough in light of hemorrhage-induced vasospasm
Matthew D Alexander, E Sander Connolly , Philip M Meyers
World Journal of Radiology , 2010,
Abstract: Cerebral arteriovenous malformations (AVMs) have abnormally enlarged arteries and veins prone to spontaneous hemorrhage. Immediately following surgical excision of a cerebral AVM, even normal brain tissue surrounding the lesion is subject to hemorrhage, a phenomenon termed normal perfusion pressure breakthrough (NPPB) syndrome. According to this theory, arteries supplying cerebral AVMs become dilated and lose their capacity to dilate or constrict to autoregulate pressure. Acutely after removal of a cerebral AVM, excessive blood pressure in these arterial feeders can cause normal brain tissue to bleed. However, this theory remains controversial. We present a patient with a cerebral AVM that demonstrated cerebrovascular reactivity and argues against an assumption underlying the theory of NPPB syndrome.
Treatment of mechanically-induced vasospasm of the carotid artery in a primate using intra-arterial verapamil: a technical case report
Alexander L Coon, Geoffrey P Colby, William J Mack, Lei Feng, Philip Meyers, E Sander Connolly
BMC Cardiovascular Disorders , 2004, DOI: 10.1186/1471-2261-4-11
Abstract: As part of a study assessing the placement feasibility and safety of a catheter capable of delivering intra-arterial cerebroprotective therapy, a female 16 kg baboon prophylaxed with intravenous nitroglycerin underwent transfemoral CCA catheterization with a metallic 6-Fr catheter without signs of acute spasm. The protocol dictated that the catheter remain in the CCA for 12 hours. Upon completion of the protocol, arteriography revealed a marked decrease in CCA size (mean cross-sectional area reduction = 31.6 ± 1.9%) localized along the catheter length. Intra-arterial verapamil (2 mg/2cc) was injected and arteriography was performed 10 minutes later. Image analysis at 6 points along the CCA revealed a 21.0 ± 1.7% mean increase in vessel diameter along the length of the catheter corresponding to a 46.7 ± 4.0% mean increase in cross-sectional area. Mean systemic blood pressure did not deviate more than 10 mm Hg during the procedure.Intraluminal CCBs like verapamil may constitute an effective endovascular treatment for mechanically-induced vasospasm in medium to large-sized vessels such as the CCA.Rapid advancements in endovascular technology and techniques allow for treatment of an ever-increasing range of neurovascular diseases. Despite improvements in the safety and efficacy of these procedures, complications such as vasospasm, stroke, and perforation still occur [1]. Vasospasm, or contraction of smooth muscle fibers in the wall of a vessel, is a commonly recognized adverse event that may complicate an endovascular procedure by limiting distal blood flow.Vasospasm complicates many disease states, particularly those affecting small vessels. Recently, treatment of small-vessel vasospasm has proven amenable to pharmacological intervention. For example, in the treatment of cerebral artery spasm, intravenous nitrates [2], intravenous calcium channel blockers (CCBs) [3], and intra-arterial papaverine [4] and CCBs [5] have been shown to prevent or mitigate this small artery
Radiotherapy plus Concomitant and Adjuvant Temozolomide for Glioblastoma – A Critical Review
Ricardo J. Komotar,Marc L. Otten,Gaetan Moise,E. Sander Connolly
Clinical Medicine : Oncology , 2008,
Abstract:
Complement Inhibition as a Proposed Neuroprotective Strategy following Cardiac Arrest
Brad E. Zacharia,Zachary L. Hickman,Bartosz T. Grobelny,Peter A. DeRosa,Andrew F. Ducruet,E. Sander Connolly
Mediators of Inflammation , 2009, DOI: 10.1155/2009/124384
Abstract: Out-of-hospital cardiac arrest (OHCA) is a devastating disease process with neurological injury accounting for a disproportionate amount of the morbidity and mortality following return of spontaneous circulation. A dearth of effective treatment strategies exists for global cerebral ischemia-reperfusion (GCI/R) injury following successful resuscitation from OHCA. Emerging preclinical as well as recent human clinical evidence suggests that activation of the complement cascade plays a critical role in the pathogenesis of GCI/R injury following OHCA. In addition, it is well established that complement inhibition improves outcome in both global and focal models of brain ischemia. Due to the profound impact of GCI/R injury following OHCA, and the relative lack of effective neuroprotective strategies for this pathologic process, complement inhibition provides an exciting opportunity to augment existing treatments to improve patient outcomes. To this end, this paper will explore the pathophysiology of complement-mediated GCI/R injury following OHCA.
The baboon (Papio anubis) extracranial carotid artery: An anatomical guide for endovascular experimentation
J Mocco, Daniel J Hoh, M Nathan Nair, Tanvir F Choudhri, William J Mack, Ilya Laufer, E Sander Connolly
BMC Cardiovascular Disorders , 2001, DOI: 10.1186/1471-2261-1-4
Abstract: We characterized the extracranial carotid system often male baboons (Papio anubis, range 15.1–28.4 kg) by early post-mortem dissection. Photographic documentation of vessel lengths, lumen diameters, and angles of origin were measured for each segment of the carotid bilaterally.The common carotid arteries averaged 94.7 ± 1.7 mm (left) and 87.1 ± 1.6 mm (right) in length. The average minimal common carotid lumen diameters were 3.0 ± 0.3 mm (left) and 2.9 ± 0.2 mm (right). Each animal had a common brachiocephalic artery arising from the aorta which bifurcated into the left common carotid artery and right braciocephalic artery after 21.5 ± 1.6 mm. The vascular anatomy was found to be consistent among animals despite a wide range of animal weights.The consistency in the Papio anubis extracranial carotid system may promote the use of this species in the preclinical investigation of neuro-interventional therapies.There has been a recent interest in developing aggressive interventional strategies for the treatment of a variety of neurological diseases including stroke, subarachnoid hemorrhage, and head trauma [1-4]. Successful translation of these therapies to the clinical arena, however, is critically dependent on the use of appropriate experimental models [5]. Non-human primate models of neurological diseases currently exist and have the advantage of most closely mimicking human physiology [6]. These models are particularly relevant to neuro-interventional research in that anatomical similarities permit routine vascular access and evaluation of devices designed on a clinically relevant scale.Conducting experimental primate endovascular studies, however, requires a comprehensive understanding of the carotid vascular system. Previous investigations of non-human primate vascular anatomy have focused primarily on the general morphology of the vessels and not on vessel angles, lengths, or lumen diameters which are necessary for guiding endovascular technology [7,8]. To answer
Nutritional support and brain tissue glucose metabolism in poor-grade SAH: a retrospective observational study
J Michael Schmidt, Jan Claassen, Sang-Bae Ko, Hector Lantigua, Mary Presciutti, Kiwon Lee, E Sander Connolly, Stephan A Mayer, David S Seres, Neeraj Badjatia
Critical Care , 2012, DOI: 10.1186/cc11160
Abstract: We used a retrospective observational cohort study of 50 mechanically ventilated poor-grade (Hunt-Hess 4 or 5) aneurysmal SAH patients who underwent brain microdialysis monitoring for an average of 109 hours. Enteral nutrition was started within 72 hours of admission whenever feasible. Intensive insulin therapy was used to maintain serum glucose levels between 5.5 and 7.8 mmol/l. Serum glucose, insulin and caloric intake from enteral tube feeds, dextrose and propofol were recorded hourly. Cerebral metabolic distress was defined as a lactate to pyruvate ratio (LPR) > 40. Time-series data were analyzed using a general linear model extended by generalized estimation equations (GEE).Daily mean caloric intake received was 13.8 ± 6.9 cal/kg and mean serum glucose was 7.9 ± 1 mmol/l. A total of 32% of hourly recordings indicated a state of metabolic distress and < 1% indicated a state of critical brain hypoglycemia (< 0.2 mmol/l). Calories received from enteral tube feeds were associated with higher serum glucose concentrations (Wald = 6.07, P = 0.048), more insulin administered (Wald = 108, P < 0.001), higher body mass index (Wald = 213.47, P < 0.001), and lower body temperature (Wald = 4.1, P = 0.043). Enteral feeding (Wald = 1.743, P = 0.418) was not related to brain glucose concentrations after accounting for serum glucose concentrations (Wald = 67.41, P < 0.001). In the presence of metabolic distress, increased insulin administration was associated with a relative reduction of interstitial brain glucose concentrations (Wald = 8.26, P = 0.017), independent of serum glucose levels.In the presence of metabolic distress, insulin administration is associated with reductions in brain glucose concentration that are independent of serum glucose levels. Further study is needed to understand how nutritional support and insulin administration can be optimized to minimize secondary injury after subarachnoid hemorrhage.Hyperglycemia, defined as serum glucose > 11 mmol/l after suba
Effects of the neurological wake-up test on clinical examination, intracranial pressure, brain metabolism and brain tissue oxygenation in severely brain-injured patients
Raimund Helbok, Pedro Kurtz, Michael J Schmidt, Morgan R Stuart, Luis Fernandez, Sander E Connolly, Kiwon Lee, Erich Schmutzhard, Stephan A Mayer, Jan Claassen, Neeraj Badjatia
Critical Care , 2012, DOI: 10.1186/cc11880
Abstract: This prospective observational study was performed in a neuroscience intensive care unit in a tertiary-care academic center. Twenty consecutive severely brain-injured patients with multimodal neuromonitoring were analyzed for levels of brain lactate, pyruvate and glucose, intracranial pressure (ICP), cerebral perfusion pressure (CPP) and brain tissue oxygen tension (PbtO2) during IS trials.Of the 82 trial days, 54 IS-trials were performed as interruption of sedation and analgesics were not considered safe on 28 days (34%). An increase in the FOUR Score (Full Outline of UnResponsiveness score) was observed in 50% of IS-trials by a median of three (two to four) points. Detection of a new neurologic deficit occurred in one trial (2%), and in one-third of IS-trials the trial had to be stopped due to an ICP-crisis (> 20 mmHg), agitation or systemic desaturation. In IS-trials that had to be aborted, a significant increase in ICP and decrease in PbtO2 (P < 0.05), including 67% with critical values of PbtO2 < 20 mmHg, a tendency to brain metabolic distress (P < 0.07) was observed.Interruption of sedation revealed new relevant clinical information in only one trial and a large number of trials could not be performed or had to be stopped due to safety issues. Weighing pros and cons of IS-trials in patients with acute brain injury seems important as related side effects may overcome the clinical benefit.Titrating sedatives and analgesics to achieve the right balance between deep sedation and wakefulness and to ameliorate patients' comfort in the intensive care unit (ICU) is an integral part of critical care [1]. Over-sedation can lead to prolonged duration of mechanical ventilation and ICU stay and increase the incidence of secondary complications, including nosocomial infections and delirium.Daily interruption of sedation trials (IS-trials) have been implemented in many surgical and medical ICUs after randomized controlled trials demonstrated that IS decreased the duration of
Endovascular Thrombectomy Following Acute Ischemic Stroke: A Single-Center Case Series and Critical Review of the Literature
Eric Sussman,Christopher Kellner,Michael McDowell,Peter Yang,Eric Nelson,Sophie Greenberg,Daniel Sahlein,Sean Lavine,Philip Meyers,E. Sander Connolly
Brain Sciences , 2013, DOI: 10.3390/brainsci3020521
Abstract: Acute ischemic stroke (AIS) due to thrombo-embolic occlusion in the cerebral vasculature is a major cause of morbidity and mortality in the United States and throughout the world. Although the prognosis is poor for many patients with AIS, a variety of strategies and devices are now available for achieving recanalization in patients with this disease. Here, we review the treatment options for cerebrovascular thromboembolic occlusion with a focus on the evolution of strategies and devices that are utilized for achieving endovascular clot extraction. In order to demonstrate the progression of this treatment strategy over the past decade, we will also present a single-center case series of AIS patients treated with endovascular thrombectomy.
Complement Inhibition Promotes Endogenous Neurogenesis and Sustained Anti-Inflammatory Neuroprotection following Reperfused Stroke
Andrew F. Ducruet, Brad E. Zacharia, Sergey A. Sosunov, Paul R. Gigante, Mason L. Yeh, Justin W. Gorski, Marc L. Otten, Richard Y. Hwang, Peter A. DeRosa, Zachary L. Hickman, Paulina Sergot, E. Sander Connolly
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0038664
Abstract: Background and Purpose The restoration of blood-flow following cerebral ischemia incites a series of deleterious cascades that exacerbate neuronal injury. Pharmacologic inhibition of the C3a-receptor ameliorates cerebral injury by attenuating post-ischemic inflammation. Recent reports also implicate C3a in the modulation of tissue repair, suggesting that complement may influence both injury and recovery at later post-ischemic time-points. Methods To evaluate the effect of C3a-receptor antagonism on post-ischemic neurogenesis and neurological outcome in the subacute period of stroke, transient focal cerebral ischemia was induced in adult male C57BL/6 mice treated with multiple regimens of a C3a receptor antagonist (C3aRA). Results Low-dose C3aRA administration during the acute phase of stroke promotes neuroblast proliferation in the subventricular zone at 7 days. Additionally, the C3a receptor is expressed on T-lymphocytes within the ischemic territory at 7 days, and this cellular infiltrate is abrogated by C3aRA administration. Finally, C3aRA treatment confers robust histologic and functional neuroprotection at this delayed time-point. Conclusions Targeted complement inhibition through low-dose antagonism of the C3a receptor promotes post-ischemic neuroblast proliferation in the SVZ. Furthermore, C3aRA administration suppresses T-lymphocyte infiltration and improves delayed functional and histologic outcome following reperfused stroke. Post-ischemic complement activation may be pharmacologically manipulated to yield an effective therapy for stroke.
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