Acute Focal Neurological Deficits in Aneurysmal Subarachnoid Hemorrhage

Sarrafzadeh, Asita; Haux, Daniel; Sakowitz, Oliver W.; Benndorf, Goetz; Herzog, H.; Kuechler, Ingeborg; Unterberg, Andreas

doi:10.1161/01.str.0000074036.97859.02

Cited by 100 publications

(32 citation statements)

References 19 publications

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“…If we make the assumption that these flow pathways must be patent for the proper maintenance of extracellular homeostasis by CSF, we can infer from our findings in this study that this function is also impaired following SAH. Clinical and animal studies that have shown a buildup of metabolic waste products, decreased available glucose, and altered ionic concentrations [7, 13, 23]—all hallmarks of EBI—support this idea.We also cannot ignore that a functional and patent CSF systemis likely critical to the clearance of toxic blood products from the initial hemorrhage itself. Any or all of these perturbations of normal physiology could contribute to the early ICP-independent vascular dysfunction that is documented in both animal [11] and clinical studies [20, 23].…”

Section: Discussionmentioning

confidence: 99%

“…Broad categories of EBI include blood brain barrier disruption [6], altered metabolic homeostasis [7], cortical spreading depression [8], and neuronal cell death [9, 10]. Global cerebral hypoperfusion, which occurs within the first minutes of SAH, is thought to be one of the primary contributors to EBI and is a strong predictor of outcome [5].…”

Section: Introductionmentioning

confidence: 99%

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Intracisternal Administration of Tissue Plasminogen Activator Improves Cerebrospinal Fluid Flow and Cortical Perfusion After Subarachnoid Hemorrhage in Mice

Siler

González

Wang

et al. 2014

Transl. Stroke Res.

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Early brain injury (EBI) during the first 72 h after subarachnoid hemorrhage (SAH) is an important determinant of clinical outcome. A hallmark of EBI, global cerebral ischemia, occurs within seconds of SAH and is thought to be related to increased intracranial pressure (ICP). We tested the hypothesis that ICP elevation and cortical hypoperfusion are the result of physical blockade of cerebrospinal fluid (CSF) flow pathways by cisternalmicrothrombi. In mice subjected to SAH, we measured cortical blood volume (CBV) using optical imaging, ICP using pressure transducers, and patency of CSF flow pathways using intracisternally injected tracer dye. We then assessed the effects of intracisternal injection of recombinant tissue plasminogen activator (tPA). ICP rose immediately after SAH and remained elevated for 24 h. This was accompanied by a decrease in CBV and impaired dye movement. Intracisternal administration of tPA immediately after SAH lowered ICP, increased CBV, and partially restored CSF flow at 24 h after SAH. Lowering ICP without tPA, by draining CSF, improved CBVat 1 h, but not 24 h after SAH. These findings suggest that blockade of CSF flow by microthrombi contributes to the early decline in cortical perfusion in an ICP-dependent and ICP-independent manner and that intracisternal tPA may reduce EBI and improve outcome after SAH.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Intracisternal Administration of Tissue Plasminogen Activator Improves Cerebrospinal Fluid Flow and Cortical Perfusion After Subarachnoid Hemorrhage in Mice

Siler

González

Wang

et al. 2014

Transl. Stroke Res.

View full text Add to dashboard Cite

show abstract

“…Similarly blood glutamate scavengers have been shown to improve neurological outcome in animal models, but the blockade of NMDA receptors may actually hinder neuronal survival [33]. In clinical studies glutamate elevation in cerebral interstitial fluid detected with microdialysis was predictive of ischemia [34] and the release of excitatory amino acid after SAH measured in interstitial and cerebrospinal fluid (CSF) correlated strongly with ICP elevation, secondary brain injury, and poor outcome [35]. …”

Section: Early Brain Injurymentioning

confidence: 99%

To Look Beyond Vasospasm in Aneurysmal Subarachnoid Haemorrhage

Cossu

Messerer

Oddo

et al. 2014

BioMed Research International

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Delayed cerebral vasospasm has classically been considered the most important and treatable cause of mortality and morbidity in patients with aneurysmal subarachnoid hemorrhage (aSAH). Secondary ischemia (or delayed ischemic neurological deficit, DIND) has been shown to be the leading determinant of poor clinical outcome in patients with aSAH surviving the early phase and cerebral vasospasm has been attributed to being primarily responsible. Recently, various clinical trials aimed at treating vasospasm have produced disappointing results. DIND seems to have a multifactorial etiology and vasospasm may simply represent one contributing factor and not the major determinant. Increasing evidence shows that a series of early secondary cerebral insults may occur following aneurysm rupture (the so-called early brain injury). This further aggravates the initial insult and actually determines the functional outcome. A better understanding of these mechanisms and their prevention in the very early phase is needed to improve the prognosis. The aim of this review is to summarize the existing literature on this topic and so to illustrate how the presence of cerebral vasospasm may not necessarily be a prerequisite for DIND development. The various factors determining DIND that worsen functional outcome and prognosis are then discussed.

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“…High lactate/pyruvate ratios in normoxic conditions have been interpreted as markers of hyperglycolysis. Elevated glutamate is a marker of cellular dysfunction, for example, delayed cerebral ischemia in high-risk SAH patients [56]. Absolute CMD values are important, but trends over time may provide more useful information.…”

Section: Monitoring Techniquesmentioning

confidence: 99%

Clinical review: Neuromonitoring - an update

et al. 2013

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Critically ill patients are frequently at risk of neurological dysfunction as a result of primary neurological conditions or secondary insults. Determining which aspects of brain function are affected and how best to manage the neurological dysfunction can often be difficult and is complicated by the limited information that can be gained from clinical examination in such patients and the effects of therapies, notably sedation, on neurological function. Methods to measure and monitor brain function have evolved considerably in recent years and now play an important role in the evaluation and management of patients with brain injury. Importantly, no single technique is ideal for all patients and different variables will need to be monitored in different patients; in many patients, a combination of monitoring techniques will be needed. Although clinical studies support the physiologic feasibility and biologic plausibility of management based on information from various monitors, data supporting this concept from randomized trials are still required.

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Acute Focal Neurological Deficits in Aneurysmal Subarachnoid Hemorrhage

Cited by 100 publications

References 19 publications

Intracisternal Administration of Tissue Plasminogen Activator Improves Cerebrospinal Fluid Flow and Cortical Perfusion After Subarachnoid Hemorrhage in Mice

Intracisternal Administration of Tissue Plasminogen Activator Improves Cerebrospinal Fluid Flow and Cortical Perfusion After Subarachnoid Hemorrhage in Mice

To Look Beyond Vasospasm in Aneurysmal Subarachnoid Haemorrhage

Clinical review: Neuromonitoring - an update

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