Asymptomatic versus Symptomatic Infarcts from Vasospasm in Patients with Subarachnoid Hemorrhage: Serial Magnetic Resonance Imaging

Shimoda, Masami; Takeuchi, Masataka; Tominaga, Jiro; Oda, Shinri; Kumasaka, Akira; Tsugane, Ryuichi

doi:10.1097/00006123-200112000-00010

Cited by 123 publications

(88 citation statements)

References 30 publications

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“…Previous studies have demonstrated that after aSAH, 30% to 65% of patients will have a cerebral infarct identified on imaging at long-term follow-up. 2,3,8,12,28,29 The rates of early infarcts from previous studies 2,8,12,13 are also comparable with our current data (17% to 34% versus 18%). In contrast to our report, earlier studies were not capable of directly comparing clipping to coiling or determining how different treatment methods may affect infarct rates and neurological outcomes.…”

Section: Discussionsupporting

confidence: 91%

Dissociation of Early and Delayed Cerebral Infarction After Aneurysmal Subarachnoid Hemorrhage

Ayling

Ibrahim

Alotaibi

et al. 2016

Stroke

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Background and Purpose-Cerebral infarction after aneurysmal subarachnoid hemorrhage is a significant cause of substantial morbidity and mortality. Because early and delayed cerebral infarction after aneurysmal subarachnoid hemorrhage may be mediated by different processes, we evaluated whether aneurysm-securing methods contributed to infarcts and whether long-term outcomes differ between early and delayed infarcts. Methods-A post hoc analysis of the CONSCIOUS-1 study (Clazosentan to Overcome Neurological Ischemia and Infarction Occurring After Subarachnoid Hemorrhage) was performed. Using multivariate logistic regression analysis and propensity matching, independent clinical risk factors associated with infarctions were identified, and the contribution of cerebral infarcts to long-term outcomes was evaluated. Results-Within the cohort of 413 subjects, early infarcts were present in 76 subjects (18%), whereas delayed infarcts occurred in 79 subjects (19%), and 36 subjects (9%) had new infarctions that were present on both early and delayed imaging. Propensity score matching revealed a significantly higher proportion of early infarcts after clipping (odds ratio, 4.62; 95% confidence interval, 1.99-11.57; P=0.00012). Multivariate logistic regressions identified clipping as an independent risk factor for early cerebral infarction (odds ratio, 0.26; 95% confidence interval, 0.15-0.48; P<0.001), and angiographic vasospasm was an independent risk factor for delayed cerebral infarction (odds ratio, 1.79; 95% confidence interval, 1.03-3.13; P=0.039). Early infarcts were a significant independent risk factor for poor long-term outcomes at 3 months (odds ratio, 2.34; 95% confidence interval, 1.18-4.67; P=0.015). Conclusions-Clipping is an independent risk factor for the development of early cerebral infarcts, whereas delayed cerebral infarcts are associated with angiographic vasospasm. Early cerebral infarcts are stronger predictors of worse outcome than delayed infarction. Clinical Trial Registration-URL: http://www.clinicaltrials.gov. Unique identifier: NCT00111085.

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Section: Discussionsupporting

confidence: 91%

Dissociation of Early and Delayed Cerebral Infarction After Aneurysmal Subarachnoid Hemorrhage

Ayling

Ibrahim

Alotaibi

et al. 2016

Stroke

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“…Therefore, there was not a robust association between delayed cerebral ischemia and outcome, but in this study the investigators were not directly examining cerebral infarction. Similar findings were reported in a retrospective review by Shimoda, et al, 52 who found that cerebral infarction was associated with poor outcome but that the relationship of delayed cerebral ischemia to outcome was less obvious. No statistical analysis of these data was performed.…”

Section: Does Cerebral Infarction Cause Poor Outcome?supporting

confidence: 89%

“…Furthermore, not all patients with angiographic vasospasm have symptoms attributable to it, and vice versa. 7,45,52 The term "symptomatic vasospasm" is more subjective, because it depends on how exhaustive the efforts are to exclude other causes of neurological worsening. Furthermore, it is complicated because there may be contributing factors, and because patients with poor-grade SAH are more difficult to assess, particularly if they are sedated.…”

Section: Definitions Of Terminologymentioning

confidence: 99%

“…Even deterioration due to ischemia has been attributed to causes other than angiographic vasospasm; these include microvascular vasospasm, thromboembolism, and delayed neuronal apoptosis triggered by global ischemia occurring at the time of SAH. 38,39,49,52 Here we use the term delayed cerebral ischemia to mean ischemia from angiographic vasospasm.…”

Section: Definitions Of Terminologymentioning

confidence: 99%

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Can angiographic vasospasm be used as a surrogate marker in evaluating therapeutic interventions for cerebral vasospasm?

Nolan

Macdonald²

2006

FOC

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✓ The authors tested the null hypothesis that published literature with a high level of evidence does not support the assertion that subarachnoid hemorrhage (SAH) causes cerebral vasospasm, which in turn causes cerebral infarction and poor outcome after aneurysmal SAH. The medical literature on SAH was searched in MEDLINE. The author's personal files of all published literature on SAH were reviewed. References cited in Cochrane reviews as well as the published papers that were reviewed were also retrieved. There is no question that SAH causes what the authors have chosen to call “angiographic vasospasm.” However, the incidence and severity of vasospasm in recent series of patients is not well defined. There is reasonable evidence that vasospasm causes infarction, but again, accurate data on how severe and how diffuse vasospasm has to be to cause infarction and how often vasospasm is the primary cause of infarction are not available. There are good data on the incidence of cerebral infarction after SAH, and these data indicate that it is highly associated with poor outcome. The link between angiographic vasospasm and poor outcome is particularly poorly described in terms of what would be considered data of a high level of evidence. The question as to whether there is a clear pathway from SAH to vasospasm to cerebral infarction to poor outcome seems so obvious to neurosurgeons as to make it one not worth asking. Nevertheless, the obvious is not always true or accurate, so it is important to note that published literature only weakly supports the causative association of vasospasm with infarction and poor outcome after SAH. It behooves neurosurgeons to document this seemingly straightforward pathway with high-quality evidence acceptable to the proponents of evidence-based medicine.

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“…CT can detect clinically asymptomatic infarcts, particularly in patients with low GCS [69,70]. MRI can detect a larger proportion of asymptomatic infarcts compared to CT [71], and importantly the overall burden of infarcts is correlated with outcome [72,73].…”

Section: Vasospasm After Subarachnoid Hemorrhagementioning

confidence: 99%

Biomarkers in Neurocritical Care

Kimberly

2012

Neurotherapeutics

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The gold standard for assessing neurological function is the bedside clinical examination. However, in neurocritical patients, the signs and symptoms related to the severity of illness can often be ambiguous. It can be hard to distinguish between a severe but stable disease state and one that is dynamic and in a critical decline. Clinicians and family members alike may struggle with the uncertainty of functional outcome prediction. Intermediate biomarkers of brain injury can assist with ongoing clinical management of patients, and in some circumstances can guide prognosis. Used in the right setting, biomarkers in neurocritical care can also aid with decisions to intensify treatment or avoid prolonged and unnecessary therapy. The term biomarker is used in various ways, and here we use it to refer to 3 general types: 1) circulating blood macromolecules, 2) brain imaging, and 3) continuous invasive monitors. Despite its promise, biomarkers have several limitations and should be interpreted in the context of the overall clinical assessment.

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Asymptomatic versus Symptomatic Infarcts from Vasospasm in Patients with Subarachnoid Hemorrhage: Serial Magnetic Resonance Imaging

Cited by 123 publications

References 30 publications

Dissociation of Early and Delayed Cerebral Infarction After Aneurysmal Subarachnoid Hemorrhage

Dissociation of Early and Delayed Cerebral Infarction After Aneurysmal Subarachnoid Hemorrhage

Can angiographic vasospasm be used as a surrogate marker in evaluating therapeutic interventions for cerebral vasospasm?

Biomarkers in Neurocritical Care

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