Dataset Information

CSF Volumetric Analysis for Quantification of Cerebral Edema After Hemispheric Infarction.

ABSTRACT: BACKGROUND:Malignant cerebral edema (CED) complicates at least 20 % of large hemispheric infarcts (LHI) and may result in neurological deterioration or death. Midline shift (MLS) is a standard but crude measure of edema severity. We propose that volumetric analysis of shifts in cerebrospinal fluid (CSF) over time provides a reliable means of quantifying the spectrum of edema severity after LHI. METHODS:We identified 38 patients from 2008 to 2014 with NIHSS ?8, baseline CT <6 h after stroke onset, at least 1 follow-up (FU) CT, and no parenchymal hematoma. The volumes of CSF (sulci, ventricles, and cisterns) ipsilateral (IL) and contralateral (CL) to infarct on baseline and FU CTs were quantified by manually assisted outlining with MIPAV image analysis software, as was infarct volume and MLS on FU CTs. Percentage change in CSF volumes (?CSF) from baseline to FU scans was correlated with MLS and compared in those with vs. without malignant edema (defined as hemicraniectomy, osmotic therapy, or death/neurological deterioration with MLS ?5 mm). RESULTS:11 of 38 subjects (29 %) developed malignant edema. Neither baseline NIHSS nor CSF volume differed between those with and without edema (median NIHSS 18 vs. 13, p = 0.12, CSF volume 102 vs. 124 ml, p = 0.16). Inter-rater reliability for CSF measurements was excellent (intraclass correlation coefficient 0.97). ?CSF correlated strongly with MLS at peak edema (r = -0.75), even adjusting for infarct volume (p = 0.009). ?CSF was also greater in those with malignant edema [-55 % (IQR -49 to -62) vs. -36 % (-27 to -45), p = 0.004]. ?CSF was the greatest within IL sulci [-97 % (-86 to -99) vs. -71 % (-41 to -79), p = 0.002] but also significantly greater within CL sulci in those with malignant edema [-50 % (-29 to -65) vs. -25 % (0 to -31), p = 0.014]. More than half this CSF volume reduction occurred by the time of first FU CT around 24 h after stroke, while MLS rose later. CONCLUSIONS:Volumetric CSF analysis reliably quantifies CED and distinguishes those with malignant edema and MLS from those with a more benign course after LHI. ?CSF may provide an earlier and more sensitive indicator of edema severity across a broader dynamic range than MLS.

SUBMITTER: Dhar R

PROVIDER: S-EPMC4821820 | biostudies-literature | 2016 Jun

REPOSITORIES: biostudies-literature

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CSF Volumetric Analysis for Quantification of Cerebral Edema After Hemispheric Infarction.

Dhar Rajat R Yuan Kristy K Kulik Tobias T Chen Yasheng Y Heitsch Laura L An Hongyu H Ford Andria A Lee Jin-Moo JM

Neurocritical care 20160601 3

<h4>Background</h4>Malignant cerebral edema (CED) complicates at least 20 % of large hemispheric infarcts (LHI) and may result in neurological deterioration or death. Midline shift (MLS) is a standard but crude measure of edema severity. We propose that volumetric analysis of shifts in cerebrospinal fluid (CSF) over time provides a reliable means of quantifying the spectrum of edema severity after LHI.<h4>Methods</h4>We identified 38 patients from 2008 to 2014 with NIHSS ≥8, baseline CT <6 h aft ...[more]

PMID: 26438467

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Project description:Glyburide (also known as glibenclamide) is a second-generation sulfonylurea drug that inhibits sulfonylurea receptor 1 (Sur1) at nanomolar concentrations. Long used to target KATP (Sur1-Kir6.2) channels for the treatment of diabetes mellitus type 2, glyburide was recently repurposed to target Sur1-transient receptor potential melastatin 4 (Trpm4) channels in acute central nervous system injury. Discovered nearly two decades ago, SUR1-TRPM4 has emerged as a critical target in stroke, specifically in large hemispheric infarction, which is characterized by edema formation and life-threatening brain swelling. Following ischemia, SUR1-TRPM4 channels are transcriptionally upregulated in all cells of the neurovascular unit, including neurons, astrocytes, microglia, oligodendrocytes and microvascular endothelial cells. Work by several independent laboratories has linked SUR1-TRPM4 to edema formation, with blockade by glyburide reducing brain swelling and death in preclinical models. Recent work showed that, following ischemia, SUR1-TRPM4 co-assembles with aquaporin-4 to mediate cellular swelling of astrocytes, which contributes to brain swelling. Additionally, recent work linked SUR1-TRPM4 to secretion of matrix metalloproteinase-9 (MMP-9) induced by recombinant tissue plasminogen activator in activated brain endothelial cells, with blockade of SUR1-TRPM4 by glyburide reducing MMP-9 and hemorrhagic transformation in preclinical models with recombinant tissue plasminogen activator. The recently completed GAMES (Glyburide Advantage in Malignant Edema and Stroke) clinical trials on patients with large hemispheric infarctions treated with intravenous glyburide (RP-1127) revealed promising findings with regard to brain swelling (midline shift), MMP-9, functional outcomes and mortality. Here, we review key elements of the basic science, preclinical experiments and clinical studies, both retrospective and prospective, on glyburide in focal cerebral ischemia and stroke.

Project description:IntroductionLarge hemispheric infarction (LHI) can lead to fatal complications such as malignant brain edema (MBE). We aimed to investigate the correlation between heart-rate-to-blood-pressure ratios and MBE or one-month death after LHI.MethodsWe prospectively included LHI patients from a registered cohort. Hourly heart-rate-to-blood-pressure ratios were recorded as a variation of the traditional shock index (SI), SIs and SId (systolic and diastolic pressures, respectively), and calculated for mean and variability (standard deviation) in 24 h and two 12 h epochs (1-12 h and 13-24 h) after onset of symptoms. MBE was defined as neurological deterioration symptoms with imaging evidence of brain swelling. We employed a generalized estimating equation to compare the trend in longitudinal collected SIs and SId between patients with and without MBE. We used multivariate logistic regression to investigate the correlation between SIs, SId and outcomes.ResultsOf the included 162 LHI patients, 28.4% (46/162) developed MBE and 25.3% (40/158) died within one month. SIs and SId increased over baseline in all patients, with a similar ascending profile during the first 12 h epoch and a more intensive increase in the MBE group during the second 12 h epoch (p < 0.05). During the overall 24 h, patients with greater SId variability had a significantly increased MBE risk after adjustment (OR 3.72, 95%CI 1.38-10.04). Additionally, during the second 12 h epoch (13-24 h after symptom onset), patients developing MBE had a significantly higher SId level (OR 1.18, 95%CI 1.00-1.39) and greater SId variability (OR 3.16, 95%CI 1.35-7.40). Higher SId and greater SId variability within 24 h independently correlated with one-month death (all p < 0.05). Within the second 12 h epoch, higher SIs, higher SId and greater SId variability independently correlated with one-month death (all p < 0.05). No significant correlation was observed in the first 12 h epoch.ConclusionsHigher and more fluctuated heart-rate-to-blood-pressure ratios independently correlated with MBE development and one-month death in LHI patients, especially during the second 12 h (13-24 h) epoch after onset.

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Project description:Research in sickle cell anemia (SCA) has used, with limited race-matched control data, binary categorization of patients according to the presence or absence of silent cerebral infarction (SCI). SCI have primarily been identified using low-resolution MRI, with radiological definitions varying in lesion length and the requirement for abnormality on both fluid attenuated inversion recovery (FLAIR) and T1-weighted images. We aimed to assess the effect of published SCI definitions on global, regional, and lobar lesion metrics and their value in predicting cognition. One hundred and six patients with SCA and 48 controls aged 8–30 years underwent 3T MRI with a high-resolution FLAIR sequence and Wechsler cognitive assessment. Prevalence, number, and volume of lesions were calculated using a semi-automated pipeline for SCI defined as: (1) Liberal: any length (L-SCI); (2) Traditional: >3 mm in greatest dimension (T-SCI); (3) Restrictive; >3 mm in greatest dimension with a corresponding T1-weighted hypo-intensity (R-SCI). Globally, as hypothesized, there were large effects of SCI definition on lesion metrics in patients and controls, with prevalence varying from 24–42% in patients, and 4–23% in controls. However, contrary to hypotheses, there was no effect of any global metric on cognition. Regionally, there was a consistent distribution of SCI in frontal and parietal deep and juxta-cortical regions across definitions and metrics in patients, but no consistent distribution in controls. Effects of regional SCI metrics on cognitive performance were of small magnitude; some were paradoxical. These findings expose the challenges associated with the widespread use of SCI presence as a biomarker of white-matter injury and cognitive dysfunction in cross-sectional high-resolution MRI studies in patients with SCA. The findings indicate that with high-resolution MRI: (1) radiological definitions have a large effect on resulting lesion groups, numbers, and volumes; (2) there is a non-negligible prevalence of lesions in young healthy controls; and (3) at the group-level, there is no cross-sectional association between global lesion metrics and general cognitive impairment irrespective of lesion definition and metric. With high-resolution multi-modal MRI, the dichotomy of presence or absence of SCI does not appear to be a sensitive biomarker for the detection of functionally significant pathology; the search for appropriate endpoints for clinical treatment trials should continue.

Dataset Information

CSF Volumetric Analysis for Quantification of Cerebral Edema After Hemispheric Infarction.

Publications

CSF Volumetric Analysis for Quantification of Cerebral Edema After Hemispheric Infarction.

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