Radiation Exposure Prior to Ischemia Decreases Lesion Volume, Brain Edema and Cell Death

2009 ◽  
pp. 51-53 ◽  
Author(s):  
E. Titova ◽  
A. Adami ◽  
R. Ostrowski ◽  
S. Lalas ◽  
R. Vlkolinsky ◽  
...  
Keyword(s):  
Cell Death ◽  
Radiation Exposure ◽  
Brain Edema ◽  
Lesion Volume

Abstract WP47: Reperfusion Following Ischemic Stroke is Associated with Reduced Brain Edema

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Hannah J Irvine ◽  
Thomas W Battey ◽  
Ann-Christin Ostwaldt ◽  
Bruce C Campbell ◽  
Stephen M Davis ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Brain Edema ◽  
Infarct Volume ◽  
Brain Magnetic Resonance Imaging ◽  
Lesion Volume ◽  
Stroke Patients ◽  
Early Reperfusion ◽  
Echoplanar Imaging ◽  
Swelling Volume

Introduction: Revascularization is a robust therapy for acute ischemic stroke, but animal studies suggest that reperfusion edema may attenuate its beneficial effects. In stroke patients, early reperfusion consistently reduces infarct volume and improves long-term functional outcome, but there is little clinical data available regarding reperfusion edema. We sought to elucidate the relationship between reperfusion and brain edema in a patient cohort of moderate to severe stroke. Methods: Seventy-one patients enrolled in the Echoplanar Imaging Thrombolysis Evaluation Trial (EPITHET) with serial brain magnetic resonance imaging and perfusion-weighted imaging (PWI) were analyzed. Reperfusion percentage was calculated based on the difference in PWI lesion volume at baseline and follow-up (day 3-5). Midline shift (MLS) was measured on the day 3-5 fluid attenuated inversion recovery (FLAIR) sequence. Swelling volume and infarct growth volume were assessed using region-of-interest analysis on the baseline and follow-up DWI scans based on our prior methods. Results: Greater percentage of reperfusion was associated with less MLS (Spearman ρ = -0.46; P <0.0001) and reduced swelling volume (Spearman ρ = -0.56; P <0.0001). In multivariate analysis, reperfusion was an independent predictor of less MLS ( P <0.006) and decreased swelling volume ( P <0.0054), after adjusting for age, baseline NIHSS, admission blood glucose, baseline DWI volume, and IV tPA treatment. Conclusions: Reperfusion is associated with reduced brain edema as measured by MLS and swelling volume. While our data do not exclude the possibility of reperfusion edema in certain circumstances, in stroke patients, reperfusion following acute stroke is predominantly linked to less brain swelling.

scholarly journals Butin attenuates brain edema in a rat model of intracerebral hemorrhage by anti inflammatory pathway

2018 ◽  
Vol 9 (1) ◽  
pp. 7-12 ◽  
Author(s):  
Peiyu Li ◽  
Cheng Jiwu
Keyword(s):  
Intracerebral Hemorrhage ◽  
Brain Edema ◽  
Treated Group ◽  
Control Group ◽  
Lesion Volume ◽  
Dependent Manner ◽  
Neurological Score ◽  
Factor Α ◽  
The Brain ◽  
Brain Tissues

Abstract Background This study evaluates the effect of butin against brain edema in intracerebral hemorrhage (ICH). Methodology ICH was induced by injecting bacterial collagenase in the brain and all the animals were separated into four groups such as control group, ICH group treated with vehicle, Butin 25 and 50 mg/kg group receives butin (25 and 50 mg/kg, i.p.)60 min after the induction of ICH in all animals. One day after neurological score, hemorrhagic injury and expressions of protein responsible for apoptosis and inflammatory cytokines were assessed in the brain tissue of ICH rats. Result Neurological scoring significantly increased and hemorrhagic lesion volume decreased in butin treated group of rats compared to ICH group. However, treatment with butin significantly decreases the ratio of Bax/Bcl-2 and protein expression of Cleaved caspase-3 than ICH group in dose dependent manner. Level of inflammatory mediators such as tumor necrosis factor-α (TNF-α) and interlukin-6 (IL-6) in the brain tissues were significantly decreased in the butin treated group than ICH group. In addition butin attenuates the altered signaling pathway of NF-κB in the brain tissues of ICH rats. Conclusion Our study concludes that butin attenuates the altered behavior and neuronal condition in ICH rats by reducing apoptosis and inflammatory response.

Ferroptosis, a new form of cell death defined after radiation exposure

2022 ◽  
pp. 1-9
Author(s):  
Xiaohong Zhang ◽  
Xin Li ◽  
Chunyan Zheng ◽  
Chunzhi Yang ◽  
Rui Zhang ◽  
...  
Keyword(s):  
Cell Death ◽  
Radiation Exposure ◽  
New Form

scholarly journals Celecoxib Induces Functional Recovery after Intracerebral Hemorrhage with Reduction of Brain Edema and Perihematomal Cell Death

2004 ◽  
Vol 24 (8) ◽  
pp. 926-933 ◽  
Author(s):  
Kon Chu ◽  
Sang-Wuk Jeong ◽  
Keun-Hwa Jung ◽  
So-Young Han ◽  
Soon-Tae Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
Intracerebral Hemorrhage ◽  
Brain Edema ◽  
Functional Recovery ◽  
Autologous Blood ◽  
Prostaglandin E ◽  
Dependent Manner ◽  
Behavioral Tests ◽  
Adult Rats ◽  
Cox 2

The selective cyclooxygenase-2 (COX-2) inhibitor has been reported to have antiinflammatory, neuroprotective, and antioxidant effects in ischemia models. In this study, the authors examined whether a selective COX-2 inhibitor (celecoxib) reduces cerebral inflammation and edema after intracerebral hemorrhage (ICH), and whether functional recovery is sustained with longer treatment. ICH was induced using collagenase in adult rats. Celecoxib (10 or 20 mg/kg) was administered intraperitoneally 20 minutes, 6 hours, and 24 hours after ICH and then daily thereafter. Seventy-two hours after ICH induction, the rats were killed for histologic assessment and measurement of brain edema and prostaglandin E2. Behavioral tests were performed before and 1, 7, 14, 21, and 28 days after ICH. The brain water content of celecoxib-treated rats decreased both in lesioned and nonlesioned hemispheres in a dose-dependent manner. Compared with the ICH-only group, the number of TUNEL-positive, myeloperoxidase-positive, or OX42-positive cells was decreased in the periphery of hematoma and brain prostaglandin E2 level was reduced in the celecoxib-treated group. Celecoxib-treated rats recovered better by the behavioral tests at 7 days after ICH throughout the 28-day period, and the earlier the drug was administered, the better the functional recovery. Evidence of similar effects in an autologous blood–injected model showed that direct collagenase toxicity was not the major cause of inflammation or cell death. These data suggest that celecoxib treatment after ICH reduces prostaglandin E2 production, brain edema, inflammation, and perihematomal cell death in the perihematomal zone and induces better functional recovery.

Attenuated neurological deficit, cell death and lesion volume in Fas-mutant mice is associated with altered neuroinflammation following traumatic brain injury

2011 ◽  
Vol 1414 ◽  
pp. 94-105 ◽  
Author(s):  
Jenna M. Ziebell ◽  
Nicole Bye ◽  
Bridgette D. Semple ◽  
Thomas Kossmann ◽  
Maria Cristina Morganti-Kossmann
Keyword(s):  
Traumatic Brain Injury ◽  
Cell Death ◽  
Brain Injury ◽  
Neurological Deficit ◽  
Mutant Mice ◽  
Lesion Volume

scholarly journals The Dichotomy of Memantine Treatment for Ischemic Stroke: Dose-Dependent Protective and Detrimental Effects

2014 ◽  
Vol 35 (2) ◽  
pp. 230-239 ◽  
Author(s):  
Melissa Trotman ◽  
Philipp Vermehren ◽  
Claire L Gibson ◽  
Robert Fern
Keyword(s):  
Cell Death ◽  
Ischemic Stroke ◽  
Focal Cerebral Ischemia ◽  
Recovery Period ◽  
Behavioral Outcomes ◽  
Lesion Volume ◽  
Low Doses ◽  
Memantine Treatment ◽  
Patients At Risk ◽  
Higher Doses

Excitotoxicity is a major contributor to cell death during the acute phase of ischemic stroke but aggressive pharmacological targeting of excitotoxicity has failed clinically. Here we investigated whether pretreatment with low doses of memantine, within the range currently used and well tolerated for the treatment of Alzheimer's disease, produce a protective effect in stroke. A coculture preparation exposed to modeled ischemia showed cell death associated with rapid glutamate rises and cytotoxic Ca2+ influx. Cell death was significantly enhanced in the presence of high memantine concentrations. However, low memantine concentrations significantly protected neurons and glia via excitotoxic cascade interruption. Mice were systemically administered a range of memantine doses (0.02, 0.2, 2, 10, and 20 mg/kg/day) starting 24 hours before 60 minutes reversible focal cerebral ischemia and continuing for a 48-hour recovery period. Low dose (0.2 mg/kg/day) memantine treatment significantly reduced lesion volume (by 30% to 50%) and improved behavioral outcomes in stroke lesions that had been separated into either small/striatal or large/striatocortical infarcts. However, higher doses of memantine (20 mg/kg/day) significantly increased injury. These results show that clinically established low doses of memantine should be considered for patients ‘at risk’ of stroke, while higher doses are contraindicated.

scholarly journals Reperfusion after ischemic stroke is associated with reduced brain edema

2017 ◽  
Vol 38 (10) ◽  
pp. 1807-1817 ◽  
Author(s):  
Hannah J Irvine ◽  
Ann-Christin Ostwaldt ◽  
Matthew B Bevers ◽  
Simone Dixon ◽  
Thomas WK Battey ◽  
...  
Keyword(s):  
Brain Edema ◽  
Animal Studies ◽  
Lesion Size ◽  
Lesion Volume ◽  
Modest Improvement ◽  
Beneficial Effects ◽  
Echoplanar Imaging ◽  
The Difference ◽  
Swelling Volume

Rapid revascularization is highly effective for acute stroke, but animal studies suggest that reperfusion edema may attenuate its beneficial effects. We investigated the relationship between reperfusion and edema in patients from the Echoplanar Imaging Thrombolysis Evaluation Trial (EPITHET) and Mechanical Retrieval and Recanalization of Stroke Clots Using Embolectomy (MR RESCUE) cohorts. Reperfusion percentage was measured as the difference in perfusion-weighted imaging lesion volume between baseline and follow-up (day 3–5 for EPITHET; day 6–8 for MR RESCUE). Midline shift (MLS) and swelling volume were quantified on follow-up MRI. We found that reperfusion was associated with less MLS (EPITHET: Spearman ρ = −0.46; P < 0.001, and MR RESCUE: Spearman ρ = −0.49; P < 0.001) and lower swelling volume (EPITHET: Spearman ρ = −0.56; P < 0.001, and MR RESCUE: Spearman ρ = −0.27; P = 0.026). Multivariable analyses performed in EPITHET and MR RESCUE demonstrated that reperfusion independently predicted both less MLS (ß coefficient = −0.056; P = 0.025, and ß coefficient = −0.38; P = 0.028, respectively) and lower swelling volumes (ß coefficient = −4.7; P = 0.007, and ß coefficient = −10.7; P = 0.009, respectively), after adjusting for age, sex, NIHSS, admission glucose and follow-up lesion size. Taken together, our data suggest that even modest improvement in perfusion is associated with less brain edema in EPITHET and MR RESCUE.

scholarly journals Release of Bradykinin and Expression of Kinin B2 Receptors in the Brain: Role for Cell Death and Brain Edema Formation After Focal Cerebral Ischemia in Mice

2005 ◽  
Vol 25 (8) ◽  
pp. 978-989 ◽  
Author(s):  
Moritz Gröger ◽  
Diane Lebesgue ◽  
Didier Pruneau ◽  
Jane Relton ◽  
Seong-Woong Kim ◽  
...  
Keyword(s):  
Cell Death ◽  
Cerebral Ischemia ◽  
Brain Edema ◽  
Brain Damage ◽  
Receptor Expression ◽  
Experimental Stroke ◽  
Edema Formation ◽  
Receptor Mrna ◽  
The Brain ◽  
Brain Edema Formation

Pharmacological studies using bradykinin B2 receptor antagonists suggest that bradykinin, an early mediator of inflammation and the main metabolite of the kallikrein-kinin system, is involved in secondary brain damage after cerebral ischemia. However, the time-course of bradykinin production and kinin receptor expression as well as the conclusive role of bradykinin B2 receptors for brain damage after experimental stroke have not been elucidated so far. C57/Bl6 mice were subjected to 45 mins of middle cerebral artery occlusion (MCAO) and 2, 4, 8, 24, and 48 h later brains were removed for the analysis of tissue bradykinin concentration and kinin B2 receptor mRNA and protein expression. Brain edema, infarct volume, functional outcome, and long-term survival were assessed in WT and B2−/− mice 24 h or 7 days after MCAO. Tissue bradykinin was maximally increased 12 h after ischemia (three-fold), while kinin B2 receptor mRNA upregulation peaked 24 to 48 h after MCAO (10- to 12-fold versus naïve brain tissue). Immunohistochemistry revealed that kinin B2 receptors were constitutively and widely expressed in mouse brain, were upregulated 2 h after ischemia in cells showing signs of ischemic damage, and remained upregulated in the penumbra up to 24 h after ischemia. B2−/− mice had improved motor function ( P<0.05), smaller infarct volumes (–38%; P<0.01), developed less brain edema (–87%; P<0.05), and survived longer ( P<0.01) as compared with wild-type controls. The current results show that bradykinin is produced in the brain, kinin B2 receptors are upregulated on dying cells, and B2 receptors are involved in cell death and brain edema formation after experimental stroke.

Establishment of novel technical methods for evaluating brain edema and lesion volume in stroked rats: A standardization of measurement procedures

2019 ◽  
Vol 1718 ◽  
pp. 12-21 ◽  
Author(s):  
Matthew Boyko ◽  
Vladislav Zvenigorodsky ◽  
Julia Grinshpun ◽  
Honore N. Shiyntum ◽  
Israel Melamed ◽  
...  
Keyword(s):  
Brain Edema ◽  
Lesion Volume

scholarly journals A systematic evaluation of intraoperative white matter tract shift in pediatric epilepsy surgery using high-field MRI and probabilistic high angular resolution diffusion imaging tractography

2017 ◽  
Vol 19 (5) ◽  
pp. 592-605 ◽  
Author(s):  
Joseph Yuan-Mou Yang ◽  
Richard Beare ◽  
Marc L. Seal ◽  
A. Simon Harvey ◽  
Vicki A. Anderson ◽  
...  
Keyword(s):  
White Matter ◽  
Brain Edema ◽  
Angular Resolution ◽  
Diffusion Imaging ◽  
Head Rotation ◽  
High Angular Resolution ◽  
Lesion Volume ◽  
White Matter Tract ◽  
The Third ◽  
The Impact

OBJECTIVECharacterization of intraoperative white matter tract (WMT) shift has the potential to compensate for neuronavigation inaccuracies using preoperative brain imaging. This study aimed to quantify and characterize intraoperative WMT shift from the global hemispheric to the regional tract-based scale and to investigate the impact of intraoperative factors (IOFs).METHODSHigh angular resolution diffusion imaging (HARDI) diffusion-weighted data were acquired over 5 consecutive perioperative time points (MR1 to MR5) in 16 epilepsy patients (8 male; mean age 9.8 years, range 3.8–15.8 years) using diagnostic and intraoperative 3-T MRI scanners. MR1 was the preoperative planning scan. MR2 was the first intraoperative scan acquired with the patient's head fixed in the surgical position. MR3 was the second intraoperative scan acquired following craniotomy and durotomy, prior to lesion resection. MR4 was the last intraoperative scan acquired following lesion resection, prior to wound closure. MR5 was a postoperative scan acquired at the 3-month follow-up visit. Ten association WMT/WMT segments and 1 projection WMT were generated via a probabilistic tractography algorithm from each MRI scan. Image registration was performed through pairwise MRI alignments using the skull segmentation. The MR1 and MR2 pairing represented the first surgical stage. The MR2 and MR3 pairing represented the second surgical stage. The MR3 and MR4 (or MR5) pairing represented the third surgical stage. The WMT shift was quantified by measuring displacements between a pair of WMT centerlines. Linear mixed-effects regression analyses were carried out for 6 IOFs: head rotation, craniotomy size, durotomy size, resected lesion volume, presence of brain edema, and CSF loss via ventricular penetration.RESULTSThe average WMT shift in the operative hemisphere was 2.37 mm (range 1.92–3.03 mm) during the first surgical stage, 2.19 mm (range 1.90–3.65 mm) during the second surgical stage, and 2.92 mm (range 2.19–4.32 mm) during the third surgical stage. Greater WMT shift occurred in the operative than the nonoperative hemisphere, in the WMTs adjacent to the surgical lesion rather than those remote to it, and in the superficial rather than the deep segment of the pyramidal tract. Durotomy size and resection size were significant, independent IOFs affecting WMT shift. The presence of brain edema was a marginally significant IOF. Craniotomy size, degree of head rotation, and ventricular penetration were not significant IOFs affecting WMT shift.CONCLUSIONSWMT shift occurs noticeably in tracts adjacent to the surgical lesions, and those motor tracts superficially placed in the operative hemisphere. Intraoperative probabilistic HARDI tractography following craniotomy, durotomy, and lesion resection may compensate for intraoperative WMT shift and improve neuronavigation accuracy.

Sign in / Sign up

Export Citation Format

Share Document