Spreading of Vasogenic Edema and Cytotoxic Edema Assessed by Quantitative Diffusion and T2 Magnetic Resonance Imaging

Loubinoux, Isabelle; Volk, Andreas; Borredon, Josiane; Guirimand, S.; Tiffon, Bernard; Seylaz, Jacques; Méric, P.

doi:10.1161/01.str.28.2.419

Cited by 182 publications

(151 citation statements)

References 45 publications

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“…This assumption is supported by previous studies, which show that in humans the maximum evolution of vasogenic edema culminates at 24 to 48 hours (28). On the contrary, the vasogenic edema contribution in the first seven hours was found to be negligible in rats (20).…”

Section: Discussionsupporting

confidence: 81%

“…On the contrary, the vasogenic edema contribution in the first seven hours was found to be negligible in rats (20). The spread of ADC would thus stop at approximately seven hours and any further increase in volume would mainly be due to edematous swelling (28). These results in animals need to be clarified in human experiments, but measures of the DWI volume clearly must take into account the expansion of vasogenic edema, especially during the first 24 hours.…”

Section: Discussionmentioning

confidence: 93%

“…The increase in lesion growth is possibly due to a persistent active ischemic process, but opinions about the time of lesion extent are discordant. Some animal experiments reported a limited ischemic evolution in the first hours after stroke onset (28), but other studies that reported a persistence of mismatch after 24 hours suggest a longer extent of the growing time process (29,30).…”

Section: Discussionmentioning

confidence: 99%

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Evolution of lesion volume in acute stroke treated by intravenous t‐PA

Pialat

Wiart

Nighoghossian

et al. 2005

Magnetic Resonance Imaging

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Purpose:To determine the evolution of the ischemic lesion volumes in a population treated with tissue plasminogen activator (t-PA), MRIs were performed before treatment and 24 hours later; final infarct size was evaluated 60 days later. Materials and Methods:A total of 42 patients with hemispheric stroke were recruited for a thrombolytic study. Intravenous t-PA was given after MRI within the first seven hours after stroke onset. Volumes were evaluated on day 0 and day 1 with diffusion-weighted imaging (DWI), on day 60 with T2-weighted imaging (T2WI), and recanalization was assessed based on day 1 MR angiography (MRA).Results: Lesion volume increased between day 0 and day 1, and decreased between day 1 and day 60. It was lower in the group of patients with recanalization on day 1 MRA. Conclusion:Volume analysis emphasizes the effectiveness of recanalization as a predictive factor for better outcome, based on final infarct size. The decrease in lesion volumes between day 1 and day 60 suggests that other factors leads to overestimation of day 1 abnormal diffusion volume. This could explain the delayed partial reversibility of the DWI abnormality.

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Section: Discussionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Evolution of lesion volume in acute stroke treated by intravenous t‐PA

Pialat

Wiart

Nighoghossian

et al. 2005

Magnetic Resonance Imaging

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show abstract

“…Although we utilized a model of a focal ischemic insult, in which the cytotoxic edema appears to be predominant (Dijkhuizen et al, 1999;Loubinoux et al, 1997), it is possible that a vasogenic component of edema was also present. Studies of brain edema have shown that the BBB remains intact during the first 6 h following MCA occlusion and reperfusion (Hatashita et al, 1988;Iannotti and Hoff, 1983).…”

mentioning

confidence: 99%

The Protein Kinase C Activator Phorbol Myristate Acetate Decreases Brain Edema by Aquaporin 4 Downregulation after Middle Cerebral Artery Occlusion in the Rat

Fazzina

Amorini

Marmarou

et al. 2010

Journal of Neurotrauma

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The protein kinase C activator phorbol 12-myristate 13-acetate (PMA) is known to interact with aquaporin 4 (AQP 4), a water-selective transporting protein that is abundant in astrocytes, and has experimentally been found to decrease osmotically-induced cell swelling. The purpose of this study was to examine whether PMA reduces brain edema following focal ischemia induced by middle cerebral artery (MCA) occlusion by modulation of AQP4 expression. Male Sprague-Dawley rats were randomly assigned to either sham surgery (n ¼ 6), or a continuous intravenous infusion of vehicle (1% dimethylsulfoxide), followed by MCA occlusion (n ¼ 18), and administration of PMA at 50 mg=kg (n ¼ 6) or at 200 mg=kg (n ¼ 6) starting 60 min before or 30 min (200 mg=kg; n ¼ 6) or 60 min (200 mg=kg; n ¼ 6) after MCA occlusion. Cerebral blood flow was monitored with laser Doppler over the MCA territory, and confirmed a 70% reduction during occlusion. After a 2-h period of ischemia and 2 h of reperfusion, the animals were sacrificed for assessment of brain water content and sodium and potassium concentration. AQP4 expression was assessed by immunoblotting and quantified by densitometry (n ¼ 24). Statistical analysis was performed by ANOVA followed by Tukey's post-hoc test. PMA treatment at 200 mg=kg significantly reduced brain water concentration in the infarcted area when started 60 min before or 30 min after occlusion ( p < 0.001 and p ¼ 0.022, respectively), and prevented the subsequent sodium shift ( p < 0.05). PMA normalized the AQP4 upregulation in ischemia ( p ¼ 0.021). A downregulation of AQP4 in the ischemic area paralleling the reduction in brain edema formation following PMA treatment suggests that the effect was mediated by AQP4 modulation.

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“…Correction for edema-induced midline shift in hemispherical volume was incorporated into infarct volume calculations as described previously. 2,20 Neurobehavioral Assessment Neurobehavioral assessment was performed by a neurologic interventional radiologist before the procedure at 24 h and 7 days following embolization. A simple 12-point canine neurobehavior scoring system (Table 1), including assessments of motor function, consciousness, head turning, circling and hemianopsia, was adapted for the canine ischemic stroke models.…”

Section: Mr Scanningmentioning

confidence: 99%

An endovascular canine stroke model: middle cerebral artery occlusion with autologous clots followed by ipsilateral internal carotid artery blockade

Liu

et al. 2013

Laboratory Investigation

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Stroke is one of the leading causes of death worldwide and the main reason for long-term disability. An appropriate animal model of stroke is urgently required for understanding the exact pathophysiological mechanism of stroke and testing any new therapeutic regimen. Our work aimed to establish a canine stroke model occluding the middle cerebral artery (MCA) and blocking the ipsilateral internal carotid artery (ICA), and to assess the infarct lesions by magnetic resonance imaging. The stroke model was generated by injecting two autologous clots into each MCA, followed by 2-h ipsilateral ICA blockade (ilICAB) using a catheter in 15 healthy adult beagles. Outcome measurements included 24-h and 7-day postocclusion T2-weighted imaging (T2WI)-based infarct volume calculation. In addition, pial collateral score, canine neurobehavioral score and histopathologic results were documented. Out of 15 dogs, 12 with successful MCA occlusion (MCAO) and ilICAB survived 7 days without complications or casualties and MCA were reperfused at 7 days after occlusion. High signal intensity in the basal ganglia and cerebral cortex on T2WI was initially observed in each dog at 6 h after the procedure. The mean percentage hemispherical infarct volume corrected for edema in all dogs on T2WI at 24 h after occlusion was 12.99 ± 1.57%, and the degree of variability was 12.08%. The infarct volumes at 24 h after occlusion correlated with pial collateral scores and canine neurobehavioral scores well. This canine stroke model with combined MCAO and ilICAB reported here were proven to be highly feasible and reproducible.

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Spreading of Vasogenic Edema and Cytotoxic Edema Assessed by Quantitative Diffusion and T2 Magnetic Resonance Imaging

Cited by 182 publications

References 45 publications

Evolution of lesion volume in acute stroke treated by intravenous t‐PA

Evolution of lesion volume in acute stroke treated by intravenous t‐PA

The Protein Kinase C Activator Phorbol Myristate Acetate Decreases Brain Edema by Aquaporin 4 Downregulation after Middle Cerebral Artery Occlusion in the Rat

An endovascular canine stroke model: middle cerebral artery occlusion with autologous clots followed by ipsilateral internal carotid artery blockade

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