Moseley ME, Cohen Y, Mintorovitch J, Chileuitt L, Shimizu H, Kucharczyk J, Wendland MF, Weinstein PREarly detection of regional cerebral ischemia in cats: comparison of diffusion-and T2-weighted MRI and spectroscopy. Magn Reson Med 14:330-346
Department of Radiology, University of California, San Francisco 94143. Magnetic Resonance in Medicine
(Impact Factor: 3.57).
05/1990; 14(2):330-46. DOI: 10.1002/mrm.1910140218
Diffusion-weighted MR images were compared with T2-weighted MR images and correlated with 1H spin-echo and 31P MR spectroscopy for 6-8 h following a unilateral middle cerebral and bilateral carotid artery occlusion in eight cats. Diffusion-weighted images using strong gradient strengths (b values of 1413 s/mm2) displayed a significant relative hyperintensity in ischemic regions as early as 45 min after onset of ischemia whereas T2-weighted spin-echo images failed to clearly demonstrate brain injury up to 2-3 h postocclusion. Signal intensity ratios (SIR) of ischemic to normal tissues were greater in the diffusion-weighted images at all times than in either TE 80 or TE 160 ms T2-weighted MR images. Diffusion- and T2-weighted SIR did not correlate for the first 1-2 h postocclusion. Good correlation was found between diffusion-weighted SIR and ischemic disturbances of energy metabolism as detected by 31P and 1H MR spectroscopy. Diffusion-weighted hyperintensity in ischemic tissues may be temperature-related, due to rapid accumulation of diffusion-restricted water in the intracellular space (cytotoxic edema) resulting from the breakdown of the transmembrane pump and/or to microscopic brain pulsations.
Available from: Arik Eisenkraft
- "It was shown that following seizure initiation there are prominent pathological changes in brain tissue including pronounced perineuronal and perivascular edema as well as swelling of astrocytes (McDonough and Shih, 1997; Petras, 1994). T2- weighted magnetic resonance imaging (MRI) and diffusionweighted MRI (DWI) are particularly sensitive to recognize areas of cerebral edema (Brant-Zawadzki et al., 1987; Moseley et al., 1990). T2 prolongation and reduced apparent diffusion coefficient, ADC, were found in brain tissue of rats exposed to the OP soman. "
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ABSTRACT: Magnetic resonance (MR) imaging is a sensitive modality for demonstrating in-vivo alterations in brain structure and function after acute organophosphate (OP) poisoning. The goals of this study were to explore early imaging findings in organophosphate-poisoned animals, to assess the efficacy of centrally acting antidotes and to find whether early MR findings can predict post-poisoning cognitive dysfunction.
Sprague-Dawley rats were poisoned with the agricultural OP paraoxon and were treated with immediate atropine and obidoxime (ATOX) to reduce acute mortality caused by peripheral inhibition of acetylcholinesterase. Animals were randomly divided into three groups based on the protocol of centrally acting antidotal treatment: group 1- no central antidotal treatment (n=10); group 2- treated with midazolam (MID) at 30minutes after poisoning (n=9), group 3-treated with a combination of MID and scopolamine (SCOP) at 30minutes after poisoning (n= 9) and controls (n=6). Each animal had a brain MR examination 3 and 24hours after poisoning. Each MR examination included the acquisition of a T2 map and a single-voxel (1)H-MR spectroscopy (localized on the thalami, to measure total creatine [Cr], N-acetyl-aspartate [NAA] and cholines [Cho] levels). Eleven days after poisoning each animal underwent a Morris Water Maze to assess hippocampal learning. Eighteen days after poisoning, animals were euthanized, and their brains were dissected, fixed and processed for histology.
All paraoxon poisoned animals developed generalized convulsions, starting within a few minutes following paraoxon injection. Brain edema was maximal on MR imaging 3hours after poisoning. Both MID and MID+SCOP prevented most of the cortical edema, with equivalent efficacy. Brain metabolic dysfunction, manifested as decreased NAA/Cr, appeared in all poisoned animals as early as 3hours after exposure (1.1±0.07 and 1.42±0.05 in ATOX and control groups, respectively) and remained lower compared to non-poisoned animals even 24hours after poisoning. MID and MID+SCOP prevented much of the 3hours NAA/Cr decrease (1.22±0.05 and 1.32±0.1, respectively). Significant correlations were found between imaging findings (brain edema and spectroscopic changes) and clinical outcomes (poor learning, weight loss and pathological score) with correlation coefficients of 0.4-0.75 (p<0.05).
MR imaging is a sensitive modality to explore organophosphate-induced brain damage. Delayed treatment with midazolam with or without scopolamine provides only transient neuroprotection with some advantage in adding scopolamine. Early imaging findings were found to correlate with clinical consequences of organophosphate poisoning and could be potentially used in the future to predict long-term prognosis of poisoned casualties.
Copyright © 2015. Published by Elsevier B.V.
NeuroToxicology 04/2015; 48. DOI:10.1016/j.neuro.2015.04.003 · 3.38 Impact Factor
- "BBB disruption in mdx mice due to reduced expression of tight junction proteins has been reported previously (Nico et al., 2003). Consequently, the osmotic influx of water into the cell causes cellular edema and a decrease in extracellular space, leading to a decrease in ADC (Kucharczyk et al., 1991; Moseley et al., 1990). While it has been shown that aqp4 facilitates the clearance of vasogenic edema as a result of BBB disruption (Papadopoulos et al., 2004), the lack of properly functioning aqp4 channels at the BBB in mdx mice (Adams et al., 2008; Frigeri et al., 2001) may prevent the removal of water from the cerebrum and therefore worsen cellular edema. "
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ABSTRACT: Dystrophin, the main component of the dystrophin–glycoprotein complex, plays an important role in maintaining the structural integrity of cells. It is also involved in the formation of the blood–brain barrier (BBB). To elucidate the impact of dystrophin disruption in vivo, we characterized changes in cerebral perfusion and diffusion in dystrophin-deficient mice (mdx) by magnetic resonance imaging (MRI). Arterial spin labeling (ASL) and diffusion-weighted MRI (DWI) studies were performed on 2-month-old and 10-month-old mdx mice and their age-matched wild-type controls (WT). The imaging results were correlated with Evan's blue extravasation and vascular density studies. The results show that dystrophin disruption significantly decreased the mean cerebral diffusivity in both 2-month-old (7.38 ± 0.30 × 10- 4 mm2/s) and 10-month-old (6.93 ± 0.53 × 10- 4 mm2/s) mdx mice as compared to WT (8.49 ± 0.24 × 10- 4, 8.24 ± 0.25 × 10- 4 mm2/s, respectively). There was also an 18% decrease in cerebral perfusion in 10-month-old mdx mice as compared to WT, which was associated with enhanced arteriogenesis. The reduction in water diffusivity in mdx mice is likely due to an increase in cerebral edema or the existence of large molecules in the extracellular space from a leaky BBB. The observation of decreased perfusion in the setting of enhanced arteriogenesis may be caused by an increase of intracranial pressure from cerebral edema. This study demonstrates the defects in water handling at the BBB and consequently, abnormal perfusion associated with the absence of dystrophin.
NeuroImage 11/2014; 102(0 2). DOI:10.1016/j.neuroimage.2014.08.053 · 6.36 Impact Factor
Available from: Qiang Shen
- "Perfusionweighted MRI can measure cerebral blood flow (CBF) at the tissue level, allowing for the detection of tissue with reduced perfusion that is at risk of ischemic brain injury. Diffusionweighted MRI (DWI), which measures water motion, is very sensitive to early ischemic brain injury in contrast to computed tomography and T2 MRI (Moseley et al., 1990). As such DWI has become the method of choice for early detection of ischemic brain injury. "
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ABSTRACT: Stroke is a leading cause of morbidity and mortality in the world. Low-dose methylene blue (MB), which has been used safely to treat methemoglobinemia and cyanide poisoning in humans, has energy enhancing and antioxidant properties. We tested the hypothesis that methylene blue treatment delays progression of at-risk tissue (ca. perfusion-diffusion mismatch) to infarct in permanent middle cerebral artery occlusion in rats at two MB treatment doses. Serial MRI was used to evaluate MB treatment efficacy. The major findings were: (i) MB significantly prolonged the perfusion-diffusion mismatch, (ii) MB mildly increased the CBF in the hypoperfused tissue, (iii) MB did not change the final infarct volume in permanent ischemic stroke, and (iv) there were no dose-dependent effects on mismatch progression for the 1 and 3 mg/kg doses studied. This neuroprotective effect is likely the result of sustained ATP production and increased CBF to tissue at risk. This work has the potential to readily lead to clinical stroke trials given MB's excellent safety profile.
Brain Research 09/2014; 1588. DOI:10.1016/j.brainres.2014.09.007 · 2.84 Impact Factor
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