Early detection of regional cerebral ischemia in cats: Comparison of diffusion- and T2-weighted MRI and spectroscopy
ABSTRACT 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.
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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; DOI:10.1016/j.neuro.2015.04.003 · 3.05 Impact Factor
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ABSTRACT: It is significantly important to define brain death with greater precision in terms of timing and accuracy. While in the past determination of brain death is simply based on conventional angiography, now with major technological advances the Diffusion-weighted MRI is a new method sensitive to cerebral ischemia which gives on the molecular level the deeply ischemic nature of the changes. Its value in brain death has been shown in various studies. In our study, we did a comparative overview of diffusion-weighted imaging (DWI) with and magnetic resonance angiography (MRA) considering the contribution of ADC measurements from brain parenchyma, in the patients diagnosed with brain death by clinical criteria. We studied 16 brain deaths in serial studies, in which there is a prominent difference between the white and gray matter ADC values on diffusion MRI. In the postmortem brains, ADC values comparing with the normal brain parenchyma, were reduced 65% in white matter and 42% in gray matter. Also, the patients’ ADC values of gray and white matter were significantly lower than those of irreversible brain-ischemia patients’ in ADC values. In comparison to most of the other studies, in our study population studied is large, in which is a comprehensive study that results consistent with the literature. As a result we propose that in the definition of brain death Diffusion MRI and ADC measurements are reliable to show diffuse ishemic changes of brain parenchyma.International Journal of Medical Physics, Clinical Engineering and Radiation Oncology 05/2015; 4(2):113-123. DOI:10.4236/ijmpcero.2015.42015
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ABSTRACT: Epilepsy is a common neurological disorder in which magnetic resonance imaging plays a key role. Diffusion imaging based on the molecular diffusion of water has been widely used clinically and in research for patients with epilepsy. Diffusion tensor imaging (DTI), the most common model, has been used for around two decades. Several parameters can be derived from DTI that are sensitive, but non-specific, to underlying structural changes. DTI assumes a single diffusion process following a Gaussian distribution within each voxel and is thus an overly simplistic representation of tissue microstructure. Several more advanced models of diffusion are now available that may have greater utility in the understanding of the effects of epilepsy on tissue microstructure. In this review, I summarise the principles, applications in epilepsy and future potential of three such techniques. Diffusion kurtosis imaging (DKI) characterises the degree to which diffusion deviates from Gaussian behaviour and gives an idea of the underlying tissue complexity. It has been used in both focal and generalised epilepsy and seems more sensitive than DTI. Multi-compartment models separate the signal from extra- and intra-axonal compartments in each voxel. The Composite Hindered and Restricted Model of Diffusion (CHARMED) can characterise axonal density but has not yet been applied in patients with epilepsy. The Neurite Orientation Dispersion and Density Imaging (NODDI) model can determine the intracellular volume fraction (ICVF) and degree of dispersion of neurite orientation. Preliminary data suggest it may more sensitive than conventional and diffusion imaging in localising focal epilepsy.04/2015; 5(2):279-87. DOI:10.3978/j.issn.2223-4292.2015.02.03