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The engineering of a novel intra-operative MRI system is described. A movable, 1.5 Tesla MRI magnet was placed in a neurosurgical operating room without affecting established neurosurgical procedure. The system allows fast, high-quality MR intra-operative imaging of the brain and spine without the necessity of patient transportation. A neuro-navigational device capable of displaying and updating spatially referenced MR images in the operating room was integrated with the MRI system. Over 100 procedures have been carried out with this system without limiting surgical access and without compromising traditional neurosurgical, nursing or anesthetic techniques. J. Magn. Reson. Imaging 2001;13:78-86.

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OBJECTIVE: The goal was to enhance a mobile magnetic resonance imaging system developed for neurosurgery. Components of the system included an actively shielded, 1.5-T superconducting magnet, a titanium operating room table, a radiofrequency (RF) head coil that could be disassembled, and local RF shielding. METHODS: The system was designed and implemented by the Division of Neurosurgery, University of Calgary (Calgary, Alberta, Canada), in collaboration with the National Research Council of Canada Institute for Biodiagnostics (Winnipeg, Manitoba, Canada). The ceiling-mounted, 1.5-T magnet was moved into and out of the surgical field as required. After initial success in monitoring the resection of various intracranial and cranial base lesions, significant modifications to the system were made by Innovative Magnetic Resonance Imaging Systems, Inc. (Winnipeg, Manitoba, Canada), and BrainLAB (Heimstetten, Germany). These modifications included the design and construction of a shorter magnet with a larger bore and stronger gradients, widening of the titanium operating room table, modification of the RF coil housing to allow vertical movement and incorporation of a three-pin head-clamp, construction of a transparent, copper-impregnated RF shield, and integration with a surgical navigation system. RESULTS: The movable intraoperative imaging system has now been used for 101 neurosurgical procedures, including the previously reported cases. CONCLUSION: The modifications to the system have enhanced its integration with established neurosurgical techniques and have improved patient safety. The larger magnet bore size, together with the ability to move the RF coil vertically, allows placement of patients in prone or lateral positions. Surgical navigation has been successfully integrated with the intraoperatively acquired high-resolution images. The ability to identify and resect residual lesions before wound closure remains a tremendous immediate advantage of this technology.

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OBJECTIVE: This study demonstrates the utility of a newly-developed moveable 1.5 Tesla intraoperative MR imaging system using a case report of a multi-lobulated parafalx meningioma. CLINICAL PRESENTATION: A 43-year-old female presented with progression of a multi-lobulated anterior parafalx meningioma several years following resection of a large left frontal convexity meningioma. INTERVENTION AND TECHNIQUE: Surgical excision of the lesion was undertaken. Following apparent total resection, intraoperative MR imaging revealed two residual dumbell shaped lobules. Using these updated MR images, the tumour was readily identified and removed. CONCLUSION: The moveable 1.5 Tesla intraoperative MR system used in the present case provides rapid, high resolution MR images during neurosurgical procedures. Moving the magnet out of the surgical field during surgery permits the use of all standard neurosurgical instruments. The ease of use and quality of images combined with minimal interference on well-established surgical techniques makes this system a valuable adjunct in the neurosurgical treatment of intracranial disease.

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BACKGROUND: In the past few years, although significant efforts have been made to assess flow distribution during retrograde cerebral perfusion with microspheres, dye, or hydrogen clearance, flow distribution in real time is still undefined. We used MR perfusion imaging to monitor flow distribution in the brain during and after deep hypothermic circulatory arrest (DHCA) with antegrade or retrograde cerebral perfusion (ACP or RCP). METHODS AND RESULTS: Thirteen pigs were divided into 2 groups and exposed to 120 minutes of either RCP (n = 7) or ACP (n = 6) at 15 degrees C, followed by 60 minutes of cardiopulmonary bypass (CPB) at 37 degrees C. During DHCA, the brain was perfused antegradely through the common carotid artery or retrogradely through the superior vena cava at pressures of 60 to 70 mm Hg and 20 to 25 mm Hg in the ACP and RCP groups, respectively. Esophageal temperature was monitored continuously. MR perfusion images were acquired every 30 minutes before, during, and after DHCA. The brain was perfusion-fixed with formaldehyde solution for histopathology at the completion of each experiment. During initial normothermic CPB, MR perfusion imaging showed a nearly uniform distribution of flow in the brain. The same pattern was maintained with a significant increase in regional cerebral blood volume during ACP and reperfusion in the ACP group. RCP provided little or no detectable blood distribution to the brain, resulting in poor reperfusion of many areas of the brain on reflow with CPB at 37 degrees C. The total area suffering poor reperfusion was significantly higher in the RCP group than the ACP group. Histopathology showed no morphological changes in any area of the brain in the ACP group, whereas varying severity of neuronal damage was observed in different regions of the brain in the RCP group. CONCLUSIONS: ACP preserves uniform blood distribution and normal morphology of brain tissue after prolonged DHCA. RCP provides very little blood to the tissue of the brain. A 120-minute period of RCP results in abnormal flow distribution and neuronal damage during reperfusion. The damage resulting from shorter periods of RCP remains to be assessed.

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Inactivation of the tumor suppressor gene p16INK4A is the most common genetic alteration in human head and neck squamous cell cancer (HNSCC), making it an ideal target for gene replacement. We constructed a replication-defective, recombinant adenovirus capable of directing a high level of p16INK4A protein expression (Ad5-p16) to investigate its benefit in treating HNSCC. Initial in vitro experiments in four human HNSCC cell lines demonstrated that Ad5-p16 treatment significantly inhibits cell growth with up to 96% efficiency. Flow cytometric analysis showed that Ad5-p16 induced a maximum G1-S cell cycle arrest of 90%. Subsequent studies in a nude mouse model demonstrated that Ad5-p16 treatment significantly reduced (cell line 011) or stabilized (cell line 012) established tumors when compared with control treatments (P < 0.008). These results demonstrate for the first time a significant antitumor effect of Ad5-p16 against human HNSCC in vivo and support the potential application of Ad5-p16 to treat locally advanced, unresectable, or metastatic head and neck cancer, as well as microscopic residual disease after surgical resection.

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Hypoxic-ischemic changes in brain are detected earlier with diffusion-weighted (DW) than with T2-weighted magnetic resonance (MR) imaging techniques in adults, whereas the response in immature brain is not known. We investigated MR imaging changes prior to, during, and/or after 2 h of hypoxia-ischemia (right carotid artery occlusion + 2 h of hypoxia) in 7-day-old rats anesthetized with isoflurane. In general, within the first 45 min of hypoxia-ischemia there were no changes in the DW or T2-weighted images. By the second hour of hypoxia-ischemia there were marked areas of increased intensity in both the T2 and the DW images, with cortex and striatum being affected prior to thalamus and hippocampus. The area of DW exceeded that of T2 hyperintensities. In the first hour after hypoxia-ischemia there was a transient recovery of hyperintensities on both T2 and DW images. Between 24 and 72 h the hyperintense area on DW images decreased, whereas that on T2-weighted images increased. The distribution of pathological damage assessed histologically correlated with the areas of hyperintensity on the MR images. In contrast to adult brain, early hypoxic-ischemic injury in immature brain is detected as an increase in intensity in both diffusion- and T2-weighted images, indicating a unique alteration in brain water dynamics in this neonatal model of hypoxia-ischemia. These imaging changes and alterations in brain water can rapidly but transiently reverse upon the start of normoxia and reperfusion, suggestive of secondary energy failure or delayed neuronal death.

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OBJECTIVE: This study was designed to determine whether simultaneous antegrade/retrograde cardioplegia improves myocardial perfusion in areas supplied by occluded vessels. METHODS: Isolated pig hearts placed in a Langendorff preparation were divided into two groups. The left anterior descending coronary artery was occluded at its origin. In group 1 (n = 7), simultaneous antegrade/retrograde cardioplegia was conducted with use of a single perfusion unit with tubing in a Y-shaped configuration at the end, joined to the aorta and the coronary sinus. In group 2 (n = 8) simultaneous antegrade/retrograde cardioplegia was performed with two separate units, one for antegrade delivery of cardioplegic solution and the other for retrograde cardioplegic solution delivery. Myocardial perfusion in the region supplied by the left anterior descending artery and the region not supplied by this artery was assessed by magnetic resonance imaging, with use of a magnetic resonance contrast agent. The contrast agent was introduced into the common perfusion line in group 1 and into the aortic line only in group 2. RESULTS: Magnetic resonance images showed that the myocardium in the region supported by the left anterior descending artery could not be perfused with antegrade cardioplegic solution because of occlusion of the artery. During simultaneous antegrade/retrograde cardioplegia, however, the myocardium in the left anterior descending region was perfused by approximately 40% to 50% (group 1) or 20% to 30% (group 2) of the degree of perfusion in the region not perfused by the left anterior descending artery (100%). Almost no cardioplegic solution was delivered to the heart through the coronary sinus route during simultaneous antegrade/retrograde cardioplegia in both groups of hearts. Myocardial perfusion in the region supported by the left anterior descending artery was heterogeneous during simultaneous antegrade/retrograde cardioplegia. CONCLUSIONS: Simultaneous antegrade/retrograde cardioplegia significantly improved myocardial perfusion in jeopardized areas of the myocardium. The jeopardized myocardium was mainly perfused by the solution drained from the adjacent normal tissue. Elevated pressure at the coronary sinus during simultaneous antegrade/retrograde cardioplegia is responsible for the redistribution of antegradely delivered cardioplegic solution.

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Signal phase variations caused by physiology are a major source of instability in fMRI images produced by multiple RF pulses. k-Space phase variation maps show cyclic phase variations at the frequency of respiration combined with a cardiac variation of lower amplitude. The amplitude of the variation increases with gradient echo time and proximity to the chest, suggesting that the dominant cause of the phase variation is a B0 shift (approximately 0.01 ppm) produced by movement of organs in the chest. A simple k-space phase correction method is proposed and demonstrated for FLASH fMRI. The retrospective method requires no pulse sequence modification, and is more effective than navigator echo correction. Physiological noise is dramatically reduced, especially at inferior slice locations.

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BACKGROUND: Neurocognitive deficits after open heart operations have been correlated to jugular venous oxygen desaturation on rewarming from hypothermic cardiopulmonary bypass (CPB). Using a porcine model, we looked for evidence of cerebral hypoxia by magnetic resonance imaging during CPB. Brain oxygenation was assessed by T2*-weighted imaging, based on the blood oxygenation level-dependent effect (decreased T2*-weighted signal intensity with increased tissue concentrations of deoxyhemoglobin). METHODS: Pigs were placed on normothermic CPB, then cooled to 28 degrees C for 2 hours of hypothermic CPB, then rewarmed to baseline temperature. T2*-weighted, imaging was undertaken before CPB, during normothermic CPB, at 30-minute intervals during hypothermic CPB, after rewarming, and then 15 minutes after death. Imaging was with a Bruker 7.0 Tesla, 40-cm bore magnetic resonance scanner with actively shielded gradient coils. Regions of interest from the magnetic resonance images were analyzed to identify parenchymal hypoxia and correlated with jugular venous oxygen saturation. Post-hoc fuzzy clustering analysis was used to examine spatially distributed regions of interest whose pixels followed similar time courses. Attention was paid to pixels showing decreased T2* signal intensity over time. RESULTS: T2* signal intensity decreased with rewarming and in five of seven experiments correlated with the decrease in jugular venous oxygen saturation. T2* imaging with fuzzy clustering analysis revealed two diffusely distributed pixel groups during CPB. One large group of pixels (50% +/- 13% of total pixel count) showed increased T2* signal intensity (well-oxygenated tissue) during hypothermia, with decreased intensity on rewarming. Changes in a second group of pixels (34% +/- 8% of total pixel count) showed a progressive decrease in T2* signal intensity, independent of temperature, suggestive of increased brain hypoxia during CPB. CONCLUSIONS: Decreased T2* signal intensity in a diffuse spatial distribution indicates that a large proportion of cerebral parenchyma is hypoxic (evidenced by an increased proportion of tissue deoxyhemoglobin) during CPB in this porcine model. Neuronal damage secondary to parenchymal hypoxia may explain the postoperative neuropsychological dysfunction after cardiac operations.

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OBJECTIVE: This study was done to determine whether retrograde delivery of cardioplegic solution provides uniform blood flow to the myocardium supplied by an occluded coronary artery and whether it maintains myocardial energy levels beyond the coronary occlusion. METHODS: Isolated pig hearts were used. A hydraulic occluder was placed at the origin of the left anterior descending coronary artery. The perfusion pressure for retrograde delivery of cardioplegic solution was controlled at 40 to 50 mm Hg. Magnetic resonance imaging and localized 31P magnetic resonance spectroscopy were used to assess myocardial perfusion and energy metabolism, respectively. RESULTS: Magnetic resonance perfusion images (n = 7) showed that the perfusion defect that occurred during antegrade delivery of cardioplegic solution (as a result of the occlusion of the left anterior descending coronary artery) resolved during retrograde delivery of cardioplegic solution. Retrograde perfusion delivered similar amounts of flow to the jeopardized myocardium as it did to other areas of the myocardium. However, the distribution of cardioplegic solution by the retrograde route was heterogeneous (cloudlike) across both ventricular walls. 31P magnetic resonance spectra showed that the ischemic changes induced by occlusion of the left anterior descending artery during antegrade perfusion were greatly alleviated by retrograde perfusion; however, it took longer for retrograde cardioplegia (n = 7, 17.08 minutes) to restore the levels of inorganic phosphate/phosphocreatine relative to the effect of releasing the left anterior descending artery occluder during antegrade delivery of cardioplegic solution (n = 7, 5.3 minutes). CONCLUSIONS: First, retrograde delivery of cardioplegic solution provides sufficient flow to the myocardium beyond a coronary occlusion to maintain near normal levels of energy metabolites, and second, the efficacy of the retrograde route of cardioplegic solution delivery (in terms of distribution of the solution and rate of myocardial energy recovery) is significantly lower than that of the antegrade route.

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31P, 1H and lactate spectroscopic imaging was used to evaluate' the effects of hypothermia on focal cerebral ischemia produced by middle cerebral artery occlusion. The effects on high energy phosphate metabolism, pH, lactate and NAA were investigated in 24 spontaneously hypertensive rats subjected to either permanent or transient ischemia. Under either normothermic (37.5 degrees C) or hypothermic (32 degrees C) conditions, with permanent 6-h occlusion, there was little difference between groups in either the NMR measurements or the volume of infarction. In animals that underwent 3 h of ischemia followed by 12 h of reperfusion, the ischemic changes in lactate, pH, NAA, and high-energy phosphate returned toward control values, and there was a protective effect of hypothermia (infarct volume of 211 +/- 26 and 40 +/- 14 mm3 in normothermic and hypothermic groups, respectively). Thus, hypothermia did not ameliorate the changes in lactate, pH, NAA, or high energy phosphate levels occurring during ischemia, however, during reperfusion there was an improvement in both the recovery of these metabolites and pathological outcome in hypothermic compared with normothermic animals.

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The theory and construction of a dual surface coil which provides good B1 homogeneity and sensitivity in a defined volume of interest is described. The probe comprises two coaxial rings, of different diameters and in different planes, which carry opposing currents of different values. Current in the second ring compensates for the roll-off of the B1 field associated with a single surface coil. Coupling between the rings and a third matching ring is by mutual inductance only. A comparison to a traditional surface coil with practical application to pig brain imaging at a field strength of 7 Tesla is shown.

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PURPOSE: The present study was carried out to evaluate a new intravascular contrast agent hydroxyethyl-starch-ferrioxamine (HES-FO) for assessment of myocardial perfusion. MATERIAL AND METHODS: Isolated pig hearts were perfused with a crystalloid cardioplegic solution in a Langendorff apparatus. MR images were acquired along the short cardiac axis using T1- and T2*-weighted methods. Gd-DTPA and HES-FO were used as the standard extracellular and test contrast agents, respectively. RESULTS: We found that T1-weighted signal intensity was not significantly affected by HES-FO, but increased significantly in presence of Gd-DTPA. On the other hand, HES-FO resulted in a rapid, transient but significant decrease in T2*-weighted signal intensity. Although Gd-DTPA also decreased T2*-weighted signal intensity considerably, it took much longer for the T2*-weighted signal intensity to return to its initial steady-state with Gd-DTPA than with HES-FO. Moreover, increasing the dose of HES-FO (from 0.0023-0.0138 mmol/kg b.w.) had no effect on the time at which the T2* effect reached its maximum or on the duration of the T2* effect. However, these times and durations were affected significantly by increasing the dose of Gd-DTPA (0.0023-0.027 mmol/kg b.w.). CONCLUSION: The results suggest that HES-FO provides information regarding myocardial vascular flow which cannot be obtained using Gd-DTPA. It is expected that the combined use of intravascular and extracellular type contrast agents will allow more complete assessment of tissue perfusion.

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OBJECTIVE: We evaluated the effect of antegrade and retrograde brain perfusion during moderate hypothermic circulatory arrest at 28 degrees C. METHODS: Phosphorus 31-magnetic resonance spectroscopy was used to follow brain energy metabolites and intracellular pH in pigs during 2 hours of ischemia and 1 hour of reperfusion. Histopathologic analysis of brain tissue fixed at the end of the experimental protocol was performed. Fourteen pigs were divided into two experimental groups subjected to antegrade (n = 6) or retrograde (n = 8) brain perfusion. Anesthesia (n = 8) and hypothermic cardiopulmonary bypass groups (15 degrees C, n = 8) served as control subjects. In the antegrade and retrograde brain perfusion groups, the initial bypass flow rate was 60 to 100 ml x kg(-1) x min(-1). In the antegrade group, the brain was perfused through the carotid arteries at a flow rate of 180 to 210 ml x min(-1) during circulatory arrest at 28 degrees C. In the retrograde group, the brain was perfused through the superior vena cava at a flow rate of 300 to 500 ml x min(-1) during circulatory arrest at 28 degrees C. RESULTS: The intracellular pH was 7.1 +/- 0.1 and 7.2 +/- 0.1 in the anesthesia and hypothermic bypass groups, respectively. Brain intracellular pH and high-energy metabolites (adenosine triphosphate, phosphocreatine) did not change during the course of the 3.5-hour study. In the antegrade group, adenosine triphosphate and intracellular pH were unchanged throughout the protocol. In the retrograde perfusion group, the intracellular pH level decreased to 6.4 +/- 0.1, and adenosine triphosphate and phosphocreatine levels decreased within the first 30 minutes of circulatory arrest and remained at low levels until the end of reperfusion. High-energy phosphates did not return to their initial levels during reperfusion. Histopathologic analysis of nine regions of the brain showed good preservation of cell structure in the anesthesia, hypothermic bypass, and antegrade perfusion groups. The retrograde perfusion group showed changes in all the regions examined. CONCLUSIONS: The study shows that moderate hypothermic circulatory arrest at 28 degrees C with antegrade brain perfusion during circulatory arrest protects the brain but that retrograde cerebral perfusion at 28 degrees C does not protect the brain.

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Neurologic and neuropsychologic impairment are important sequelae of cardiac surgery in general and of coronary artery bypass graft surgery in particular. Although estimates of incidence vary, the numbers affected are considerable. Despite the ubiquity of such effects and the general consensus that impairments originate from ischemic injury secondary to microemboli produced during surgery, the nature of the underlying brain injuries remains poorly understood. Precise, and preferably quantitative, definition of the localization and nature of the underlying injuries is a precondition for the rigorous evaluation of the efficacy of prophylactic measures. The ability of magnetic resonance imaging (MRI) to detect surgically related lesions and the course of brain swelling is described, as are potential improvements in imaging sensitivity. Results of an experimental program studying chemical sequelae of surgery in a pig model are presented. MR spectroscopy can provide noninvasive information on the biochemical changes in brain and brain metabolism that permit empirical evaluation of various neuroprotective interventions. Functional MRI provides a means of studying the neuropsychologic mechanisms most often affected by cardiac surgery. Experimental data are presented that demonstrate that two such mechanisms, selective attention and working memory, can be imaged successfully. Perfusion mapping, combined with functional imaging, allows for the quantitative study of flow and functional activation. Applied to structures such as the cingulate, these techniques permit comparison of surgical sequelae with processes such as normal aging. MRI technology offers the possibility of improved anatomic, chemical, and functional definition of the effects of cardiac surgery on the brain.

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To evaluate the effect of hypothermic circulatory arrest on brain metabolism, we used 31P-magnetic resonance spectroscopy to monitor brain metabolites in pigs during 2 hours of ischemia and 1 hour of reperfusion. Twenty-eight pigs were divided into five groups. Anesthesia (n = 5) and hypothermic cardiopulmonary bypass groups (n = 5) served as controls. In the circulatory arrest (n = 6), antegrade perfusion (n = 6), and retrograde (n = 6) brain perfusion groups, the bypass flow rate was 60 to 100 ml.kg-1.min-1. In the antegrade group, the brain was perfused via the carotid arteries at a blood flow rate of 180 to 200 ml.min-1 during circulatory arrest at 15 degrees C. In the retrograde group, the brain was perfused through the superior vena cava at a flow rate of 300 to 500 ml.min-1 during circulatory arrest at 15 degrees C. The intracellular pH was 7.1 +/- 0.1 and 7.3 +/- 0.1 in the anesthesia and hypothermic cardiopulmonary bypass groups, respectively. In the circulatory arrest group, the intracellular pH decreased to 6.2 +/- 0.1 and did not recover to its initial value (7.0 +/- 0.1) during reperfusion (p < 0.05 compared with the value obtained from the control groups at the corresponding time). Inorganic phosphate did not return to its initial level during reperfusion. In three animals in this group, levels of high-energy phosphates, adenosine triphosphate and phosphocreatine, recovered partially but did not reach the levels observed before arrest. In the group receiving antegrade perfusion, cerebral metabolites and intracellular pH were unchanged throughout the protocol. During circulatory arrest in the retrograde perfusion group the intracellular pH decreased to 6.4 +/- 0.1 and recovered fully during reperfusion (7.1 +/- 0.1). High-energy phosphates also returned to their initial levels during reperfusion. These studies show that deep hypothermic circulatory arrest with antegrade brain perfusion provides the best brain protection of the options investigated.

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Chronic brain ischemia (CBI) was induced in aging (13 month) rats by ligating the left subclavian artery and placing temporary occluders in each common carotid artery [three-vessel occlusion (3-VO)]. Carotid artery occluders were removed after 1, 2, or 3 weeks following brain ischemia or maintained for 9 weeks. Two rats were kept with their occluders in place for 25 weeks. On weeks 3 and 9 after CBI, 31P-/1H-nuclear magnetic resonance (NMR) spectroscopy and high resolution diffusion weighted imaging were performed in vivo, non-invasively for detection of hippocampal high energy phosphates, lactate, intracellular pH, N-acetyl-aspartate, choline, glutamate, creatine, and structural alterations of the brain following CBI. Brains were histologically processed for morphometry of glial fibrillary acidic protein (GFAP) and CA1 damaged neurons 9 weeks after CBI. 31P-/1H-NMR spectroscopy showed that high energy substrates remained normal in ischemic animals when compared to non-ischemic controls except for an elevation of phosphomonesters in the hippocampal region. Rats deoccluded 1 and 2 weeks after initiation of CBI had no NMR spectroscopic or imaging changes. Rats kept ischemic for 9 weeks showed high signal intensities in the parietal cortex detected by diffusion weighted imaging as well as CA1 damage and increased GFAP density but no cortical atrophy or neuronal damage could be detected histologically. Rats kept ischemic for 25 weeks showed extensive cortical atrophy which corresponded to the high signal intensity observed with diffusion weighted imaging in the group kept ischemic for 9 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)

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RATIONALE AND OBJECTIVES: Phosphorus magnetic resonance spectroscopy has been used noninvasively to determine characteristic spectral parameters for untreated human brain tumors as a prelude to its use in clinical diagnosis. METHODS: The spectra, which reflect the relative amounts of phosphorus-containing compounds, and the pH within and surrounding the tumors, were obtained in vivo using the localization technique of one-dimensional chemical shift imaging applied with a surface coil. Phosphorus-31 chemical shift imaging was performed successfully in vivo on 9 volunteers and 27 patients with untreated brain tumors, including 7 with astrocytoma, 4 with glioblastoma, 3 with meningioma, and 11 with metastases. This study provides spectra from within and surrounding the brain tumors, and allows accountability for the heterogeneity of brain tumors by the selection of the maximum data point for each parameter. RESULTS: The ratios of resonance areas, phosphodiesters over nucleoside triphosphate (NTP), and phosphomonoesters over NTP, were found to be higher in glioblastomas (2.55 +/- 0.22, 1.06 +/- 0.09) and astrocytomas (3.04 +/- 0.36, 1.28 +/- 0.36) than in normal brain (2.00 +/- 0.32, 0.79 +/- 0.22). The ratios of areas due to inorganic phosphate and NTP, and phosphocreatine and NTP, also were higher in astrocytomas (1.16 +/- 0.40, 1.17 +/- 0.41) compared with glioblastomas (0.68 +/- 0.01, 0.88 +/- 0.19) and normal brain (0.61 +/- 0.03, 0.77 +/- 0.03). The pH of brain tumors ranged from alkaline to neutral, with meningiomas consistently having alkaline pH. CONCLUSIONS: These data show that there are statistically significant differences in the magnetic resonance parameters of the affected brain hemispheres of patients with astrocytomas, glioblastomas, meningiomas, and normal brain tissue, and underline the need for a multisite clinical trial to establish clinical criteria for diagnosis.

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Lung parenchyma is, structurally and magnetically, a very inhomogeneous system. The strong local field gradients due to magnetic susceptibility variation across the air-tissue interfaces impose a spatially dependent phase on spins that are inhomogeneously distributed. As a result, the slice selection process can cause destructive interference and corresponding partial cancellation of the NMR signals from different parts of the slice. The mechanism of this effect was studied by expanding the internal magnetic field gradient as a Fourier series and determining the Fourier components with a foam model, which consists of air bubbles preferentially at the alveolar diameter. The effect of signal cancellation as a function of slice thickness is characterized by a sinc-like function with destructive interference of higher orders shown as lobes and the zeroth order as the main peak. Computer simulation of the slice selection process was conducted to illustrate the combined effects of signal cancellation and spatial average, and their dependence on slice thickness. Finally, images of rat lungs are presented to demonstrate the significant improvement in image quality by avoiding the high order destructive interference of NMR signals in the slice selection process.

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