Partial Volume Effect Correction Research Articles

Cortical dysfunction in non-demented Parkinson's disease patients: a combined (31)P-MRS and (18)FDG-PET study.

Regional cerebral phosphorus-31 magnetic resonance spectroscopy ((31)P-MRS) was performed in 10 non- demented Parkinson's disease patients and nine age-matched control subjects. Five of the patients undergoing (31)P-MRS and four additional Parkinson's disease patients had cerebral 2-[(18)F]fluoro-2-deoxy-D-glucose PET ((18)FDG-PET), the results of which were compared with those of eight age-matched control subjects. All Parkinson's disease patients underwent neuropsychological testing including performance and verbal subtests of the Wechsler Adult Intelligence Scale-Revised, Boston Naming Test, Controlled Oral Word Association test (FAS Test) and California Learning Test to exclude clinical dementia. (31)P MR spectra from right and left temporo-parietal cortex, occipital cortex and a central voxel incorporating basal ganglia and brainstem were obtained. (31)P MR peak area ratios of signals from phosphomonoesters (PMEs), inorganic phosphate (P(i)), phosphodiesters (PDEs), alpha-ATP, gamma-ATP and phosphocreatine (PCr) relative to beta-ATP were measured. Relative percentage peak areas of PMEs, P(i), PDEs, PCr, and alpha-, beta- and gamma-ATP signals were also measured with respect to the total (31)P-MRS signal. Significant bilateral increases in the P(i)/beta-ATP ratio were found in temporoparietal cortex (P = 0.002 right and P = 0.014 left cortex) for the non-demented Parkinson's disease patients compared with controls. In the right temporoparietal cortex, there was also a significant increase in the mean relative percentage P(i) (P = 0.001). (18)FDG-PET revealed absolute bilateral reductions in glucose metabolism after partial volume effect correction in posterior parietal and temporal cortical grey matter (P < 0.01 and P < 0.05, respectively) for the Parkinson's disease group, using both volume of interest analysis and statistical parametric mapping. There were significant correlations between right temporoparietal P(i)/beta-ATP ratios and estimated reductions in performance IQ (r = 0.96, P < 0.001). Left temporoparietal P(i)/beta-ATP ratios correlated with full scale IQ and verbal IQ (r = -0.82, P = 0.006, r = -0.86, P = 0.003, respectively). In summary, temporoparietal cortical hypometabolism was seen in non-demented Parkinson's disease patients with both (31)P-MRS and (18)FDG-PET, suggesting that both glycolytic and oxidative pathways are impaired. This dysfunction may reflect either the presence of primary cortical pathology or deafferentation of striato-cortical projections. (31)P-MRS and (18)FDG-PET may both provide useful predictors of future cognitive impairment in a subset of Parkinson's disease patients who go on to develop dementia.

Effect of partial volume correction on estimates of the influx and cerebral metabolism of 6-[18F]fluoro-L-dopa studied with PET in normal control and Parkinson's disease subjects

The poor spatial resolution of positron emission tomography (PET) is a limiting factor in the accurate assay of physiological processes investigated by compartmental modeling of tracer uptake and metabolism in living human brain. The radioactivity concentration in a region-of-interest is consequently altered by loss of signal from that structure and contamination from adjacent brain regions, phenomena known as partial volume effects. We now apply an MRI-based algorithm to compensate for partial volume effects in the special case of compartmental modeling of the cerebral uptake of 6-[(18)F]fluoro-L-dopa (FDOPA), an exogenous substrate of dopa decarboxylase. High-resolution MRI scans were obtained from normal volunteers (n = 4) and patients with Parkinson's disease (n = 4) in order to segment specific brain regions and calculate the partial volume correction factors. Dynamic 2D PET scans were acquired during 90 min following intravenous infusion of FDOPA. After partial volume correction, the apparent net blood-brain clearance of FDOPA (K(i)) was greatly increased in caudate and putamen of normal subjects and in caudate of Parkinson's disease patients. The equilibrium distribution volume of FDOPA (V(D)(e)) in cerebral cortex increased by 35% in all subjects. Using a two-compartment model, the relative activity of dopa decarboxylase with respect to FDOPA (k(D)(3)) in the basal ganglia was increased 2-3 times in normal subjects, to the range obtained previously in brain of living rat. The partial volume correction also increased the magnitude of k(D)(3) in caudate of Parkinson's disease patients, but did not alter k(D)(3) in putamen. A three-compartment model correcting for elimination of decarboxylated metabolites also yielded higher estimates of k(D)(3), but with a penalty in precision of the estimates. Together, these observations suggest that the limited spatial resolution of PET results in substantial underestimation of the true rate of FDOPA uptake and metabolism in vivo, and may also tend to obscure regional heterogeneity in the neurochemical pathology of Parkinson's disease.

Measurement of the tricarboxylic acid cycle rate in human grey and white matter in vivo by 1H-[13C] magnetic resonance spectroscopy at 4.1T.

13C isotopic labeling data were obtained by 1H-observed/13C-edited magnetic resonance spectroscopy in the human brain in vivo and analyzed using a mathematical model to determine metabolic rates in human grey matter and white matter. 22.5-cc and 56-cc voxels were examined for grey matter and white matter, respectively. When partial volume effects were ignored, the measured tricarboxylic acid cycle rate was 0.72+/-0.22 (mean +/- SD) and 0.29+/-0.09 micromol min(-1) g(-1) (mean +/- SD) in voxels of approximately 70% grey and approximately 70% white matter, respectively. After correction for partial volume effects using a model with two tissue compartments, the tricarboxylic acid cycle rate in pure grey matter was higher (0.80+/-0.10 mol min(-1) g(-1); mean +/- SD) and in white matter was significantly lower (0.17+/-0.01 micromol min(-1) g(-1); mean +/- SD). In 1H-observed/13C-edited magnetic resonance spectroscopy labeling studies, the larger concentrations of labeled metabolites and faster metabolic rates in grey matter biased the measurements heavily toward grey matter, with labeling time courses in 70% grey matter appearing nearly identical to labeling in pure grey matter.

Robustness of Anatomically Guided Pixel-by-Pixel Algorithms for Partial Volume Effect Correction in Positron Emission Tomography

Several algorithms have been proposed to improve positron emission tomography quantification by combining anatomical and functional information in a pixel-by-pixel correction scheme. The precision of these methods when applied to real data depends on the precision of the manifold correction steps, such as full-width half-maximum modeling, magnetic resonance imaging-positron emission tomography registration, tissue segmentation, or background activity estimation. A good understanding of the influence of these parameters thus is critical to the effective use of the algorithms. In the current article, the authors present a monodimensional model that allows a simple theoretical and experimental evaluation of correction imprecision. The authors then assess correction robustness in three dimensions with computer simulations, and evaluate the validity of regional SD as a correction performance criterion.

Correction of partial volume effects in myocardial SPECT

Background. Marked partial volume effects occur in myocardial single photon emission computed tomographic (SPECT) studies because of limited resolution in imaging the myocardial wall and contractile motion of the heart. Little work has been undertaken to develop correction techniques for SPECT except for efforts to improve the reconstructed resolution. Our purpose was to examine the extent of the problem and propose a correction method. Methods and Results. A potential correction method, developed initially for positron emission tomography, involved estimation of extravascular density by means of subtracting vascular density derived in a blood pool study from total density derived from a transmission study. Provided partial volume errors are the same for transmission and emission data, activity per gram of extravasclar tissue can be obtained by means of dividing the perfusion regional data by extravascular density for the same region. Simulations were designed to assess the importance of partial volume errors and the use of extravascular density to correct the errors. Recovery coefficients for the myocardium were estimated by means of simulation of the beating heart on the basis of published values for ventricular dimensions. Resolution for transmission with a scanning line source system was compared with emission resolution. The effect of spillover on measured partial volume losses was assessed, and a method for matching spillover for emission and extravascular density was demonstrated. Correction for partial volume effects was demonstrated for a phantom with variable wall thickness. Significant variation in recovery coefficient was demonstrated between posterior and septal walls for individual patients independent of heart size. Filtering was necessary to account for the difference in transmission resolution measured in the axial direction. Spillover effects had a significant influence on the measured recovery for small objects; however, for a specific reconstruction algorithm and defined region size, correction was implemented to match the spillover effects for emission and extravascular density. Use of extravascular density for correction of partial volume loss, for ordered subsets expectation maximization reconstruction with compensation for resolution, was demonstrated to be accurate to within 10%. Conclusions. The feasibility of correcting partial volume effects with extravascular density was demonstrated. Correction is effective provided care is taken to match both resolution and spillover for emission and extravascular density.

Regional glucose metabolic abnormalities are not the result of atrophy in Alzheimer's disease.

To determine whether the hypometabolism observed in PET images of patients with Alzheimer's disease (AD) is due entirely to brain atrophy. Reduced brain glucose metabolism in AD patients measured using PET has been reported by numerous authors. Actual glucose metabolic values in AD may be reduced artificially because of brain atrophy, which accentuates the partial volume effect (PVE) on data collected by PET. Using segmented MR images, we corrected regional cerebral metabolic rates for glucose for PVEs to evaluate the effect of atrophy on uncorrected values for brain metabolism in AD patients and healthy control subjects. Global glucose metabolism was reduced significantly before and after correction in AD patients compared with controls. Before PVE correction, glucose metabolic values in patients were lower than in control subjects in the inferior parietal, frontal, and lateral temporal cortex; in the posterior cingulate; and in the precuneus. These reductions remained significantly lower after PVE correction, although in the posterior cingulate the difference in metabolism between AD patients and control subjects lessened. Regional glucose metabolism of these areas with PVE correction was lower in moderately-severely demented patients than in mildly demented patients. Reduced glucose metabolism measured by PET in AD is not simply an artifact due to an increase in CSF space induced by atrophy, but reflects a true metabolic reduction per gram of tissue.

Compartmental analysis of dopa decarboxylation in living brain from dynamic positron emission tomograms.

The trapping of decarboxylation products of radiolabelled dopa analogs in living human brain occurs as a function of the activity of dopa decarboxylase. This enzyme is now understood to regulate, with tyrosine hydroxylase, cerebral dopamine synthesis. Influx into brain of dopa decarboxylase substrates such as 6-[18F]fluorodopa and beta-[11C]dopa measured by positron emission tomography can be analyzed by solution of linear differential equations, assuming irreversible trapping of the decarboxylated products in brain. The isolation of specific physiological steps in the pathway for catecholamine synthesis requires compartmental modelling of the observed dynamic time-activity curves in plasma and in brain. The several approaches to the compartmental modelling of the kinetics of labelled substrates of dopa decarboxylase are now systematically and critically reviewed. Labelled catechols are extensively metabolized by hepatic catechol-O-methyltransferase yielding brain-penetrating metabolites. The assumption of a fixed blood-brain permeability ratio for O-methyl-6-[18F]fluorodopa or O-methyl-beta-[11C]dopa to the parent compounds eliminates several parameters from compartmental models. However, catechol-O-methyltransferase activity within brain remains a possible factor in underestimation of cerebral dopa decarboxylase activity. The O-methylation of labelled catechols is blocked with specific enzyme inhibitors, but dopa decarboxylase substrates derived from m-tyrosine may supplant the catechol tracers. The elimination from brain of decarboxylated tracer metabolites can be neglected without great prejudice to the estimation of dopa decarboxylase activity when tracer circulation is less than 60 minutes. However, elimination of dopamine metabolites from brain occurs at a rate close to that observed previously for metabolites of glucose labelled in the 6-position. This phenomenon can cause systematic underestimation of the rate of dopa decarboxylation in brain. The spillover of radioactivity due to the limited spatial resolution of tomographs also results in underestimation of dopa decarboxylase activity, but correction for partial volume effects is now possible. Estimates of dopa decarboxylase activity in human brain are increased several-fold by this correction. Abnormally low influx of dopa decarboxylase tracers in the basal ganglia is characteristic of Parkinson's disease and other movement disorders. Consistent with postmortem results, the impaired retention of labelled dopa is more pronounced in the putamen than in the caudate nucleus of patients with Parkinson's disease; this heterogeneity persists after correction for spillover. Current in vivo assays of dopa decarboxylase activity fail to discriminate clinically distinct stages in the progression of Parkinson's disease and are, by themselves, insufficient for differential diagnosis of Parkinson's disease and other subcortical movement disorders. However, potential new avenues for therapeutics can be tested by quantifying the rate of metabolism of exogenous dopa in living human brain.

Do people with epilepsy know more about the condition than people without epilepsy?

s 77 Do people with epilepsy know more about the condition than people without epilepsy? T. Duthie*, S. Jarvie+ & H. Kent’ * Glaxo Welcome UK Ltd, Uxbridge, Middlesex, UK, ‘Department of Clinical Psychology The Grail Street Centre, Glasgow, UK and $British Epilepsy Association, Anstey House, Leeds, UK The level of knowledge of epilepsy among patients has been shown to be key to the management of the condition. However, few studies have assessed the level of knowledge of epilepsy in a large population sample. The objectives of this study (which was part of a larger research project) were first to compare the level of epilepsy-related knowledge between people with epilepsy and people without epilepsy in a general population. Secondly, to ascertain whether people with epilepsy feel satisfied with their knowledge of the condition and with their access to information on the condition. A questionnaire containing the Epilepsy Knowledge Profile---General (EKP-G) and additional questions on information access was designed and pilot tested. The additional questions were only given to the epilepsy sample. The final questionnaire was sent by post to a general population sample of 893 people with epilepsy and 1200 people without epilepsy. The nonepilepsy sample was drawn to match the demographics of the epilepsy sample. Responses from 287 people with epilepsy and 383 people without epilepsy were received, representing a response rate of 32.1% and 32.0% respectively. The mean number of correct responses to the questionnaire are: people with epilepsy (n = 287), medical (n = 34), 25.6 (75.3%) social (n = 21), 14.5 (69%), total (n = 55), 40.2 (73.1%); people without epilepsy (n = 383), medical (n = 34) 25.6 (75.3%), social (n = 21) 14.3 (68.1%), total (n = 55) 39.9 (72.5%). The results from the questionnaire indicate that there is no statistically significant difference in the medical knowledge (P = 0.31) or the social knowledge (P = 0.15) of epilepsy, between the two samples. The relationship between knowledge levels and the epilepsy sample’s satisfaction with their understanding of the condition will be explored. The findings from the study will generate suggestions to improve the focus and target of information provided on epilepsy. In addition, the results will help patient organizations to identify issues for future campaigns. Correlation of l1 C-FMZ-PET and 3H-FMZ autoradiography in temporal-lobe epilepsy M.J. Koepp, K.S.P. Hand, M.l? Richardson, N.G. Bowery & J.S. Duncan Epilepsy Research Group, Institute of Neurology, Queen Square, London, UK We used llC-Flumazenil (FMZ) PET and 3H-FMZ autoradiography in patients with mesial temporal lobe epilepsy (mTLE) to compare in viva and ex viva determination of central benzodiazepine receptors (cBZR). Comparing autoradiography and quantitative neuropathology we demonstrated that there is loss of cBZR in CA1 over and above loss of neurons. In order to determine cBZR density within the body of the hippocampus we applied an MRI-based, four-compartment method for partial volume effect (PVE) correction to ” C-FMZ volume of distribution (FMZ-Vd) images from 10 patients with refractory mTLE due to unilateral, histologically verified hippocampal sclerosis (HS) and 15 age-matched healthy volunteers. Saturation autoradiography was performed in the hippocampal specimens from the same patients and six controls with calculation of receptor availability (Bniax). Reductions of FMZ-Vd after correction for PVE were compared with reductions of Bmax in relation to available control data. FMZ-Vd in the body of the epileptogenic hippocampus was reduced by a mean of 41.7% compared with healthy volunteers. FMZ-B max determined autoradiographically in available hippocampal tissue was reduced by a mean of 41.2% compared to normal control data. In conclusion, down-regulation of cBZR on remaining neurones in HS can be detected in viva using ’ ‘C-FMZ PET corrected for PVE. Memory testing with intra-carotid sodium amytal: A non-mnestic factor S. Oxbury, E. Burkitt, J.M. Oxbury, & A.J. Molyneux The Radcliffe Infirmary, Oxford, UK Intracarotid sodium amytal (ISA) inactivates the injected hemisphere enabling measurement of the mnestic capacity of the other. It is used to check that the hemisphere contralateral to planned temporal lobe surgery (TLS) is free from pathology which might cause postoperative amnesia. An apparently normal non-dominant hemisphere (ND) may score unexpectedly low on memory tests, possibly because it has a lower capacity than the dominant hemisphere (D) or because incidental effects of D injection, e.g. aphasia, complicate assessment. We therefore analysed the post-recovery scores of 22 pre-TLS patients for recognition of eight three-dimensional common objects, initially presented immediately after ISA injection (175200 mg), according to whether the non-injected (i.e. functioning) side was ND or D and pathological or intact. We also

Blood flow distribution in the normal human preterm brain.

Disturbances in cerebral blood flow (CBF) are a major factor in the etiology and pathogenesis of cerebral damage in the neonate. As most animals are more mature at birth than man, extrapolation from animal studies to the human is questionable. Therefore, we have measured regional CBF (rCBF) in preterm infants. rCBF flow was measured in 12 normotensive and normoxic preterm infants [mean birth weight 915 g (range 550 to 2680 g), mean gestational age 27.7 wk (25 to 32 wk)]. All infants had a normal cerebral ultrasound examination. rCBF was measured using a mobile brain dedicated fast-rotating four-head multidetector system specially designed for neonatal studies. The tracer was 99mTc-labeled D,L-hexamethylpropylenamine oxime in a dose of 4 Mbq/kg. rCBF of the subcortical white matter was 0.53 (0.48-0.58) of the global CBF. After correction for scattered radiation, the estimate of rCBF to the white matter was reduced to 0.39 (0.36-0.42). The flow to the basal ganglia was 2.33 (2.08-2.59) times the global CBF. After correction for partial volume effect, the cortical flow was higher than the flow to the basal ganglia and highest in the frontotemporal cortex (motor cortex). The flow to the cerebellum was of the same magnitude as the flow to the basal ganglia, but with a significantly higher variation. rCBF in 12 preterm infants showed a flow distribution similar to flow in other newborn mammals. The gray-white matter contrast, however, was greater. This new information, combined with existing data showing low global CBF, suggests that blood flow to the white matter in the preterm human neonate is extremely low.

Regional hippocampal [11C]flumazenil PET in temporal lobe epilepsy with unilateral and bilateral hippocampal sclerosis.

Using statistical parametric mapping and [11C]flumazenil (FMZ) PET we have previously shown reduction of central benzodiazepine receptor (cBZR) binding restricted to the hippocampus in mesial temporal lobe epilepsy due to unilateral hippocampal sclerosis. However, bilateral hippocampal pathology can be present in up to 50% of patients with mesial temporal lobe epilepsy. Additionally, the limited spatial resolution of PET results in a partial volume effect that affects quantitative analysis of cBZRs and such an effect can mask hippocampal dysfunction. We analysed changes in the [11C]FMZ volume of distribution (FMZ-Vd) before and after correction for partial volume effect in six patients with refractory mesial temporal lobe epilepsy and a quantitative MRI diagnosis of bilateral hippocampal sclerosis, which appeared either symmetrical on MRI (bilateral symmetrical hippocampal sclerosis; three patients) or bilateral but asymmetrical (asymmetrical hippocampal sclerosis; three patients), and in nine patients with refractory mesial temporal lobe epilepsy and unilateral hippocampal sclerosis on MRI than was subsequently histologically verified. Fifteen healthy controls were also studied for comparison. Before correction for partial volume effects, significant unilateral reductions of FMZ-Vd were found in one of the three patients with bilateral symmetrical hippocampal sclerosis, in one of the three asymmetrical hippocampal sclerosis patients and in six of the nine unilateral hippocampal sclerosis patients. No significant bilateral reductions of hippocampal FMZ-Vd were detected. After correction for partial volume effect, all three patients with bilateral symmetrical hippocampal sclerosis showed significant bilateral reductions of FMZ-Vd, and these were asymmetrical in two. All three patients with asymmetrical hippocampal sclerosis and all nine patients with unilateral hippocampal sclerosis on MRI showed unilateral reductions of FMZ-Vd concordant with the side of the EEG focus. In addition one of the three patients with asymmetrical hippocampal sclerosis and three of the nine patients with unilateral hippocampal sclerosis showed significant reductions of FMZ-Vd in the hippocampus contralateral to the side of the EEG focus. Absolute quantification of [11C]FMZ-PET, corrected for partial volume effect, within multiple hippocampal volumes of interest was necessary in order to detect bilateral changes of cBZR in mesial temporal lobe epilepsy due to hippocampal sclerosis with optimal sensitivity. This [11C]FMZ-PET approach was able to demonstrate subtle contralateral abnormalities in one-third of patients thought to have unilateral or bilateral asymmetrical hippocampal sclerosis on MRI. Reduction of cBZR binding was consistently over and above loss of hippocampal volume indicating that atrophy is not the sole determinant of cBZR loss in mesial temporal lobe epilepsy.

Effect of partial volume correction on muscarinic cholinergic receptor imaging with single-photon emission tomography in patients with temporal lobe epilepsy

Effect of partial volume correction on muscarinic cholinergic receptor imaging with single-photon emission tomography in patients with temporal lobe epilepsy

11C-flumazenil PET, volumetric MRI, and quantitative pathology in mesial temporal lobe epilepsy.

Using statistical parametric mapping and 11C-flumazenil (FMZ) PET we have previously shown reduction of central benzodiazepine receptor (cBZR) binding restricted to the hippocampus in mesial temporal lobe epilepsy (mTLE) due to hippocampal sclerosis (HS). The limited spatial resolution of PET, however, results in partial-volume averaging that affects quantitative analysis of cBZR density. We determined hippocampal volume loss and reduction in cBZR binding using an MRI-based method for partial-volume effect correction of 11C-FMZ volume of distribution (FMZ-Vd) in 17 patients with refractory mTLE and an MRI diagnosis of HS that was subsequently histologically verified in all cases. Quantitative neuropathology was performed with assessment of neuron density in 14 of the 17 patients. Absolute FMZ-Vd and asymmetry indices (FMZ-AI) were compared before and after partial-volume effect correction with MRI-determined hippocampal volumes (HCV), hippocampal T2 measurements, and, if available, neuronal cell densities. Compared with 15 age-matched healthy volunteers, significant reductions of absolute hippocampal FMZ-Vd were found before correction for partial-volume effects in 11 of 17 patients (65%) and only abnormal FMZ-AI in the other six patients. After partial-volume effects correction all 17 patients (100%) showed both significant unilateral reduction of absolute FMZ-Vd and abnormal FMZ-AI. There was no correlation between corrected absolute FMZ-Vd and HCV or neuronal cell density. After correction for partial-volume effect we found a mean 38% reduction of FMZ-Vd in the sclerosed hippocampus, over and above the reduction of HCV. Correction for partial-volume effect allows absolute quantitation of FMZ-PET and increases its sensitivity for detecting abnormalities in TLE due to HS. The lack of correlation between cBZR binding and neuronal density implies that atrophy with neuron loss is not the sole determinant of reduced cBZR binding in patients with mTLE and hippocampal sclerosis.

Effect of partial volume correction on muscarinic cholinergic receptor imaging with single-photon emission tomography in patients with temporal lobe epilepsy.

Animal experiments and preliminary results in humans have indicated alterations of hippocampal muscarinic acetylcholine receptors (mAChR) in temporal lobe epilepsy. Patients with temporal lobe epilepsy often present with a reduction in hippocampal volume. The aim of this study was to investigate the influence of hippocampal atrophy on the quantification of mAChR with single photon emission tomography (SPET) in patients with temporal lobe epilepsy. Cerebral uptake of the muscarinic cholinergic antagonist [123I]4-iododexetimide (IDex) was investigated by SPET in patients suffering from temporal lobe epilepsy of unilateral (n=6) or predominantly unilateral (n=1) onset. Regions of interest were drawn on co-registered magnetic resonance images. Hippocampal volume was determined in these regions and was used to correct the SPET results for partial volume effects. A ratio of hippocampal IDex binding on the affected side to that on the unaffected side was used to detect changes in muscarinic cholinergic receptor density. Before partial volume correction a decrease in hippocampal IDex binding on the focus side was found in each patient. After partial volume no convincing differences remained. Our results indicate that the reduction in hippocampal IDex binding in patients with epilepsy is due to a decrease in hippocampal volume rather than to a decrease in receptor concentration.

16 SPECTにおける部分容積効果の補正

16 SPECTにおける部分容積効果の補正

Improved 3D correction for partial volume effects in brain SPECT

An improved method for correction of partial volume effects (PVE) in brain SPECT is proposed. It is fully three-dimensional, does not require particular patient positioning, and works with scans only partially covering the brain. The location of functionally inactive brain regions (primarily cerebrospinal fluid) is extracted from high-resolution MRI. An automatic 3D registration algorithm then determines the geometric transformation between MRI and SPECT. Correction consists of: 1) counting the volumetric active/inactive ratio in each volume element of the functional scan using the measured SPECT point spread function; 2) correcting the functional measures according to these ratios; 3) fusing functional and anatomical information at the resolution of MRI. Quantitative validation was performed using a phantom containing a test region in which multiple parallel acrylic plates thinner than SPECT resolution created high PVE, as well as a large reference region not suffering from PVE. Reference activity was recovered in the test region with an accuracy of 1-3%. The method was applied to clinical images demonstrating a combination of hypoperfusion and cortical atrophy. The composite anatomical-functional corrected images, in which the main sulci are visible, yield better differentiation between decreased function and focal atrophy.

230 心筋SPECT画像における部分容積効果の補正 : 肥大型心筋症への応用

230 心筋SPECT画像における部分容積効果の補正 : 肥大型心筋症への応用

NMR measurements of flow profiles in a coarse bed of packed spheres

The velocity profiles of water flowing in a circular pipe filled with coarse, uniform, spherical beads, as well as the evolution of velocity profiles from clear flow into the bed of beads and visa versa, were measured by nuclear magnetic resonance (NMR) imaging using the phase-encoding method. Corrections for partial-volume effects were necessary in order to obtain accurate flow parameters. Phase errors due, for example, to electrical eddy currents induced by switching gradients, were minimized by the use of a static reference sample. For a tube diameter that is eight times the particle diameter, the flow reaches a steady state condition within one bead diameter into the packed bed after having a parabolic velocity profile only 1.5 tube diameters before encountering the bed. Within the packed bed, there are velocity spikes up to 16 times the average velocity in the unobstructed part of the pipe. The velocity distribution in the packed bed has a maximum that approaches the average velocity in the bed for increasing slice thickness along the flow. This distribution decreases exponentially with increasing velocity on the high-velocity side of the maximum. Even at modest flows, where velocity is steady upstream of the packed bed as well as in the bed, unsteady flow is detected downstream of the beads.

Attenuation correction of SPECT using X-ray CT on an emission-transmission CT system: myocardial perfusion assessment

The authors present experimental results for attenuation correction of emission tomography through use of an attenuation map derived from X-ray CT data. The X-ray and gamma-ray data were obtained from a third-generation X-ray CT scanner and a single-headed SPECT Scanner juxtaposed to enable systematic registration of SPECT and X-ray CT Images. CT measurements were obtained from known materials at a given X-ray technique, then related to attenuation coefficients at 140 keV. The resulting calibration data were used to generate attenuation maps for the coregistered SPECT data. In addition, phantom studies provided recovery coefficients as a function of object size to compensate for partial volume effects in the coregistered radionuclide data. This technique has been applied to a torso phantom, yielding attenuation maps with an average accuracy error <1%. Reconstruction of the SPECT image without attenuation correction underestimated the regional myocardial activity errors with an average accuracy error of -90%. Reconstruction with attenuation correction reduced the average accuracy error to -37%, but addition of a partial volume correction overestimated the regional myocardial activity concentration by an average error of 94%. The technique has also been applied to small pigs in myocardial perfusion studies by correlating the image-derived myocardial activity concentrations with those obtained directly from excised tissue samples. Correcting for attenuation increased the slope of the regression line from 0.16 to 0.36 (compared with an ideal slope of 1.00.) Adding an additional correction for partial volume effects improved the slope of the regression line to 0.93. The absolute precision error (standard error of the estimate) obtained without correction (2.14 /spl mu/Ci/ml) was degraded by attenuation correction (4.23 /spl mu/Ci/ml) and was also degraded by adding a correction for partial volume errors (10 89 /spl mu/Ci/ml), although the relative precision error without correction (31.2%) was improved by attenuation correction to 27.6% when the images were reconstructed with attenuation correction alone or with a combination of attenuation correction and compensation for partial volume effects.

Positron emission tomography metabolic data corrected for cortical atrophy using magnetic resonance imaging.

The correct interpretation of clinical positron emission tomography (PET) data depends largely on the physical limits of the PET scanner. The partial volume effect (PVE) is related to the size of the studied object compared to the spatial resolution. It represents one of the most important limiting factors in quantitative data analysis. This effect is increased in the case of atrophy, as in patients with Alzheimer disease (AD), and it influences measurement of the metabolic reduction generally seen in cerebral degeneration. In this case, interpretation can be biased, because cortical activity will be underestimated due to the atrophy. In general, anatomical images of AD patients have shown diffuse atrophy, while PET studies have found widespread hypometabolism affecting the parietal and temporal lobes. Although hypometabolic areas usually correspond to atrophic regions, they also occur without such changes. Thus, the aim is to differentiate authentic hypometabolism (decrease of glucose consumption per unit volume of gray matter) from that due to PVE from atrophy (cell loss). Consequently, we are using a method for three-dimensional (3D) correction of human PET data with 3D magnetic resonance imaging (MRI). We measured atrophy and metabolism by using both T1-weighted MR images and high and medium resolution PET scans. We injected 12 patients and controls with [18F]fluorodeoxyglucose for glucose consumption measurements. Atrophy was estimated in the following way. We isolated the cerebral structures, using a segmentation technique on the MRI scans, into gray matter (GM), white matter, and cerebrospinal fluid. We superimposed the PET images onto the MR images to obtain anatomo-functional correlations. We degraded the segmented MR images to the resolution of the PET images by a convolution process to create a PET image correction map. We corrected the metabolic PET data for the PVE. We studied the cerebral metabolic rate of glucose in the GM where metabolic variation is the most relevant to AD. By dealing with problems relating to the sensitivity to the segmentation and to the PET-MRI coregistration, computation of MRI convolution processes provided the degree of PVE on a pixel-by-pixel basis, allowing correction of hypometabolisms contained in GM PET values. Global cortical metabolism increased after correction for PVE by, on average, 29 and 24% for tomographs acquired with medium (TTV03 LETI) and high (ECAT 953B CTI/Siemens) resolution, respectively, whereas the cortical metabolism increased by 75 and 65% for the respective tomographs in AD patients. The difference of metabolism between scans after correction for PVE was less than before correction, decreasing from 31 to 17%. This difference was most marked in the frontal and temporal lobes. Fusion imaging allowed correction for PVE in metabolic data using 3D MRI and determination of whether a change in the apparent radiotracer concentration in PET data reflected an alteration in GM volume, a change in radiotracer concentration per unit volume of GM, or both.

Investigation of partial volume correction methods for brain FDG PET studies

The use of positron emission tomography (PET) in quantitative fluorodeoxyglucose (FDG) studies of aging and dementia has been limited by partial volume effects. A general method for correction of partial volume effects (PVE) in PET involves the following common procedures: segmentation of MRI brain images into gray matter (GM), white matter (WM), cerebral spinal fluid (CSF), and muscle (MS) components: MRI PET registration; and generation of simulated PET images. Afterward, two different approaches can be taken. The first approach derives first a pixel-by-pixel correction map as the ratio of the measured image to the simulated image [with realistic full-width at half-maximum (FWHM)]. The correction map was applied to the MRI segmentation image. Regions of interest (ROI's) can then be applied to give results free of partial volume effects. The second approach uses the ROI values of the simulated pure image (with negligible FWHM) and those of the simulated and the measured PET images to correct for the PVE effect. By varying the ratio of radiotracer concentrations for different tissue components, the in-plane FWHM's of a three-dimensional point spread function, and the ROI size, the authors evaluated the performance of these two approaches in terms of their accuracy and sensitivity to different simulation configurations. The results showed that both approaches are more robust than the approach developed by Muller-Gartner et al. (1992), and the second approach is more accurate and more robust than the first. In conclusion, the authors recommend that the second approach should be used on FDG PET images to correct for partial volume effects and to determine whether an apparent change in GM radiotracer concentration is truly due to metabolic changes.