In this work we demonstrate the proof of principle of CT-based attenuation correction of 3D positron emission tomography (PET) data by using scans of bone and soft tissue equivalent phantoms and scans of humans. This method of attenuation correction is intended for use in a single scanner that combines volume-imaging (3D) PET with x-ray computed tomography (CT) for the purpose of providing accurately registered anatomical localization of structures seen in the PET image. The goal of this work is to determine if we can perform attenuation correction of the PET emission data using accurately aligned CT attenuation information. We discuss possible methods of calculating the PET attenuation map at 511 keV based on CT transmission information acquired from 40 keV through 140 keV. Data were acquired on separate CT and PET scanners and were aligned using standard image registration procedures. Results are presented on three of the attenuation calculation methods: segmentation, scaling, and our proposed hybrid segmentation/scaling method. The results are compared with those using the standard 3D PET attenuation correction method as a gold standard. We demonstrate the efficacy of our proposed hybrid method for converting the CT attenuation map from an effective CT photon energy of 70 keV to the PET photon energy of 511 keV. We conclude that using CT information is a feasible way to obtain attenuation correction factors for 3D PET.
A method for scatter correction using dual energy window acquisition has been developed and implemented on data collected with a brain-PET tomograph operated in the septa retracted, 3D mode. Coincidence events are assigned to (i) an upper energy window where both photons deposit energy between 380 keV and 850 keV or (ii) a lower energy window where one or both photons deposit within 200 keV and 380 keV. Scaling parameters are derived from measurements of the ratios of counts from line sources due to scattered and unscattered events in the two energy windows in head-sized phantoms. A scaled subtraction of the two energy windows produces a distribution of scatter which is smoothed prior to subtraction from the upper energy window. In phantoms, the correction was found to restore the uniformity, contrast and linearity of activity concentration. Relative activity concentrations were restored to within 7% of their true values in a multicompartment phantom. The method was found to provide accurate correction for scattered events arising from activity outside the direct detector field of view. In a three-compartment phantom containing water, 18F and 11C scanned in dynamic, multiframe mode, the half-lives of the two isotopes were restored to within 2% of their true value.
Cerebrovascular reserve (CVR) and oxygen extraction fraction (OEF) are used to identify hemodynamic compromise in symptomatic patients with carotid occlusive vascular disease, but evidence suggests that they are not equivalent. The authors studied the relationship between CVR and OEF to evaluate their equivalence and stages of hemodynamic compromise. Symptomatic patients (N = 12) with carotid occlusion were studied by stable xenon-computed tomography CBF after intravenous acetazolamide administration for CVR, followed within 24 hours by positron emission tomography (PET) for OEF. Middle cerebral artery territories were analyzed by hemisphere and level. Hemispheric subcortical white matter infarctions were graded with magnetic resonance imaging. Both hemispheric and level analysis of CVR and OEF showed a significant (P = 0.001), negative linear relationship [CVR (%) = -1.5 (OEF) + 83.4, (r = -0.57, P = 0.001, n = 24]. However, 37.5% of the hemispheres showed compromised CVR but normal OEF and were associated (P = 0.019) with subcortical white matter infarction. CMRO2 was elevated in stage II hemodynamic compromise (CVR < 10%, OEF > 50%). CVR and OEF showed a significant negative linear relationship in stage II hemodynamic compromise but revealed hemispheres in hemodynamic compromise by CVR but normal OEF that were associated with subcortical white matter infarction.
This report deals with the analysis of data from a 3-year clinical trial on the effect of walking on postmenopausal bone loss. Two hundred fifty-five women, with an average age of 57 at entry, were randomized into two groups, a walking and a control group. Bone measures in the shaft of the radius were carried out with a CT scanner in search of generalized skeletal effects rather than effects localized to the bones of the leg. Although bone density losses were comparable in the two randomized groups, changes in the cross-sectional area of the radius were significantly greater in the walkers with high grip strength (greater than 25 Kg) than in the controls with comparable high grip strength which corresponded to the upper half range of the grip-strength distribution. It is concluded that the moderate activity of walking exerted systemically positive effects on the radius which, within the protocol of the study, could be substantiated only when synergized with inherent muscle strength.
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