POSITRON EMISSION TOMOGRAPHY METABOLIC DATA CORRECTED FOR CORTICAL ATROPHY USING MAGNETIC-RESONANCE-IMAGING

The correct interpretation of clinical positron emission tomography (P ET) data depends largely on the physical limits of the PET scanner. Th e partial volume effect (PVE) is related to the size of the studied ob ject 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 di sease (AD), and it influences measurement of the metabolic reduction g enerally seen in cerebral degeneration. In this case, interpretation c an be biased, because cortical activity will be underestimated due to the atrophy. in general, anatomical images of AD patients have shown d iffuse atrophy, while PET studies have found widespread hypometabolism affecting the parietal and temporal lobes. Although hypometabolic are as usually correspond to atrophic regions, they also occur without suc h 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 3 D magnetic resonance imaging (MRI). We measured atrophy and metabolism by using both T1-weighted MR images and high and medium resolution PE T scans. We injected 12 patients and controls with [F-18]fluorodeoxygl ucose for glucose consumption measurements. Atrophy was estimated in t he following way. We isolated the cerebral structures, using a segment ation technique on the MRI scans, into gray matter (GM), white matter, and cerebrospinal fluid. We superimposed the PET images onto the MR i mages to obtain anatomo-functional correlations. We degraded the segme nted MR images to the resolution of the PET images by a convolution pr ocess to create a PET image correction map. We corrected the metabolic PET data for the PVE. We studied the cerebral metabolic rate of gluco se 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 proc esses provided the degree of PVE on a pixel-by-pixel basis, allowing c orrection of hypometabolisms contained in GM PET values. Global cortic al metabolism increased after correction for PVE by, on average, 29 an d 24% for tomographs acquired with medium (TTV03 LETI) and high (ECAT 953B CTI/Siemens) resolution, respectively, whereas the cortical metab olism increased by 75 and 65% for the respective tomographs in AD pati ents. The difference of metabolism between scans after correction for PVE was less than before correction, decreasing from 31 to 17%. This d ifference was most marked in the frontal and temporal lobes. Fusion im aging allowed correction for PVE in metabolic data using 3D MRI and de termination of whether a change in the apparent radiotracer concentrat ion in PET data reflected an alteration in GM volume, a change in radi otracer concentration per unit volume of GM, or both.