Purpose: To compare the apparent diffusion coefficient (ADC) in non-small cell lung cancer lesions with standardized uptake values (SUV) derived from combined 18F-fluoro-deoxy-glucose-positron emission tomography/magnetic resonance imaging (FDG-PET/MRI) and those derived from FDG-PET/CT.
Materials and Methods: In 18 consecutive patients with histologically proven NSCLC (17 men, 1 woman; mean age, 61???12 years), whole-body FDG-PET/MRI was performed after whole-body FDG-PET/CT. Regions of interest (ROI) encompassing the entire primary tumor were drawn into FDG-PET/CT and FDG-PET/MR images to determine the maximum and mean standardized uptake value (SUVmax; SUVmean) and into ADC parameter maps to assess mean ADC values. Pearson?s correlation coefficients were calculated to compare SUV and ADC values.
Results: The SUVmax of NSCLC was 12.3???4.8 [mean ?SD], and the SUVmean was 7.2???2.8 as assessed by FDG-PET/MRI. The SUVmax and SUVmean derived from FDG-PET/CT and FDG-PET/MRI correlated well (R?=?0.93; p?0.001 and R?=?0.92; p?0.001, respectively). The ADCmean of the pulmonary tumors was 187.9???88.8???10?5?mm?/s [mean???SD]. The ADCmean exhibited a significant inverse correlation with the SUVmax (R?=??0.72; p?0.001) as well as with the SUVmean assessed by FDG-PET/MRI (R?=??0.71; p?0.001).
Conclusion: This simultaneous PET/MRI study corroborates the assumed significant inverse correlation between increased metabolic activity on FDG-PET and restricted diffusion on DWI in NSCLC.
Citation Format:
Canavan's disease is an autosomal recessive hereditary leukodystrophy resulting from deficiency of the enzyme aspartoacylase. Two children suffering from this metabolic brain disease were examined using image-guided localized proton spectroscopy. The absolute concentrations of metabolites were determined. These data demonstrate, for the first time, that the well known increase of the N-acetylaspartic acid (NAA)/Cho ratio in this disease may be not only due to a reduction of choline-containing compounds in brain tissue but, at least in specific cases, also due to an increase of the NAA concentration, which is a result of the enzyme defect.
BackgroundPain is a complex experience with sensory, emotional and cognitive aspects. Genetic and environmental factors contribute to pain-related phenotypes such as chronic pain states. Genetic variations in the gene coding for catechol-O-methyltransferase (COMT) have been suggested to affect clinical and experimental pain-related phenotypes including regional μ-opioid system responses to painful stimulation as measured by ligand-PET (positron emission tomography). The functional val158met single nucleotide polymorphism has been most widely studied. However, apart from its impact on pain-induced opioid release the effect of this genetic variation on cerebral pain processing has not been studied with activation measures such as functional magnetic resonance imaging (fMRI), PET or electroencephalography. In the present fMRI study we therefore sought to investigate the impact of the COMT val158met polymorphism on the blood oxygen level-dependent (BOLD) response to painful laser stimulation.Results57 subjects were studied. We found that subjects homozygous for the met158 allele exhibit a higher BOLD response in the anterior cingulate cortex (ACC), foremost in the mid-cingulate cortex, than carriers of the val158 allele.ConclusionThis result is in line with previous studies that reported higher pain sensitivity in homozygous met carriers. It adds to the current literature in suggesting that this behavioral phenotype may be mediated by, or is at least associated with, increased ACC activity. More generally, apart from one report that focused on pain-induced opioid release, this is the first functional neuroimaging study showing an effect of the COMT val158met polymorphism on cerebral pain processing.
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