Differentiation of Glioblastomas from Metastatic Brain Tumors by Tryptophan Uptake and Kinetic Analysis: A Positron Emission Tomographic Study with Magnetic Resonance Imaging Comparison

Differentiating high-grade gliomas from solitary brain metastases is often difficult by conventional magnetic resonance imaging (MRI); molecular imaging may facilitate such discrimination. We tested the accuracy of α[ 11 C]methyl-L-tryptophan (AMT)–positron emission tomography (PET) to differentiate newly diagnosed glioblastomas from brain metastases. AMT-PET was performed in 36 adults with suspected brain malignancy. Tumoral AMT accumulation was measured by standardized uptake values (SUVs). Tracer kinetic analysis was also performed to separate tumoral net tryptophan transport (by AMT volume of distribution [VD]) from unidirectional uptake rates using dynamic PET and blood input function. Differentiating the accuracy of these PET variables was evaluated and compared to conventional MRI. For glioblastoma/metastasis differentiation, tumoral AMT SUV showed the highest accuracy (74%) and the tumor/cortex VD ratio had the highest positive predictive value (82%). The combined accuracy of MRI (size of contrast-enhancing lesion) and AMT-PET reached up to 93%. For ring-enhancing lesions, tumor/cortex SUV ratios were higher in glioblastomas than in metastatic tumors and could differentiate these two tumor types with > 90% accuracy. These results demonstrate that evaluation of tryptophan accumulation by PET can enhance pretreatment differentiation of glioblastomas and metastatic brain tumors. This approach may be particularly useful in patients with a newly diagnosed solitary ring-enhancing mass

Cerebral glucose metabolism measured by positron emission tomography in term newborn infants with hypoxic ischemic encephalopathy

Total and regional cerebral glucose metabolism (CMRgl) was measured by positron emission tomography with 2-(F-18) fluoro-2-deoxy-D-glucose ((18)FDG) in 20 term infants with hypoxic ischemic encephalopathy (HIE) after perinatal asphyxia. All infants had signs of perinatal distress, and 15 were severely acidotic at birth. Six infants developed mild HIE, twelve moderate HIE, and two severe HIE during their first days of life. The positron emission tomographic scans were performed at 4-24 d of age (median, 11 d). One hour before scanning, 2-3.7 MBq/kg (54-100 µCi/kg) (18)FDG was injected i.v. No sedation was used. Quantification of CMRgl was based on a new method employing the glucose metabolism of the erythrocytes, requiring only one blood sample. In all infants, the most metabolically active brain areas were the deep subcortical parts, thalamus, basal ganglia, and sensorimotor cortex. Frontal, temporal, and parietal cortex were less metabolically active in all infants. Total CMRgl was inversely correlated with the severity of HIE (p mol.min(-1).100 g(-1), 11 with moderate HIE had 26.6 (13.0-65.1) µmol.min(-1).100 g(-1), and two with severe HIE had 10.4 and 15.0 µmol.min(-1).100 g(-1), respectively. Five of six infants who developed cerebral palsy had a mean (range) CMRgl of 18.1 (10.2-31.4) µmol.min(-1).100 g(-1) compared with 41.5 (13.0-100.8) µmol.min(-1).100 g(-1) in the infants with no neurologic sequela at 2 y. We conclude that CMRgl measured during the subacute period after perinatal asphyxia in term infants is highly correlated with the severity of HIE and short-term outcome

Abnormal Retinal Optic Nerve Morphology in Young Adults after Intrauterine Growth Restriction

Intrauterine growth restriction (IUGR) is a recognized risk factor for neurologic deficits later in life. Abnormal fetal blood flow in the presence of fetal growth retardation helps to distinguish true fetal growth impairment from small but normally grown infants. The present study aimed to investigate the influence of IUGR with abnormal fetal blood flow on retinal optic nerve morphology at 18 y of age. A prospective study was performed in 19 subjects with IUGR [abnormal fetal aortic blood flow velocity; median birth weight deviation of -31% (-22 to -42%; median (range)] and in 23 subjects with a normal birth weight for gestational age [normal fetal aortic blood flow velocity; median birth weight deviation of -2% (-10 to 22%)]. All subjects were previously examined concerning minor neurologic dysfunction (MND) at 7 y of age. The ocular fundus was examined by ophthalmoscopy, and the optic nerve morphology was evaluated by digital image analysis. Decrease in neuroretinal rim area at 18 y of age was associated with increasing negative birth weight deviation (r = 0.71, p < 0.0001). The subjects with severe MND at 7 y had a reduced neuroretinal rim area [median (range), 1.57 mm(2) (1.37-1.78 mm(2))] compared with those with less severe MND [1.94 mm(2) (1.33-2.71 mm(2))] and with those with normal neurologic function [2.18 mm(2) (1.75-2.70 mm(2)); P < 0.05 and p < 0.0001, respectively]. A decrease in neuroretinal rim area reflects either a reduction in axonal volume or a decrease in the number of axons in the optic nerve. It is yet unclear whether this finding represents neuronal changes within other cerebral regions in subjects with IUGR