RESUMO
BACKGROUND AND PURPOSE: Hypoxia and cerebral ischemia (HI) events are capable of triggering important changes in brain metabolism, including glucose metabolism abnormalities, which may be related to the severity of the insult. Using positron emission microtomography (microPET) with [18F]fluorodeoxyglucose (18F-FDG), this study proposes to assess abnormalities of brain glucose metabolism in adult rats previously submitted to the neonatal HI model. We hypothesize that cerebral metabolic outcomes will be associated with cognitive deficits and magnitude of brain injury. METHODS: Seven-day-old rats were subjected to an HI model, induced by permanent occlusion of the right common carotid artery and systemic hypoxia. 18F-FDG-microPET was used to assess regional and whole brain glucose metabolism in rats at 60 postnatal days (PND 60). An interregional cross-correlation matrix was utilized to construct metabolic brain networks (MBN). Rats were also subjected to the Morris Water Maze (MWM) to evaluate spatial memory and their brains were processed for volumetric evaluation. RESULTS: Brain glucose metabolism changes were observed in adult rats after neonatal HI insult, limited to the right brain hemisphere. However, not all HI animals exhibited significant cerebral hypometabolism. Hippocampal glucose metabolism was used to stratify HI animals into HI hypometabolic (HI-h) and HI non-hypometabolic (HI non-h) groups. The HI-h group had drastic MBN disturbance, cognitive deficit, and brain tissue loss, concomitantly. Conversely, HI non-h rats had normal brain glucose metabolism and brain tissue preserved, but also presented MBN changes and spatial memory impairment. Furthermore, data showed that brain glucose metabolism correlated with cognitive deficits and brain volume outcomes. CONCLUSIONS: Our findings demonstrated that long-term changes in MBN drive memory impairments in adult rats subjected to neonatal hypoxic ischemia, using in vivo imaging microPET-FDG. The MBN analyses identified glucose metabolism abnormalities in HI non-h animals, which were not detected by conventional 18F-FDG standardized uptake value (SUVr) measurements. These animals exhibited a metabolic brain signature that may explain the cognitive deficit even with no identifiable brain damage.
Assuntos
Encéfalo/metabolismo , Hipóxia-Isquemia Encefálica/metabolismo , Transtornos da Memória/metabolismo , Rede Nervosa/metabolismo , Animais , Encéfalo/diagnóstico por imagem , Modelos Animais de Doenças , Glucose/metabolismo , Hipóxia-Isquemia Encefálica/complicações , Hipóxia-Isquemia Encefálica/diagnóstico por imagem , Masculino , Transtornos da Memória/diagnóstico por imagem , Transtornos da Memória/etiologia , Rede Nervosa/diagnóstico por imagem , Tomografia por Emissão de Pósitrons , Ratos , Ratos WistarRESUMO
Posterior reversible encephalopathy syndrome (PRES) is a clinical-radiologic entity not yet understood, that presents with transient neurologic symptoms and particular radiological findings. Few papers show the differences between pregnant and non-pregnant patients. We review the cases of 38 women diagnosed with PRES, in order to find significant differences between pregnant (18) and non-pregnant (20) patients. We found differences among the age of patients (25.83 years old in pregnant and 29.31 years old in non pregnant; P=0.001); in the mean of highest systolic blood pressure, that was higher in non-pregnant group (185:162 mmHg; P=0.121); and in creatinine levels that was higher in non-pregnant group (3.47:1.04 mg/dL; P=0.001). To our knowledge, just a few papers analyzed whether PRES syndrome presented in the same way in pregnant and non-pregnant patients. The differences and the possible pathophisiology of this syndrome still remain enigmatic.