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Cerebral Structure (cerebral + structure)
Selected AbstractsInsights into the acute cerebral metabolic changes associated with childhood diabetesDIABETIC MEDICINE, Issue 5 2005F. J. Cameron Abstract Aims Type 1 diabetes is a prevalent chronic disease in childhood with the commonest single cause of death being cerebral oedema in the context of diabetic ketoacidosis (DKA). The nature of the alterations in cerebral metabolism that may result in vulnerability to neuronal injury remains unknown. The aim of this study was to analyse the magnetic resonance imaging (MRI) and magnetic resonance spectroscopy (MRS) brain data from eight children with diabetes following acute presentation with hyperglycaemia with or without ketoacidosis, to determine the nature and timing of any alterations in cerebral structure and metabolism. Methods This study used MRI and MRS to investigate regional cerebral abnormalities in a small series of diabetic patients with and without DKA. Changes were compared with the clinical and biochemical features of the patients studied. Results Our small series of patients all demonstrated abnormal signal changes in the frontal region on fluid attenuated inversion recovery (FLAIR) MR imaging, suggestive of oedema, and spectroscopic abnormalities of increased taurine, myoinositol and glucose levels. The MR abnormalities varied in severity but did not correlate with any clinical or biochemical parameters. Conclusions These changes indicate that many diabetic children, particularly at presentation, may have alterations in cerebral metabolism with implications for the pathogenesis and treatment of the cerebral complications of DKA. In addition, our findings suggest that increased taurine may be one of the important differentiating factors in the response of the brain of diabetic children to DKA that may reflect an increase in their vulnerability to cerebral oedema compared with diabetic adults. [source] Difluoromethylornithine Decreases Long-Lasting Protein Oxidation Induced by Neonatal Ethanol Exposure in the Hippocampus of Adolescent RatsALCOHOLISM, Issue 5 2007Carlos Fernando Mello Background: Ethanol exposure and withdrawal during central nervous system development can cause oxidative stress and produce severe and long-lasting behavioral and morphological alterations in which polyamines seem to play an important role. However, it is not known if early ethanol exposure causes long-lasting protein oxidative damage and if polyamines play a role in such a deleterious effect of ethanol. Methods: In this study we investigated the effects of early ethanol exposure (6 g/kg/d, by gavage), from postnatal day (PND) 1 to 8, and of the administration of difluoromethylornithine (DFMO, 500 mg/kg, i.p., on PND 8), a polyamine biosynthesis inhibitor, on the extent of oxidative modification of proteins. Indices of oxidative modification of proteins included protein carbonyls, 3-nitrotyrosine (3-NT), and protein bound 4-hydroxynonenal (HNE) in the hippocampus, cerebellum, hypothalamus, striatum, and cerebral cortex of Sprague,Dawley rats at PND 40. Results: Both ethanol and DFMO administration alone increased protein carbonyl immunoreactivity in the hippocampus at PND 40, but the combination of DFMO and ethanol resulted in no effect on protein carbonyl levels. No alterations in the content of protein-bound HNE, 3-NT, or carbonyl were found in any other cerebral structure. Conclusions: These results suggest that the hippocampus is selectively affected by early ethanol exposure and by polyamine synthesis inhibition. In addition, the results suggest a role for polyamines in the long-lasting increase of protein carbonyls induced by ethanol exposure and withdrawal. [source] Increased midbrain gray matter in Tourette's syndromeANNALS OF NEUROLOGY, Issue 2 2006Gaėtan Garraux MD Objective To investigate cerebral structure in Tourette's syndrome (TS). Methods Voxel-based morphometry study of high-resolution MRIs in 31 TS patients compared with 31 controls. Results Increased gray matter mainly in the left mesencephalon in 31 TS patients. Interpretation This result constitutes strong and direct evidence supporting Devinsky's hypothesis (Devinsky O. Neuroanatomy of Gilles de la Tourette's syndrome. Possible midbrain involvement. Arch Neurol 1983;40:508,514) according to which midbrain disturbances play an important pathogenic role in TS. Ann Neurol 2006;59:381,385 [source] Reliving lifelong episodic autobiographical memories via the hippocampus: A correlative resting PET study in healthy middle-aged subjectsHIPPOCAMPUS, Issue 5 2008Pascale Piolino Abstract We aimed at identifying the cerebral structures whose synaptic function subserves the recollection of lifetime's episodic autobiographical memory (AM) via autonoetic consciousness. Twelve healthy middle-aged subjects (mean age: 59 years ± 2.5) underwent a specially designed cognitive test to assess the ability to relive richly detailed episodic autobiographical memories from five time periods using the Remember/Know procedure. We computed an index of episodicity (number of Remember responses justified by the recall of specific events and details) and an index of retrieval spontaneity, and additionally an index of semanticized memories (number of Know responses). The regional cerebral blood flow (rCBF) was measured in the resting state, with H2O15 as part of an activation PET study. The indexes were correlated with blood flow using volumes of interest in frontotemporal regions, including hippocampus and voxel-wise analyses in SPM. With both analyses, significant correlations were mainly found between the index of episodicity and rCBF in the medial temporal lobe, including hippocampus, across the five time periods (unlike the index of semanticized memories) and between the spontaneity index and rCBF in the prefrontal areas. These results highlight, in healthy subjects, the distinct role of these two structures in AM retrieval and support the view that the hippocampus is needed for reexperiencing detailed episodic memories no matter how old they are. © 2008 Wiley-Liss, Inc. [source] Focal Cortical Dysplasia: Improving Diagnosis and Localization With Magnetic Resonance Imaging Multiplanar and Curvilinear ReconstructionJOURNAL OF NEUROIMAGING, Issue 3 2002Maria Augusta Montenegro MD ABSTRACT Objective. To establish the contribution of multiplanar reconstruction (MPR) and curvilinear reformatting (CR) to the MRI investigation of focal cortical dysplasia (FCD). Methods. From a group of patients with intractable frontal lobe epilepsy, we selected patients with neuroimaging diagnosis of FCD. The diagnosis of FCD was based on the neuroimaging findings after a three step evaluation, always in the same order: (a) plain MRI films, (b) MPR, and (c) CR. After the selection of patients, the process of reviewing all the images in the three stages described above was performed by one of us, who did not take part on the selection of patients nor on the initial evaluation, and who was blind to the clinical and EEG findings of the patients. For data analysis, we first assessed the contribution of the additional findings of MPR analysis compared to the results of the evaluation using only plain MRI films, as is usually done in routine practice. Second, we assessed the contribution of CR to the findings of plain MRI films plus MPR. After completing the multistep evaluation, we all went back to review the plain MRI films with knowledge of lesion topography, in order to identify possible subtle features associated with FCD. Results. Seventeen patients met the inclusion criteria. Twelve had imaging diagnosis of FCD and were included in the second step of this project. Plain films of high resolution MRI showed the lesion in 6 (50%) of the 12 patients. By adding MPR to the plain MRI films, we identified lesions in all 12 patients. Furthermore, we found that MPR provided a better lesion localization and ascertainment of its relationship to other cerebral structures in 5 of 6 (83%) patients who had a lesion identified on plain films. By adding CR to the plain MRI films plus MPR analysis, we observed that (a) CR also allowed the identification of the dysplastic lesion in all patients, (b) CR improved lesion localization in one patient, and (c) CR provided a better visualization of the lesion extent in 4 patients (33%), showed a larger lesion in 3, and demonstrated that part of the area suspected as abnormal was more likely volume averaging in 2. Conclusion. MPR and CR analysis add to the neuroimaging evaluation of FCD by improving the lesion diagnosis and localization. CR helps to establish the extent of the lesion more precisely, allowing the visualization of some areas not shown on high resolution MRI and MPR. These techniques are complementary and do not replace the conventional wisdom of MRI analysis. 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