Literature DB >> 20959972

Proton MR spectroscopic imaging of basal ganglia and thalamus in neurofibromatosis type 1: correlation with T2 hyperintensities.

Charlotte Barbier1, Camille Chabernaud, Laurent Barantin, Philippe Bertrand, Catherine Sembely, Dominique Sirinelli, Pierre Castelnau, Jean-Philippe Cottier.   

Abstract

INTRODUCTION: Neurofibromatosis type 1 (NF1) is frequently associated with hyperintense lesions on T2-weighted images called "unidentified bright objects" (UBO). To better characterize the functional significance of UBO, we investigate the basal ganglia and thalamus using spectroscopic imaging in children with NF1 and compare the results to anomalies observed on T2-weighted images.
METHODS: Magnetic resonance (MR) data of 25 children with NF1 were analyzed. On the basis of T2-weighted images analysis, two groups were identified: one with normal MR imaging (UBO- group; n = 10) and one with UBO (UBO+ group; n = 15). Within the UBO+ group, a subpopulation of patients (n = 5) only had lesions of the basal ganglia. We analyzed herein seven regions of interest (ROIs) for each side: caudate nucleus, capsulo-lenticular region, lateral and posterior thalamus, thalamus (lateral and posterior voxels combined), putamen, and striatum. For each ROI, a spectrum of the metabolites and their ratio was obtained.
RESULTS: Patients with abnormalities on T2-weighted images had significantly lower NAA/Cr, NAA/Cho, and NAA/mI ratios in the lateral right thalamus compared with patients with normal T2. These abnormal spectroscopic findings were not observed in capsulo-lenticular regions that had UBO but in the thalamus region that was devoid of UBO.
CONCLUSION: Multivoxel spectroscopic imaging using short-time echo showed spectroscopic abnormalities in the right thalamus of NF1 patients harboring UBO, which were mainly located in the basal ganglia. This finding could reflect the anatomical and functional interactions of these regions.

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Year:  2010        PMID: 20959972     DOI: 10.1007/s00234-010-0776-4

Source DB:  PubMed          Journal:  Neuroradiology        ISSN: 0028-3940            Impact factor:   2.804


  35 in total

1.  Proton magnetic resonance spectroscopy of brain lesions in children with neurofibromatosis type 1.

Authors:  I D Wilkinson; P D Griffiths; J K Wales
Journal:  Magn Reson Imaging       Date:  2001-10       Impact factor: 2.546

Review 2.  Brain structure and function in neurofibromatosis type 1: current concepts and future directions.

Authors:  Jonathan M Payne; Mahendranath D Moharir; Richard Webster; Kathryn N North
Journal:  J Neurol Neurosurg Psychiatry       Date:  2010-03       Impact factor: 10.154

3.  Inactivation of NF1 in CNS causes increased glial progenitor proliferation and optic glioma formation.

Authors:  Yuan Zhu; Takayuki Harada; Li Liu; Mark E Lush; Frantz Guignard; Chikako Harada; Dennis K Burns; M Livia Bajenaru; David H Gutmann; Luis F Parada
Journal:  Development       Date:  2005-12       Impact factor: 6.868

4.  Reduced striatal dopamine underlies the attention system dysfunction in neurofibromatosis-1 mutant mice.

Authors:  Jacquelyn A Brown; Ryan J Emnett; Crystal R White; Carla M Yuede; Sara B Conyers; Karen L O'Malley; David F Wozniak; David H Gutmann
Journal:  Hum Mol Genet       Date:  2010-09-07       Impact factor: 6.150

5.  Thalamic involvement in neurofibromatosis type 1: evaluation with proton magnetic resonance spectroscopic imaging.

Authors:  P Y Wang; W E Kaufmann; C W Koth; M B Denckla; P B Barker
Journal:  Ann Neurol       Date:  2000-04       Impact factor: 10.422

6.  Visual-spatial performance deficits in children with neurofibromatosis type-1.

Authors:  Gregory W Schrimsher; Rebecca L Billingsley; John M Slopis; Bartlett D Moore
Journal:  Am J Med Genet A       Date:  2003-07-30       Impact factor: 2.802

Review 7.  Genetic and epigenetic mechanisms in the pathogenesis of neurofibromatosis type I.

Authors:  L J Metheny; A J Cappione; G R Skuse
Journal:  J Neuropathol Exp Neurol       Date:  1995-11       Impact factor: 3.685

8.  Neurofibromatosis type 1: pathologic substrate of high-signal-intensity foci in the brain.

Authors:  D P DiPaolo; R A Zimmerman; L B Rorke; E H Zackai; L T Bilaniuk; A T Yachnis
Journal:  Radiology       Date:  1995-06       Impact factor: 11.105

9.  Proton MR spectroscopy in patients with neurofibromatosis type 1: evaluation of hamartomas and clinical correlation.

Authors:  M Castillo; C Green; L Kwock; K Smith; D Wilson; S Schiro; R Greenwood
Journal:  AJNR Am J Neuroradiol       Date:  1995-01       Impact factor: 3.825

10.  Metabolite changes in normal-appearing gray and white matter are linked with disability in early primary progressive multiple sclerosis.

Authors:  J Sastre-Garriga; G T Ingle; D T Chard; Lí Ramió-Torrentà; M A McLean; D H Miller; A J Thompson
Journal:  Arch Neurol       Date:  2005-04
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  3 in total

1.  Multivariate pattern analysis reveals subtle brain anomalies relevant to the cognitive phenotype in neurofibromatosis type 1.

Authors:  João V Duarte; Maria J Ribeiro; Inês R Violante; Gil Cunha; Eduardo Silva; Miguel Castelo-Branco
Journal:  Hum Brain Mapp       Date:  2012-09-11       Impact factor: 5.038

2.  Evaluation of the basal ganglia in neurofibromatosis type 1.

Authors:  Francesco Nicita; Claudio Di Biasi; Saadi Sollaku; Stefano Cecchini; Vincenzo Salpietro; Angelo Pittalis; Laura Papetti; Fabiana Ursitti; Fiorenza Ulgiati; Anna Maria Zicari; Gian Franco Gualdi; Enrico Properzi; Marzia Duse; Martino Ruggieri; Alberto Spalice
Journal:  Childs Nerv Syst       Date:  2013-07-27       Impact factor: 1.475

3.  GABA deficiency in NF1: A multimodal [11C]-flumazenil and spectroscopy study.

Authors:  Inês R Violante; Miguel Patricio; Inês Bernardino; José Rebola; Antero J Abrunhosa; Nuno Ferreira; Miguel Castelo-Branco
Journal:  Neurology       Date:  2016-07-29       Impact factor: 9.910

  3 in total

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