, Volume 53, Issue 2, pp 141–148 | Cite as

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

  • Charlotte Barbier
  • Camille Chabernaud
  • Laurent Barantin
  • Philippe Bertrand
  • Catherine Sembely
  • Dominique Sirinelli
  • Pierre CastelnauEmail author
  • Jean-Philippe Cottier
Paediatric Neuroradiology



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.


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.


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.


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.


Neurofibromatosis MRI Spectroscopy Basal ganglia Thalamus 



The authors thank the CIC INSERM 202, Tours, 37000, France, which is responsible for the study monitoring. The authors are grateful to Marc Sitbon and Devika Jutagir (USA) for careful reading and correction of the manuscript. This work was supported by the PHRC grant from the Region Centre and CHU de Tours & a fellowship of the Association Neurofibromatoses et Recklinghausen (ANR), France, to C. Chabernaud.

Conflict of interest

We declare that we have no conflict of interest.


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Copyright information

© Springer-Verlag 2010

Authors and Affiliations

  • Charlotte Barbier
    • 1
  • Camille Chabernaud
    • 2
  • Laurent Barantin
    • 1
  • Philippe Bertrand
    • 3
  • Catherine Sembely
    • 4
  • Dominique Sirinelli
    • 4
  • Pierre Castelnau
    • 2
    • 5
    • 6
    Email author
  • Jean-Philippe Cottier
    • 1
    • 5
  1. 1.Department of NeuroradiologyCHRU & Tours UniversityToursFrance
  2. 2.Department of Pediatric NeurologyCHRU & Tours University and INSERM U930ToursFrance
  3. 3.Department of RadiologyCHRU & Tours UniversityToursFrance
  4. 4.Department of Pediatric RadiologyCHRU & Tours UniversityToursFrance
  5. 5.CHRU & Tours University and INSERM U930ToursFrance
  6. 6.Neurologie Pediatrique & INSERM U930, Hopital d’Enfants Gatien de ClochevilleTours cedex 09France

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