American Journal of Neuroradiology 28:773-776, April 2007
© 2007 American Society of Neuroradiology
BRAIN
Contribution of Diffusion Tensor MR Imaging in Detecting Cerebral Microstructural Changes in Adults with Neurofibromatosis Type 1
a MR Center, University Children's Hospital, Zurich, Switzerland
b Center for Integrative Human Physiology, University of Zurich, Zurich, Switzerland
c Department of Neurology, University Children's Hospital, Zurich, Switzerland
d Department of Diagnostic Imaging, Medical Physics, University Hospital, Freiburg, Germany
Address correspondence to Thomas Loenneker, MR-Center, University Children's Hospital, Steinwiesstr 75, 8032 Zurich, Switzerland; e-mail: thomas.loenneker{at}kispi.unizh.ch
BACKGROUND AND PURPOSE: After an early progression of signal intensity changes in T2-weighted MR images, also known as "neurofibromatosis bright objects," in patients with neurofibromatosis type 1 (NF-1), there is a tendency toward regression or even disappearance in early adulthood. The purpose of this study was to investigate whether adult patients with NF-1 exhibit generalized microstructural alterations even in normal-appearing brain regions.
MATERIALS AND METHODS: Conventional and diffusion tensor MR imaging of the brain was obtained in 10 adult patients with NF-1 and 10 age-matched healthy volunteers. Apparent diffusion coefficient (ADC) and fractional anisotropy (FA) were measured in brain stem, basal ganglia, thalamus, corpus callosum, and frontal and parietooccipital white matter regions.
RESULTS: Significantly increased ADC and decreased FA values were found in all regions of interest and in all patients with NF-1, irrespective of their scholastic achievement and subsequent professional performance, compared with control subjects (P < .001). There were no significant correlations with the age (P > .1) or with the lateralization between brain hemispheres (P > .05).
CONCLUSION: Diffusion tensor imaging reveals globally elevated FA and decreased ADC values in the mature brains of patients with NF-1, which is most likely a consequence of diffuse and basic alterations in cerebral microstructure that result from the underlying gene mutation.
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