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Adaptive metabolic changes in CADASIL white matter

Akhvlediani, Tamar ; Henning, Anke ; Sándor, Peter ; Boesiger, Peter ; Jung, Hans

In: Journal of Neurology, 2010, vol. 257, no. 2, p. 171-177

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    Title
    • Adaptive metabolic changes in CADASIL white matter
    Author
    • Akhvlediani, Tamar. Department of Neurology, University Hospital Zürich, Frauenklinikstrasse 26, 8091, Zurich, Switzerland
    • Henning, Anke. Institute for Biomedical Engineering, University and Swiss Federal Institute of Technology Zürich, Zurich, Switzerland
    • Sándor, Peter. Department of Neurology, University Hospital Zürich, Frauenklinikstrasse 26, 8091, Zurich, Switzerland
    • Boesiger, Peter. Institute for Biomedical Engineering, University and Swiss Federal Institute of Technology Zürich, Zurich, Switzerland
    • Jung, Hans. Department of Neurology, University Hospital Zürich, Frauenklinikstrasse 26, 8091, Zurich, Switzerland
    Document Type
    • Postprint
    OAI-PMH Identifier
    • oai:doc.rero.ch:319699
    Summary
    Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an important genetic cause of stroke, but pathogenic mechanisms and functional alterations remain poorly characterized. The purpose of this study was to investigate adaptive metabolic and functional changes in white matter hyperintensities and normal-appearing white matter in CADASIL patients using 1H-magnetic resonance spectroscopic imaging (MRSI). Eight CADASIL patients and eight matched healthy controls were studied. 1H-MRSI data were acquired on a 3T scanner using high-resolution multi-spin echo spectroscopic imaging (T E=288ms) and non-accelerated medium-resolution MRSI (T E=35ms). MRI of all CADASIL patients demonstrated characteristic white matter hyper-intensities (WMH) in the subcortical periventricular white matter. Cre/Cho, Glx/Cho and Glx/Cre ratios were significantly decreased in WMH compared to normal-appearing white matter (NAWM) in patients, while Glx/Cre and mI/Cho ratios in NAWM showed a significant increase compared to healthy controls. In severely affected patients derived spectra reflected a decrease of NAA concentrations inside WMH when compared to healthy white matter. Metabolic abnormalities in WMH of CADASIL patients are compatible with axonal loss due to chronic micro-infarctions. Increased Glx/Cre and mI/Cho ratios in NAWM indicate an augmented glial cell density and decreased neuronal cell density. This altered tissue composition might be interpreted as adaptation to hypoperfusion and impaired vasoreactivity in NAWM of CADASIL patients. Our data might contribute to the general understanding of adaptive processes induced by hypoperfusion and chronic ischemia