Detecting white matter injury in sickle cell disease using voxel-based morphometry
Article first published online: 31 JAN 2006
Copyright © 2006 American Neurological Association
Annals of Neurology
Volume 59, Issue 4, pages 662–672, April 2006
How to Cite
Baldeweg, T., Hogan, A. M., Saunders, D. E., Telfer, P., Gadian, D. G., Vargha-Khadem, F. and Kirkham, F. J. (2006), Detecting white matter injury in sickle cell disease using voxel-based morphometry. Ann Neurol., 59: 662–672. doi: 10.1002/ana.20790
- Issue published online: 24 MAR 2006
- Article first published online: 31 JAN 2006
- Manuscript Accepted: 2 DEC 2005
- Manuscript Revised: 16 NOV 2005
- Manuscript Received: 12 OCT 2005
- Action Medical Research (UK)
- Wellcome Trust
- Children NHS Trust
- NHS Executive
Sickle cell disease (SCD) is associated with cerebrovascular disease, cerebral infarction, and cognitive dysfunction. This study aimed to detect the presence and extent of white matter abnormalities in individuals with SCD using voxel-based morphometry (VBM).
Thirty-six children and adolescents with SCD (age range, 9–24 years) and 31 controls (8–25 years) underwent magnetic resonance investigations using T1- and T2-weighted protocols. White and gray matter density maps were obtained from three-dimensional magnetic resonance imaging (MRI) data sets. Using VBM, we compared the maps between controls and SCD individuals with silent white matter infarct lesions (SCD+L; n = 16), and those without visible abnormality (SCD−L; n = 20).
In comparison with controls, intelligence quotients (IQs) were lower in both SCD groups irrespective of presence of visible lesions. VBM showed widespread bilateral white matter abnormalities in the SCD+L group, extending beyond the regions of focal infarction in the deep anterior and posterior white matter borderzones. Bilateral white matter abnormalities were also observed in the SCD−L group, in locations similar to those in the SCD+L group.
VBM is sensitive to detection of widespread white matter injury in SCD patients in borderzones between arterial territories even in the absence of evidence of infarction. Those changes may contribute to cognitive deficits in this population. Ann Neurol 2006