Accrual of MRI white matter abnormalities in elderly with normal and impaired mobility Leslie Wolfson a, T , Xingchang Wei b , Charles B. Hall d , Victoria Panzer a , Dorothy Wakefield a , Randall R. Benson e , Julia A. Schmidt a , Simon K. Warfield b,c , Charles R.G. Guttmann b,c a Department of Neurology, University of Connecticut Health Center, Farmington, CT 06030-1840, United States b Center for Neurological Imaging, Department of Radiology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115, United States c Computational Radiology Laboratory, Department of Radiology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115, United States d Departments of Neurology and Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY 10461, United States e Department of Neurology, Wayne State University, Detroit, MI 48201, United States Received 27 August 2004; received in revised form 30 November 2004; accepted 30 December 2004 Available online 31 March 2005 Abstract White matter signal abnormality (WMSA) is often present in the MRIs of older persons with mobility impairment. We examined the relationship between impaired mobility and the progressive accrual of WMSA. Mobility was assessed with the Short Physical Performance Battery (SPPB) and quantitative measures of gait and balance. Fourteen subjects had baseline and follow-up MRI scans performed 20 months apart. WMSA was detected and quantified using automated computer algorithms. In the control subjects, WMSA volume increased by 0.02F0.05% ICCV (percent intracranial cavity volume)/year while the WMSA of mobility impaired subjects increased five-times faster (0.10F0.10 ICCV/year, p =0.03). WMSA volume was related to some of the mobility measures and was sensitive to change which was not true of the other MRI variables. The study demonstrates the sensitivity of longitudinal automated volumetric analysis of WMSA to differentiate differences in the accrual rate of WMSA in groups selected on the basis of mobility. Based on these results, we propose that a subset of subjects with mobility impairment have accelerated, disease related WMSA accrual, thus explaining the rapid progression of mobility impairment in some older persons without apparent cause. This study demonstrates that quantitative MRI and performance measures can provide valuable insight into the rate of progression and pathophysiologic abnormalities underlying mobility impairment. D 2005 Elsevier B.V. All rights reserved. Keywords: Elderly; Normal and impaired-mobility; Automated; Longitudinal; Volumetric; Determination; White matter signal abnormality 1. Introduction Impaired balance and gait result in limited mobility or falls thereby restricting the lives of older persons. The prevalence of impaired mobility is 14% at age 75 and involves almost half of the populace over 84 years [1]. Impaired mobility may result from one or more of the following deficits: deconditioning, arthritis, neuromuscular disease and CNS diseases that compromise postural control. Many individuals present with mobility impairment with non-specific neurological signs that cannot be explained by known etiology. These mobility deficits progress over time often with a cautious, unsteady gait and inability to respond to environmental hazards resulting in falls [2]. CNS diseases known to cause mobility dysfunction, such as Parkinson’s disease, account for only a small portion of older persons with failing mobility [2], underscoring the importance of identifying alternative causes of impaired mobility in this population. A number of imaging studies have demonstrated a relationship between lesions of the cerebral white matter (WM) and impaired mobility [3–8]. A 4-year longitudinal study of normal older subjects demonstrated an increase in WM signal abnormalities (WMSA) associated with gait 0022-510X/$ - see front matter D 2005 Elsevier B.V. All rights reserved. doi:10.1016/j.jns.2004.12.017 DOI of original article: 10.1016/j.jns.2005.01.011. T Corresponding author. Tel.: +1 860 679 3186; fax: +1 860 679 4446. E-mail address: wolfson@nso.uchc.edu (L. Wolfson). Journal of the Neurological Sciences 232 (2005) 23 – 27 www.elsevier.com/locate/jns