A voxel-based morphometry study of patterns of brain atrophy in ALS and ALS/FTLD
J. L. Chang, MEng,
C. Lomen-Hoerth, MD, PhD,
J. Murphy, PhD,
R. G. Henry, PhD,
J. H. Kramer, PsyD,
B. L. Miller, MD and
M. L. Gorno-Tempini, MD, PhD
From the Departments of Neurology (J.L. Chang, and Drs. Lomen-Hoerth, Murphy, Kramer, Miller, and Gorno-Tempini) and Radiology (Dr. Henry), University of California San Francisco.
Address correspondence and reprint requests to Dr. Maria Luisa Gorno-Tempini, UCSF Memory and Aging Center, 350 Parnassus Ave., Suite 706, San Francisco, CA 94143-1207; e-mail: marilu{at}memory.ucsf.edu
Objective: To investigate the patterns of MRI brain atrophyin patients with ALS with and without clinically evident frontotemporallobar dementia (FTLD) using voxel-based morphometry (VBM).
Methods: Voxel-based morphometry was used to compare T1-weightedMRI images obtained from ten ALS patients with FTLD, ten ALSpatients who were cognitively and behaviorally normal, and 22control subjects. Images from patients and controls were spatiallypre-processed using a study-specific, customized template anda priori images. A statistical threshold of p < 0.05 correctedfor multiple comparisons determined significance.
Results: A common pattern of gray matter atrophy was seen inboth ALS and ALS/FTLD patients when compared to controls thatinvolved the bilateral motor/premotor cortices, the left middleand inferior frontal gyri, the anterior portion of the superiorfrontal gyri, the superior temporal gyri, the temporal polesand left posterior thalamus. Most of the frontal regions weresignificantly more atrophied in the ALS/FTLD group than in theALS group. No significant differences were found in white mattervolumes.
Conclusions: Patients with ALS and ALS associated with frontotemporallobar degeneration exhibit widespread gray matter atrophy infrontotemporal regions. This finding supports the idea of aclinical and anatomic continuum between ALS and frontotemporallobar degeneration.
Supported by the ALS Association, The McBean Family Foundation,The Sandler Foundation, the John Douglas French Alzheimer'sAssociation, the National Institute on Aging (5P01 AG019724-02and 1 P50 AG-03-006-01), the California Department of Health(DHS 04-35516), the UCSF General Clinical Research Center (M01RR00079), and the National Institute of Neurologic Diseasesand Stroke (R01 NS50915).
Received May 27, 2004. Accepted in final form March 29, 2005.
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