NEUROLOGY 2005;65:75-80
© 2005 American Academy of Neurology
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 atrophy in patients with ALS with and without clinically evident frontotemporal lobar dementia (FTLD) using voxel-based morphometry (VBM).
Methods: Voxel-based morphometry was used to compare T1-weighted MRI images obtained from ten ALS patients with FTLD, ten ALS patients who were cognitively and behaviorally normal, and 22 control subjects. Images from patients and controls were spatially pre-processed using a study-specific, customized template and a priori images. A statistical threshold of p < 0.05 corrected for multiple comparisons determined significance.
Results: A common pattern of gray matter atrophy was seen in both ALS and ALS/FTLD patients when compared to controls that involved the bilateral motor/premotor cortices, the left middle and inferior frontal gyri, the anterior portion of the superior frontal gyri, the superior temporal gyri, the temporal poles and left posterior thalamus. Most of the frontal regions were significantly more atrophied in the ALS/FTLD group than in the ALS group. No significant differences were found in white matter volumes.
Conclusions: Patients with ALS and ALS associated with frontotemporal lobar degeneration exhibit widespread gray matter atrophy in frontotemporal regions. This finding supports the idea of a clinical and anatomic continuum between ALS and frontotemporal lobar degeneration.
Supported by the ALS Association, The McBean Family Foundation, The Sandler Foundation, the John Douglas French Alzheimer's Association, the National Institute on Aging (5P01 AG019724-02 and 1 P50 AG-03-006-01), the California Department of Health (DHS 04-35516), the UCSF General Clinical Research Center (M01 RR00079), and the National Institute of Neurologic Diseases and Stroke (R01 NS50915).
Received May 27, 2004. Accepted in final form March 29, 2005.
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