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The Effect of Brain Atrophy on Cerebral Hypometabolism in the Visual Variant of Alzheimer Disease
Arun L. W. Bokde, PhD;
Pietro Pietrini, MD, PhD;
Vicente Ibáñez, MD, PhD;
Maura L. Furey, PhD;
Gene E. Alexander, PhD;
Neill R. Graff-Radford, MD;
Stanley I. Rapoport, MD;
Mark B. Schapiro, MD;
Barry Horwitz, PhD
Arch Neurol. 2001;58:480-486.
Background Brain glucose metabolic rates measured by positron emission tomography
can be more affected by partial volume effects in Alzheimer disease (AD) than
in healthy aging because of disease-associated brain atrophy.
Objective To determine whether the distinct distribution of cerebral metabolic
lesions in patients with the visual variant of AD (AD + VS) represents a true
index of neuronal/synaptic dysfunction or is the consequence of brain atrophy.
Setting Government research hospital.
Design Resting cerebral metabolic rate for glucose was measured with positron
emission tomography in a cross-sectional study of AD and AD + VS groups and
in healthy control subjects. Segmented magnetic resonance images were used
to correct for brain atrophy.
Patients Patients with AD + VS had prominent visual and visuospatial symptoms.
There were 15 patients with AD, 10 with AD + VS, and 37 age-matched control
subjects.
Main Outcome Measure Measurement of the rate of cerebral glucose metabolism.
Results Before atrophy correction, the AD + VS group, compared with the control
subjects, showed hypometabolism in primary and extrastriate visual areas and
in parietal and superior temporal cortical areas. Compared with the AD group,
the AD + VS group showed hypometabolism in visual association areas. After
atrophy correction, hypometabolism remained significantly different between
patients and controls and between the 2 AD groups.
Conclusions The reductions in cerebral hypometabolism represent a true loss of functional
activity and are not simply an artifact caused by brain atrophy. The different
patterns of hypometabolism indicate the differential development of the lesions
between the AD and AD + VS groups.
From the Laboratory of Neurosciences, National Institute on Aging,
National Institutes of Health, Bethesda, Md (Drs Bokde, Pietrini, Furey, Rapoport,
Schapiro, and Horwitz); Department of Human and Environmental Sciences, University
of Pisa, Pisa, Italy (Dr Pietrini); Division de Neuropsychiatrie, Belle Idée,
Geneve, Switzerland (Dr Ibáñez); Arizona Alzheimer's Disease
Research Center and Department of Psychology, Arizona State University, Tempe
(Dr Alexander); and Department of Neurology, Mayo Clinic–Jacksonville,
Jacksonville, Fla (Dr Graff-Radford). Dr Horwitz is now with the Language
Section, National Institute on Deafness and Other Communication Disorders,
National Institutes of Health.
Corresponding author and reprints: Barry Horwitz, PhD, Language Section,
National Institute on Deafness and Other Communication Disorders, NIH, Bldg
10, Room 6C420, Bethesda, MD 20892 (e-mail: horwitz{at}helix.nih.gov).
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