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Brain 18F-FDG PET in the Diagnosis of Neurodegenerative Dementias: Comparison with Perfusion SPECT and with Clinical Evaluations Lacking Nuclear Imaging*

Daniel H.S. Silverman, MD, PhD

Department of Molecular and Medical Pharmacology, David Geffen School of Medicine at UCLA, Los Angeles, California



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FIGURE 1. Normal adult pattern of cerebral glucose metabolism measured with 18F-FDG. Images are shown from the most superior (far left column) to most inferior (far right column) planes of the brain. In this and later figures, images are cross-sectional and are displayed with the anterior brain at the top of each image and the left side of the brain on the right of each image. Normal aging is associated with some increased generalized cortical atrophy, as evidenced by moderate widening (arrow) of the interthalamic distances in the 85-y-old patient (middle right). Additional arrows highlight the progression of mild metabolic decline, also attributable to normal aging, in the medial prefrontal cortex bilaterally (middle left, ages 53 and 85 y) and in the left anterior prefrontal cortex (middle left, age 85 y). Otherwise, in healthy adults, the pattern of regional cerebral metabolism changes little throughout adulthood.

 


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FIGURE 2. 18F-FDG PET images of early AD. Early Alzheimer’s typically affects the parietal, temporal, and posterior cingulate cortices. Brain images of this 80-y-old woman demonstrate hypometabolism of the parietal cortex, bilaterally (left and middle), with relative sparing of the primary visual cortex, sensorimotor cortex, thalamus, and basal ganglia. In the early stages of AD, deficits often appear asymmetrically, as evidenced here by mild hypometabolism of the left temporal cortex (right). In later stages of the disease, degeneration will be apparent bilaterally.

 


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FIGURE 3. 18F-FDG PET images of early- and late-stage dementia with Lewy bodies. Typical cerebral metabolic patterns for patients with dementia with Lewy body disease are similar to AD patterns, but with less sparing of the occipital cortex. A patient with early-stage disease (top row; 63-y-old woman) was clinically followed up for 28 mo, during which her MMSE score dropped from 23 to 14, of 30 possible points. The arrows on her scan highlight bilateral hypometabolism of the parietal (left) and occipital (middle) cortices, as well as hypometabolism of the posterior temporal cortex (right). A patient in a later stage of the disease (bottom row; 71-y-old man) has moderate to severe bilateral hypometabolism in the parietal cortex (left) and in the temporooccipital cortex (right), as similarly seen in the early-stage patient. Additional arrows in the left image refer to progression of hypometabolism in the occipital and prefrontal cortices, bilaterally.

 


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FIGURE 4. 18F-FDG PET images of Parkinson’s disease dementia. Typical patterns of regional cerebral metabolism are similar in Parkinson’s dementia and AD, with less sparing of the occipital cortex and more sparing of the mesiotemporal area. The diagnosis of Parkinson’s disease in this patient (72-y-old woman) was subsequently confirmed by autopsy. The arrows on her scan indicate parietal (left and middle images) and occipital (middle and right images) hypometabolism, whereas the 18F-FDG uptake in basal ganglia is undiminished at this stage of her disease.

 


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FIGURE 5. 18F-FDG PET images of vascular dementia. Hypometabolism affecting cortical, subcortical, and cerebellar areas is often seen in vascular dementia. This patient (65-y-old woman) was followed for 10 mo, and vascular dementia was diagnosed both clinically and by structural imaging. Arrows indicate hypometabolism of the right frontal cortex (far left, middle right), right parietal cortex (far left, middle left), right basal ganglia and thalamus (middle right), and right temporal cortex (far right). The hypometabolism of the left cerebellum (far right) is characteristic of cross-cerebellar diaschisis, caused by diminished afferent input from the contralateral cortex.

 


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FIGURE 6. 18F-FDG PET images of early frontotemporal dementia. This patient (66-y-old man) was diagnosed both clinically and by PET as having frontotemporal disease. The patient’s MMSE score at the time of PET was 27 of a possible 30 points. Arrows indicate bilateral hypometabolism of the frontal cortex (far left), at a time that the remainder of the cerebral activity is not appreciably affected (middle left, middle right, and far right).

 


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FIGURE 7. 18F-FDG PET images of Huntington’s disease. This patient (43-y-old man) has an 8-y history of progressive Huntington’s disease. Arrows highlight the typical metabolic pattern of hypometabolism severely affecting the basal ganglia (right) at a time that cortical metabolism is still relatively intact (left and middle). As the disease progresses, diffuse cortical involvement gradually develops.

 


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FIGURE 8. Distribution of 111 scan-positive cases among 170 patients undergoing PET for cognitive evaluation. TP = true positives; FP = false positives.

 


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FIGURE 9. 18F-FDG PET scans of a patient with false-positive findings and an AD patient. Shown are representative axial (left) and sagittal (middle) slices through an 18F-FDG PET brain scan of a 79-y-old woman undergoing clinical evaluation for cognitive impairment. The patient had a history of depression and thyroid disease and was receiving thyroid hormone replacement therapy at time of PET. The interpreting nuclear medicine physician had read the scan as consistent with early neurodegenerative changes in an Alzheimer-like pattern, because of the apparent relative decreased activity in the parietal cortex (bold white arrows), relative to the adjacent frontal and temporal cortex (thin white arrows). Longitudinal clinical follow-up for 2.5 y after the scan showed no progressive dementia, so the scan interpretation was classified as false positive. If this scan were being read now, the false-positive interpretation might have been avoided by comparing the thalamic activity (red arrows) to the parietal activity, with which it is approximately isometabolic, and to the (higher) frontal activity—in contrast to the pattern found in AD (right), in which parietal cortex becomes hypometabolic relative to the (preserved and normally isometabolic) thalamus.

 





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