Article Figures & Data
Figures
- FIGURE 1.
Typical regional cerebral 18F-FDG hypometabolism patterns in AD, DLB, and frontal and temporal FTD. Patterns are presented as z score maps based on significantly hypometabolic voxels relative to nondemented comparison population. AD pattern of glucose hypometabolism involves predominantly temporoparietal association cortices and posterior cingulate and precuneus cortices. In advanced disease, prefrontal association cortices show additional hypometabolism. Primary sensorimotor and visual neocortices are relatively spared. DLB has cortical hypometabolism similar to that of AD but with additional involvement of occipital cortex. FTD demonstrates frontal lobar or frontal and temporal polar cortical hypometabolism with relative sparing of parietal association cortex and preservation of primary somatomotor and visual cortices. ANT = anterior; INF = inferior; LAT = lateral; MED = medial; POST = posterior; SUP = superior.
Tables
Reference Cohort A Cohort B TP FN FP TN Sensitivity Specificity Accuracy Mosconi et al., 2007 (88) AD Healthy control 33 0 0 19 100% 100% 100% Ng et al., 2007 (94) AD Healthy control 12 3 10 15 80% 60% 68% Chen et al., 2008 (95) AD Healthy control 47 5 9 51 90% 85% 88% Mosconi et al., 2008 (52) AD Healthy control 192 2 2 108 99% 98% 99% McMurtray et al., 2008 (90) AD Elderly control with only subjective memory complaints 25 2 4 23 93% 85% 89% Total 309 12 25 216 96% 90% 93% FN = false-negative; FP = false-positive; TN = true-negative; TP = true-positive.
Reference and AAN level Diagnostic standard and study type Subjects Major findings Dobert et al., 2005 (34), AAN level II Longitudinal clinical diagnosis; prospective cohort study in primary care–like setting Twenty-four patients with initial clinical suspicion of beginning dementia, 12 of whom had mild cognitive impairment, underwent 18F-FDG PET at baseline. Final diagnosis was based on variable longitudinal clinical follow-up (average, 16 ± 12 mo) and included 9 patients with pure AD, 7 with mixed AD and vascular-type dementia, 6 without dementia, and remainder with FTD or pure vascular dementia. For diagnosis of more purely defined AD, 18F-FDG PET had sensitivity of 44% and specificity of 83%. For diagnosis of mixed AD and vascular dementia, 18F-FDG PET had sensitivity of 71% and specificity of 78%. For diagnosis of AD and mixed vascular/AD dementia vs. absence of dementia, 18F-FDG PET had sensitivity of 91.7% and specificity of 88.9%. Panegyres et al., 2009 (35), AAN level I Longitudinal clinical diagnosis with average clinical follow-up of 5–6 y; prospective cohort study of 18F-FDG PET diagnostic utility in primary care setting Community-dwelling subjects presented to primary care center for cognitive complaints. Final clinical diagnosis was early-stage AD (n = 49), non-AD dementia (n = 29), depression (n = 11), or miscellaneous (n = 13). For diagnosis of AD, 18F-FDG PET had sensitivity of 78% and specificity of 81% in this heterogeneous population. For differential diagnosis of other dementias, including FTD, 18F-FDG PET had specificity > 95%. Reference and AAN level Diagnostic standard Study type Subjects Major findings Silverman et al., 2001 (42), AAN level II Autopsy confirmation and clinical follow-up Multicenter retrospective analysis based on postmortem diagnosis AD (n = 97); non-AD (n = 41), such as progressive supranuclear palsy, Parkinson disease, cerebrovascular disease, or mixed AD was identified in 85/89 (sensitivity, 96%) AD-only cases and 6/8 AD-plus cases (overall sensitivity, 94%). Absence of AD was confirmed in 30/41 cases (specificity, 73%), including 23 with other neurodegenerative dementias. Absence of neurodegenerative disease was confirmed in 14/18 cases (specificity, 78%). Negative PET scan indicated that pathologic progression of cognitive impairment during mean 3-y follow-up was unlikely. Jagust et al., 2007 (39), AAN level II Autopsy confirmation Retrospective study with 4-y clinical follow-up and 5 y until death and autopsy Forty-four subjects with dementia, cognitive impairment, or normal cognitive functions; postmortem diagnosis included AD (n = 20), FTD, DLB, mixed, and vascular dementia For diagnosing AD, accuracy of 18F-FDG PET (sensitivity, 84%; specificity, 74%) was better than that of initial clinical evaluation (sensitivity, 76%; specificity, 58%). 18F-FDG PET (78%) also had better NPV than did initial clinical evaluation (65%). Minoshima et al., 2001 (41), AAN level II Autopsy confirmation and clinical follow-up Retrospective 18F-FDG PET analysis based on postmortem diagnosis, and retrospective 18F-FDG PET diagnosis based on clinical follow-up AD (n = 10); autopsy-confirmed DLB (n = 11); additional 53 patients with clinically probable diagnosis of AD (n = 40) or DLB (n = 13) based on follow-up evaluation 18F-FDG PET can distinguish AD from DLB with 90% sensitivity and 80% specificity. Foster et al., 2007 (16), AAN level II Autopsy confirmation Retrospective consensus study of 6 dementia experts reviewing clinical history and 18F-FDG PET studies AD (n = 31); FTD (n = 14); controls (n = 33) 18F-FDG PET is significantly more accurate in distinguishing FTD from AD than clinical methods. 18F-FDG PET adds important information that appropriately increases diagnostic confidence, even among experienced dementia specialists. Mean interrater κ was 0.31–0.42 for clinical information and 0.73–0.78 for 18F-FDG PET. For AD diagnosis compared with FTD, sensitivity was 96.7% and specificity was 85.7%. Reference and AAN level Cohort A Cohort B TP FN FP TN Sensitivity Specificity Accuracy Silverman et al., 2001 (42), AAN level II AD Non-AD/nondementia 91 11 6 30 89% 83% 88% Minoshima et al., 2001 (41), AAN level II AD DLB 9 1 2 9 90% 82% 86% Foster et al., 2007 (16), AAN level II AD FTD 30 1 2 12 97% 86% 93% Jagust et al., 2007 (39), AAN level II AD and mixed Non-AD 21 4 5 14 84% 74% 80% Panegyres et al., 2009 (35), AAN level I AD Non-AD 38 11 10 43 78% 81% 79% Total 189 28 25 108 87% 81% 85% FN = false-negative; FP = false-positive; TN = true-negative; TP = true-positive.
Reference and study type Diagnostic standard Subjects Likelihood ratios Panegyres et al. 2009 (35), prospective cohort study of diagnostic utility of 18F-FDG PET Clinical diagnosis based on longitudinal long-term assessment Community-dwelling subjects presented to primary care center for cognitive complaints. Final clinical diagnosis was early-stage AD (n = 49), non-AD dementia (n = 29), depression (n = 11), or miscellaneous (n = 13). Positive likelihood ratio for 18F-FDG PET scan considered consistent with AD was 4.11 (95% CI, 2.29–7.32), suggesting increase in likelihood of final diagnosis of AD when diagnosed on 18F-FDG PET with AD. Negative likelihood ratio for AD was 0.27 (95% CI, 0.16–0.46), suggesting more significant decrease in likelihood of final diagnosis of AD when 18F-FDG PET findings are negative for AD. Probability before 18F-FDG PET that patient had AD was 48%. After 18F-FDG PET, probability increased to 79%, indicating that 18F-FDG PET increases diagnosis probability of early-onset AD from 48% to 79%. Jagust et al., 2007 (39), historical cohort study Postmortem diagnosis Forty-four individuals with dementia, cognitive impairment, or normal cognitive function underwent clinical initial evaluation and PET and were followed up for approximately 4 y until final evaluation and 5 y until death and autopsy. Clinical, pathologic, and imaging diagnoses were categorized as AD or not AD. Positive likelihood ratio of 18F-FDG PET for AD diagnosis was 3.2, and negative likelihood ratio was 0.21. Silverman et al., 2001 (42), multicenter retrospective analysis Postmortem diagnosis Multicenter retrospective analysis was performed on heterogeneous patient population. Positive likelihood ratio of 18F-FDG PET for AD diagnosis was 3.5, and negative likelihood ratio was 0.08. Positive likelihood ratio of 18F-FDG PET for presence of neurodegenerative disease of any kind was 4.2, and negative likelihood ratio was 0.075.
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- Article
- Abstract
- CLINICAL GUIDELINES FOR THE DIAGNOSIS OF AD AND DEMENTIA AND THE ROLE OF IMAGING
- OBJECTIVES OF THIS REVIEW
- 18F-FDG PET CROSS-SECTIONAL CASE-CONTROL STUDIES USING CLINICAL ASSESSMENT AS DIAGNOSTIC REFERENCE STANDARD
- 18F-FDG PET STUDIES USING LONGITUDINAL CLINICAL FOLLOW-UP ASSESSMENT AS DIAGNOSTIC REFERENCE STANDARD
- 18F-FDG PET STUDIES OF AD AND DEMENTIA USING PATHOLOGIC CONFIRMATION AS THE REFERENCE STANDARD
- 18F-FDG PET DIFFERENTIAL DIAGNOSIS OF AD VERSUS OTHER DEMENTIAS
- LARGE MULTICENTER STUDIES
- PHYSICIAN CONFIDENCE LEVEL AND PREDICTIVE VALUE OF 18F-FDG PET
- COMPUTER-ASSISTED QUANTITATIVE INTERPRETATION OF BRAIN 18F-FDG PET
- PATHOPHYSIOLOGY OF 18F-FDG METABOLISM AND INVESTIGATIONAL STUDIES
- SAFETY
- LIMITATIONS
- TEMPORAL PROFILE OF 18F-FDG PET IN RELATIONSHIP TO OTHER BIOMARKERS OF AD
- LITERATURE REVIEW AND COMMENTS
- CONCLUSION
- Acknowledgments
- Footnotes
- REFERENCES
- Figures & Data
- Supplemental
- Info & Metrics
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