The online version of this article (doi:10.1186/1750-1326-9-10) contains supplementary material, which is available to authorized users.
The authors declare that they have no competing interests.
EMM contributed to acquisition of data, drafted the manuscript and agrees to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. HB conducted neuropsychological evaluation of patients and provided revisions to initial drafts of the manuscript. JM, MCS, JW conducted neuropsychological evaluation of patients. LK and JM read the results of each patient’s [18 F] florbetapir scan and provided feedback to the manuscript. MG and AA provided patients for the series and feedback on manuscript draft. MS participated in the case series design and provided critical feedback to initial drafts. SG participated in the case series design and coordination and provided critical feedback to initial and subsequent drafts. All authors read and approved the final manuscript.
Identification and quantification of fibrillar amyloid in brain using positron emission tomography (PET) imaging and Amyvid™ ([18 F] Amyvid, [18 F] florbetapir, 18 F-AV-45) was recently approved by the US Food and Drug Administration as a clinical tool to estimate brain amyloid burden in patients being evaluated for cognitive impairment or dementia. Imaging with [18 F] florbetapir offers in vivo confirmation of the presence of cerebral amyloidosis and may increase the accuracy of the diagnosis and likely cause of cognitive impairment (CI) or dementia. Most importantly, amyloid imaging may improve certainty of etiology in situations where the differential diagnosis cannot be resolved on the basis of standard clinical and laboratory criteria.
A consecutive case series of 30 patients (age 50-89; 16 M/14 F) were clinically evaluated at a cognitive evaluation center of urban dementia center and referred for [18 F] florbetapir PET imaging as part of a comprehensive dementia workup. Evaluation included neurological examination and neuropsychological assessment by dementia experts. [18 F] florbetapir PET scans were read by trained nuclear medicine physicians using the qualitative binary approach. Scans were rated as either positive or negative for the presence of cerebral amyloidosis. In addition to a comprehensive dementia evaluation, post [18 F] florbetapir PET imaging results caused diagnoses to be changed in 10 patients and clarified in 9 patients. Four patients presenting with SCI were negative for amyloidosis. These results show that [18 F] florbetapir PET imaging added diagnostic clarification and discrimination in over half of the patients evaluated.
Amyloid imaging provided novel and essential data that: (1) caused diagnosis to be revised; and/or (2) prevented the initiation of incorrect or suboptimal treatment; and/or (3) avoided inappropriate referral to an anti-amyloid clinical trial.
Additional file 1: Table S1: Patient demographics, scan outcomes. (PDF 104 KB)13024_2013_523_MOESM1_ESM.pdf
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