Brain 18F-FDG PET/CT usefulness in primary progressive aphasia variant diagnosis and in their development into Alzheimer’s disease or fronto-temporal dementia

Background-Aim: Primary Progressive Aphasia (PPA) is a heterogeneous clinical entity that includes different variants such as
Logopenic Aphasia (LPA) that could develop into Alzheimer’s disease (AD) and Progressive Non-Fluent Aphasia (PNFA) variant and
Semantic Variant (SV) that could develop into Fronto-Temporal
Dementia (FTD). We investigated brain 18F-FDG PET/CT usefulness
in patients with uncertain PPA diagnosis and in those with already
ascertained diagnosis to evaluate a possible early development into
AD or FTD.
Methods: We retrospectively enrolled 49 consecutive patients: 15
cases with uncertain symptoms attributable to PPA variants of recent
appearance (Group A) and 34 with PPA already ascertained with
suspicious clinical signs for early development into AD or FTD
(Group B). All patients underwent PET/CT after i.v. injection of
370 MBq dose of 18F-FDG using a Discovery tomograph (GE).
Images were analyzed both qualitatively (QL) and quantitatively
(QN), the latter by an automated software (Cortex ID, GE Healthcare,
USA) that produces brain metabolic map compared with normal age
matched controls.
Results: QL and QN analyses of PET/CT showed different patterns of
cortical hypometabolism in the two Groups of patients. In particular,
in Group A, 8/15 patients showed a selective hypometabolism in
fronto-temporal and fronto-parietal regions (6 bilateral and 2 in left
hemisphere) and were classified as PNFA and SV variants, respectively. In 5/15 cases hypometabolic areas were detected in temporoparietal regions (3 bilaterally and 2 in left hemisphere), in 1/15 cases
in right temporo-parietal regions with the patients classified as
affected by LPA variant, while hypometabolism was diffuse in the remaining 1/15 cases. QN analysis could better discriminate the areas
of bilateral hypometabolism including the apparent diffuse hypometabolism evidenced at QL in one case; thus, 9/15 patients were
classified as at higher risk of early progressing into AD (6 cases) or
FTD (3 cases), confirming the initial suspect clinical symptoms of
disease. In 18/34 Group B cases, PET/CT evidenced areas of hypometabolism in fronto-temporal and fronto-parietal regions (14
bilateral and 4 in left hemisphere) and the classification in PNFA and
SV patients was confirmed, while the 13/34 cases with reduced FDG
uptake in temporo-parietal regions (8 bilateral, 3 in left and 2 in right
hemispheres) were classified as LPA variant. Considering the data of
QN analysis, 22/31 (71%) cases showed a considerable hypometabolism in bilateral brain areas and were classified as high risk of
progressing into AD ( 8 cases) or FTD (14 cases). Moreover, in the
2/34 cases with diffuse hypometabolism the diagnosis was uncertain
also at QN analysis as well as in the remaining case in whom FDG
uptake was apparently normal despite suspect symptoms of disease.
Conclusions: 18F-FDG PET/CT proved a valuable diagnostic tool to
give a useful support for PPA variant diagnosis and for establishing
the development of PPA into FTD or AD in both recent and advanced
stage of diseases with QN analysis representing the best methods to
reach the diagnosis. However, the finding of diffuse hypometabolism
in two cases and normal cortical FDG uptake in one case despite the
symptoms of PPA remains to clarify with a close follow up. A larger
number of cases and a longer follow up is necessary to confirm the
present data