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Degeneration patterns on [ 18 F]FDG‐PET predict amyloid deposition in corticobasal syndrome
Author(s) -
Parmera Jacy Bezerra,
Coutinho Artur M,
Neto Adalberto Studart,
Carneiro Camila de Godoi,
de Almeida Isabel Junqueira,
Aranha Mateus Rozalem,
Barbosa Egberto Reis,
Buchpiguel Carlos A,
Nitrini Ricardo,
Brucki Sonia MD
Publication year - 2020
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1002/alz.041878
Subject(s) - progressive supranuclear palsy , corticobasal degeneration , pittsburgh compound b , medicine , positron emission tomography , nuclear medicine , pet imaging , pathology , cognitive impairment , psychology , disease
Background Corticobasal Syndrome (CBS) is a neurodegenerative disease which phenotype is related to multiple pathologies, including 4‐repeat tauopathies ‐ Corticobasal Degeneration (CBD) and Progressive Supranuclear Palsy (PSP) ‐ and Alzheimer’s disease (AD). Previous works with post‐mortem analysis established [ 18 F]FDG‐PET patterns closely related to CBD, PSP or AD pathology. Methods Forty patients with probable CBS were evaluated concerning their movement disorders and cognition. They were underwent [ 18 F]FDG‐PET/CT and, according to their brain metabolic patterns, distributed into two groups: likely related to AD (CBS FDG‐PET AD) (figure 1) and likely unrelated to AD (CBS FDG‐PET nonAD) (figure 2). Twenty‐five patients underwent [ 11 C]PIB‐PET on a hybrid PET/MRI equipment to assess their amyloid status. Both [ 18 F]FDG‐PET and [ 11 C]PIB‐PET were analyzed based on visual and 3D‐SSP semi‐quantitative parameters. Each examination was blind to other modalities. Results Based on the patterns at [ 18 F]FDG‐PET, we classified 12 patients (30%) in the CBS FGD‐PET AD group and 28 patients (70%) in the CBS FDG‐PET nonAD group. All patients (100%) previously classified as CBS FDG‐PET AD tested positive for amyloid deposition at [ 11 C]PIB‐PET and 88,9% classified as CBS FDG‐PET nonAD tested negative (p=0,001 for [ 11 C]PIB positive status; sensitivity 77,8%; specificity 100%). There were no significant differences in age, gender, symptoms duration and schooling at CBS FDG‐PET groups or [ 11 C]PIB status. Demography is shown in table 1. Functional and cognitive impairment was markedly more severe in the CBS FDG‐PET AD group, which had worst scores regarding memory, attention and visuospatial domains (table 2). CBS FDG‐PET AD group also presented more frequently myoclonus (100% vs. 53,6%, p=0,004), displayed less frequently dystonia (16,7% vs. 57,1%, p=0,035) and had more neglect syndrome (p =0,041) and hallucinations (p=0,039) (figure 3). Patients with positive status at [ 11 C]PIB also presented worst cognitive performance on memory, attention and visuospatial domains. Conclusion [ 18 F]FDG‐PET was useful to predict CBS variants depicting their degeneration patterns, being able to detect a CBS‐AD group with brain amyloid deposition, worst functional and cognitive decline, also showing high accuracy to exclude AD pathology in the CBS‐nonAD group. Motor and cortical symptoms such as dystonia, myoclonus and neglect syndrome might potentially aid biomarkers in distinguishing pathologic variants.