Functional neuroimaging using F-18 FDG PET/CT in amnestic mild cognitive impairment: A preliminary study.

Background and Objective: People with amnestic mild cognitive impairment (aMCI) are at a higher risk of developing Alzheimers Dementia (AD) than their cognitively normal peers. Decreased glucose metabolism with F‑18 fluorodeoxyglucose (FDG) positron emission tomography (PET) is a downstream marker of neuronal injury and neurodegeneration. The risk of developing AD is higher in patients with aMCI who have a pattern of AD related glucose metabolic changes on FDG‑PET than those who do not have these changes. We evaluated the utility of visual and ‘statistical parametric mapping (SPM)‑supported reading’ of the FDG‑PET scans of patients clinically classified as aMCI for identification of predementia patterns and for prediction of their progression to AD (PTAD). Patients and Methods: A total of 35 patients diagnosed as aMCI (mini mental state examination (MMSE) score ≥ 25) at the cognitive disorders and memory (CDM) clinic of speciality neurology centers were referred for a resting FDG‑PET study. All patients had a detailed neurological, neuropsychological, and magnetic resonance imaging (MRI) evaluation prior to referral. Mean age of patients was 67.9 ± 8.7 (standard deviation (SD)) years, male: female (M: F) =26:9. Twenty healthy age‑matched controls were included in the study for SPM (http://www.fil.ion.ucl.ac.uk/spm/) . Scans were interpreted visually and using SPM. Each scan was classified as high, intermediate, or low likelihood for PTAD. Results: On visual analysis, four scans were classified as high likelihood of PTAD and reveled hypometabolism in AD related territories. Seven patients had hypometabolism in at least one AD related territory and were classified as intermediate likelihood for PTAD. Two patients had hypometabolism in other than AD territories, while 22 patients did not show any significant hypometabolism on their FDG‑PET scans and were classified as low likelihood for PTAD. SPM analysis of these cases confirmed the areas hypometabolism in all 13 patients compared to a normal subgroup (P < 0.05). On follow‑up of 24 months, all four cases with high likelihood scans had progression of cognitive deficits and were confirmed as AD in the CDM clinic while none of the others showed cognitive decline. Interpretation and Conclusion: A pattern of AD hypometabolism on the FDG‑PET study is useful for predicting PTAD. A longer follow‑up of patients with hypometabolism in single AD territories is needed to predict their clinical behavior.