OBJECTIVE: The aim of this study was to analyze cerebral perfusion and glucose metabolism in patients with cognitive impairment using cerebral blood flow (99m)Tc-HMPAO SPECT and (18)F-FDG PET/CT scans. MATERIAL AND METHODS: Twenty-two patients with cognitive impairment were included: 4 subjective memory complaints (SMC), 8 amnestic mild cognitive impairment (MCI), 5 prodromic Alzheimer's disease (AD) and 5 AD. In each clinical group, (99m)Tc-HMPAO SPECT and (18)F-FDG PET/CT scans were performed. RESULTS: (99m)Tc-HMPAO SPECT showed regions of cerebral hypoperfusion in 15 patients and was normal in 7 of the 22 patients. (18)F-FDG PET/CT scan showed cerebral regional hypometabolism in 19 patients and was normal in the other 3 patients. The distribution of abnormalities on (99m)Tc-HMPAO SPECT and (18)F-FDG PET/CT scans was similar in 9 patients (2 SMC, 2 amnestic MCI, 2 prodromic AD, and 3 AD). In 6 patients (1 amnestic MCI, 2 prodromic AD, and 3 AD), FDG hypometabolism was more extensive than the cerebral hypoperfusion. Four patients (1SMC, 3 amnestic MCI) had an abnormal (18)F-FDG PET/CT scan and normal (99m)Tc-HMPAO SPECT. There were 3 patients (1 SMC 2, amnestic MCI) with normal (99m)Tc-HMPAO SPECT and (18)F-FDG PET/CT scans. CONCLUSION: (99m)Tc-HMPAO SPECT and (18)F-FDG PET/CT scans showed cerebral hypoperfusion and hypometabolism in patients with cognitive impairment, even in patients with clinical diagnosis of SMC. In patients with a normal cerebral blood flow SPECT, brain glucose cerebral hypometabolism can be detected. In some patients, the extension of FDG hypometabolism is more pronounced than that corresponding to the hypoperfusion area.
OBJECTIVE: The aim of this study was to analyze cerebral perfusion and glucose metabolism in patients with cognitive impairment using cerebral blood flow (99m)Tc-HMPAO SPECT and (18)F-FDG PET/CT scans. MATERIAL AND METHODS: Twenty-two patients with cognitive impairment were included: 4 subjective memory complaints (SMC), 8 amnestic mild cognitive impairment (MCI), 5 prodromic Alzheimer's disease (AD) and 5 AD. In each clinical group, (99m)Tc-HMPAO SPECT and (18)F-FDG PET/CT scans were performed. RESULTS: (99m)Tc-HMPAO SPECT showed regions of cerebral hypoperfusion in 15 patients and was normal in 7 of the 22 patients. (18)F-FDG PET/CT scan showed cerebral regional hypometabolism in 19 patients and was normal in the other 3 patients. The distribution of abnormalities on (99m)Tc-HMPAO SPECT and (18)F-FDG PET/CT scans was similar in 9 patients (2 SMC, 2 amnestic MCI, 2 prodromic AD, and 3 AD). In 6 patients (1 amnestic MCI, 2 prodromic AD, and 3 AD), FDG hypometabolism was more extensive than the cerebral hypoperfusion. Four patients (1SMC, 3 amnestic MCI) had an abnormal (18)F-FDG PET/CT scan and normal (99m)Tc-HMPAO SPECT. There were 3 patients (1 SMC 2, amnestic MCI) with normal (99m)Tc-HMPAO SPECT and (18)F-FDG PET/CT scans. CONCLUSION: (99m)Tc-HMPAO SPECT and (18)F-FDG PET/CT scans showed cerebral hypoperfusion and hypometabolism in patients with cognitive impairment, even in patients with clinical diagnosis of SMC. In patients with a normal cerebral blood flow SPECT, brain glucose cerebral hypometabolism can be detected. In some patients, the extension of FDG hypometabolism is more pronounced than that corresponding to the hypoperfusion area.
Authors: Yvonne Höller; Arne C Bathke; Andreas Uhl; Nicolas Strobl; Adelheid Lang; Jürgen Bergmann; Raffaele Nardone; Fabio Rossini; Harald Zauner; Margarita Kirschner; Amirhossein Jahanbekam; Eugen Trinka; Wolfgang Staffen Journal: Front Aging Neurosci Date: 2017-09-07 Impact factor: 5.750