Matteo Pardini1, Edward D Huey2, Salvatore Spina2, William C Kreisl2, Silvia Morbelli2, Eric M Wassermann2, Flavio Nobili2, Bernardino Ghetti2, Jordan Grafman2. 1. From the Departments of Neuroscience, Rehabilitation, Ophthalmology, Genetics, and Maternal and Child Health (M.P., F.N.) and Health Sciences (S.M.), University of Genoa; IRCCS Ospedale Policlinico San Martino (M.P., S.M., F.N.), Genoa, Italy; Cognitive Neuroscience Division, Department of Neurology (E.D.H.), Gertrude H. Sergievsky Center, New York; Taub Institute for Research on Alzheimer's Disease and the Aging Brain (E.D.H., W.C.K.), Columbia University Medical Center, New York, NY; Department of Neurology (S.S.), UCSF Memory and Aging Center, UCSF, San Francisco, CA; Department of Pathology and Laboratory Medicine (S.S., B.G.), Indiana University School of Medicine, Indianapolis; Nuclear Medicine Unit (S.M.), IRCCS AOU San Martino, IST, Genoa, Italy; Behavioral Neurology Unit (E.M.W.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD; Psychiatry and Behavioral Sciences & Cognitive Neurology/Alzheimer's Disease Research Center (J.G.), Feinberg School of Medicine and Department of Psychology, Northwestern University; and Brain Injury Research, Cognitive Neuroscience Lab, Think and Speak Lab (J.G.), Shirley Ryan AbilityLab, Chicago, IL. matteo.pardini@unige.it. 2. From the Departments of Neuroscience, Rehabilitation, Ophthalmology, Genetics, and Maternal and Child Health (M.P., F.N.) and Health Sciences (S.M.), University of Genoa; IRCCS Ospedale Policlinico San Martino (M.P., S.M., F.N.), Genoa, Italy; Cognitive Neuroscience Division, Department of Neurology (E.D.H.), Gertrude H. Sergievsky Center, New York; Taub Institute for Research on Alzheimer's Disease and the Aging Brain (E.D.H., W.C.K.), Columbia University Medical Center, New York, NY; Department of Neurology (S.S.), UCSF Memory and Aging Center, UCSF, San Francisco, CA; Department of Pathology and Laboratory Medicine (S.S., B.G.), Indiana University School of Medicine, Indianapolis; Nuclear Medicine Unit (S.M.), IRCCS AOU San Martino, IST, Genoa, Italy; Behavioral Neurology Unit (E.M.W.), National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD; Psychiatry and Behavioral Sciences & Cognitive Neurology/Alzheimer's Disease Research Center (J.G.), Feinberg School of Medicine and Department of Psychology, Northwestern University; and Brain Injury Research, Cognitive Neuroscience Lab, Think and Speak Lab (J.G.), Shirley Ryan AbilityLab, Chicago, IL.
Abstract
OBJECTIVE: To evaluate brain 18Fluorodeoxyglucose PET (FDG-PET) differences among patients with a clinical diagnosis of corticobasal syndrome (CBS) and distinct underling primary pathologies. METHODS: We studied 29 patients with a diagnosis of CBS who underwent FDG-PET scan and postmortem neuropathologic examination. Patients were divided into subgroups on the basis of primary pathologic diagnosis: CBS-corticobasal degeneration (CBS-CBD) (14 patients), CBS-Alzheimer disease (CBS-AD) (10 patients), and CBS-progressive supranuclear palsy (CBS-PSP) (5 patients). Thirteen age-matched healthy patients who underwent FDG-PET were the control group (HC). FDG-PET scans were compared between the subgroups and the HC using SPM-12, with a threshold of p FWE < 0.05. RESULTS: There were no differences in Mattis Dementia Rating Scale or finger tapping scores between CBS groups. Compared to HC, the patients with CBS presented significant hypometabolism in frontoparietal regions, including the perirolandic area, basal ganglia, and thalamus of the clinically more affected hemisphere. Patients with CBS-CBD showed a similar pattern with a more marked, bilateral involvement of the basal ganglia. Patients with CBS-AD presented with posterior, asymmetric hypometabolism, including the lateral parietal and temporal lobes and the posterior cingulate. Finally, patients with CBS-PSP disclosed a more anterior hypometabolic pattern, including the medial frontal regions and the anterior cingulate. A conjunction analysis revealed that the primary motor cortex was the only common area of hypometabolism in all groups, irrespective of pathologic diagnosis. DISCUSSION AND CONCLUSIONS: In patients with CBS, different underling pathologies are associated with different patterns of hypometabolism. Our data suggest that FDG-PET scans could help in the etiologic diagnosis of CBS.
OBJECTIVE: To evaluate brain 18Fluorodeoxyglucose PET (FDG-PET) differences among patients with a clinical diagnosis of corticobasal syndrome (CBS) and distinct underling primary pathologies. METHODS: We studied 29 patients with a diagnosis of CBS who underwent FDG-PET scan and postmortem neuropathologic examination. Patients were divided into subgroups on the basis of primary pathologic diagnosis: CBS-corticobasal degeneration (CBS-CBD) (14 patients), CBS-Alzheimer disease (CBS-AD) (10 patients), and CBS-progressive supranuclear palsy (CBS-PSP) (5 patients). Thirteen age-matched healthy patients who underwent FDG-PET were the control group (HC). FDG-PET scans were compared between the subgroups and the HC using SPM-12, with a threshold of p FWE < 0.05. RESULTS: There were no differences in Mattis Dementia Rating Scale or finger tapping scores between CBS groups. Compared to HC, the patients with CBS presented significant hypometabolism in frontoparietal regions, including the perirolandic area, basal ganglia, and thalamus of the clinically more affected hemisphere. Patients with CBS-CBD showed a similar pattern with a more marked, bilateral involvement of the basal ganglia. Patients with CBS-AD presented with posterior, asymmetric hypometabolism, including the lateral parietal and temporal lobes and the posterior cingulate. Finally, patients with CBS-PSP disclosed a more anterior hypometabolic pattern, including the medial frontal regions and the anterior cingulate. A conjunction analysis revealed that the primary motor cortex was the only common area of hypometabolism in all groups, irrespective of pathologic diagnosis. DISCUSSION AND CONCLUSIONS: In patients with CBS, different underling pathologies are associated with different patterns of hypometabolism. Our data suggest that FDG-PET scans could help in the etiologic diagnosis of CBS.
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