OBJECTIVE: A subgroup of patients with Alzheimer's disease present with visual disturbances at onset. This study investigated whether specific cortical networks associated with visual processes are preferentially affected in this subgroup and determined the clinical implications of such abnormalities. METHOD: Regional cerebral glucose metabolic rates were assessed with positron emission tomography and [18F]2-fluoro-2-deoxy-D-glucose, and general intellectual functions, memory, and visual skills were measured with cognitive tests in patients with probable Alzheimer's disease-10 with and 22 without prominent visual symptoms-and in 25 healthy comparison subjects. RESULTS: Both patient groups showed reduced glucose metabolism in parietal regions and in middle and superior temporal regions in comparison with the healthy subjects. The Alzheimer's disease patients without visual symptoms also showed reductions in inferior temporal, frontal, and limbic structures, as is typical of Alzheimer's disease. In contrast, the patients with visual symptoms had larger metabolic deficits than the patients without visual symptoms in the parietal and occipital cortices (including the primary visual cortex), with a relative sparing of inferior temporal, frontal, and limbic regions. Consistently, the patients with visual symptoms had significantly greater visuospatial deficits and less severe memory impairments than the patients without visual symptoms. CONCLUSIONS: Alzheimer's disease patients with visuospatial deficits who are studied while alive have a distinctive regional distribution of cerebral metabolic impairment that is related to specific cognitive deficits and that distinguishes them from patients with typical Alzheimer's disease. These findings imply that regional variations in brain dysfunction can occur in Alzheimer's disease, with differential involvement of cortical systems resulting in distinctive clinical subgroups.
OBJECTIVE: A subgroup of patients with Alzheimer's disease present with visual disturbances at onset. This study investigated whether specific cortical networks associated with visual processes are preferentially affected in this subgroup and determined the clinical implications of such abnormalities. METHOD: Regional cerebral glucose metabolic rates were assessed with positron emission tomography and [18F]2-fluoro-2-deoxy-D-glucose, and general intellectual functions, memory, and visual skills were measured with cognitive tests in patients with probable Alzheimer's disease-10 with and 22 without prominent visual symptoms-and in 25 healthy comparison subjects. RESULTS: Both patient groups showed reduced glucose metabolism in parietal regions and in middle and superior temporal regions in comparison with the healthy subjects. The Alzheimer's diseasepatients without visual symptoms also showed reductions in inferior temporal, frontal, and limbic structures, as is typical of Alzheimer's disease. In contrast, the patients with visual symptoms had larger metabolic deficits than the patients without visual symptoms in the parietal and occipital cortices (including the primary visual cortex), with a relative sparing of inferior temporal, frontal, and limbic regions. Consistently, the patients with visual symptoms had significantly greater visuospatial deficits and less severe memory impairments than the patients without visual symptoms. CONCLUSIONS:Alzheimer's diseasepatients with visuospatial deficits who are studied while alive have a distinctive regional distribution of cerebral metabolic impairment that is related to specific cognitive deficits and that distinguishes them from patients with typical Alzheimer's disease. These findings imply that regional variations in brain dysfunction can occur in Alzheimer's disease, with differential involvement of cortical systems resulting in distinctive clinical subgroups.
Authors: Mark W Albers; Grover C Gilmore; Jeffrey Kaye; Claire Murphy; Arthur Wingfield; David A Bennett; Adam L Boxer; Aron S Buchman; Karen J Cruickshanks; Davangere P Devanand; Charles J Duffy; Christine M Gall; George A Gates; Ann-Charlotte Granholm; Takao Hensch; Roee Holtzer; Bradley T Hyman; Frank R Lin; Ann C McKee; John C Morris; Ronald C Petersen; Lisa C Silbert; Robert G Struble; John Q Trojanowski; Joe Verghese; Donald A Wilson; Shunbin Xu; Li I Zhang Journal: Alzheimers Dement Date: 2014-07-09 Impact factor: 21.566
Authors: F Sartucci; D Borghetti; T Bocci; L Murri; P Orsini; V Porciatti; N Origlia; L Domenici Journal: Brain Res Bull Date: 2010-04-10 Impact factor: 4.077
Authors: Harald Hampel; Nicola Toschi; Claudio Babiloni; Filippo Baldacci; Keith L Black; Arun L W Bokde; René S Bun; Francesco Cacciola; Enrica Cavedo; Patrizia A Chiesa; Olivier Colliot; Cristina-Maria Coman; Bruno Dubois; Andrea Duggento; Stanley Durrleman; Maria-Teresa Ferretti; Nathalie George; Remy Genthon; Marie-Odile Habert; Karl Herholz; Yosef Koronyo; Maya Koronyo-Hamaoui; Foudil Lamari; Todd Langevin; Stéphane Lehéricy; Jean Lorenceau; Christian Neri; Robert Nisticò; Francis Nyasse-Messene; Craig Ritchie; Simone Rossi; Emiliano Santarnecchi; Olaf Sporns; Steven R Verdooner; Andrea Vergallo; Nicolas Villain; Erfan Younesi; Francesco Garaci; Simone Lista Journal: J Alzheimers Dis Date: 2018 Impact factor: 4.472
Authors: Emiliano Ricciardi; Pietro Pietrini; Mark B Schapiro; Stanley I Rapoport; Maura L Furey Journal: Brain Res Bull Date: 2009-02-07 Impact factor: 4.077