To examine the neuroanatomical correlates of spatial and temporal disorientation in Alzheimer’s disease (AD), we performed an anterograde clinicopathological study of 29 patients with clinically and neuropathologically confirmed AD. Spatial and temporal disorientation was assessed using the locational orientation subtests of the Mini Mental State Examination and the Benton’s test for temporal orientation. Quantitative analysis of neurofibrillary tangles and senile plaques were performed in the CA1 field of the hippocampus, layers II and V of the entorhinal cortex, and layers II–III and V–VI of areas 9, 7, 39, 19, 37, 20 and 23 in the right hemisphere. Forward stepwise logistic regression was used to assess the relationship between lesion densities and the presence of either spatial or temporal disorientation; severity scores and brain weight were included as covariants. A statistically significant relationship was found between neurofibrillary tangle densities in Brodmann’s areas 7, 23 and the CA1 field of hippocampus and both spatial and temporal disorientation. Senile plaque counts did not correlate with any of the neuropsychological parameters. Both temporal and spatial disorientation in AD are related to the degeneration of the same pathways linking the hippocampus with the superior parietal and posterior cingulate cortex in the right hemisphere. These observations are discussed with respect to the notion of global corticocortical disconnection in AD.
To examine the neuroanatomical correlates of impaired processing of famous faces in Alzheimer’s disease (AD), we performed an anterograde clinicopathological study of 25 patients with clinically and neuropathologically confirmed AD. Famous face recognition, identification and naming was assessed using the Famous Face Test. The assessment of neurofibrillary tangle (NFT) and senile plaque (SP) densities was performed in ten cortical areas in both hemispheres, and statistical analysis was made using forward stepwise logistic regression models. A statistically significant relationship was found between NFT densities in Brodmann’s areas 9 and 24 in both hemispheres and impaired famous face naming and identification. SP counts did not correlate with any of the neuropsychological parameters. These data suggest that NFT formation in prefrontal and anterior cingulate cortex, two areas involved in semantic memory processes, is a key event in famous face naming and identification deficits. In agreement with previous studies, they also indicate that SP densities are not a good pathological correlate of neuropsychological deficits in AD.
Objective: To examine the neuroanatomic correlates of visual agnosia in AD. Methods: The authors performed an anterograde clinicopathologic study of 23 patients with clinically and neuropathologically confirmed AD in a 305-bed acute care geriatric hospital and a 165-bed acute care psychiatric hospital. The presence of apperceptive visual agnosia was assessed using the Ghent's overlapping figure test and the Gottschaldt's hidden figure test. Associative visual agnosia was examined using the conceptual items of the Columbia Mental Maturity Test. Correlations between neurofibrillary tangle (NFT) and senile plaque (SP) densities and visual agnosia were studied using forward stepwise logistic regression. Results: A statistically significant relation was found between NFT densities in Brodmann's areas 18, 19, and 37, and associative visual agnosia, whereas NFT densities in the areas studied did not correlate with the presence of apperceptive visual agnosia. Senile plaque counts did not correlate with any of the neuropsychological parameters. Conclusions: These results support the existence of a dichotomy between associative and apperceptive agnosia, and show that only the former is related to the damage of secondary and high-order visual association areas in AD. In addition, the results suggest that SP densities do not represent a valuable pathologic correlate of visual agnosia in this disorder.
Objective: To examine the neuroanatomical correlates of apraxia in Alzheimer disease.Patients: Twenty-three patients with clinically overt Alzheimer disease.Design: Anterograde study and neuropathologic case series. Clinical severity was assessed using the Global Deterioration Scale. Ideomotor praxis was examined on transitive and intransitive movements and meaningless gestures, and dressing ability was evaluated clinically. Constructive praxis was tested using a 3-dimensional figure copying task. Correlations between neurofibrillary tangle and senile plaque densities and praxis test performance were studied using stepwise logistic regression models.Setting: Studies were conducted at the Psychiatric and Geriatric Hospitals of the University of Geneva School of Medicine, Geneva, Switzerland.Main Outcome Measures: Odds ratios to estimate the associations between neurofibrillary tangle and senile plaque densities in each neocortical area and the presence of ideomotor, dressing, and constructional apraxia.Results: Statistically significant relationships were found between neurofibrillary tangle densities in the anterior cingulate cortex and ideomotor and dressing apraxia and between neurofibrillary tangle densities in the superior parietal, posterior cingulate, and occipital cortex and constructional apraxia. Senile plaque counts did not correlate with praxic performance.Conclusions: These results suggest that ideomotor and dressing apraxia are associated with mild damage of the anterior cingulate cortex, whereas constructional apraxia is related to the disruption of cortical pathways mediating visuospatial cognition in Alzheimer disease. Senile plaque densities do not represent a valuable pathologic correlate of apraxia in this disorder.