PATHOLOGICAL CORRELATES OF APRAXIA IN ALZHEIMER-DISEASE

Citation
P. Giannakopoulos et al., PATHOLOGICAL CORRELATES OF APRAXIA IN ALZHEIMER-DISEASE, Archives of neurology, 55(5), 1998, pp. 689-695
Citations number
63
Categorie Soggetti
Clinical Neurology
Journal title
ISSN journal
00039942
Volume
55
Issue
5
Year of publication
1998
Pages
689 - 695
Database
ISI
SICI code
0003-9942(1998)55:5<689:PCOAIA>2.0.ZU;2-E
Abstract
Objective: To examine the neuroanatomical correlates of apraxia in Alz heimer 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 mo vements and meaningless gestures, and dressing ability was evaluated c linically. 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 stepwi se 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 ideomot or, dressing, and constructional apraxia. Results: Statistically signi ficant relationships were found between neurofibrillary tangle densiti es 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. Conc lusions: 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 pathw ays mediating visuospatial cognition in Alzheimer disease. Senile plaq ue densities do not represent a valuable pathologic correlate of aprax ia in this disorder.