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Item and associative encoding in amnestic mild cognitive impairment: a volumetric and functional MRI study
Poster Presentations P4 ordysfunctional mechanisms. The aim of the current study was to examineactivation differences between early AD patients and controls using avisuospatial task with increasing task demand. We focussed on functionalcharacteristics of the parietal lobe and examined potential compensation ordisconnection mechanisms by combining a parametric fMRI task with effectiveconnectivity measures via Granger Causality Mapping (GCM). Methods: Eighteen male patients withamnestic MCI and 18 male cognitively healthy older individuals were given anevent-related parametric ^ , 40A ^ , 60A ^ and mental rotation task with different rotation angles (0A ^ ) in the MRI scanner. Neural activity per angle rotation for the total 120A group and the comparison between the MCI patients and the controls was calculated, as well as the parametric effects for the total group and the comparison between both groups. Parietal regions significant in the parametric group comparison were used as reference region of interest for the GCM analysis. Results: Separate measurements of eachrotation angle revealed widespread neural activation differences between thegroups. More temporal and parietal activation in the higher rotation anglecondition was observed in MCI patients compared to controls. The parametric modulation, which identifies regions associated with increasing angle,confirmed these results, and showed that MCI patients recruited larger regions within the parietal and temporal lobes. MCI patients showed more deactivationin frontal areas. GCM analyses with parietal regions as reference ROI showed anincreased parietal-temporal effective connectivity in MCI patients compared tocontrols, but a decreased connectivity between the inferior parietal lobule andthe posterior cingulate gyrus. Conclusions: We conclude that early ADpatients compensate parietal-posterior cingulate disconnection with increasedtemporo-parietal connectivity to maintain adequate task performance.
P4-127
ITEM AND ASSOCIATIVE ENCODING IN AMNESTIC MILD COGNITIVE IMPAIRMENT: A VOLUMETRIC AND FUNCTIONAL MRI STUDY
Laurence Dricot*1, Martin Kavec2, Cecile Grandin3, Xavier Seron3, Adrian Ivanoiu3, 1Universite Catholique de Louvain, Bruxelles, Belgium; 2 Erasme Hospital University, Bruxelles, Belgium; 3Cliniques Universitaires Saint-Luc, Bruxelles, Belgium. Background: Associative memory is impaired in amnestic mild cognitive impairment (aMCI). Anterior hippocampus seems to be involved with associative memory in young subjects and appears atrophic in aMCI patients. However, the relationship between anterior hippocampus dysfunction and associative memory has never been studied in aMCI. Methods: We conducted a volumetric and functional magnetic resonance imaging studyinvestigating associative encoding in 32 subjects (16 aMCI and 16 elderly controls) while controlling for item encoding. Results: Behaviorally, we confirmed the presence of an associative impairment in aMCI even after controlling for item memory differences between groups. Functionally, we found a lower activation in the left anterior hippocampus in aMCI than in controls in response to successful associative encoding, even after controlling for atrophy. Structurally, we observed anterior hippocampus atrophy in aMCI. We found that associative encoding activation correlated with anterior hippocampus volume and with associative memory score. Conclusions: This convergence between behavioral, functional and structural data emphasizes the preeminence of associative encoding deficits in aMCI. Results are discussed in the context of functional activity modifications in normal and pathological aging.
P4-128
THE OVERLAP BETWEEN THE CORTICOBASAL DEGENERATION SYNDROME AND NONFLUENT APHASIA
Federica Agosta*1, Giulia Longoni1, Flavia Mattioli2, Giancarlo Comi1, Roberto Gasparotti2, Massimo Filippi1, 1Hospital San Raffaele, Milan, Italy; 2Spedali Civili of Brescia, Brescia, Italy.
S749
Background: Recent clinicopathological studies demonstrated an association between the presenting syndrome of nonfluent aphasia and the pathological diagnosis of corticobasal degeneration. In this study, we present clinical, neuropsychological, and structural MRI data of patients with nonfluent aphasia, apraxia of speech, ideomotor limb apraxia and extrapyramidal signs at presentation compared to those of patients with the classic primary progressive aphasia (PPA). Methods: Four patients with a CBSnonfluent aphasia syndrome at presentation and three patients with the nonfluent PPA variant were studied. Structural MRI scans were obtained also from 10 age- and sex-matched healthy controls were studied. Grey matter (GM) atrophy patterns were assessed using voxel-based morphometry. Results: Compared with controls, both CBS-nonfluent and nonfluent PPA patients showed atrophy of the left insula. In addition, CBS-nonfluent patients had GM atrophy involving the left rolandic operculum, precentral and postcentral gyri, superior temporal gyrus, middle cingulum, and inferior parietal lobule, while patients with nonfluent PPA experienced atrophy of the left superior frontal gyrus, inferior temporal gyrus, anterior/middle cingulum, and bilateral amygdala. The direct comparison between the two patient groups showed that CBS-nonfluent patients had a greater atrophy of the left rolandic operculum, postcentral gyrus, and inferior parietal lobule compared with nonfluent PPA. On the contrary, patients with nonfluent PPA had a greater tissue loss of the left superior frontal gyrus, inferior temporal gyrus, and bilateral amygdala compared with those with the CBS-nonfluent variant. Conclusions: Our findings corroborate the overlap between nonfluent PPA and CBS. This study also suggests that specific anatomical substrates are associated with different clinical symptoms in these patients. The damage to the left insula in all patients highlights its role in motor speech deficits, while the parietal damage is likely to be related to limb apraxia.
P4-129
THE PRE-DEMENTIA STAGE OF DEMENTIAWITH LEWY BODIES
Arvid Rognve*1, Eirik Auning2, Tormod Fladby3, Clive Ballard4, Dag Aarsland5, 1Haugesund hospital, Helse fonna, haugesund, Norway; 2 Ahus, University of Oslo, Oslo, Norway; 3Ahus, University of Oslo, Lørenskog, Norway; 4Kings college London, dementia research center, london, United Kingdom; 5Stavanger University hospital, University of Oslo, Stavanger, Norway. Background: Objective: To explore the presenting and early symptoms in patients diagnosed with mild dementia with Lewy bodies (DLB). Methods: Patients with mild dementia fullfilling diagnostic criteria for DLB (n ¼ 61) and Alzheimers disease (AD) (n ¼ 109), were recruited from dementia clinics in western Norway. At diagnosis, caregivers were asked which symptoms had been the presenting symptom of dementia, and which other symptoms had occurred prior to diagnosis. DLB patients were grouped as mild and very mild based on the median MMSE total score, and the proportions with core and suggestive DLB features in these subgroups were recorded.
Table 1 Demographics and clinical characteristics of patients with DLB and AD Variables
DLB (n¼61)
AD (n¼109)
Age Sex, female, n (%) MMSE score Education, years UPDRS III total score NPI total score, median (range) Disease duration, years
75.75 6 7.71 75.64 6 7.81 26 (42.6 %) 82 (75.2 %) 23.19 6 3.18 23.84 6 2.23 9.79 6 3.12 9.69 6 2.91 15.54 6 14.00 1.96 6 3.19 22.00 (89) 8.00 (63) 3.28 6 2.05 2.37 61.65
P-value * .436 .000 .045 .416 .000 .047 .038
DLB ¼ Dementia with Lewy bodies, AD ¼ Alzheimer disease dementia Numbers represent mean 6 standard deviation (SD) if not indicated otherwise * DLB and AD compared
P4-127
ITEM AND ASSOCIATIVE ENCODING IN AMNESTIC MILD COGNITIVE IMPAIRMENT: A VOLUMETRIC AND FUNCTIONAL MRI STUDY
Laurence Dricot*1, Martin Kavec2, Cecile Grandin3, Xavier Seron3, Adrian Ivanoiu3, 1Universite Catholique de Louvain, Bruxelles, Belgium; 2 Erasme Hospital University, Bruxelles, Belgium; 3Cliniques Universitaires Saint-Luc, Bruxelles, Belgium. Background: Associative memory is impaired in amnestic mild cognitive impairment (aMCI). Anterior hippocampus seems to be involved with associative memory in young subjects and appears atrophic in aMCI patients. However, the relationship between anterior hippocampus dysfunction and associative memory has never been studied in aMCI. Methods: We conducted a volumetric and functional magnetic resonance imaging studyinvestigating associative encoding in 32 subjects (16 aMCI and 16 elderly controls) while controlling for item encoding. Results: Behaviorally, we confirmed the presence of an associative impairment in aMCI even after controlling for item memory differences between groups. Functionally, we found a lower activation in the left anterior hippocampus in aMCI than in controls in response to successful associative encoding, even after controlling for atrophy. Structurally, we observed anterior hippocampus atrophy in aMCI. We found that associative encoding activation correlated with anterior hippocampus volume and with associative memory score. Conclusions: This convergence between behavioral, functional and structural data emphasizes the preeminence of associative encoding deficits in aMCI. Results are discussed in the context of functional activity modifications in normal and pathological aging.
P4-128
THE OVERLAP BETWEEN THE CORTICOBASAL DEGENERATION SYNDROME AND NONFLUENT APHASIA
Federica Agosta*1, Giulia Longoni1, Flavia Mattioli2, Giancarlo Comi1, Roberto Gasparotti2, Massimo Filippi1, 1Hospital San Raffaele, Milan, Italy; 2Spedali Civili of Brescia, Brescia, Italy.
S749
Background: Recent clinicopathological studies demonstrated an association between the presenting syndrome of nonfluent aphasia and the pathological diagnosis of corticobasal degeneration. In this study, we present clinical, neuropsychological, and structural MRI data of patients with nonfluent aphasia, apraxia of speech, ideomotor limb apraxia and extrapyramidal signs at presentation compared to those of patients with the classic primary progressive aphasia (PPA). Methods: Four patients with a CBSnonfluent aphasia syndrome at presentation and three patients with the nonfluent PPA variant were studied. Structural MRI scans were obtained also from 10 age- and sex-matched healthy controls were studied. Grey matter (GM) atrophy patterns were assessed using voxel-based morphometry. Results: Compared with controls, both CBS-nonfluent and nonfluent PPA patients showed atrophy of the left insula. In addition, CBS-nonfluent patients had GM atrophy involving the left rolandic operculum, precentral and postcentral gyri, superior temporal gyrus, middle cingulum, and inferior parietal lobule, while patients with nonfluent PPA experienced atrophy of the left superior frontal gyrus, inferior temporal gyrus, anterior/middle cingulum, and bilateral amygdala. The direct comparison between the two patient groups showed that CBS-nonfluent patients had a greater atrophy of the left rolandic operculum, postcentral gyrus, and inferior parietal lobule compared with nonfluent PPA. On the contrary, patients with nonfluent PPA had a greater tissue loss of the left superior frontal gyrus, inferior temporal gyrus, and bilateral amygdala compared with those with the CBS-nonfluent variant. Conclusions: Our findings corroborate the overlap between nonfluent PPA and CBS. This study also suggests that specific anatomical substrates are associated with different clinical symptoms in these patients. The damage to the left insula in all patients highlights its role in motor speech deficits, while the parietal damage is likely to be related to limb apraxia.
P4-129
THE PRE-DEMENTIA STAGE OF DEMENTIAWITH LEWY BODIES
Arvid Rognve*1, Eirik Auning2, Tormod Fladby3, Clive Ballard4, Dag Aarsland5, 1Haugesund hospital, Helse fonna, haugesund, Norway; 2 Ahus, University of Oslo, Oslo, Norway; 3Ahus, University of Oslo, Lørenskog, Norway; 4Kings college London, dementia research center, london, United Kingdom; 5Stavanger University hospital, University of Oslo, Stavanger, Norway. Background: Objective: To explore the presenting and early symptoms in patients diagnosed with mild dementia with Lewy bodies (DLB). Methods: Patients with mild dementia fullfilling diagnostic criteria for DLB (n ¼ 61) and Alzheimers disease (AD) (n ¼ 109), were recruited from dementia clinics in western Norway. At diagnosis, caregivers were asked which symptoms had been the presenting symptom of dementia, and which other symptoms had occurred prior to diagnosis. DLB patients were grouped as mild and very mild based on the median MMSE total score, and the proportions with core and suggestive DLB features in these subgroups were recorded.
Table 1 Demographics and clinical characteristics of patients with DLB and AD Variables
DLB (n¼61)
AD (n¼109)
Age Sex, female, n (%) MMSE score Education, years UPDRS III total score NPI total score, median (range) Disease duration, years
75.75 6 7.71 75.64 6 7.81 26 (42.6 %) 82 (75.2 %) 23.19 6 3.18 23.84 6 2.23 9.79 6 3.12 9.69 6 2.91 15.54 6 14.00 1.96 6 3.19 22.00 (89) 8.00 (63) 3.28 6 2.05 2.37 61.65
P-value * .436 .000 .045 .416 .000 .047 .038
DLB ¼ Dementia with Lewy bodies, AD ¼ Alzheimer disease dementia Numbers represent mean 6 standard deviation (SD) if not indicated otherwise * DLB and AD compared