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Guillaume Turc,
Marion Apoil,
Olivier Naggara,
David Calvet,
Catherine Lamy,
Alina M Tataru,
Jean-François Méder,
Jean-Louis Mas, Jean-Claude Baron,
Catherine Oppenheim,
Emmanuel Touzé
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ABSTRACT: BACKGROUND AND PURPOSE: The DRAGON score, which includes clinical and computed tomographic scan parameters, showed a high specificity to predict 3-month outcome in patients with acute ischemic stroke treated by intravenous tissue plasminogen activator. We adapted the score for patients undergoing MRI as the first-line diagnostic tool. METHODS: We reviewed patients with consecutive anterior circulation ischemic stroke treated ≤4.5 hour by intravenous tissue plasminogen activator between 2003 and 2012 in our center, where MRI is systematically implemented as first-line diagnostic work-up. We derived the MRI-DRAGON score keeping all clinical parameters of computed tomography-DRAGON (age, initial National Institutes of Health Stroke Scale and glucose level, prestroke handicap, onset to treatment time), and considering the following radiological variables: proximal middle cerebral artery occlusion on MR angiography instead of hyperdense middle cerebral artery sign, and diffusion-weighted imaging Alberta Stroke Program Early Computed Tomography Score (DWI ASPECTS) ≤5 instead of early infarct signs on computed tomography. Poor 3-month outcome was defined as modified Rankin scale >2. We calculated c-statistics as a measure of predictive ability and performed an internal cross-validation. RESULTS: Two hundred twenty-eight patients were included. Poor outcome was observed in 98 (43%) patients and was significantly associated with all parameters of the MRI-DRAGON score in multivariate analysis, except for onset to treatment time (nonsignificant trend). The c-statistic was 0.83 (95% confidence interval, 0.78-0.88) for poor outcome prediction. All patients with a MRI-DRAGON score ≤2 (n=22) had a good outcome, whereas all patients with a score ≥8 (n=11) had a poor outcome. CONCLUSIONS: The MRI-DRAGON score is a simple tool to predict 3-month outcome in acute stroke patients screened by MRI then treated by intravenous tissue plasminogen activator and may help for therapeutic decision.
Stroke 03/2013; · 5.73 Impact Factor
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ABSTRACT: A wide range of experimental studies have provided evidence that a night of sleep contributes to memory consolidation. Mental rotation (MR) skill is characterized by fundamental aspect of both cognitive and motor abilities which can be improved within practice sessions, but little is known about the effect of consolidation after MR practice. In the present study, we investigated the effect of MR training and the following corresponding day-and sleep-related time consolidations in taking into account the well-established gender difference in MR. Forty participants (20 women) practiced a computerized version of the Vandenberg and Kuse MR task. Performance was evaluated before MR training, as well as prior to, and after a night of sleep or a similar daytime interval. Data showed that while men outperformed women during the pre-training test, brief MR practice was sufficient for women to achieve equivalent performance. Only participants subjected to a night of sleep were found to enhance MR performance during the retest, independently of gender. These results provide first evidence that a night of sleep facilitates MR performance compared with spending a similar daytime interval, regardless gender of the participants. Since MR is known to involve motor processes, the present data might contribute to schedule relevant mental practice interventions for fruitful applications in rehabilitation and motor learning processes.
PLoS ONE 03/2013; 8(3):1-8. · 4.09 Impact Factor
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ABSTRACT: A wide range of experimental studies have provided evidence that a night of sleep contributes to memory consolidation. Mental rotation (MR) skill is characterized by fundamental aspect of both cognitive and motor abilities which can be improved within practice sessions, but little is known about the effect of consolidation after MR practice. In the present study, we investigated the effect of MR training and the following corresponding day- and sleep-related time consolidations in taking into account the well-established gender difference in MR. Forty participants (20 women) practiced a computerized version of the Vandenberg and Kuse MR task. Performance was evaluated before MR training, as well as prior to, and after a night of sleep or a similar daytime interval. Data showed that while men outperformed women during the pre-training test, brief MR practice was sufficient for women to achieve equivalent performance. Only participants subjected to a night of sleep were found to enhance MR performance during the retest, independently of gender. These results provide first evidence that a night of sleep facilitates MR performance compared with spending a similar daytime interval, regardless gender of the participants. Since MR is known to involve motor processes, the present data might contribute to schedule relevant mental practice interventions for fruitful applications in rehabilitation and motor learning processes.
PLoS ONE 01/2013; 8(3):e60296. · 4.09 Impact Factor
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ABSTRACT: In acute stroke, diffusion-weighted imaging (DWI) lesions are commonly considered markers of irreversible ischemia yet can occasionally reverse. However, the extent and clinical correlates of DWI reversal in thrombolyzed patients remain unclear. We assessed the extent of reversible acute DWI lesions (RADs) and their relationships with clinical outcome in patients thrombolyzed ≤4.5 hours from onset.
Data were retrospectively analyzed. RAD was defined as an acute DWI lesion not part of a 24-hour DWI lesion as determined voxelwise. Associations with an early neurological improvement (early neurological improvement=ΔNational Institutes of Health Stroke Scale ≥8 or National Institutes of Health Stroke Scale ≤2 at 24 hours) or an excellent outcome (modified Rankin Scale ≤1) were assessed in multivariate analyses.
One hundred seventy-six patients were included. The median (interquartile range) time to treatment from onset was 150 minutes (120-194). Eighty-nine patients (50%) exhibited visually-detectable RAD irrespective of its extent. Over the whole population, the median percentage and volume of RAD were 11% (4-36) and 2.4mL (0.5-8). Subtracting RAD from initial DWI altered perfusion-weighted imaging-DWI classification in 5 of 100 patients (shift from "no mismatch" to "mismatch" profile in all). Percent RAD was significantly greater in patients treated ≤3 hours (P=0.049), without proximal occlusion (P=0.003), and in 24-hour recanalizers (P<0.001). Early neurological improvement was independently associated with percent RAD. This association increased with percent RAD split in quartiles in a "dose-dependent" manner (P for trend=0.01). Excellent outcome was independently associated with percent RAD (P for trend <0.001).
DWI reversal was often sizeable in patients treated ≤4.5 hours. It was strongly associated with, albeit not necessarily causal for, early neurological improvement.
Stroke 09/2012; 43(11):2986-91. · 5.73 Impact Factor
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Marine Fouquet,
Béatrice Desgranges,
Renaud La Joie,
Denis Rivière,
Jean-François Mangin,
Brigitte Landeau,
Florence Mézenge,
Alice Pélerin,
Vincent de La Sayette,
Fausto Viader, Jean-Claude Baron,
Francis Eustache,
Gaël Chételat
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ABSTRACT: Identifying the specific substrates of memory deficits in early Alzheimer's disease would help to develop clinically-relevant therapies. The present study assesses the relationships between encoding versus retrieval deficits in patients with amnestic Mild Cognitive Impairment (aMCI) and atrophy specifically within the hippocampus and throughout the white matter. Twenty-two aMCI patients underwent T1-weighted MRI scans and neuropsychological testing. Grey matter and white matter segments obtained from the MRI images were each entered in correlation analyses, assessed only in the hippocampus for grey matter segments, with encoding and retrieval memory performances. For the grey matter segments, the resulting spmT correlation maps were then superimposed onto a 3D surface view of the hippocampus to identify the relative involvement of the different subfields, a method already used and validated elsewhere. Memory encoding deficits specifically correlated with CA1 subfield atrophy, while no relationship was found with white matter atrophy. In contrast, retrieval deficits were weakly related to hippocampal atrophy and did not involve a particular subfield, while they strongly correlated with loss of white matter, specifically in medial parietal and frontal areas. In aMCI patients, encoding impairment appears specifically related to atrophy of the CA1 hippocampal subfield, consistent with the predominance of encoding deficits and CA1 atrophy in aMCI. In contrast, episodic retrieval deficits seem to be underlain by more distributed tissue losses, consistent with a disruption of a hippocampo-parieto-frontal network.
NeuroImage 11/2011; 59(4):3309-15. · 5.89 Impact Factor
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ABSTRACT: To provide guidance regarding the most appropriate voxel-based morphometry (VBM)-derived method for assessing hippocampal atrophy in early Alzheimer's disease (AD).
T1-MRI volume data were collected in 23 patients with amnestic mild cognitive impairment (aMCI) and 18 controls. Three types of data (unmodulated and 2 types of modulated MRI) and 2 extraction methods (with reference to the hippocampal peak of atrophy identified from a preliminary whole-brain analysis, or using a template region of interest-ROI-approach) were compared to the gold-standard individual ROI (ROI-i) method through 2 statistical approaches (ANOVA and Pearson's R).
First, whole-brain analyses performed on modulated data are as sensitive as the ROI-i approach in detecting aMCI patients' hippocampal atrophy. Second, values extracted from the ROI-template applied to modulated data provide measures of hippocampal volume comparable to those obtained using the ROI-i approach.
This study provides guidance on how to extract accurate hippocampal measures from VBM-derived data in early AD, as a time-saving and easy alternative to the reference ROI-i method.
Journal of neuroimaging: official journal of the American Society of Neuroimaging 07/2011; 21(4):310-6. · 1.72 Impact Factor
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Gaël Chételat,
Victor L Villemagne,
Kerryn E Pike, Jean-Claude Baron,
Pierrick Bourgeat,
Gareth Jones,
Noel G Faux,
Kathryn A Ellis,
Olivier Salvado,
Cassandra Szoeke,
Ralph N Martins,
David Ames,
Colin L Masters,
Christopher C Rowe
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ABSTRACT: β-Amyloid deposition is one of the main hallmarks of Alzheimer's disease thought to eventually cause neuronal death. Post-mortem and neuroimaging studies have consistently reported cases with documented normal cognition despite high β-amyloid burden. It is of great interest to understand what differentiates these particular subjects from those without β-amyloid deposition or with both β-amyloid deposition and cognitive deficits, i.e. what allows these subjects to resist the damage of the pathological lesions. [¹¹C]Pittsburgh compound B positron emission tomography and magnetic resonance brain scans were obtained in 149 participants including healthy controls and patients with subjective cognitive impairment, mild cognitive impairment and Alzheimer's disease. Magnetic resonance data were compared between high versus low-[11C]Pittsburgh compound B cases, and between high-[¹¹C]Pittsburgh compound B cases with versus those without cognitive deficits. Larger temporal (including hippocampal) grey matter volume, associated with better episodic memory performance, was found in high- versus low-[¹¹C]Pittsburgh compound B healthy controls. The same finding was obtained using different [¹¹C]Pittsburgh compound B thresholds, correcting [¹¹C]Pittsburgh compound B data for partial averaging, using age, education, Mini-Mental State Examination, apolipoprotein E4 and sex-matched subsamples, and using manual hippocampal delineation instead of voxel-based analysis. By contrast, in participants with subjective cognitive impairment, significant grey matter atrophy was found in high-[¹¹C]Pittsburgh compound B cases compared to low-[¹¹C]Pittsburgh compound B cases, as well as in high-[¹¹C]Pittsburgh compound B cases with subjective cognitive impairment, mild cognitive impairment and Alzheimer's disease compared to high-[¹¹C]Pittsburgh compound B healthy controls. Larger grey matter volume in high-[¹¹C]Pittsburgh compound B healthy controls may reflect either a tissue reactive response to β-amyloid or a combination of higher 'brain reserve' and under-representation of subjects with standard/low temporal volume in the high-[¹¹C]Pittsburgh compound B healthy controls. Our complementary analyses tend to support the latter hypotheses. Overall, our findings suggest that the deleterious effects of β-amyloid on cognition may be delayed in those subjects with larger brain (temporal) volume.
Brain 11/2010; 133(11):3349-58. · 9.46 Impact Factor
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ABSTRACT: Hippocampal atrophy, posterior cingulate and frontal glucose hypometabolism, and white-matter tract disruption are well described early macroscopic events in Alzheimer's disease. The relationships between these three types of alterations have been documented in previous studies, but their chronology still remains to be established. The present study used multi-modal fluorodeoxyglucose-positron emission tomography and magnetic resonance imaging longitudinal data to address this question in patients with amnestic mild cognitive impairment. We found unidirectional, specific sequential relationships between: (i) baseline hippocampal atrophy and both cingulum bundle (r = 0.70; P = 3 × 10⁻³) and uncinate fasciculus (r = 0.75; P = 7 × 10⁻⁴) rate of atrophy; (ii) baseline cingulum bundle atrophy and rate of decline of posterior (r = 0.72; P = 2 × 10⁻³); and anterior (r = 0.74; P = 1 × 10⁻³) cingulate metabolism; and (iii) baseline uncinate white matter atrophy and subgenual metabolism rate of change (r = 0.65; P = 6 × 10⁻³). Baseline local grey matter atrophy was not found to contribute to hypometabolism progression within the posterior and anterior cingulate as well as subgenual cortices. These findings suggest that hippocampal atrophy progressively leads to disruption of the cingulum bundle and uncinate fasciculus, which in turn leads to glucose hypometabolism of the cingulate and subgenual cortices, respectively. This study reinforces the relevance of remote mechanisms above local interactions to account for the pattern of metabolic brain alteration observed in amnestic mild cognitive impairment, and provides new avenues to assess the sequence of events in complex diseases characterized by multiple manifestations.
Brain 11/2010; 133(11):3301-14. · 9.46 Impact Factor
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Brain 10/2009; 132(Pt 12):e133; author reply e134. · 9.46 Impact Factor
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ABSTRACT: A sensitive marker for monitoring progression of early Alzheimer's disease would help to develop and test new therapeutic strategies. The present study is aimed at investigating brain metabolism changes over time, as a potential monitoring marker, in patients with amnestic mild cognitive impairment, according to their clinical outcome (converters or non-converters), and in relation to their cognitive decline. Seventeen amnestic mild cognitive impairment patients underwent magnetic resonance imaging and 18FDG-positron emission tomography scans both at inclusion and 18 months later. Baseline and follow-up positron emission tomography data were corrected for partial volume effects and spatially normalized using magnetic resonance imaging data, scaled to the vermis and compared using SPM2. 'PET-PAC' maps reflecting metabolic per cent annual changes were created for correlation analyses with cognitive decline. In the whole sample, the greatest metabolic decrease concerned the posterior cingulate-precuneus area. Converters had significantly greater metabolic decrease than non-converters in two ventro-medial prefrontal areas, the subgenual (BA25) and anterior cingulate (BA24/32). PET-PAC in BA25 and BA24/32 combined allowed complete between-group discrimination. BA25 PET-PAC significantly correlated with both cognitive decline and PET-PAC in the hippocampal region and temporal pole, while BA24/32 PET-PAC correlated with posterior cingulate PET-PAC. Finally, the metabolic change in BA8/9/10 was inversely related to that in BA25 and showed relative increase with cognitive decline, suggesting that compensatory processes may occur in this dorso-medial prefrontal region. The observed ventro-medial prefrontal disruption is likely to reflect disconnection from the hippocampus, both indirectly through the cingulum bundle and posterior cingulate cortex for BA24/32, and directly through the uncinate fasciculus for BA25. Altogether, our findings emphasize the potential of 18FDG-positron emission tomography for monitoring early Alzheimer's disease progression.
Brain 06/2009; 132(Pt 8):2058-67. · 9.46 Impact Factor
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ABSTRACT: Gray matter volume studies have been limited to few brain regions of interest, and white matter and glucose metabolism have received limited research attention in Korsakoff's syndrome (KS). Because of the lack of brain biomarkers, KS was found to be underdiagnosed in postmortem studies.
Nine consecutively selected patients with KS and 22 matched controls underwent both structural magnetic resonance imaging and (18)F-fluorodeoxyglucose positron emission tomography examinations. Using a whole-brain analysis, the between-group comparisons of gray matter and white matter density and relative glucose uptake between patients with KS and controls showed the involvement of both the frontocerebellar and the Papez circuits, including morphological abnormalities in their nodes and connection tracts and probably resulting hypometabolism. The direct comparison of the regional distribution and degree of gray matter hypodensity and hypometabolism within the KS group indicated very consistent gray matter distribution of both abnormalities, with a single area of significant difference in the middle cingulate cortex showing greater hypometabolism than hypodensity. Finally, the analysis of the variability in the individual patterns of brain abnormalities within our sample of KS patients revealed that the middle cingulate cortex was the only brain region showing significant GM hypodensity and hypometabolism in each of our 9 KS patients.
These results indicate widespread brain abnormalities in KS including both gray and white matter damage mainly involving two brain networks, namely, the fronto-cerebellar circuit and the Papez circuit. Furthermore, our findings suggest that the middle cingulate cortex may play a key role in the pathophysiology of KS and could be considered as a potential in vivo brain biomarker.
PLoS ONE 01/2009; 4(11):e7748. · 4.09 Impact Factor
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Circulation 09/2008; 118(6):678-83. · 14.74 Impact Factor
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ABSTRACT: In early Alzheimer's disease (AD), the hippocampal region is the area most severely affected by cellular and structural alterations, yet glucose hypometabolism predominates in the posterior association cortex and posterior cingulate gyrus. One prevalent hypothesis to account for this discrepancy is that posterior cingulate hypometabolism results from disconnection from the hippocampus through disruption of the cingulum bundle. However, only partial and indirect evidence currently supports this hypothesis. Thus, using structural magnetic resonance imaging and 2-[(18)F]fluoro-2-deoxy-D-glucose positron emission tomography in 18 patients with early AD, we assessed the relationships between hippocampal atrophy, white matter integrity, and gray matter metabolism by means of a whole-brain voxel-based correlative approach. We found that hippocampal atrophy is specifically related to cingulum bundle disruption, which is in turn highly correlated to hypometabolism of the posterior cingulate cortex but also of the middle cingulate gyrus, thalamus, mammillary bodies, parahippocampal gyrus, and hippocampus (all part of Papez's circuit), as well as the right temporoparietal associative cortex. These results provide the first direct evidence supporting the disconnection hypothesis as a major factor contributing to the early posterior hypometabolism in AD. Disruption of the cingulum bundle also appears to relate to hypometabolism in a large connected network over and above the posterior cingulate cortex, encompassing the whole memory circuit of Papez (consistent with the key location of this white matter tract within this loop) and also, but indirectly, the right posterior association cortex.
Journal of Neuroscience 07/2008; 28(24):6174-81. · 7.11 Impact Factor
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ABSTRACT: Although the penumbra can be saved by early reperfusion, in the rat it is consistently affected by selective neuronal loss. Mapping selective neuronal loss in the living primate would be desirable.
Five young adult baboons underwent (15)O positron emission tomography for cerebral blood flow, cerebral oxygen consumption, and oxygen extraction fraction mapping at baseline and serially during and after 20-hour temporary middle cerebral artery occlusion. At approximately day 30, (11)C-flumazenil (FMZ), a potential positron emission tomography marker of selective neuronal loss, and structural magnetic resonance-based infarct mapping were obtained, and the brain was perfused-fixed. Reduced FMZ binding in noninfarcted cortical middle cerebral artery areas was searched voxel-wise, and specific binding was assessed using compartmental modeling of FMZ time-activity curves.
Visual inspection revealed reduced late FMZ uptake in the affected cortical territory, extending well beyond the infarct. Accordingly, the incidence of selected voxels was greater than chance, documenting mildly but significantly reduced FMZ uptake and specific binding. Serial (15)O positron emission tomography revealed moderately severe acute ischemia followed by reperfusion. Histopathology documented only mild neuronal changes in or near the affected areas.
We document moderate but definite late FMZ binding decrements in noninfarcted cortical areas in the baboon, consistent with previous rat and human studies. These were acutely characterized by moderate ischemia followed by reperfusion, consistent with neuronal damage from ischemic or reperfusion injury in the salvaged at-risk tissue. Only mild histopathological changes subtended these FMZ alterations suggesting subtle processes such as isolated dendrite or synapse loss. Whether these changes impact on clinical outcome deserves studying because they may be targeted by specific neuroprotection.
Stroke 04/2008; 39(3):991-9. · 5.73 Impact Factor
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ABSTRACT: We aimed at identifying the cerebral structures whose synaptic function subserves the recollection of lifetime's episodic autobiographical memory (AM) via autonoetic consciousness. Twelve healthy middle-aged subjects (mean age: 59 years +/- 2.5) underwent a specially designed cognitive test to assess the ability to relive richly detailed episodic autobiographical memories from five time periods using the Remember/Know procedure. We computed an index of episodicity (number of Remember responses justified by the recall of specific events and details) and an index of retrieval spontaneity, and additionally an index of semanticized memories (number of Know responses). The regional cerebral blood flow (rCBF) was measured in the resting state, with H(2)O(15) as part of an activation PET study. The indexes were correlated with blood flow using volumes of interest in frontotemporal regions, including hippocampus and voxel-wise analyses in SPM. With both analyses, significant correlations were mainly found between the index of episodicity and rCBF in the medial temporal lobe, including hippocampus, across the five time periods (unlike the index of semanticized memories) and between the spontaneity index and rCBF in the prefrontal areas. These results highlight, in healthy subjects, the distinct role of these two structures in AM retrieval and support the view that the hippocampus is needed for reexperiencing detailed episodic memories no matter how old they are.
Hippocampus 02/2008; 18(5):445-59. · 5.18 Impact Factor
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ABSTRACT: Over and above typical motor alterations, executive and working memory (WM) impairment can also occur in early idiopathic Parkinson's disease (PD). We aimed to investigate the compensatory neural processes involved in WM performance, as well as the networks involved in the long-term memory transfer from short-term stores in PD.
Relative cerebral blood flow (rCBF) was mapped with H2O(15)-PET in eight treated nondemented PD patients while performing a WM verbal double-task (Brown-Peterson paradigm) using both short (6-second) and long (18-second) delays.
As compared to nine age-matched healthy subjects, performance of the PD group was only slightly reduced on the short-delay but markedly impaired on the long-delay task. Underlying the relatively preserved short-delay performance, the PD group exhibited overactivation of prefrontal and parietal areas involved in attention-demanding processes, suggestive of efficient compensatory processes. Further supporting this, significant positive correlations were found between short-delay performance and rCBF in the bilateral inferior parietal cortex. In contrast, the lack of overactivation with the long-delay task together with posterior cingulate hypoactivation would support the idea of functional disconnection impairing transfer of information from prefrontal onto (para)limbic areas. These findings suggest novel areas of investigation into early cognitive impairments in PD.
Journal of Neuroimaging 11/2007; 17(4):277-85. · 1.51 Impact Factor
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ABSTRACT: Using PET, we have determined the neural substrates of age-related verbal episodic memory decline. Twelve young and twelve older healthy volunteers (mean age; 22 and 59 years, respectively) were scanned while performing encoding and retrieval tasks. Retrieval performance was lower in old than in young subjects. The PET data were analyzed using a combined subtraction/correlation approach. Classic subtraction disclosed prefrontal rCBF increases common to both groups, distributed bilaterally during encoding and exclusively right-sided during retrieval, without between-group differences. The correlation analysis between PET activity during encoding and subsequent retrieval performance revealed significant correlations for the left hippocampal region in both groups, but for the right inferior frontal gyrus in the older subjects only. Thus, lower performance in older subjects during an episodic retrieval task may reflect a combination of (i) subtle encoding dysfunction, evidenced by more widespread activity-performance correlations and (ii) less efficient retrieval, as evidenced by unaltered activation pattern (as revealed by the classic subtraction method) despite reduced performance. These exploratory findings suggest the aged brain may be unable to compensate for reduced efficiency of right prefrontal cortex by additional left frontal activation.
Neurobiology of aging 11/2007; 28(10):1568-76. · 5.94 Impact Factor
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ABSTRACT: While the hippocampus is constantly reported as the site of earliest and highest structural alteration in Alzheimer's disease (AD), findings regarding the metabolic status of this region are rather heterogeneous. It has been proposed that only a time-consuming individual region-of-interest (ROI) approach would allow the detection of hypometabolism in this complex and small area. Our main goal with this study is to assess whether more automatic and clinically useful methods would be sensitive enough when considering other methodological confounds. From a single PET data set collected in 28 patients with amnestic Mild Cognitive Impairment (aMCI) and 19 controls, we assessed the effects of partial volume effect (PVE) correction, scaling (using vermis or global means), and analysis method (individual ROI versus more automatic template-based ROI or voxel-based approaches) on hippocampal hypometabolism detection in aMCI. PVE correction and scaling both showed a significant effect on group comparison, while the analysis method (individual versus template-based ROI) surprisingly did not. Hippocampal metabolic decrease was significant in all vermis-scaled conditions, and more so after PVE correction. Our findings highlight the crucial relevance of using reference-region-based (instead of global) scaling, and the higher sensitivity of PVE-corrected PET measures, to detect hippocampal hypometabolism in aMCI. They also show that hippocampal metabolic decline can be detected using template-based ROI as well as voxel-based methods. These findings have clinical relevance since they support the validity of more automatic and time-saving approaches to assess hippocampal metabolism changes in aMCI and early AD.
NeuroImage 09/2007; 37(1):18-25. · 5.89 Impact Factor
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Grégoria Kalpouzos,
Gaël Chételat, Jean-Claude Baron,
Brigitte Landeau,
Katell Mevel,
Christine Godeau,
Louisa Barré,
Jean-Marc Constans,
Fausto Viader,
Francis Eustache,
Béatrice Desgranges
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ABSTRACT: With age, the brain undergoes both structural and functional alterations, probably resulting in reported cognitive declines. Relatively few investigations have sought to identify those areas that remain intact with aging, or undergo the least deterioration, which might underlie cognitive preservations. Our aim here was to establish a comprehensive profile of both structural and functional changes in the aging brain, using up-to-date voxel-based methodology (i.e. optimized voxel-based morphometry (VBM) procedure; resting-state (18)FDG-PET with correction for partial volume effects (PVE)) in 45 optimally healthy subjects aged 20-83 years. Negative and positive correlations between age and both gray matter (GM) volume and (18)FDG uptake were assessed. The frontal cortex manifested the greatest deterioration, both structurally and functionally, whereas the anterior hippocampus, the thalamus and (functionally) the posterior cingulate cortex were the least affected. Our results support the developmental theory which postulates that the first regions to emerge phylogenetically and ontogenetically are the most resistant to age effects, and the last ones the most vulnerable. Furthermore, the lesser affected anterior hippocampal region, together with the lesser functional alteration of the posterior cingulate cortex, appear to mark the parting of the ways between normal aging and Alzheimer's disease, which is characterized by early and prominent deterioration of both structures.
Neurobiology of aging 08/2007; 30(1):112-24. · 5.94 Impact Factor
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ABSTRACT: The brain metabolic pattern of vascular dementia (VaD) remains poorly characterized. Univariate voxel-based analysis ignores the functional correlations among structures and may lack sensitivity and specificity. Here, we applied a novel voxel-based multivariate technique to a large ((18)F)2-fluoro-2-deoxy-D-glucose positron emission tomography data set. The sample consisted of 153 subjects, one-third each being probable subcortical VaD, probable Alzheimer disease (AD) (matched for Mini-Mental-State examination (MMSE) and age), and normal controls (NCs). We first applied principal component (PC) analysis and removed PCs significantly correlated to age. The remainders were used as feature vectors in a canonical variate analysis to generate canonical variates (CVs), that is, linear combinations of PC-scores. The first two CVs efficiently separated the groups. CV(1) separated VaD from AD with 100% accuracy, whereas CV(2) separated NC from demented subjects with 72% sensitivity and 96% specificity. Images depicting CV(1) and CV(2) showed that lower metabolism differentiating VaD from AD mainly concerned the deep gray nuclei, cerebellum, primary cortices, middle temporal gyrus, and anterior cingulate gyrus, whereas lower metabolism in AD versus VaD concerned mainly the hippocampal region and orbitofrontal, posterior cingulate, and posterior parietal cortices. The hypometabolic pattern common to VaD and AD mainly concerned the posterior parietal, precuneus, posterior cingulate, prefrontal, and anterior hippocampal regions, and linearly correlated with the MMSE. This study shows the potential of voxel-based multivariate methods to highlight independent functional networks in dementing diseases. By maximizing the separation between groups, this method extracted a metabolic pattern that efficiently differentiated VaD and AD.
Journal of Cerebral Blood Flow & Metabolism 10/2006; 26(9):1213-21. · 5.01 Impact Factor
