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F Pasquier

Publications and source records attributed to F Pasquier.

At least 19 recordsLinked to original sources
PubMed2006

Influence of cognitive impairment on the institutionalisation rate 3 years after a stroke.

BACKGROUND AND PURPOSE: Pre-existing cognitive decline and new-onset dementia are common in patients with stroke, but their influence on institutionalisation rates is unknown. OBJECTIVE: To evaluate the influence of cognitive impairment on the institutionalisation rate 3 years after a stroke. DESIGN: (1) The previous cognitive state of 192 consecutive patients with stroke living at home before the stroke (with the Informant Questionnaire on COgnitive Decline in the Elderly (IQCODE)), (2) new-onset dementia occurring within 3 years and (3) institutionalisation rates within 3 years in the 165 patients who were discharged alive after the acute stage were prospectively evaluated. RESULTS: Independent predictors of institutionalisation over a 3-year period that were available at admission were age (adjusted odds ratio (adjOR) for 1-year increase = 1.08; 95% confidence interval (CI) 1.03 to 1.15), severity of the neurological deficit (adjOR for 1-point increase in Orgogozo score = 0.97; 95% CI 0.96 to 0.99) and severity of cognitive impairment (adjOR for 1-point increase in IQCODE score = 1.03; 95% CI 1 to 1.06). Factors associated with institutionalisation at 3 years that were present at admission or occurred during the follow-up were age (adjOR for 1-year increase = 1.17; 95% CI 1.07 to 1.27) and any (pre-existing or new) dementia (adjOR = 5.85; 95% CI 1.59 to 21.59), but not the severity of the deficit of the neurological deficit. CONCLUSION: Age and cognitive impairment are more important predictors of institutionalisation 3 years after a stroke than the severity of the physical disability.

Adult↗
PubMed2006

Poststroke dementia.

The association between stroke and dementia is frequent. The prevalence of poststroke dementia (PSD) ranges from 6 to 32%, depending on the population studied, the criteria used for the diagnosis of dementia, and the time interval between the stroke and the neuropsychological assessment. The risk of PSD is high immediately after stroke and remains higher than in controls in stroke patients nondemented 3 months after stroke. Not all cases of PSD are vascular in origin, with about one third of demented patients diagnosed as having Alzheimer's disease plus stroke. The pathophysiology of PSD is probably multifactorial, with an influence of vascular lesions, associated Alzheimer's lesions and white matter changes. The risk of dementia is higher in older patients and in patients with preexisting cognitive decline - no dementia, severe stroke, a history of stroke, white matter changes and cerebral atrophy. The influence of stroke location, vascular risk factors and silent infarcts remains to be determined. PSD adversely influences the outcome in stroke patients.

Dementia↗
PubMed2006

Diabetes mellitus and dementia.

Alzheimer's disease (AD) and diabetes mellitus (DM) are two of the most common and devastating health problems in the elderly. They share a number of common features amongst which high prevalence after 65 years, important impact of patient's quality of life, substantial health care costs. Reviews on the epidemiological studies on cognitive impairment in patients with DM found evidence of cross-sectional and prospective associations between type 2 DM and moderate cognitive impairment, on memory and executive functions. There is also evidence for an elevated risk of both vascular dementia and AD in patients with type 2 DM, albeit with strong interaction of other factors such as hypertension, dyslipidaemia and ApoE genotype. DM is an independent predictor of post-stroke dementia. DM being an atherogenic risk factor, it may increase the risk of dementia through associations with stroke, causing vascular dementia. In addition, vascular reactivity may be adversely affected by advanced glycosylation end products resulting in more subtle perfusion abnormalities. Cerebrovascular disease may exacerbate AD through direct interactions between the two pathological processes or through cognitive impairment secondary to cerebrovascular disease "unmasking" AD at an earlier stage than it would otherwise become apparent. The increased risk of AD may also be mediated by the exacerbation of B-amyloid neurotoxicity by advanced glycosylation end products identified in the matrix of neurofibrillary tangles and amyloid plaques in AD brains, or associations with insulin functions. Decreased cholinergic transport across the blood-brain barrier observed in diabetic animals may exacerbate cognitive impairment in AD. Many interventions could reduce the cognitive decline associated with DM, yet not enough are taken into account so far.

Alzheimer Disease↗
PubMed2006

Biochemical staging of synucleinopathy and amyloid deposition in dementia with Lewy bodies.

The primary feature of dementia with Lewy bodies (DLB) is the aggregation of alpha-synuclein into characteristic lesions: Lewy bodies (LBs) and Lewy neurites. However, in most of DLB cases, LBs are associated with neurofibrillary tangles and amyloid plaques (both Alzheimer disease [AD]-related lesions). We wanted to determine if this overlap of lesions is statistical, as a result of the late onset of both diseases, or results from a specific physiopathological synergy between synucleinopathy and either tauopathy or amyloid pathology. All patients with DLB from our prospective and multidisciplinary study were analyzed. These cases were compared with cases with pure AD and patients with Parkinson disease and controls. All cases were analyzed thoroughly at the neuropathologic and biochemical levels with a biochemical staging of aggregated alpha-synuclein, tau, and Abeta species. All sporadic cases of DLB were associated with abundant deposits of Abeta x-42 that were similar in quality and quantity to those of AD. Amyloid precursor protein (APP) dysfunction is a risk factor for AD as demonstrated by pathogenic mutations and Abeta accumulation. The constant and abundant Abeta x-42 deposition in sporadic DLB suggests that synucleinopathy is also promoted by APP dysfunction. Therefore, we conclude that APP is a therapeutic target for both AD and DLB.

Aged↗
PubMed2006

Different patterns of Mini Mental Status Examination responses in primary progressive aphasia and Alzheimer's disease.

Primary progressive aphasia (PPA) syndrome is frequently misdiagnosed--particularly in favour of Alzheimer's disease (AD). Misdiagnosis is related to the heterogeneity of language disorders at onset, variability in the rate of clinical progression and the low prevalence of PPA syndrome, compared with AD. The aim of this study was to determine whether a patient's first Mini Mental Status Examination (MMSE) might provide insight into differentiating between PPA and AD. We compared item scores for the first, complete MMSE in consecutive patients with PPA versus matched patients with AD. Word recall and constructional praxis were significantly better in patients subsequently diagnosed as suffering from PPA. Patients with AD performed significantly better in terms of word registration, object naming, repetition and verbal direction. Our findings indicate that the various MMSE item scores may be helpful in differentiating PPA and AD in the first few years of the disease.

Aged↗
PubMed2005

Diagnosis and management of dementia with Lewy bodies: third report of the DLB Consortium.

The dementia with Lewy bodies (DLB) Consortium has revised criteria for the clinical and pathologic diagnosis of DLB incorporating new information about the core clinical features and suggesting improved methods to assess them. REM sleep behavior disorder, severe neuroleptic sensitivity, and reduced striatal dopamine transporter activity on functional neuroimaging are given greater diagnostic weighting as features suggestive of a DLB diagnosis. The 1-year rule distinguishing between DLB and Parkinson disease with dementia may be difficult to apply in clinical settings and in such cases the term most appropriate to each individual patient should be used. Generic terms such as Lewy body (LB) disease are often helpful. The authors propose a new scheme for the pathologic assessment of LBs and Lewy neurites (LN) using alpha-synuclein immunohistochemistry and semiquantitative grading of lesion density, with the pattern of regional involvement being more important than total LB count. The new criteria take into account both Lewy-related and Alzheimer disease (AD)-type pathology to allocate a probability that these are associated with the clinical DLB syndrome. Finally, the authors suggest patient management guidelines including the need for accurate diagnosis, a target symptom approach, and use of appropriate outcome measures. There is limited evidence about specific interventions but available data suggest only a partial response of motor symptoms to levodopa: severe sensitivity to typical and atypical antipsychotics in approximately 50%, and improvements in attention, visual hallucinations, and sleep disorders with cholinesterase inhibitors.

Brain↗
PubMed2005

Prestroke dementia in patients with atrial fibrillation. Frequency and associated factors.

BACKGROUND AND PURPOSE: Prestroke dementia is frequent but usually not identified. Non-valvular atrial fibrillation (NVAF) is independently associated with an increased risk for dementia. However, the frequency and determinants of prestroke dementia in patients with NVAF have never been evaluated. OBJECTIVE: The aim of this study was to determine the frequency of prestroke dementia and associated factors in patients with a previously known NVAF. METHODS: This is an ancillary study of Stroke in Atrial Fibrillation Ensemble II (SAFE II), an observational study conducted in patients with a previously known NVAF, consecutively admitted for an acute stroke in French and Italian centers. Prestroke dementia was evaluated by the IQCODE in patients with a reliable informant. Patients were considered as demented before stroke when their IQCODE score was > or = 104. RESULTS: of 204 patients, 39 (19.1%; 95% confidence interval [CI]: 13.7%-24.5%) patients met criteria for prestroke dementia. The only variable independently associated with prestroke dementia was increasing age (adjusted odds ratio for 1 year increase in age: 1.10; 95 % CI: 1.04-1.17), and there was a nonsignificant tendency for previous ischemic stroke or TIA and arterial hypertension. CONCLUSION: One fifth of stroke patients with a previously known NVAF were already demented before stroke. The main determinant of prestroke dementia is increasing age. A large cohort is necessary to identify other determinants.

Age Factors↗
PubMed2005

Disturbance of sensory filtering in dementia with Lewy bodies: comparison with Parkinson's disease dementia and Alzheimer's disease.

INTRODUCTION: Prepulse inhibition (PPI) is considered to mirror an organism's ability to filter out irrelevant sensory or cognitive information. The disruption of PPI has never been studied in individuals suffering from dementia with Lewy bodies (DLB). As attention deficits largely contribute to cognitive impairment in DLB, an investigation with a PPI paradigm is useful for differential diagnosis of DLB versus Alzheimer's disease (AD) and Parkinson's disease dementia (PDD). OBJECTIVE AND METHODS: PPI of the N1/P2 component of auditory evoked potentials was used to investigate the early stages of attention selectivity in 10 DLB, 10 AD, and 10 PDD patients, as well as in 10 healthy controls. The PPI paradigm consisted of the presentation of sound pulses (40 ms, 115 dB) preceded by a prepulse (40 ms, 80 dB). Sound stimuli were presented in a total of 80 trials in a pseudo-random order. RESULTS: Non-parametric analyses of variance revealed a significant group effect on the 120 ms lead interval. Retrospective analyses revealed that PPI was significantly reduced in DLB compared to healthy controls and AD. In the PDD group, the disturbance was of intermediate intensity. CONCLUSION: The present study revealed a severe disturbance of PPI in DLB patients. The DLB patients displayed a specific disruption profile in terms of magnitude as well as time course.

Acoustic Stimulation↗
PubMed2005

Lipid lowering agents are associated with a slower cognitive decline in Alzheimer's disease.

BACKGROUND: Data from epidemiological studies and animal models imply that disturbances in cholesterol metabolism are linked to Alzheimer's disease susceptibility. Lipid lowering agents (LLAs) may have implications for the prevention of Alzheimer's disease. OBJECTIVE: To investigate whether LLAs are associated with a slower cognitive decline in Alzheimer's disease. METHODS: An observational study in 342 Alzheimer patients followed in a memory clinic for 34.8 months (mean age 73.5 years, mini-mental state examination score (MMSE) 21.3 at entry); 129 were dyslipaemic treated with LLAs (47% with statins), 105 were untreated dyslipaemic, and 108 were normolipaemic. The rate of cognitive decline was calculated as the difference between the first and last MMSE score, divided by the time between the measurements, expressed by year. Patients were divided into slow and fast decliners according to their annual rate of decline (lower or higher than the median annual rate of decline in the total population). RESULTS: Patients treated with LLAs had a slower decline on the MMSE (1.5 point/year, p = 0.0102) than patients with untreated dyslipaemia (2.4 points/year), or normolipaemic patients (2.6 points/year). Patients with a slower decline were more likely to be treated with LLAs. Logistic regression analysis, with low annual cognitive decline as the dependent variable, showed that the independent variable LLA (treated with or not) was positively associated with the probability of lower cognitive decline (odds ratio = 0.45, p = 0.002). CONCLUSIONS: LLAs may slow cognitive decline in Alzheimer's disease and have a neuroprotective effect. This should be confirmed by placebo controlled randomised trials in patients with Alzheimer's disease and no dyslipaemia.

Aged↗
PubMed2005

Influence of pre-existing dementia on the risk of post-stroke epileptic seizures.

BACKGROUND: Seizures occur in 10% of stroke patients, but their predictors have not been clearly identified. Pre-existing dementia is present in 12-16% of stroke patients and, at the community level, patients with dementia have increased risk of seizures. However, the question of whether pre-existing dementia is associated with a higher risk of seizures after stroke has never been studied. AIM: To evaluate whether pre-existing dementia is associated with an increased risk of seizures after stroke. METHODS: The study was conducted on 202 consecutive stroke patients recruited to the Lille stroke/dementia study (97 men; median age, 75 years; range, 42-100). Pre-stroke cognitive functions were evaluated using the Informant Questionnaire on Cognitive Decline in the Elderly, with a cutoff value of 104 for the diagnosis of dementia. Seizures were defined as early seizures when occurring within seven days of stroke onset, and as late seizures when occurring more than seven days after stroke. RESULTS: Of 202 patients, 33 (16.3%) met the criteria for pre-existing dementia, and 11 (5.4%) developed early seizures. During 289 person-years of follow up, 14 patients developed late seizures, resulting in an incidence rate of 4.8 new cases/100 person-years. Pre-existing dementia was not associated with the occurrence of early seizures, but was independently associated with the occurrence of late seizures (adjusted odds ratio, 4.66; 95% confidence interval, 1.34 to 16.21). CONCLUSION: Stroke patients with pre-existing dementia have an increased risk of late seizures. Any factor increasing the risk of seizures (drugs, metabolic changes) should be avoided in these patients.

Adult↗
PubMed2004

Perception of emotion on faces in frontotemporal dementia and Alzheimer's disease: a longitudinal study.

UNLABELLED: Frontotemporal dementia (FTD) is a neurodegenerative disease characterised by behavioural disorders that suggest abnormalities of emotional processing. In a previous study, we showed that patients with Alzheimer's disease (AD) and with FTD were equally able to distinguish a face displaying affect from one not displaying affect. However, recognition of emotion was worse in patients with FTD than in patients with AD who did not differ significantly from controls. The aim of this study was to follow up the perception of emotions on faces in these patients. The poor perception of emotion could worsen differently in AD and in FTD, with the progression of atrophy of the amygdala, the anterior temporal cortex and the orbital frontal cortex, structures that are components of the brain's emotional processing systems. METHODS: Patients with AD or with FTD had to recognise and point out the name of one of seven basic emotions (anger, disgust, happiness, fear, sadness, surprise and contempt) on a set of 28 faces presented on slides at the first visit and 3 years later. RESULTS: Thirty-seven patients (AD = 19, FTD = 18) performed the tests initially. The two patient groups did not differ for age, sex and duration of the disease. During the follow-up, 12 patients died, 4 patients refused to perform the tests and 8 could not be tested because of the severity of the disease. Finally, 7 patients with AD and 6 patients with FTD performed the two tests at a mean delay of 40 months. All patients with AD had worse results at follow-up on the perception of emotion despite the prescription of inhibitors of cholinesterase in all patients and of selective serotonin reuptake inhibitors (SSRIs) in 4 patients. As a whole, patients with FTD had better results in the second than in the first assessment (however, 3 of them had worse results) independently of the prescription of trazodone (n = 2), other SSRIs (n = 2), or the absence of treatment (n = 2), and of possible cognitive change. CONCLUSIONS: Recognition of emotion on faces in AD decreases with the progression of dementia and could be related to the progression of the degeneration of the structures implicated in emotional processing systems. Inconsistency of the results in FTD may be related to impulsiveness, lack of consistency of the patients and to heterogeneity of the progression of the lesions.

Aged↗
PubMed2004

Depressive symptoms after stroke and relationship with dementia: A three-year follow-up study.

OBJECTIVE: To determine frequency, determinants, and time course of poststroke depressive symptoms (DS) and their relationship with dementia. METHODS: Two hundred two consecutive stroke patients were prospectively evaluated for DS, followed up over a 3-year period. Patients with Montgomery and Asberg Depression Rating Scale (MADRS) scores of >/==" BORDER="0">7 were considered as having DS. The severity of the neurologic deficit, functional outcome, and dementia were quantified with the Orgogozo Scale, modified Rankin Scale, Informant Questionnaire on Cognitive Decline in the Elderly, and an extensive battery of neuropsychological tests. RESULTS: DS were present in 43% of survivors after 6 months, 36% after 12 months, 24% after 24 months, and 18% after 36 months. The severity of the neurologic deficit at admission was the only independent predictor of DS at month 6. DS at month 6 were more frequent in patients with previous depression, dementia, and right superficial lesions. Younger age and right superficial lesions were the two variables independently associated with the presence of DS at month 36. The time course of the various DS differed, sadness remaining frequent 3 years after stroke (50%), whereas slowness, psychic slowness, lack of energy, and concentration difficulties remained frequent at month 36 in patients with dementia. CONCLUSION: DS are frequent after stroke. Their time course varies and depends on the cognitive status; this variation contributes to differences among previous studies on poststroke depression.

Adult↗
PubMed2003

Leukoaraiosis more than dementia is a predictor of stroke recurrence.

BACKGROUND AND PURPOSE: It has been suggested that poststroke dementia is associated with a higher risk of stroke recurrence. Leukoaraiosis, however, might be a confounding factor because it is a risk factor for stroke recurrence and cognitive decline. Our aim was to determine the influence of prestroke and poststroke dementia on the 3-year risk of stroke recurrence. METHODS: We evaluated prestroke cognitive functions in 202 stroke patients >or=40 years of age using the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE), with a cutoff of 104 for the diagnosis of dementia. Patients were followed up for 3 years. Dementia was diagnosed on the basis of International Classification of Diseases, 10th revision, criteria in survivors who underwent a neurologist visit or from the IQCODE score in survivors who did not. The severity of leukoaraiosis was assessed with a visual rating scale on CT scans without contrast performed at the acute stage of stroke. At each follow-up contact, stroke recurrences were recorded. RESULTS: During 385 person-years of follow-up, a total of 29 patients developed 33 stroke recurrences, resulting in an incidence rate of 8.6 per 100 person-years. We did not find any influence of dementia on the risk of stroke recurrence. Leukoaraiosis, however, was a strong predictor of stroke recurrence within 3 years after stroke. CONCLUSIONS: Dementia was not a predictor of stroke recurrence, but leukoaraiosis was strongly associated with stroke recurrence. Special attention in the secondary prevention of stroke must be given to patients with leukoaraiosis with or without dementia.

Adult↗
PubMed2003

Association of 3'-UTR polymorphisms of the oxidised LDL receptor 1 (OLR1) gene with Alzheimer's disease.

Although possession of the epsilon 4 allele of the apolipoprotein E gene appears to be an important biological marker for Alzheimer's disease (AD) susceptibility, strong evidence indicates that at least one additional risk gene exists on chromosome 12. Here, we describe an association of the 3'-UTR +1073 C/T polymorphism of the OLR1 (oxidised LDL receptor 1) on chromosome 12 with AD in French sporadic (589 cases and 663 controls) and American familial (230 affected sibs and 143 unaffected sibs) populations. The age and sex adjusted odds ratio between the CC+CT genotypes versus the TT genotypes was 1.56 (p=0.001) in the French sample and 1.92 (p=0.02) in the American sample. Furthermore, we have discovered a new T/A polymorphism two bases upstream of the +1073 C/T polymorphism. This +1071 T/A polymorphism was not associated with the disease, although it may weakly modulate the impact of the +1073 C/T polymorphism. Using 3'-UTR sequence probes, we have observed specific DNA protein binding with nuclear proteins from lymphocyte, astrocytoma, and neuroblastoma cell lines, but not from the microglia cell line. This binding was modified by both the +1071 T/A and +1073 C/T polymorphisms. In addition, a trend was observed between the presence or absence of the +1073 C allele and the level of astrocytic activation in the brain of AD cases. However, Abeta(40), Abeta(42), Abeta total, and Tau loads or the level of microglial cell activation were not modulated by the 3'-UTR OLR1 polymorphisms. Finally, we assessed the impact of these polymorphisms on the level of OLR1 expression in lymphocytes from AD cases compared with controls. The OLR1 expression was significantly lower in AD cases bearing the CC and CT genotypes compared with controls with the same genotypes. In conclusion, our data suggest that genetic variation in the OLR1 gene may modify the risk of AD.

3' Untranslated Regions↗
PubMed2003

[The profile of memory disturbance in early Lewy body dementia differs from that in Alzheimer's disease].

It may be difficult to distinguish Lewy body dementia (LBD) from Alzheimer's disease (AD) especially at an early stage. Clinical diagnostic criteria for LBD still lack sensitivity. We compared memory performance in early AD and LBD to identify features that may help to distinguish these two conditions. Patients with Mini Mental State scores equal or above 18 were consecutively selected retrospectively from the University Out-patient Memory Clinic database. Probable LBD and AD were respectively diagnosed according to the international consensus criteria and the NINCDS-ADRDA criteria. Short-term memory was assessed with the digit span subtest of the Wechsler Memory Scale and the Corsi block-tapping test. Long term verbal memory was assessed with a French version of the Grober and Buschke test. Long-term visual memory was tested with the recall of four geometric figures of the CERAD battery. There was no difference between the two groups in short-term or long-term visual memory. Except for the immediate and first free recalls, DCL patients performed significantly better than AD patients in all subtests of the Grober and Buschke test. The more striking differences were seen with the third total and delayed total recall. These results highlight the differences of memory impairment pattern in early LBD and AD. Episodic verbal memory is better in LBD patients who benefit more from cues, reflecting the subcortical component of the disease. Such neuropsychological data should be validated prospectively and further be part of the diagnostic criteria.

Aged↗
PubMed2002

Nonoverlapping but synergetic tau and APP pathologies in sporadic Alzheimer's disease.

OBJECTIVE: To determine the spatiotemporal mapping of tau pathologies and insoluble pools of Abeta in aging and sporadic AD, and their contribution to the physiopathologic, clinical, and neuropathologic features. METHODS: The authors studied 130 patients of various ages and different cognitive status, from nondemented controls (n = 60) to patients with severe definite AD (n = 70) who were followed prospectively. Insoluble Abeta 42 and 40 species were fully solubilized and quantified in the main neocortical areas, with a new procedure adapted to human brain tissue. Tau pathology staging was determined in 10 different brain areas, using Western blots. RESULTS: In AD, there is a constellation of amyloid phenotypes, extending from cases with exclusively aggregated Abeta 42 to cases with, in addition, large quantities of insoluble Abeta 40 species. Five other points were observed: 1) There was no spatial and temporal overlap in the distribution of these two insoluble Abeta species in cortical brain areas. 2) In contrast to solubilized Abeta 40 aggregates composed essentially of monomers and dimers, solubilized Abeta 42 was essentially observed as dimers and multimers. 3) Abeta 42 aggregates were observed at the early stages of tau pathology, whereas the insoluble Abeta 40 pool was found at the last stages. 4) During the progression of the disease, Abeta aggregates increase in quantity and heterogeneity, in close parallel to the extension of tau pathology. 5) There was no spatial overlap between Abeta aggregation that is widespread and heterogeneously distributed in cortical areas and tau pathology that is progressing sequentially, stereotypically, and hierarchically. CONCLUSIONS: These observations demonstrate that Abeta 42 aggregation, and not Abeta 40, is the marker that is close to Alzheimer etiology. It should be the main target for the early biological diagnosis of AD and modeling. Furthermore, the spatial mismatch between amyloid ss-precursor protein (APP) and tau pathologies in cortical brain areas demonstrates that neurodegeneration is not a direct consequence of extracellular Abeta neurotoxicity. Hence, there is a synergetic effect of APP dysfunction, revealed by Abeta aggregation, on the neuron-to-neuron propagation of tau pathology.

Alzheimer Disease↗