Biomedical subjects

Florence Pasquier

Publications and source records attributed to Florence Pasquier.

23 records · Page 2Linked to original sources

PubMed2003

Influence of prestroke dementia on early and delayed mortality in stroke patients.

Causes of early and delayed death after stroke differ. It has been suggested that delayed mortality rate was increased in patients with post-stroke dementia. Prestroke dementia is frequent: its influence on survival in stroke patients has never been evaluated. The aim of this study was to evaluate the influence of prestroke dementia on early and delayed mortality rate after stroke. In a cohort of 202 consecutive stroke patients aged >or= 40 years admitted between November 1995 and May 1996 in a primary care center, the prevalence of prestroke dementia was determined using the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE) with a cut-off of 104. Patients were followed-up for 3 years. Statistics were performed using life-table methods. Of 202 patients, 33 had prestroke dementia. Of 142 survivors at month-6, 44 were demented, of them 15 having prestroke and 29 new-onset post-stroke dementia. No patient was lost to follow-up. The risk of death at month-6 was higher in patients with prestroke dementia (RR 2.7; 95 % CI: 1.6-4.8). However, independent predictors of early death were age, severity of the deficit at admission, type and etiology of stroke. The risk of delayed death was higher in patients with prestroke dementia (RR 4.97; 95 % CI: 1.76-13.98) as in patients with new-onset post-stroke dementia (RR 6.24; 95 % CI: 2.67-14.57), compared with non-demented patients. The mortality rate did not differ between patients with prestroke and new-onset post-stroke dementia. Dementia at month-6 was an independent predictor of delayed death (RR 5.7; 95 % CI: 2.4-13.4), with age and stroke recurrence. Causes of death did not differ between demented and non-demented patients. Dementia adversely influences vital outcome in stroke patients, perhaps partly because the therapeutic approach differs between demented and non-demented patients.

Adult↗

PubMed2002

Mutation analysis and association studies of the ubiquitin carboxy-terminal hydrolase L1 gene in Huntington's disease.

Huntington's disease (HD) is attributed to a triplet CAG repeat mutation, and about 70% of the variance in age-at-onset can be explained by the size of the repeat expansion. Among potential candidates as modifier genes, we investigated the role of ubiquitin carboxy-terminal hydrolase L1 (UCH-L1) gene. We examined the association of HD with the I93M mutation and S18Y polymorphism in 138 HD patients and 136 control subjects, but we did not identify the I93M mutation. The S18Y polymorphism was present in 17% of HD patients. Of the variance in the age-at-onset that was not accounted for by the CAG repeat, 13% could be attributed to S18Y polymorphism. We sequenced the entire coding region of the UCH-L1 gene in seven HD patients with unexplained older or younger onset age. The S18Y polymorphism was found in three out of the four patients presenting with a later age-at-onset. We conclude that the UCH-L1 gene may be a genetic factor that influences the variability in age-at-onset of HD.

Adult↗

PubMed2002

The dynamic time course of semantic memory impairment in Alzheimer's disease: clues from hyperpriming and hypopriming effects.

The nature of semantic memory deficit in Alzheimer's disease is still a matter of controversy. To clarify this issue, we examined the evolution of semantic memory impairment in 24 Alzheimer's disease patients by means of a longitudinal study. We used two semantic tasks, one explicit and the other implicit, to evaluate the integrity of the same concepts. The explicit task was a semantic knowledge task composed of naming and questions, involving superordinate and attribute knowledge of concepts. The implicit task, a lexical decision task, assessed semantic priming and allowed a very pure measurement of semantic memory. In this task, related pairs of words had coordinate (e.g. "tiger-lion") or attribute ("tiger-stripe") relationships. In the coordinate relation between two words, the semantic priming performances were at first paradoxical: they increased abnormally (hyperpriming) before falling down, whereas in the attribute condition, the priming effects were first normal and then started to decrease in the final sessions (hypopriming). Compared with the semantic knowledge performance, these apparently disconcerting results reflect a coherent pattern of semantic memory degradation in Alzheimer's disease that is a progressive deterioration starting with specific attribute information. The data reveal in an astonishing yet striking manner the dynamic semantic memory degradation in Alzheimer's disease through the apparently paradoxical semantic priming effects.

Aged↗

PubMedDate not supplied

Prevalence of risk factors of prion-related disease according to the French circular 138 (DGS/DH/5C/DHOS/E2/2001/138) among patients referred for gastrointestinal endoscopy.

AIM OF THE STUDY: To assess the prevalence of risk factors of prion-related disease transmission in a gastrointestinal endoscopy unit. METHODS: Clinical evaluation of the risk of transmission of prion-related diseases using the criteria defined by the French circular 138 in patients referred for digestive endoscopy without anesthesia. RESULTS: 1017 patients were included in this study. According to circular 138, 7 patients (0.68%) were at high risk of transmitting prion-related disease. According to these criteria, a high index of suspicion of prion-related disease was detected in 26 patients (2.55%). Clinical evaluation of risk was not possible for 56 patients (5.51%), due to coma or sedation (38 patients) or communication impairment (18 patients). CONCLUSIONS: Application of circular 138 led us to consider that 2.55% of patients in this study had a high risk of prion-related disease. The circular criteria cannot be assessed in patients with sedation for mechanical ventilation, coma or communication impairment.

Endoscopy, Gastrointestinal↗

PubMedDate not supplied

Tau aggregation in the hippocampal formation: an ageing or a pathological process?

Tauopathy is a concept to describe different genetic or metabolic dysfunctions of tau proteins that generate most of the known dementing disorders. Tauopathy is a degenerating process that also affects the entorhinal formation, and then the hippocampal formation in ageing. In Alzheimer's disease (AD), a disease due to APP dysfunction, a similar tauopathy process in observed in neocortical areas, well correlated to cognitive impairment. One important gap of knowledge is the relationship between tauopathy in the hippocampal formation, ageing, AD, and cognitive impairment. Here we show that the multidisciplinary analysis of numerous brains from non-demented and demented patients suggests the following observations: tauopathy of the hippocampal formation in humans is age-related but not an age-dependent process, also independent of AD, but amplified by APP dysfunctions. Tauopathy in the entorhinal and hippocampal formation could be another type of pathological dysfunction of tau proteins, and a therapeutic target to delay AD. Relevant animal models are desperately needed to address this issue.

Aged↗