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Biomedical subjects

Hilde Hénon

Publications and source records attributed to Hilde Hénon.

10 recordsLinked to original sources

Antithrombotic agents' use in patients with atrial fibrillation and acute cerebral ischemia.

BACKGROUND: although trials suggest a benefit of aspirin, and not of anticoagulation (AC), in the acute stage of cerebral ischemia associated with atrial fibrillation (AF), many neurologists still use heparin. OBJECTIVE: to evaluate how antithrombotic agents were used at the acute stage of cerebral ischemia in AF patients after the publication of trials and guidelines. METHODS: we reviewed the charts of all patients with AF who were admitted between 1996 and 2002 as primary care patients, within 48 hours after onset of an ischemic stroke (IS) or transient ischemic attacks (TIAs). We recorded the first antithrombotic treatment prescribed at admission. RESULTS: in 763 consecutive patients (42% men; median age 79 years), the use of AC on admission decreased over time from 70% to 22% (p<0.001), while antiplatelet agents increased from 27% to 78% (p<0.001). Patients who received AC were more likely to be younger, to have a Barthel index >60, no hemorrhagic changes, and to have been admitted in 1996 or 1997. Results were similar between patients with IS and TIAs and in patients who were not under AC before. In patients who were under oral AC before, AC use at admission did not decline over time (p=0.366). CONCLUSION: there was a clear decrease in AC use during the study period, except in patients who were already under AC before, and in TIA patients.

Acute Disease↗

Influence of dementia on antithrombotic therapy prescribed before stroke in patients with atrial fibrillation.

BACKGROUND AND PURPOSE: Oral anticoagulation (OAC) decreases the risk of stroke in patients with nonvalvular atrial fibrillation (NVAF), but remains underused in practice. The aim of this study was to test the hypothesis that prestroke dementia influenced the nonprescription of OAC before stroke. METHODS: This is an ancillary study of Stroke in Atrial Fibrillation Ensemble II, an observational study conducted in patients with a previously known NVAF, consecutively admitted for an acute stroke to French and Italian centers. Prestroke dementia was evaluated by the clinical physician and validated by an Informant Questionnaire for Cognitive Decline in the Elderly score of >or=104 in patients with a reliable informant. RESULTS: Of 204 patients, 24 patients met criteria for prestroke dementia according to GP's opinion. The only variables independently associated with OAC before stroke were follow-up by a cardiologist (adjusted OR: 3.33; 95% CI: 1.47-7.53) and a younger age of patients (adjusted OR: 0.94; 95% CI: 0.89-0.99). Variables independently associated with any antithrombotic drug therapy before stroke were follow-up by a general practitioner (adjusted OR: 2.78; 95% CI: 1.09-7.11), and by a cardiologist (adjusted OR: 3.15; 95% CI: 1.48-6.69). CONCLUSION: In daily practice, the under-prescription of OAC in patients with NVAF mainly depends on co-morbidity and on characteristics of the physician, not on prestroke dementia.

Administration, Oral↗

Secondary prevention after ischemic stroke. Evolution over time in practice.

BACKGROUND AND OBJECTIVE: An optimal management of vascular risk factors, associated with antithrombotic drugs and carotid surgery when appropriate, reduces the risk of a new vascular event after stroke. Although secondary prevention is not optimal in many patients in practice, the question of whether there is an improvement over time remains unanswered. The aim of our study was to test the hypothesis that secondary prevention measures after cerebral ischemia improve over time. METHOD: We included 123 consecutive patients in 1994, and 125 consecutive patients in 2002, who were admitted to a neurological department for any reason and had had an episode of cerebral ischemia less than 6 years earlier. We compared the groups for the management of arterial hypertension, hypercholesterolemia, diabetes mellitus and smoking. We recorded the values of blood pressure, biological parameters, and presence of antithrombotic therapy, lipid-lowering and anti-hypertensive drugs. Whether patients were properly treated or not, was determined by a comparison between their current treatment and guidelines available when recruited. RESULTS: Prevention was not optimal in 96 of 123 (78%) patients in 1994, and in 77 of 125 (62 %) in 2002. Vascular risk factors were better identified and managed in 2002 than in 1994, especially for hypercholesterolemia. Antithrombotic therapies, statins and antihypertensive drugs, except calcium channel blockers, were more often used in 2002. The proportion of patients in whom arterial hypertension and hypercholesterolemia were identified was higher in 2002, but the proportion of patients identified as diabetics remained stable. However, the proportion of patients with blood pressure >140/90 mmHg, glycemia >or = 126 mg/dl, total cholesterol level > or = 240 mg/dl, or being current smokers, were significantly lower in 2002 than in 1994. CONCLUSION: Although most of patients with previous cerebral ischemia did not receive an optimal management of their risk factors in 2002, there was an improvement over an 8-year period.

Aged↗

Poststroke dementia.

Dementia is one of the major causes of dependency after stroke. The prevalence of poststroke dementia (PSD)-defined as any dementia occurring after stroke-is likely to increase in the future. In community-based studies, the prevalence of PSD in stroke survivors is about 30% and the incidence of new onset dementia after stroke increases from 7% after 1 year 48% after 25 years. Having a stroke doubles the risk of dementia. Patient-related variables associated with an increased risk of PSD are increasing age, low education level, dependency before stroke, prestroke cognitive decline without dementia, diabetes mellitus, atrial fibrillation, myocardial infarction, epileptic seizures, sepsis, cardiac arrhythmias, congestive heart failure, silent cerebral infarcts, global and medial-temporal-lobe atrophy, and white-matter changes. Stroke-related variables associated with an increased risk of PSD are stroke severity, cause, location, and recurrence. PSD might be the result of vascular lesions, Alzheimer pathology, white-matter changes, or combinations of these. The cause of PSD differs among studies in relation to the mean age of patients, ethnicity, criteria used, and time after stroke. In developed countries, the proportion of patients with presumed Alzheimer's disease among those with PSD is between 19% and 61%. Patients with PSD have high mortality rates and are likely to be functionally impaired. These patients should be treated according to the current guidelines for stroke prevention.

Dementia↗

Poststroke dementia in the elderly.

Risk of dementia increases after stroke, and poststroke dementia (PSD) is an important cause of disability in the elderly. The prevalence rates of PSD vary from 12.2% to 31.8% within 3 months to 1 year after stroke, depending on patient populations and the diagnostic criteria used in the numerous studies. Incidence rates of PSD increase with time after the stroke. Although vascular lesions and white matter changes can explain the cognitive disorders seen in stroke patients, an underlying neurodegenerative disorder may contribute to the development of PSD. Cognitive decline may pre-date the stroke and follow a progressive course after the stroke. The vascular and degenerative processes involved share common environmental and genetic risk factors. This review explains the mechanisms of dementia in stroke patients and identifies predictive factors for PSD. The following points are successively considered: (i) demographic characteristics of the patients, including age and level of education; (ii) prestroke cognitive decline; (iii) vascular risk factors, including diabetes mellitus and prior strokes; (iv) stroke characteristics, including severity and location of the vascular lesion; (v) co-morbid disorders; and (vi) abnormalities on brain imaging, including location, size and number of vascular lesions, white matter changes and cerebral atrophy. Older age, prestroke cognitive decline, stroke recurrence, hypoxic-ischaemic disorders, left-side infarcts, strategic infarcts and white matter lesions appear to be the main predictive factors of PSD. Prevention of stroke should reduce the morbidity and mortality associated with PSD. In addition, management of PSD with secondary prevention treatments could reduce occurrence of further strokes. Cholinesterase inhibitors may be beneficial not only in Alzheimer's disease associated with cerebrovascular lesions, but also for the treatment of cholinergic dysfunction arising from pure vascular dementia. Better knowledge of the risk factors for PSD, including environmental and genetic factors, should increase the effectiveness of preventive strategies in patients with this condition.

Aged↗

Poststroke dementia: influence of hippocampal atrophy.

BACKGROUND: The prevalence of dementia is increased after stroke. Medial temporal lobe atrophy (MTLA) is associated with Alzheimer disease, and with prestroke dementia in patients who have had a stroke. OBJECTIVE: To determine the influence of MTLA on the long-term risk of dementia after stroke, after excluding the patients who had prestroke dementia. METHODS: The study was conducted in 144 consecutive patients who had a stroke, who were aged 40 years or older (66 women and 78 men; median age, 72 years), and who had an Informant Questionnaire on Cognitive Decline in the Elderly score lower than 104. On admission to the hospital all patients underwent a noncontrast computed tomographic scan including temporal lobe-positioned slices. A cut-off of 11.5 mm was used to differentiate patients with MTLA from those without MTLA. Patients were followed up with clinical and cognitive assessments over a 3-year period. RESULTS: Three years after stroke, 34 patients (23.6%) had developed new-onset dementia. The cumulative proportion of survivors without dementia was 57.6% in patients with MTLA and 80.8% in patients without MTLA (P =.02). The unadjusted relative risk of poststroke dementia associated with MTLA was 2.3 (95% confidence interval, 1.1-4.7). However, using the Cox proportional hazards model, MTLA did not seem to be an independent predictor of poststroke dementia. Independent predictors of poststroke dementia were increasing age, diabetes mellitus, severity of the clinical deficit at admission, and severity of leukoaraiosis on computed tomography. CONCLUSIONS: Patients who had a stroke and MTLA more frequently develop dementia than patients without MTLA, but our study does not suggest that MTLA independently contributes to dementia. A longer follow-up may be necessary to reevaluate the influence of MTLA.

Adult↗

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↗

Influence of eye orientation on pain as a function of anxiety.

The effect of eye orientation on pain was investigated as a function of the stimulus intensity and the subjects' anxiety. Right-handed female subjects received sequences of electric shocks gradually increasing in intensity. Unpleasantness threshold, pain threshold, tolerance threshold and pain range were obtained when eyes were directed towards a target LED situated in the direction of, or away from, the source of stimulation, in the ipsi- or contralateral hemispace. Directing the eyes ipsilaterally to the stimulated hand yielded a lower unpleasantness threshold when the right hand was stimulated. No significant effect was observed in high trait anxiety subjects. These results are interpreted in terms of hemispatial attention bias. Moreover, an ipsilateral eye orientation increased pain range but this effect reversed in the highest state anxiety subjects. These latter observations could reflect the interacting influences of both spatial attention and state anxiety in selecting the processing mode of painful stimuli.

Adolescent↗

Neuroimaging predictors of dementia in stroke patients.

The risk of dementia is increased in stroke patients. Dementia syndromes associated with cerebrovascular diseases were commonly recognized as an immediate consequence of stroke. However, more and more data suggest that degenerative pathology and white matter changes (WMC) may play a role in the development of dementia in stroke patients. The aim of this paper was to review the literature concerning the neuroimaging predictors of dementia in stroke patients. From the literature data, it appears that although vascular lesions alone may lead to dementia, in stroke patients, no clear association between stroke location and size has yet been identified, even if the role of the left hemisphere has been suggested. The influence of silent infarcts remains undetermined while more and more data suggest that global cerebral atrophy and WMC are predictive factors of post-stroke dementia (PSD). The influence of medial temporal lobe atrophy on the risk of PSD has until now never been evaluated.

Dementia, Vascular↗