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Biomedical subjects

D Deplanque

Publications and source records attributed to D Deplanque.

18 recordsLinked to original sources
PubMed2006

Prior TIA, lipid-lowering drug use, and physical activity decrease ischemic stroke severity.

OBJECTIVE: To determine clinical and pharmacologic factors that could influence the initial severity and short-term outcome of cerebral ischemia. METHODS: In a cross-sectional hospital-based study of patients with acute supratentorial ischemic stroke, we systematically collected medical history, previous leisure-time physical activity, current and previous treatments, blood pressure, temperature, blood glucose, fibrinogen, NIH Stroke Scale (NIHSS) score at admission, and outcome at day 8. Factors potentially associated with initial stroke severity and outcome were selected by univariate analyses and then validated in logistic regression analyses with lower severity of stroke at admission (NIHSS 0 to 5) or good outcome at day 8 (modified Rankin Scale 0 to 1, Barthel Index 95 to 100) as dependent variables. RESULTS: In 362 consecutive patients (median age 70 years, range 16 to 97 years; 195 women), independent factors associated with a lower severity at admission were previous leisure-time physical activity (adjusted odds ratio [OR] 1.67, 95% CI 1.07 to 2.66), TIA (adjusted OR 2.28, 95% CI 1.06 to 4.87) and treatment with lipid-lowering drug (adjusted OR 1.76, 95% CI 1.02 to 3.03). Previous treatment with lipid-lowering drug and leisure-time physical activity were also independent factors associated with a good short-term outcome. CONCLUSION: Both regular physical activity and lipid-lowering drugs should be prospectively evaluated to determine whether they reduce the severity of ischemic stroke.

Adolescent↗
PubMed2006

PPAR: a new pharmacological target for neuroprotection in stroke and neurodegenerative diseases.

PPARs (peroxisome-proliferator-activated receptors) are ligand-activated transcriptional factor receptors belonging to the so-called nuclear receptor family. The three isoforms of PPAR (alpha, beta/delta and gamma) are involved in regulation of lipid or glucose metabolism. Beyond metabolic effects, PPARalpha and PPARgamma activation also induces anti-inflammatory and antioxidant effects in different organs. These pleiotropic effects explain why PPARalpha or PPARgamma activation has been tested as a neuroprotective agent in cerebral ischaemia. Fibrates and other non-fibrate PPARalpha activators as well as thiazolidinediones and other non-thiazolidinedione PPARgamma agonists have been demonstrated to induce both preventive and acute neuroprotection. This neuroprotective effect involves both cerebral and vascular mechanisms. PPAR activation induces a decrease in neuronal death by prevention of oxidative or inflammatory mechanisms implicated in cerebral injury. PPARalpha activation induces also a vascular protection as demonstrated by prevention of post-ischaemic endothelial dysfunction. These vascular effects result from a decrease in oxidative stress and prevention of adhesion proteins, such as vascular cell adhesion molecule 1 or intercellular cell-adhesion molecule 1. Moreover, PPAR activation might be able to induce neurorepair and endothelium regeneration. Beyond neuroprotection in cerebral ischaemia, PPARs are also pertinent pharmacological targets to induce neuroprotection in chronic neurodegenerative diseases.

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

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↗
PubMed2003

Angioplasty and stenting for high-grade internal carotid artery stenosis: safety study in 39 selected patients.

BACKGROUND: Carotid angioplasty and stenting (CAS) is sometimes used as an alternative to surgery, despite the lack of evidence for its safety and efficacy. METHOD: Over a 33-month period, 39 consecutive patients with a stenosis >/=70% underwent CAS (4 in a randomized trial and 35 because of contra-indications for surgery). RESULTS: In 5 patients (13%; 95% CI: 3-23), a major complication occurred (3 disabling ischaemic strokes, 1 myocardial infarction, 1 acute interstitial nephropathy). In 7 patients (18%; 95% CI: 6-30), a minor complication occurred (5 transient ischaemic attacks, 1 transient confusional state, 1 non-disabling ischaemic stroke). CONCLUSION: CAS cannot be considered as a routine procedure and should be restricted to high-risk patients unfit for surgery.

Adult↗
PubMed2003

[Peripheral haemosiderosis of the central nervous system].

We report 2 cases of patients with hemosiderosis of the central nervous system. The diagnosis was made in 1999 in a stroke unit. The patients had both deafness, but their clinical presentation was different, due to heterogeneous features of this pathology. Hemosiderosis of the central nervous system is due to chronic subarachnoidal hemorrhage. Magnetic resonance imaging is extremely sensitive to the presence of hemosiderin and is the investigation of choice enabling diagnosis and sometimes bleeding source (50 p. cent). The interest of our observations concerned the source of bleeding. In the first patient, diagnostic work-up was negative. For the second one, the deposition of hemosiderin was explained by 3 possible sources. If a bleeding source can be identified, surgery is the optimal treatment. Copper chelation, like Trientine can be used, but there is no evidence-based for using this treatment.

Adolescent↗
PubMed2001

Successes and setbacks of the falls consultation: report on the first 150 patients.

OBJECTIVE: We report the results of a Falls Consultation. DESIGN: Data concerning the first 150 patients are reported. Each patient was assessed by a geriatrician, a neurologist, and a physiatrist, who visited him or her at home, and was reassessed by the same geriatrician 6 mo later. RESULTS: Of the 150 patients, 135 patients completed the initial evaluation. Most of them were frequent fallers. The population was very heterogeneous regarding the health status and the degree of disability. In most cases, falls were the result of several interacting factors. The most frequent recommendations from the staff were physical therapy, environmental changes, and medication changes. Over the following 6 mo, approximately one out of four patients had experienced new falls. However, the risk of falling was significantly reduced (5.3 +/- 7.3 falls in 6 mo before vs. 0.8 +/- 1.6 falls in 6 mo after the intervention). The Activities of Daily Living score was a predictor of recurrent falls, hospitalization, and institutionalization. CONCLUSION: Our results show that a multidisciplinary falls consultation can be efficient in reducing the risk of falls in nonselected elderly fallers but suggest that differential strategies are needed to manage adequately the more vigorous and the frail old person as well.

Accidental Falls↗
PubMed2001

Relationship between leuko-araiosis and blood pressure variability in the elderly.

Although leuko-araiosis is a common finding on computed tomographic (CT) scans of the brain, its pathogenesis remains uncertain. To investigate the association between blood pressure (BP) disturbances and leuko-araiosis, we retrospectively reviewed CT scans and 24-hour ambulatory blood pressure monitorings of 79 elderly patients (57 women and 22 men; mean age: 83.3 +/- 6.4 years). Of the 79 patients, 50 were demented (30 had Alzheimer's disease and 18 vascular dementia) and 29 were not demented. The leuko-araiosis score (LA score) was determined by using Rezek's scale. To evaluate short-term variation of BP, we determined (1) the variability of systolic and diastolic BPs (SBP, DBP; within-subject standard deviation of all readings over a 24-hour period), (2) the coefficient of variability (variability of BP/mean BP) and (3) the maximal variation of BP (difference between the maximum and minimum 24-hour BPs). Higher LA scores were associated with higher SBPs in 24-hour, diurnal and nocturnal periods, higher maximal variation of SBP, greater variability of SBP during 24-hour, diurnal and nocturnal periods and greater coefficient of variability of SBP during sleep. Our study suggests that elevations and short-term variations of SBP may contribute to the pathogenesis of white matter lesions in elderly persons.

Aged↗
PubMed2000

Differential role of nitric oxide pathway and heat shock protein in preconditioning and lipopolysaccharide-induced brain ischemic tolerance.

The purposes of this study were to investigate the role of nitric oxide (NO), nitric oxide synthase (NOS), and 70 kDa heat shock protein in brain ischemic tolerance induced by ischemic preconditioning and lipopolysaccharide. Focal cerebral ischemia was induced in rats by intraluminal middle cerebral artery occlusion. Infarct volume was significantly reduced (1) in rats subjected to 3 min ischemia 72 h prior to 60 min ischemia; (2) in rats administered lipopolysaccharide (0.5 mg/kg; i.p.) 72 h prior to 60 min ischemia compared with controls. The beneficial effect of ischemic preconditioning was unchanged despite prior administration of nitro-L-arginine methyl ester (L-NAME), a NOS inhibitor. Conversely, the protective effect of lipopolysaccharide was nullified by L-NAME. Using immunohistochemical techniques, we observed that (1) ischemic preconditioning but not lipopolysaccharide induces the expression of 70 kDa heat shock protein in cerebral cortex and (2) lipopolysaccharide induces early increased expression of endothelial NOS in cerebral blood vessels. The results suggest that (1) endothelium-derived NO plays a role of a trigger in the brain tolerance induced by lipopolysaccharide, and (2) 70 kDa heat shock protein is involved in the protection afforded by ischemic preconditioning but not by lipopolysaccharide.

Animals↗
PubMed2000

Increase in endogenous brain superoxide dismutase as a potential mechanism of lipopolysaccharide-induced brain ischemic tolerance.

A low dose (0.5 mg/kg) of lipopolysaccharide (LPS), administered 72 hours before 60-minute middle cerebral artery occlusion, induced a delayed neuroprotection proven by the significant decrease (-35%) of brain infarct volume in comparison with control, whereas infarct volumes remained unchanged in rats treated 12, 24, or 168 hours before ischemia. This delayed neuroprotective effect of LPS was induced only with low doses (0.25 to 1 mg/kg), whereas this effect disappeared with a higher dose (2 mg/kg). The delayed neuroprotection of LPS was induced in the cortical part of the infarcted zone, not in the subcortical part. The beneficial effect of LPS on consequences of middle cerebral artery occlusion was suppressed by dexamethasone (3 mg/kg) and indomethacin (3 mg/ kg) administered 1 hour before LPS, whereas both drugs had no direct effect on infarct volume by themselves, suggesting that activation of inflammatory pathway is involved in the development of LPS-induced brain ischemic tolerance. Preadministration of cycloheximide, an inhibitor of protein synthesis, also blocked LPS-induced brain ischemic tolerance suggesting that a protein synthesis is also necessary as a mediating mechanism. Superoxide dismutase (SOD) could be one of the synthesized proteins because lipopolysaccharide increased SOD brain activity 72 hours, but not 12 hours, after its administration, which paralleled the development of brain ischemic tolerance. In contrast, catalase brain activity remained unchanged after LPS administration. The LPS-induced delayed increase in SOD brain content was suppressed by a previous administration of indomethacin. These data suggest that the delayed neuroprotective effect of low doses of LPS is mediated by an increased synthesis of brain SOD that could be triggered by activation of inflammatory pathway.

Adaptation, Physiological↗
PubMed1999

Stroke and atrial fibrillation: is stroke prevention treatment appropriate beforehand? SAFE I Study Investigators.

OBJECTIVE: To undertake a pilot study before conducting a large European multicentre prospective study, to determine the proportion of patients with atrial fibrillation who were not receiving antithrombotic treatment before stroke onset, and their characteristics. DESIGN AND PATIENTS: The stroke in atrial fibrillation ensemble (SAFE) I study was an observational study conducted in 213 patients with atrial fibrillation consecutively admitted in 1997 to three European centres for an acute stroke or transient ischaemic attack (TIA). It was determined whether they were receiving prior antithrombotic treatment. RESULTS: Atrial fibrillation was known before stroke in 148 patients (69.5%). Of 213 patients, 34 (16.0%) were receiving anticoagulation treatment before stroke, but only six had an international normalised ratio between 2. 0 and 3.5; 65 (30.5%) were receiving antiplatelet treatment; and three (1.4%) were receiving both anticoagulation and antiplatelet treatment. Of 137 patients eligible for oral anticoagulation, 108 (78.8%) did not receive treatment. Of 142 patients eligible for any antithrombotic treatment, 62 (43.7%) were not treated. The logistic regression analysis, assuming anticoagulation treatment as a dependent variable, found digoxin treatment, absence of arterial hypertension, mitral stenosis, and cardioversion as independent factors. Assuming any antithrombotic treatment as a dependent variable, previously known atrial fibrillation, lower age, being a non-smoker, and absence of arterial hypertension were found to be independent factors. CONCLUSION: More than half of the patients with atrial fibrillation admitted for acute stroke or TIA were not receiving any antithrombotic treatment beforehand. New onset atrial fibrillation and contraindications account for a minority of non-prescriptions; thus, other reasons should be identified to improve stroke prevention in the community.

Adult↗
PubMed1998

Stroke patterns of internal carotid artery dissection in 40 patients.

BACKGROUND AND PURPOSE: Internal carotid artery dissection (ICAD) is a frequent cause of ischemic stroke in young patients. Whether cerebral ischemia is of embolic or hemodynamic origin remains to be determined. Heparin is often administered in ICAD; however, a drug trial can hardly be conducted because of the low recurrence rate after the acute stage. Therefore, the best therapeutic approach should be determined on the basis of the presumed mechanism of cerebral ischemia. One way to approach the mechanism of stroke in ICAD is to determine stroke patterns. We postulated that most cortical and large subcortical infarcts (>/=15 mm) are of embolic origin and that small subcortical infarcts (<15 mm) and junctional infarcts are not. The aim of our study was to determine the stroke patterns in 40 consecutive patients with ICAD. METHODS: The patients (26 women and 14 men; mean age, 42.8 years) had a total of 65 ICADs. Seventeen patients were free of any vascular risk factor. CT scans, MRI scans, and angiographic features were analyzed by observers who were blinded to the clinical findings. RESULTS: We found 34 cortical infarcts, 25 large subcortical infarcts, 1 small subcortical infarct, and 5 junctional infarcts. CONCLUSIONS: Most infarcts related to ICAD are cortical infarcts or large subcortical infarcts; small subcortical infarcts and junctional infarcts are infrequent. Therefore, these findings suggest that most infarcts occurring in carotid artery dissection (CAD) are probably embolic rather than hemodynamic in origin. According to this presumed mechanism, anticoagulation seems a logical treatment at the early stage of CAD.

Adolescent↗
PubMed1996

[Benign angiopathy of the puerperium: a clinicoradiological case associated with ingestion of bromocriptine].

We report a case of benign cerebral angiopathy in a 37 year-old woman in the postpartum period occurring after bromocriptine therapy to suppress lactation. She presented with severe headache, hyperthermia and bradycardia. She had partial seizure. Angiography excluded cortical vein thrombosis but revealed multiple narrowing of intracerebral arteries. Bromocriptine was stopped. The patient totally recovered. A second angiography performed 3 months later was normal. Postpartum cerebral angiopathy is considered as rare but the prevalence is probably underestimated. Neurological features of this affection are multiple. Diagnosis is made by angiography performed in emergency and which showed narrowing of intracerebral arteries which are reversible. Prognosis is good. Reversible vasoconstriction may be due to acute arterial hypertension, sometimes triggered by ergot derivatives.

Adult↗
PubMedDate not supplied

Susceptibility to provoked cerebral infarction is not increased in a rat model of pharmacologically-induced hypertension despite endothelial dysfunction.

An increase in susceptibility to provoked stroke has been described in a genetically-determined rat model of hypertension. We investigated whether the susceptibility to provoked cerebral ischaemia was also increased in a rat model of pharmacologically-induced hypertension with endothelial dysfunction. Chronic inhibition of nitric oxide synthase induced by N(omega)-nitro-L-arginine methyl ester (L-NAME) administration (50 or 75 mg.kg(-1) x day(-1)) in drinking water for 6 weeks caused a sustained hypertension, comparable in the two groups. Endothelium-dependent relaxation induced by acetylcholine or A23187 was significantly, and dose-dependently, impaired in rats receiving L-NAME, as proven by a decrease in maximal relaxation and increase of EC50, as compared to control. Endothelium-independent relaxation induced by sodium nitroprusside was not different in the three groups. Aortic media area was significantly, and dose-dependently, increased following chronic nitric oxide inhibition. Cerebral infarct volumes were not increased in L-NAME-treated groups independently of the level of endothelial dysfunction induced by chronic L-NAME administration. These data demonstrate that susceptibility to cerebral infarction was not increased in a non-genetically determined hypertension model in spite of the development of endothelial dysfunction and vascular structure alterations.

Animals↗