Christian Lucas
university of lille
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Featured researches published by Christian Lucas.
Stroke | 1998
Christian Lucas; Thierry Moulin; Dominique Deplanque; Laurent Tatu; Didier Chavot
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.
European Neurology | 1997
Didier Leys; Christian Lucas; Marc Gobert; Ghislaine Deklunder; Jean-Pierre Pruvo
Cervical artery dissection (CAD) accounts for up to one fifth of ischemic strokes occurring before 45 years. Their increasing recognition is probably due to an increased clinical awareness of this condition in patients with painful ischemic events. The internal carotid artery is the most commonly affected vessel. Cerebral ischemia is the most serious consequence of a CAD. It may be due to hemodynamic factors or emboli. The enlargement of the artery may lead to a direct compression of the lower cranial nerves. CAD typically occurs in young adults with a mean age of 40 years with a male:female ratio of 1.5. After exclusion of traumatic cases, the average annual incidence rate of CAD is 2.6 per 100,000, but the reported incidence figures in the literature are likely to be an underestimation of the incidence of CAD. A spontaneous dissection is assumed when no or only minor trauma preceded the onset. However, the differentiation between spontaneous and traumatic dissections is artificial because of a continuum between both forms. The pathogenesis of dissections remains unknown in most cases. However, traumas and primary diseases of the arterial wall are the main predisposing factors. The clinical presentation of spontaneous dissections of the internal carotid artery includes cerebral ischemia, cervical or cranial pain, Horners syndrome and cranial nerve palsy; CAD may also be silent. Brainstem ischemic deficits and occipital pain are the most common findings in vertebral artery dissections, but these features may be biased because the most benign and the most severe cases may escape detection. The favorable natural history of CAD emphasizes the need for a noninvasive approach to the detection, monitoring and follow-up. This noninvasive approach can be obtained by means of CT scan, MRI, magnetic resonance angiography and ultrasonography, although angiography remains the gold standard for the diagnosis of arterial dissections. Follow-up studies suggest a fairly good overall prognosis in adults and in children. In many centers, CAD are treated by heparin at the acute stage, although the benefit of such a potentially dangerous treatment has never been proven by a randomized trial.
Journal of Headache and Pain | 2010
Denys Fontaine; Yves Lazorthes; Patrick Mertens; Serge Blond; Gilles Géraud; Nelly Fabre; Malou Navez; Christian Lucas; F. Dubois; Sebastien Gonfrier; P. Paquis; Michel Lanteri-Minet
Chronic cluster headache (CCH) is a disabling primary headache, considering the severity and frequency of pain attacks. Deep brain stimulation (DBS) has been used to treat severe refractory CCH, but assessment of its efficacy has been limited to open studies. We performed a prospective crossover, double-blind, multicenter study assessing the efficacy and safety of unilateral hypothalamic DBS in 11 patients with severe refractory CCH. The randomized phase compared active and sham stimulation during 1-month periods, and was followed by a 1-year open phase. The severity of CCH was assessed by the weekly attacks frequency (primary outcome), pain intensity, sumatriptan injections, emotional impact (HAD) and quality of life (SF12). Tolerance was assessed by active surveillance of behavior, homeostatic and hormonal functions. During the randomized phase, no significant change in primary and secondary outcome measures was observed between active and sham stimulation. At the end of the open phase, 6/11 responded to the chronic stimulation (weekly frequency of attacks decrease >50%), including three pain-free patients. There were three serious adverse events, including subcutaneous infection, transient loss of consciousness and micturition syncopes. No significant change in hormonal functions or electrolytic balance was observed. Randomized phase findings of this study did not support the efficacy of DBS in refractory CCH, but open phase findings suggested long-term efficacy in more than 50% patients, confirming previous data, without high morbidity. Discrepancy between these findings justifies additional controlled studies (clinicaltrials.gov number NCT00662935).
Stroke | 1996
Xavier Leclerc; Olivier Godefroy; A. Salhi; Christian Lucas; Didier Leys; Jean-Pierre Pruvo
BACKGROUND AND PURPOSE We attempted to evaluate the sensitivity of helical CT for the diagnosis of extracranial internal carotid artery (ICA) dissection. METHODS Sixteen consecutive patients with 18 angiographically confirmed extracranial ICA dissections were studied with a helical CT protocol with large-volume acquisition and thin axial slice reconstructions. A control group including normal and atherosclerotic ICAs was formed for comparison, and a blind interpretation of CT images was made by two observers. We evaluated the presence of stenosis, eccentric lumen, mural thickening, aneurysm, occlusion, and annular contrast enhancement. When the artery seemed to be occluded, we measured the external diameter of the ICA (1) on the occluded side, at its upper portion and most enlarged level, (2) at its lower portion, beyond the bulb, and (3) on the contralateral side, at is upper portion. RESULTS Interobserver agreement was good except for the presence of annular contrast enhancement. In the stenotic dissection group (n=12), the presence of a narrowed eccentric lumen at the upper portion of the ICA on axial CT images was classified correctly in all cases (sensitivity, 100%; specificity, 100%). An arterial wall thickening was seen in all cases of dissection but also in three cases of the control group. In the occlusive dissection group (n=6), the enlargement of the dissected artery was the best criterion (sensitivity, 100%, specificity, 100%) for occlusive dissection. CONCLUSIONS Helical CT seems to be a reliable method for evaluating extracranial ICA dissection. The analysis of the residual arterial lumen and the measurement of the external diameter of the carotid artery were the best criteria for the diagnosis. Further studies with larger groups are required to determine whether ICA dissections might be diagnosed using helical CT as a first procedure.
Journal of Neurology | 2003
Breteau G; Mounier-Vehier F; Olivier Godefroy; Jean-Yves Gauvrit; Marie-Anne Mackowiak-Cordoliani; Marie Girot; Bertheloot D; Hilde Hénon; Christian Lucas; Xavier Leclerc; Fourrier F; Jean-Pierre Pruvo; Didier Leys
Abstract. An early diagnosis and heparin therapy have contributed to a decreased mortality in cerebral venous thrombosis (CVT). However, predictors of outcome are difficult to identify, because most studies suffered heterogeneity in diagnostic findings and treatments, retrospective design, and recruitment bias. The aim of this study was to evaluate the clinical outcome in 55 consecutive patients with CVT admitted over a 4-year period. The study population consisted of 42 women and 13 men, with a median age of 39 years (range 16–68). The diagnosis was performed with MRI in 53 patients, and angiography in 2. The outcome was assessed with the modified Rankin scale (mRs). After a median follow-up of 36 months (range: 12–60), 45 patients were independent (mRS 0–2), and 10 were dependent or dead (mRS 3–6). Of 48 survivors, 7 had seizures, 6 motor deficits, 5 visual field defects, 29 headache (migraine in 14, tension headache in 13, other in 2). The logistic regression analysis found focal deficits and cancer at time of diagnosis, as independent predictors of dependence or death at year 3, and isolated intra-cranial hypertension as an independent predictor of survival and independence. Mortality rates are low in the absence of cancer and focal deficits, and more than 80 % of survivors are independent after 3 years. However, 3/4 of survivors have residual symptoms. Therefore, despite a low mortality rate, CVT remains a serious disorder.
Stroke | 1999
Hilde Hénon; Florence Lebert; I. Durieu; Olivier Godefroy; Christian Lucas; Florence Pasquier; Didier Leys
BACKGROUND AND PURPOSE Acute confusional state (ACS) is frequent in hospitalized stroke patients. We previously showed that 16% of patients admitted for a stroke have preexisting dementia. The extent to which preexisting cognitive decline is associated with a risk of ACS at the acute stage of stroke remains to be systematically examined. The aim of this study was to evaluate the prevalence of ACS in acute stroke patients, to study the influence of preexisting cognitive decline and other patient characteristics, and to evaluate the influence of ACS on outcome. METHODS We diagnosed ACS using DSM-IV criteria and the Delirium Rating Scale with a cutoff of 10 in 202 consecutive stroke patients aged 40 years or older (median age, 75 years; range, 42 to 101 years). Cognitive functioning before stroke was assessed with the Informant Questionnaire on Cognitive Decline in the Elderly. RESULTS Forty-nine stroke patients (24.3%; 95% CI, 18.3% to 30.2%) had an ACS during hospitalization. Using logistic regression analysis, we found preexisting cognitive decline (P=0.006) and metabolic or infectious disorders (P=0.008) to be independent predictors of ACS. Functional, but not vital, prognosis was worse in patients with ACS at discharge and 6 months after stroke. CONCLUSIONS ACS occurs in one fourth of stroke patients older than 40 years. Its occurrence requires inquiry for a preexisting cognitive decline, which usually remains unrecognized in the absence of a systematic evaluation.
Journal of Neurology | 2003
Didier Leys; Dominique Deplanque; Marie-Anne Mackowiak-Cordoliani; Christian Lucas; Régis Bordet; C. Mounier-Vehier
Stroke prevention is a crucial issue because (i) stroke is a frequent and severe disorder, and (ii) acute stroke therapies that are effective at the individual level have only a little impact in term of public health. Stroke prevention consists of the combination of 3 strategies: an optimal management of vascular risk factors, associated when appropriate with antithrombotic therapies, carotid surgery, or both. Primary prevention trials have shown that reducing blood pressure in hypertensive subjects reduces their vascular risk, including stroke. The association of perindopril plus indapamide reduces the vascular risk in patients who have had a stroke or TIA during the last 5 years, irrespective of their baseline blood pressure. Lowering serum cholesterol with statins or gemfibrozil in patients with hypercholesterolemia or coronary heart disease (CHD), reduces the risk of stroke. However, no trial of cholesterol-lowering therapy has been completed in stroke patients. A strict control of high cholesterol levels should be encouraged, because of benefits in terms of CHD. Statins should be prescribed for stroke patients with CHD, or increased cholesterol levels. Cigarette smoking is associated with an increased risk of stroke and should be avoided. Careful control of all risk factors, especially arterial hypertension in type 1 and type 2 diabetics is recommended, together with a strict glycemic control to reduce systemic microvascular complications. Estrogens prescribed in hormone replacement or oral contraceptive therapies are not recommended after an ischemic stroke. It is also recommended to reduce alcohol consumption and obesity, and to increase physical activity in patients at risk for first-ever or recurrent stroke. An optimal management of risk factors for stroke is crucial to reduce the risks of first-ever stroke, recurrent stroke, any vascular event after stroke and vascular death. One of the major public health issues for the coming years will be to focus more on risk factor recognition and management.
Cerebrovascular Diseases | 2004
Christian Lucas; J.L. Lecroart; C. Gautier; Xavier Leclerc; M. Dauzat; Didier Leys; G. Deklunder
Background and Purpose: Cervical artery dissection (CAD) accounts for 10–20% of ischemic strokes in young adults. Although trauma and preexisting disorders of the arterial wall are the main predisposing factors, most CADs are considered ‘spontaneous’. We hypothesized that CAD could originate in systemic vascular disease bound to the intima–media interface without clinical signs. If this hypothesis is true, endothelium-dependent vasodilation would be impaired in response to a physiological stimulus such as an increase in blood flow. Methods: Flow-mediated arterial dilation was studied in 65 consecutive patients with spontaneous CAD: 26 with carotid artery dissection (ICAD), and 39 with vertebral artery dissection (VAD). CAD patients with vascular risk factors, trivial or obvious cervical trauma, or connective tissue disease were excluded. Twenty-three patients with ischemic stroke of unknown cause were included as controls. Using high-resolution ultrasonography, brachial artery diameter was measured at rest, during post-ischemic hyperemia (flow-mediated endothelium-dependent dilation), and after sublingual glyceryl trinitrate spray (endothelium-independent dilation). Results: The mean ± SD values of the flow-mediated vasodilation index were 5.7 ± 6.2% in ICAD, 5.0 ± 9.3% in VAD and 13.2 ± 6.5% in controls (p < 0.0005), without any difference between ICAD and VAD. Endothelium-independent dilation mean values were 21.5 ± 9.5% in ICAD, 25.1 ± 12.5% in VAD, and 20.8 ± 8.4% in controls, without a significant difference between groups (p = 0.49). Conclusions: These results give evidence of impaired endothelium-dependent vasodilation in CAD patients that is not the result of stroke, and suggest that an underlying abnormality of the arterial wall layers may predispose to CAD.
Neuroradiology | 1999
J. de Seze; Christian Lucas; X. Leclerc; A. Sahli; P. Vermersch; Didier Leys
Abstract The one-and-a-half syndrome is characterised by a lateral gaze palsy in one direction and internuclear ophthalmoplegia in the other. It is due to a unilateral lesion of the dorsal pontine tegmentum, involving the ipsilateral paramedian pontine reticular formation, internuclear fibres of the ipsilateral medical longitudinal fasciculus and, usually, the abducens nucleus. The main causes of this rare syndrome are stroke and multiple sclerosis. Few cases have been reported since the introduction of MRI. Our aim was to examine clinicoradiological correlations in six patients with a one-and-a-half syndrome due to a stroke. Ophthalmological symptoms were diplopia, oscillopsia or blurred vision. Four patients had an associated facial nerve palsy, three a hemiparesis and one a unilateral hemihypoaesthesia. MRI revealed an infarct in the pons in all patients. The cause of the infarct was a basilar artery dissection in one patient, bilateral vertebral artery dissection in a second and unknown in the other four. All patients recovered within 2 days to 8 weeks. This study showed a good correlation between the site of the lesion (superior, inferior or extensive pontine ischaemia) and clinical deficits.
Cerebrovascular Diseases | 2010
Marie Bodenant; Didier Leys; Stéphanie Debette; Charlotte Cordonnier; Frédéric Dumont; Hilde Hénon; Marie Girot; Christian Lucas; David Devos; Luc Defebvre; Dominique Deplanque; Xavier Leclerc; Régis Bordet
Background: Stroke outcomes are worse in patients admitted at nonworking hours (NWH), but whether this is also true in patients treated with intravenous (i.v.) thrombolysis has not been definitely proven. Objective: Our aim was to test the hypothesis that stroke patients treated by i.v. rt-PA at NWH have a worse outcome than those treated at working hours (WH). Methods: We compared outcomes at 7 days and at 3 months, between patients treated at NWH and at WH in the stroke unit of the Lille University Hospital. Results: Of 252 consecutive patients [median age: 69 years; 132 men (52.4%); median National Institutes of Health Stroke Scale score: 14; median onset-to-needle time: 150 min], 134 (53.2%) were treated at NWH. They did not differ for baseline characteristics and proportion of patients with modified Rankin Scale scores 0–1 and 0–2 at 3 months. Patients treated at WH were more likely to die before 7 days (12.7 vs. 4.5%; adjusted odds ratio: 3.6; 95% confidence interval: 1.2–10.4) and at 3 months (21.6 vs. 11.4%; adjusted odds ratio: 2.2; 95% confidence interval: 1.02–4.7). The causes of death did not differ between NWH and WH. At NWH, there was no difference in baseline characteristics and outcomes of patients treated by stroke- and nonstroke neurologists. Conclusion: The case fatality rates were unexpectedly higher at WH than at NWH. If this finding can be reproduced and is not a chance finding, we should identify explanations, especially organisational issues, chronobiological factors or summation of subtle – nonsignificant – baseline differences.