Trouvé à l'intérieur – Page 38... du fait d'une hypoperfusion cérébrale engendrée par l'hypertension intracrâ- nienne. L'évaluation de l'importance de l'œdème cérébral diffus est difficile en imagerie, aussi bien en tomodensitométrie qu'en IRM. Les signes tomodensi- ... (MP4 940 KB). In four cases there was hypoperfusion in the non-dominant hemisphere and the predomi-nance of pain symptoms took place in the contralateral hemibody. Trouvé à l'intérieur – Page 38La médicalisation doit être systématique quels que soient les signes à l'appel. ... Les signes neurologiques sont le fait d'une toxicité directe ou les témoins de l'hypoperfusion cérébrale : troubles de conscience, confusion, ... On the right upper corner of C, the partial 3-D reconstruction shows the exact localization of cortical microinfarcts, bilaterally, in the watershed zone of anterior and middle cerebral arteries. Karize Uy Cerebral palsy can be caused by cerebral hypoperfusion. Use the link below to share a full-text version of this article with your friends and colleagues. Mild chronic cerebral hypoperfusion caused a general dysfunction in brain capillaries, which was characterized by exacerbated IgG entrapment in these capillaries. It is a sub-type of stroke along with subarachnoid hemorrhage and intracerebral hemorrhage.. GSK3β has been widely investigated in AD and is the target of several pharmacological compounds aiming to inhibit its kinase activity [32]. Conclusions— In AD, cerebral hypoperfusion induces not only white matter changes but cortical watershed microinfarcts as well, further aggravating the degenerative process and worsening dementia. c. Un aspect S1Q3. PubMed  From the formalin-fixed brains, in all cases at least 12 different samples, including cortical areas outside of watershed zones, basal ganglia, thalamus, cerebellum, and at least 1 level of the brain stem, were taken for a detailed neuropathological investigation. Objective . capillaries) isolation buffer (MIB; 15 mM Hepes, 147 mM NaCl, 4 mM KCl, 3 mM CaCl2, and 12 mM MgCl2) supplemented with 5% Protease Inhibitor Cocktail (P8340; Sigma) and 1% Phosphatase Inhibitor Cocktail 2 (P5726; Sigma). The combinatory use of diffusion-weighted MRI (DWI) and PWI is invariably suggested in an attempt to differentiate ischemic from infarcted area, and this may require more imaging time and a high standard for cooperation patients. Intellectual changes observed in progressive supranuclear palsy (PSP) are sometimes seen with lesser intensity in Parkinson's disease (PD). In the other three patients . Evaluation of CCCI can be accomplished with PET, which estimates cerebral perfusion via measuring the CBF and oxygen extraction fraction (OEF).88 However, it is not considered as a first-line option because of a relatively high cost and demand for technique as well as a low penetration rate. It should be noted that amelioration of cognitive dysfunction and neuronal injury secondary to CCCI is likely to be accomplished via enhancing GABAergic expression and transmission in the hippocampal CA1 area with clonidine or bone marrow mesenchymal stem cells (BMSCs).66, 67 Glutamate is a well-known excitatory neurotransmitter in the CNS, and impaired activity of glutamate transporters may induce glutamate excitotoxicity, followed by apoptosis of glutamatergic neurons. The 3-D reconstruction shows that the cortical microinfarcts were restricted to the watershed cortical zones in both AD cases (compare their distribution in C with the schematic illustration of watershed zones in Figure 1). (C) Thioflavin S positive Aβ deposits are localized in the perivascular space of brain capillaries within GFAP positive astrocytic endfeet. The 3-D reconstruction shows that the cortical microinfarcts were restricted to the watershed cortical zones in both AD cases (compare their distribution in C with the schematic illustration of watershed zones in Figure 1). cortex surface) to 250 μm (inside the cortex), for a total depth of 200 μm. Increased blood levels of Aβ have been reported in AD patients at the early stages of the disease [35]. By using this website, you agree to our Atherosclerosis of the large cerebral arteries was noted on macroscopic examination, and the detection of congophilic angiopathy was performed on sections stained with Congo red, stained with thioflavin S, and immunostained with monoclonal antibody to β-amyloid. Hypoperfusion triggers vascular deposition of peripherally applied human Aβ Small cortical infarctions in watershed zones between the major cerebral arteries are known to occur in cerebral hypoperfusion. The neuropathological assessment of the AD-type cortical changes was made by 2 different investigators following criteria previously described in detail.14 The analysis of watershed cortical infarcts was also performed in all cases and in all sections independently by 2 different investigators. The microinfarcts were more numerous in the parieto-occipital region, particularly in the watershed zones of anterior and middle cerebral arteries. Immunofluorescence analysis examining endogenous IgG entrapment in brain capillaries shows that brain reperfusion, or glucose administration decreases IgG entrapment in the brain capillaries of the cortex (A), and similarly decreases IgG entrapment in the brain capillaries of the hippocampus (B). 1 VO, one vessel occlusion for 24 hours; S, saline; R, brain reperfusion; G, glucose administration. Hartz AM, Miller DS, Bauer B: Restoring blood–brain barrier P-glycoprotein reduces brain amyloid-beta in a mouse model of Alzheimer's disease. 10.1371/journal.pone.0053942, Wyss-Coray T, Masliah E, Mallory M, McConlogue L, Johnson-Wood K, Lin C, Mucke L: Amyloidogenic role of cytokine TGF-beta1 in transgenic mice and in Alzheimer's disease. Perfusion imaging modalities such as computed tomography perfusion (CTP) and perfusion-weighted MRI (PWI) are noninvasive techniques that enable the documentation of perfusion parameters including CBF, CBV, mean transit time (MTT), and time to peak (TTP) (Figure 4B,C). Hypoperfusion cérébrale à l'effort (bas débit) Trouble du rythme (Hypertrophie Ventriculaire Gauche) Trouble de la conduction Utilisation des vasodilatateurs (Dérivés Nitrés) Signes cliniques: Auscultation: temps essentiel : Souffle systolique: Méso-systolique : débute après B1 et se termine avant B2 Histology and 3-D distribution of watershed cortical infarcts in AD. angiopathie amyloide cerebrale avec hemorragie : a propos d'un cas (book, ) [] The pathogenesis of CAA-related disorders consists of two steps: Finding libraries that hold this item Fresh arrow and old arrowhead amyloude macrohemorrhages in the frontal lobes on CT A. Relative frequency of watershed cortical infarcts in AD. Local Info Ann Nucl Med 2007, 21: 15–23. There exist several differences in presenting symptoms, clinical evaluation, and diagnostic testing between them. Our results show that cerebral hypoperfusion may generate not only white matter changes but cortical watershed infarcts as well and, together with the severely disturbed cortical microcirculation, will further worsen cognitive decline in AD. In the 2VO model, inhibition of autophagy was able to attenuate microglial activation, decrease WMLs, and improve cognitive deficits of experimental mice.56 In addition, it has been demonstrated that MCP-1-mediated microglia activation worsened WMLs and impaired working memory, possibly via p38MAPK/PKC pathway.57, Accumulating evidence has implied that apoptosis of oligodendrocytes, a group of myelin-forming cells in the brain that are more susceptible to ischemic insults than other glia cells, can contribute to WMLs formation. Bars=300 μm, 100 μm, 50 μm, respectively. Figure 1. In agreement with previous observations,22–24,32 the morphological analysis of the cortical vascular network showed a strongly disturbed capillary network. Amyloid deposits and neurofibrillary tangles formation are the core pathological hallmarks of Alzheimer's disease (AD) [1]. A scheme illustrating the different protocols used to perform this study. A and C, 3-D reconstructions of the cortical outlines and microinfarcts observed on H&E-stained, serial (spaced at 3 mm) sections of the cerebrums of 2 AD cases with watershed infarcts using computer maps. Animal models demonstrated that neuronal death was present at 1 week and continued for up to 3 months after CCCI,60 especially in the striatum, hippocampus, and cortex, indicating that neurons in these 3 regions are especially vulnerable to CCCI.61, 62 In addition, CCCI-induced neuronal loss might be correlated with abnormal phosphorylation of tau protein. Such a hypothesis suggests that several risk factors affecting vascular functions are involved in AD pathogenesis. For molecular analysis, mice were perfused with saline (0.9% NaCl), brains were removed and immediately frozen in dry ice (Additional file 1: Figure S1; Protocol A). For nuclear protein analysis, nuclear fraction was extracted using commercially available kit (Thermo Scientific, IL, USA). Trouvé à l'intérieur – Page 606La leucoaraïose résulte d'une hypoperfusion cérébrale diffuse, plus particulièrement pour les lésions qui siègent dans le ... l'imagerie démontre des signes d'athérosclérose au niveau des vaisseaux de la base (dolichotronc basilaire et ... appelé « attaque cérébrale », est défini par un déficit neurologique d'apparition brutale, dû à une ischémie ou une hémorragie cérébrale. Download figureDownload PowerPointFigure 1. We thank E. Bernardi for his help with photography and B. Bolliger, who developed the volume program in the framework of a joint project between the Institute of Anatomy, University of Lausanne and the Computer Graphics Laboratory of the Swiss Federal Institute of Technology (EPFL, Lausanne, Switzerland). alzheimers.ca. Miyamoto et al demonstrated that 8-month-old mice were more susceptible to prolonged cerebral hypoperfusion than 2-month-old mice, with decreased oligodendrogenesis, more severe WMLs, and worse deficits in working memory. To analyze the morphology of the cortical vascular network, from formalin-fixed brains, 3×2×1-cm samples were taken from the frontal and parietal cortical regions of 3 AD cases with congophilic angiopathy and in 1 age-matched control case without AD and without congophilic angiopathy. Masimo (NASDAQ : MASI) a annoncé aujourd'hui le marquage CE et le lancement en Europe de l'Ouest, de Masimo SafetyNet Alert™, un système de surveillan 10.1126/science.1228541. Brain capillaries from contralateral and ipsilateral hemispheres were isolated on dextran gradient as described previously [24]. Les signes cliniques du choc cardiogénique représentent les manifestations d'une hypoperfusion tissulaire : - Signes cardiovasculaire : hypotension artérielle (PAS< 90 mmHg) et tachycardie avec pouls petit et filant, l'auscultation cardiaque retrouve des bruits lointains (baisse de la contractilité) ; The size (diameter of the maximum extent) of the small watershed cortical infarcts varied from 300 μm to 2 mm (Figure 3B). A reduction in CBF, at least induces rapid neuronal stress, which can evolve to an irreversible damage if this reduction persisted and/or is greater than 80% [10]. Mol Pharmacol 2010, 77: 715–23. There were no cortical infarcts on the convexity of the occipital poles supplied by the posterior cerebral artery. Studies have denoted that oxidative stress is involved in brain injury during sustained cerebral hypoperfusion. L'AVC ischémique représente environ 87% de tous les AVC, il est causé par l'occlusion localisée d'un vaisseau conduisant à un arrêt de l'apport en oxygène et en To analyze the intrahemispheric and interhemispheric distribution of the small cortical infarcts, their 3-dimensional (3-D) localization was visualized in 5 randomly selected AD brains from the group of AD cases in which standard analysis revealed the presence of watershed infarcts. For this purpose, we used C57BL/6J mice subjected to right common carotid artery (rCCA) permanent ligation (i.e. It is often associated with cerebral hypoxia, in which the brain receives an insufficient supply of oxygen carried by the blood. Detector sensitivity and gain were set to achieve the optimal dynamic range of detection. D and E illustrate a larger penetrating cortical artery in AD (D) and in control (E) subjects. In line with these observations, we investigated the role of brain perfusion and glucose in inducing NVU dysfunction and Aβ deposition cascade in ipsilateral brain capillaries. Major etiologies can be summarized as follows:5, 6 (i) cerebrovascular pathological changes, mainly including vascular spasm, stenosis, or occlusion in either the vertebral or carotid artery system secondary to multiple factors such as atherosclerosis, vasculitic disease, moyamoya disease, and arteriovenous malformation; (ii) cardiovascular factors such as long-standing hypertension or hypotension, and cerebral hypoperfusion induced by cardiac failure and arrhythmia; (iii) systemic diseases such as obstructive sleep apnea-hypopnea syndrome (OSAHS), chronic obstructive pulmonary ventilation disorder, anemia, abnormal blood composition, chronic carbon monoxide poisoning, diabetes, smoking, and obesity. Trouvé à l'intérieur – Page 545Après l'anamnèse de la personne âgée et de son entourage, l'examen clinique recherche des signes neurologiques ... Parallèlement, il faut rechercher un trouble hémodynamique responsable d'une hypoperfusion cérébrale, par exemple un ... In these 6 cases, 30-μm-thick, 3-mm-spaced serial sections were cut from the whole cerebrum (Polycat macrotome) and stained with H&E. Mild chronic cerebral hypoperfusion initiates Aβ deposition and aggregation. Hyperperfusion definition The intrahemispheric and interhemispheric distribution of cortical watershed infarcts varied from case to case. C57BL/6J mice (20–25 g) were housed and acclimated to standard laboratory conditions (12-hour light/dark cycle / lights on at 7:00 AM and off at 7:00 PM) with free access to chow and water. These samples were heated for all protein analysis studies except for those involving ABCB1, for which samples were loaded without heating to avoid aggregation of these highly glycosylated transmembrane proteins. To rigorously rule out the possibility that atherosclerosis may play a role in the association between AD and cortical watershed infarcts, a second statistical analysis was also performed by eliminating all AD and control cases in which the neuropathological examination showed the presence of atherosclerosis, including those with both atherosclerosis and amyloid angiopathy (Table 1). To analyze the occurrence of cortical watershed infarcts in AD, 184 autopsy cases (105 definite AD cases [aged 54 to 98 years; mean age, 78 years] and 79 age-matched control cases [aged 57 to 87 years; mean age, 72 years]) were selected (Table 1). 10.1172/JCI25247, Vogelgesang S, Warzok RW, Cascorbi I, Kunert-Keil C, Schroeder E, Kroemer HK, Siegmund W, Walker LC, Pahnke J: The role of P-glycoprotein in cerebral amyloid angiopathy; implications for the early pathogenesis of Alzheimer's disease. For instance, impairment of the WM tracts joining motor regions is considered to be accountable for gait disturbance in a subset of patients with CCCI-related cerebral small-vessel disease.33 Compared with the GM, the WM appears to be less vulnerable to ischemic insults, depicted by lower infarction threshold values for CBF, cerebral blood volume (CBF), and apparent diffusion coefficient, as well as slower evolution of ischemic penumbra.34-37 This different vulnerability is likely attributable to the differing cellular constituents and neurochemical cascades between the WM and the GM. Une maladie cérébrale vasculaire - ATCD d'AIC ou AVC hémorragique et FDR vasculaire (HTA) - Signes neurologiques focaux : déficit moteur et/ou sensitif HLH sd pyramidal sd pseudobulbaire - Imagerie cérébrale (TDM ou . Objective . This syndrome can develop at any time, from immediately after surgery to up to a month later. Un syndrome démentiel avec trouble de la personnalité et de l'humeur, associé à une labilité émotionnelle 2. SR is a Full Professor and Principal Investigator at the Department of Molecular Medicine, Faculty of Medicine, University of Laval, and the Director of CHU de Québec Research Center (CHUL). The implication of an impaired ISF-mediated Aβ drainage along the perivascular space of brain arteries in our animal model is highly probable, which would amplify the impact of ABCB1 reduction, therefore further increasing the accumulation Aβ peptides in the brain. Learn faster with spaced repetition. Kalman filter was used during scanning in order to reduce background. Science 2006, 313: 1781–4. Some studies discovered that the cholinergic system underwent changes in CCCI, as reflected by alterations in cholinergic markers such as Ach, acetylcholinesterase (AchE), choline acetyl-transferase (ChAT) as well as M-type ACh receptors in both mRNA and protein forms,63 suggesting that central cholinergic system dysfunction poses a significant effect on the pathogenesis of cognitive deficits and neuropathological lesions in CCCI.64 Furthermore, protection or reversal of the significantly decreased expression of vesicular acetylcholine transporter (vAChT) and vAChT-positive neurons in hippocampal subregions such as CA1 is able to mitigate cognitive impairments related to the possible mechanism in CCCI-induced VD. The occurrence of cortical watershed infarcts (WI+) was >10-fold higher in the group of AD cases (34/105) than in the controls (2/79). Blots were digitized, densitometrically analyzed with ImageJ image analysis software (NIH), corrected for protein loading by means of Lamin B (nuclear β-catenin), or β-actin (all others) blots, and expressed as relative values comparing ipsilateral (hypoperfused) with contralateral (non hypoperfused). Our results show that the incidence of small cortical watershed infarcts in definite AD is >10-fold higher than in age-matched controls without any AD-type cortical changes. (Début rapide ne veut pas forcément dire sans prodromes = signes qui annoncent la perte de connaissance (PC) comme les nausées, mal être, sueurs). peptides. 10.2174/1567205043332225, Hooper C, Killick R, Lovestone S: The GSK3 hypothesis of Alzheimer's disease. © American Heart Association, Inc. All rights reserved. Cerebral small vessel disease (CSVD) is a generic term that refers to intracranial vascular disease based on various pathological and neurological processes, as well as a syndrome referring to different clinical manifestations and neuroimaging features caused by the structural changes of vascular and brain parenchyma. As such, NVU/BBB dysfunction, associated to irregularities in cerebral blood flow (CBF), has been proposed to contribute in the pathogenesis of Alzheimer’s disease (AD), mainly by impairing cerebral Aβ clearance. Data are means ± SEM (n = 5 animals per group, 5 sections per animal’s brain). Sepsis in the "moment" in which the hemodynamic . We show here that mild chronic cerebral hypoperfusion induces GSK3β activation via tyrosine phosphorylation, leading to β-catenin degradation. Imagerie cérébrale en URGENCE TDM SANS inj (si IRM non dispo) • NORMALE dans les 1ères h en cas d'IC mais : • AH = hyperdensité spontanée • Signes d'IC précoces : • Hypodensité systématisée au territoire artériel • Effacement noyau lenticulaire • '' ruban insulaire • Dédifférenciation SB/SG • Effacement sillons corticaux • "Trop belle" artère = thrombus Indeed, brain reperfusion and the administration of high dose of glucose inhibited GSK3β activation, re-established β-catenin nuclear translocation, and rescued ABCB1 protein levels. For instance, it was found that repair of WM damage was interfered by disruptive compensatory mechanisms of oligodendrocyte precursor cells to oligodendrocyte renewal secondary to oxidative stress during prolonged cerebral hypoperfusion stress induced by the microcoil with an inner diameter of 0.18 mm in a mice model, while astrocytes might facilitate oligodendrogenesis through secreting brain-derived neurotrophic factor (BNDF).12, 13. (hypoperfusion) avec oedèmes réfractaires et anorexie, le niveau de soins est à repréciser. The target artery of CCCI is located in the vertebrobasilar arterial system, in which posterior circulation ischemia-associated symptoms are the main clinical manifestations (Table. non hypoperfused) brain capillaries (Figure 1A), which persisted 48 hours after 1 VO (Figure 1A). WMLs can be seen in both human brains with CCCI and animal models with experimental CCCI.38, 39 It has been demonstrated that WMLs secondary to CCCI can be predictive of ischemic events and be correlated with cognitive decline, the degree of which is positively related to the lesion severity. 10.1007/s00401-009-0532-1, CAS  ( Cochez la réponse juste ) a. Une onde P en DII de 0,09 s de durée et de 3mm d'amplitude. Ann Neurol 1997, 42: 85–94. Moreover, cerebral hypoperfusion triggered early vascular deposition of peripherally applied human Aβ1-42 peptides, which has shifted from highly vascular to the parenchyma 6 weeks later, forming small stable Aβ deposits. Acta Neuropathologica Communications A systolic blood pressure <90 mmHg or reduction in pressure> 40 mmHg from baseline value, in the absence of other causes of hypotension. We would like to thank J. Bogousslavsky, F. Regli, M. Kiraly, M. Maurin, and K. Meagher-Villemure for reviewing our manuscript and for the helpful critical comments. Neuron 2010, 67: 181–98. 1. Cases with discrete vascular amyloid deposition visible with β-amyloid immunostaining or thioflavin S, but negative for Congo red, were not considered to exhibit congophilic angiopathy. CCCI: chronic cerebral circulation insufficiency; SPECT: single-photon emission computed tomography; CTP: computed tomography perfusion; CBF: cerebral blood flow; CBV: cerebral blood volume; MTT: mean transit time; TTP: time to peak; MRA: magnetic resonance angiography; DWI: diffusion-weighted MR; PWI: perfusion-weighted MR, I have read and accept the Wiley Online Library Terms and Conditions of Use, Effects of Yangxue Qingnao Granules on chronic cerebral circulation insufficiency: a randomized, double-blind, double-dummy, controlled multicentre trial, Chronic brain hypoperfusion due to multi-vessel extracranial atherosclerotic disease: a potentially reversible cause of cognitive impairment, Prevalence and outcomes of symptomatic intracranial large artery stenoses and occlusions in China: the Chinese Intracranial Atherosclerosis (CICAS) Study, Major pathogenic mechanisms in vascular dementia: roles of cellular stress response and hormesis in neuroprotection, Cognitive impairment and chronic cerebral hypoperfusion: what can be learned from experimental models, The acetazolamide challenge: techniques and applications in the evaluation of chronic cerebral ischemia, Global burden of intracranial atherosclerosis, Predictors of ischemic stroke in the territory of a symptomatic intracranial arterial stenosis, Dual antiplatelet therapy in stroke and ICAS: subgroup analysis of CHANCE, Reversal of ischemic-induced chronic memory dysfunction in aging rats with a free radical scavenger-glycolytic intermediate combination, Oxidative stress interferes with white matter renewal after prolonged cerebral hypoperfusion in mice, Astrocytes promote oligodendrogenesis after white matter damage via brain-derived neurotrophic factor, A new rat model of chronic cerebral hypoperfusion associated with arteriovenous malformations, Vascular endothelial growth factor expression and angiogenesis induced by chronic cerebral hypoperfusion in rat brain, Chronic cerebral hypoperfusion induced by right unilateral common carotid artery occlusion causes delayed white matter lesions and cognitive impairment in adult mice, Oligodendroglial cell death with DNA fragmentation in the white matter under chronic cerebral hypoperfusion: comparison between normotensive and spontaneously hypertensive rats, Chronic cerebral hypoperfusion accelerates Alzheimer's disease pathology with cerebrovascular remodeling in a novel mouse model, Synergistic memory impairment through the interaction of chronic cerebral hypoperfusion and amyloid toxicity in a rat model, Diabetes augments cognitive dysfunction in chronic cerebral hypoperfusion by increasing neuronal cell death: implication of cilostazol for diabetes mellitus-induced dementia, Experimental models of vascular dementia and vascular cognitive impairment: a systematic review, Astroglial and cognitive effects of chronic cerebral hypoperfusion in the rat, Selective impairment of working memory in a mouse model of chronic cerebral hypoperfusion, Characterization of white matter injury in a rat model of chronic cerebral hypoperfusion, Long-term cilostazol treatment reduces gliovascular damage and memory impairment in a mouse model of chronic cerebral hypoperfusion, A mouse model characterizing features of vascular dementia with hippocampal atrophy, Adams and Victor's Principles of Neurology, Experimental evidence of ischemic thresholds and functional recovery, Viability thresholds and the penumbra of focal ischemia, Type 2 diabetes reduces the proliferation and survival of oligodendrocyte progenitor cells in ischemic white matter lesions, Icariin, a major constituent of flavonoids from Epimedium brevicornum, protects against cognitive deficits induced by chronic brain hypoperfusion via its anti-amyloidogenic effect in rats, Relief of carotid stenosis improves impaired cognition in a rat model of chronic cerebral hypoperfusion, Ischemic thresholds for gray and white matter: a diffusion and perfusion magnetic resonance study, The resistance to ischemia of white and gray matter after stroke, The existence and evolution of diffusion-perfusion mismatched tissue in white and gray matter after acute stroke, MR perfusion and diffusion in acute ischemic stroke: human gray and white matter have different thresholds for infarction, White matter lesions in an unselected cohort of the elderly: molecular pathology suggests origin from chronic hypoperfusion injury, Damage to white matter pathways in subacute and chronic spatial neglect: a group study and 2 single-case studies with complete virtual “in vivo” tractography dissection, White matter lesions and glial activation in a novel mouse model of chronic cerebral hypoperfusion, Pathologic correlates of incidental MRI white matter signal hyperintensities, Cerebral white matter lesions may be partially reversible in patients with carotid artery stenosis, What are white matter hyperintensities made of?

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