Attachement amoureux et comportements suicidaires dans un contexte de rupture amoureuse

Les ruptures amoureuses et les divorces sont très fréquents dans la société actuelle. La rupture d’une relation amoureuse est une épreuve difficile (Holmes & Rahe, 1967; Scully, Tosi, & Banning, 2000) qui génère une détresse émotionnelle importante (Birnbaum, Orr, Mikulincer, & Florian, 1997; Sbarra, 2006). Certains individus qui vivent une rupture iront même jusqu’à poser un geste suicidaire. En effet, le lien entre la rupture amoureuse et le comportement suicidaire est bien documenté à ce jour (Ide, Wyder, Kolves, & De Leo, 2010). La présente étude a investigué le rôle des insécurités d’attachement amoureux (anxiété d’abandon, évitement de l’intimité) dans la survenue des symptômes dépressifs et des comportements suicidaires (pensées et tentatives) à la suite d’une rupture. Pour ce faire, 50 participants adultes ayant vécu une rupture amoureuse dans les six derniers mois ont été recrutés auprès d’organismes d’aide (centre de prévention de suicide, centre psychologique, organisme communautaire), ainsi qu’à l’aide de publicités affichées en milieu universitaire, sur les réseaux sociaux et sur des réseaux de partenaires. Un intervenant formé en crise suicidaire a administré verbalement des questionnaires validés d’attachement amoureux, de symptômes dépressifs et de comportements suicidaires lors d’une entrevue individuelle. Les résultats des analyses de régressions multiples ont montré que l’anxiété d’abandon des adultes qui vivent une rupture est liée à davantage de symptômes dépressifs, ainsi qu’à la sévérité et l’intensité des idées suicidaires. Ces effets demeurent lorsque l’utilisation du réseau social est contrôlée. L’évitement de l’intimité n’est pas lié à ces variables. La discussion porte sur l’importance de l’anxiété d’abandon comme facteur de vulnérabilité dans les difficultés d’adaptation à la rupture, au-delà du réseau social, et propose des pistes d’évaluation et d’intervention pour les cliniciens.

Rapport d'intervention Après la pluie ... Le beau temps! : programme de prévention universelle du deuil pathologique post-ruptures amoureuses chez les adolescents de 15 à 17 ans.

Rapport d'analyse d'intervention présenté à la Faculté des arts et sciences en vue de l'obtention du grade de Maîtrise ès sciences (M. Sc.) en psychoéducation.

Entre l'idée de rompre et la rupture définitive : l'histoire de trois femmes liées pendant quinze ans et plus à un conjoint qu'elles considèrent alcoolique

Intriguée par la statistique couramment rapportée dans le domaine de l'intervention en toxicomanie à l'effet qu'une seule femme sur dix quitte un conjoint alcoolique alors que neuf hommes sur dix quittent une conjointe aux prises avec le même problème, nous nous sommes demandé quels facteurs entraient en ligne de compte quand cette petite proportion de femmes posait ce geste. Nous avons, dans ce sens, entrepris la présente étude qualitative, laquelle nous a permis d'explorer, de décrire puis de comparer l'expérience de femmes en regard de leur vie et de leur rupture temporaire ou définitive avec un partenaire qu'elles considèrent alcoolique. Bien que la documentation regorge d'hypothèses au sujet de la relation et de l'évolution du couple où le mari est alcoolique, peu d'écrits portent sur les facteurs associés au maintien de cette union et aucun n'aborde les facteurs associés à la rupture de celle-ci. Les écrits que nous avons consultés nous ayant, de plus, amenée à constater que les épouses d'alcooliques ont rarement été interrogées sur leur expérience, il nous est apparu tout à fait indiqué d'interpeller quelques-unes de ces femmes directement concernées par la question qui nous intéresse, d'écouter et de recueillir leur version à propos de leur réalité. Nous avons ainsi rencontré trois femmes qui ont accepté de nous raconter, dans le cadre d'entrevues semi-dirigées, leur histoire en regard de leur vie liée à un conjoint qu'elles considèrent alcoolique. Ces trois informatrices ont vécu au moins quinze ans avec leur conjoint et l'ont quitté à une ou à quelques reprises pour des périodes plus ou moins prolongées: la première (Édith), pour quelques heures à quelques reprises: la seconde (Hélène), quelques fois pour peu de temps puis définitivement; la troisième (Solange) a divorcé puis repris la vie commune deux mois plus tard. Leur expérience respective ajoutée à celle de deux autres femmes rapportée dans la littérature populaire québécoise nous a permis d'atteindre notre objectif de recherche, à savoir identifier des facteurs associés à la décision de quitter un conjoint alcoolique et d'autres associés au maintien de cette décision. Au terme de cette étude, l'alcoolisme nous apparaît être un facteur relativement secondaire dans la décision de quitter un partenaire aux prises avec ce problème. Il semble plutôt que l'insatisfaction conjugale et la baisse ou la perte d'espoir d'une amélioration de sa situation développée au fil des ans de même que le désir de provoquer un changement soient des facteurs déterminants dans la décision de quitter son conjoint alcoolique. D'autre part, l'acquisition d'une plus grande autonomie à divers niveaux, l'incapacité à entrevoir l'avenir auprès de son conjoint sans la présence des enfants, un réseau social de support étendu et diversifié et le développement d'une autre relation amoureuse satisfaisante semblent être des facteurs susceptibles de favoriser le maintien de ce choix. Il ressort de notre étude que la décision de quitter un partenaire alcoolique serait le fruit d'un long processus et résulterait de l'impact simultané de plusieurs facteurs d'ordres divers. Il nous semble, en outre, que la compréhension que nous avons développée de la situation des femmes que nous avons rencontrées pourrait se transposer à celle d'autres femmes vivant une relation conjugale dysfonctionnelle. Nous pensons, entre autres, aux femmes violentées par leur conjoint. Violence conjugale et alcoolisme ne sont-ils pas d'ailleurs des phénomènes souvent entrecroisés (MacLeod, 1987; Forest, 1986)? Finalement, de la présente recherche ont émergé certaines questions qui mériteraient, à notre avis, d'être examinées de près.

Early-mid Cretaceous tectonic evolution of eastern Gondwana : from silicic LIP magmatism to continental rupture

The Early–mid Cretaceous marks the confluence of three major continental-scale events in eastern Gondwana: (1) the emplacement of a Silicic Large Igneous Province (LIP) near the continental margin; (2) the volcaniclastic fill, transgression and regression of a major epicontinental seaway developed over at least a quarter of the Australian continent; and (3) epeirogenic uplift, exhumation and continental rupturing culminating in the opening of the Tasman Basin c. 84 Ma. The Whitsunday Silicic LIP event had widespread impact, producing both substantial extrusive volumes of dominantly silicic pyroclastic material and coeval first-cycle volcanogenic sediment that accumulated within many eastern Australian sedimentary basins, and principally in the Great Australian Basin system (>2 Mkm3 combined volume). The final pulse of volcanism and volcanogenic sedimentation at c. 105–95 Ma coincided with epicontinental seaway regression, which shows a lack of correspondence with the global sea-level curve, and alternatively records a wider, continental-scale effect of volcanism and rift tectonism. Widespread igneous underplating related to this LIP event is evident from high paleogeothermal gradients and regional hydrothermal fluid flow detectable in the shallow crust and over a broad region. Enhanced CO2 fluxing through sedimentary basins also records indirectly, large-scale, LIP-related mafic underplating. A discrete episode of rapid crustal cooling and exhumation began c. 100–90 Ma along the length of the eastern Australian margin, related to an enhanced phase of continental rifting that was largely amagmatic, and probably a switch from wide–more narrow rift modes. Along-margin variations in detachment fault architecture produced narrow (SE Australia) and wide continental margins with marginal, submerged continental plateaux (NE Australia). Long-lived NE-trending cross-orogen lineaments controlled the switch from narrow to wide continental margin geometries.

Continuity, Rupture, or just more of the 'Volatile and Contradictory': Glimpses of New South Wales' Penal Practice behind and through the Discursive

Throughout much of the western world more and more people are being sent to prison, one of a number of changes inspired by a 'new punitiveness' in penal and political affairs. This book seeks to understand these developments, bringing together leading authorities in the field to provide a wide-ranging analysis of new penal trends, compare the development of differing patterns of punishment across different types of societies, and to provide a range of theoretical analyses and commentaries to help understand their significance. As well as increases in imprisonment this book is also concerned to address a number of other aspects of 'the new punitiveness': firstly, the return of a number of forms of punishment previously thought extinct or inappropriate, such as the return of shaming punishments and chain gangs (in parts of the USA); and secondly, the increasing public involvement in penal affairs and penal development, for example in relation to length of sentences and the California Three Strikes Law, and a growing accreditation of the rights of victims. The book will be essential reading for students seeking to understand trends and theories of punishment on law, criminology, penology and other courses.

Fatigue crack growth under pulsatile pressure and plaque rupture

Identification of vulnerable plaque pre-rupture is extremely important for patient risk stratification. The mechanism of plaque rupture is still not entirely clear, but it is thought to be a process involving multiple factors. From a biomechanical viewpoint, plaque rupture is usually seen as a structural failure when the plaque cannot resist the hemodynamic blood pressure and shear stress exerted on it. However, the cardiovascular system is naturally a cyclical hemodynamic environment, and myocardial infarction can be a symptomatically quiescent but potentially progressive process when plaque ruptures at stresses much lower than its strength. Therefore, fatigue accumulation is a possible mechanism for plaque rupture. In this study, a crack growth model was developed, and the previously-mentioned hypothesis was tested by conducting a comparative study between 18 symptomatic and 16 asymptomatic patients with carotid stenosis.

Fatigue crack propagation analysis of plaque rupture

Rupture of atheromatous plaque is the major cause of stroke or heart attack. Considering that the cardiovascular system is a classic fatigue environment, plaque rupture was treated as a chronic fatigue crack growth process in this study. Fracture mechanics theory was introduced to describe the stress status at the crack tip and Paris' law was used to calculate the crack growth rate. The effect of anatomical variation of an idealized plaque cross-section model was investigated. The crack initiation was considered to be either at the maximum circumferential stress location or at any other possible locations around the lumen. Although the crack automatically initialized at the maximum circumferential stress location usually propagated faster than others, it was not necessarily the most critical location where the fatigue life reached its minimum. We found that the fatigue life was minimum for cracks initialized in the following three regions: the midcap zone, the shoulder zone, and the backside zone. The anatomical variation has a significant influence on the fatigue life. Either a decrease in cap thickness or an increase in lipid pool size resulted in a significant decrease in fatigue life. Comparing to the previously used stress analysis, this fatigue model provides some possible explanations of plaque rupture at a low stress level in a pulsatile cardiovascular environment, and the method proposed here may be useful for further investigation of the mechanism of plaque rupture based on in vivo patient data.

Stress analysis of carotid atheroma in transient ischemic attack patients: Evidence for extreme stress-induced plaque rupture

Plaque rupture has been considered to be the result of its structural failure. The aim of this study is to suggest a possible link between higher stresses and rupture sites observed from in vivo magnetic resonance imaging (MRI) of transient ischemic attack (TIA) patients, by using stress analysis methods. Three patients, who had recently suffered a TIA, underwent in vivo multi-spectral MR imaging. Based on plaque geometries reconstructed from the post-rupture status, six pre-rupture plaque models were generated for each patient dataset with different reconstructions of rupture sites to bridge the gap of fibrous cap from original MRI images. Stress analysis by fluid structure interaction simulation was performed on the models, followed by analysis of local stress concentration distribution and plaque rupture sites. Furthermore, the sensitivity of stress analysis to the pre-rupture plaque geometry reconstruction was examined. Local stress concentrations were found to be located at the plaque rupture sites for the three subjects studied. In the total of 18 models created, the locations of the stress concentration regions were similar in 17 models in which rupture sites were always associated with high stresses. The local stress concentration region moved from circumferential center to the shoulder region (slightly away from the rupture site) for a case with a thick fibrous cap. Plaque wall stress level in the rupture locations was found to be much higher than the value in non-rupture locations. The good correlation between local stress concentrations and plaque rupture sites, and generally higher plaque wall stress level in rupture locations in the subjects studied could provide indirect evidence for the extreme stress-induced plaque rupture hypothesis. Local stress concentration in the plaque region could be one of the factors contributing to plaque rupture.

The mechanical triggers of plaque rupture: Shear stress vs pressure gradient

The aim of this study was to evaluate the mechanical triggers that may cause plaque rupture. Wall shear stress (WSS) and pressure gradient are the direct mechanical forces acting on the plaque in a stenotic artery. Their influence on plaque stability is thought to be controversial. This study used a physiologically realistic, pulsatile flow, two-dimensional, cine phase-contrast MRI sequence in a patient with a 70% carotid stenosis. Instead of considering the full patient-specific carotid bifurcation derived from MRI, only the plaque region has been modelled by means of the idealised flow model. WSS reached a local maximum just distal to the stenosis followed by a negative local minimum. A pressure drop across the stenosis was found which varied significantly during systole and diastole. The ratio of the relative importance of WSS and pressure was assessed and was found to be less than 0.07% for all time phases, even at the throat of the stenosis. In conclusion, although the local high WSS at the stenosis may damage the endothelium and fissure plaque, the magnitude of WSS is small compared with the overall loading on plaque. Therefore, pressure may be the main mechanical trigger for plaque rupture and risk stratification using stress analysis of plaque stability may only need to consider the pressure effect.

The Pathobiology of the Saccular Cerebral Artery Aneurysm Rupture and Repair : A Clinicopathological and Experimental Approach

Backround and Purpose The often fatal (in 50-35%) subarachnoid hemorrhage (SAH) caused by saccular cerebral artery aneurysm (SCAA) rupture affects mainly the working aged population. The incidence of SAH is 10-11 / 100 000 in Western countries and twice as high in Finland and Japan. The estimated prevalence of SCAAs is around 2%. Many of those never rupture. Currently there are, however, no diagnostic methods to identify rupture-prone SCAAs from quiescent, (dormant) ones. Finding diagnostic markers for rupture-prone SCAAs is of primary importance since a SCAA rupture has such a sinister outcome, and all current treatment modalities are associated with morbidity and mortality. Also the therapies that prevent SCAA rupture need to be developed to as minimally invasive as possible. Although the clinical risk factors for SCAA rupture have been extensively studied and documented in large patient series, the cellular and molecular mechanisms how these risk factors lead to SCAA wall rupture remain incompletely known. Elucidation of the molecular and cellular pathobiology of the SCAA wall is needed in order to develop i) novel diagnostic tools that could identify rupture-prone SCAAs or patients at risk of SAH, and to ii) develop novel biological therapies that prevent SCAA wall rupture. Materials and Methods In this study, histological samples from unruptured and ruptured SCAAs and plasma samples from SCAA carriers were compared in order to identify structural changes, cell populations, growth factor receptors, or other molecular markers that would associate with SCAA wall rupture. In addition, experimental saccular aneurysm models and experimental models of mechanical vascular injury were used to study the cellular mechanisms of scar formation in the arterial wall, and the adaptation of the arterial wall to increased mechanical stress. Results and Interpretation Inflammation and degeneration of the SCAA wall, namely loss of mural cells and degradation of the wall matrix, were found to associate with rupture. Unruptured SCAA walls had structural resemblance with pads of myointimal hyperplasia or so called neointima that characterizes early atherosclerotic lesions, and is the repair and adaptation mechanism of the arterial wall after injury or increased mechanical stress. As in pads of myointimal hyperplasia elsewhere in the vasculature, oxidated LDL was found in the SCAA walls. Immunity against OxLDL was demonstrated in SAH patients with detection of circulating anti-oxidized LDL antibodies, which were significantly associated with the risk of rupture in patients with solitary SCAAs. Growth factor receptors associated with arterial wall remodeling and angiogenesis were more expressed in ruptured SCAA walls. In experimental saccular aneurysm models, capillary growth, arterial wall remodeling and neointima formation were found. The neointimal cells were shown to originate from the experimental aneurysm wall with minor contribution from the adjacent artery, and a negligible contribution of bone marrow-derived neointimal cells. Since loss of mural cells characterizes ruptured human SCAAs and likely impairs the adaptation and repair mechanism of ruptured or rupture-prone SCAAs, we investigated also the hypothesis that bone marrow-derived or circulating neointimal precursor cells could be used to enhance neointima formation and compensate the impaired repair capacity in ruptured SCAA walls. However, significant contribution of bone marrow cells or circulating mononuclear cells to neointima formation was not found.