168 resultados para adversity


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We report four cases of surgically treated intracranial arachnoid cysts, one with cyst-peritoneal shunt and three with craniotomy and arachnoid membrane resection. Their classification and etiopathogeny are discussed, and especially the different methods of treatment comparing the drastic complications (adversities) with the favorable solutions in severe clinical cases (plasticity) treated at our institution.

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Purpose: To test whether the association between childhood adversity and positive and negative psychotic experiences is due to genetic confounding. Method: Childhood adversity and psychotic experiences were assessed in a sample of 226 twins from the general population. A monozygotic (MZ) twin differences approach was used to assess possible genetic confounding. Results: In the whole sample, childhood adversity was significantly associated with positive (β =.45; SE=.16; p=.008) and negative psychotic experiences (β=.77; SE=.18; p<.01). Within-pair MZ twin differences in exposure to childhood adversity were significantly associated with differences in positive (β =.71; SE=.29; p=.016) and negative psychotic experiences (β =.98; SE=.38; p=.014) in a subsample of 86 MZ twin pairs. Conclusions: Individuals exposed to childhood adversity are more likely to report psychotic experiences. Furthermore, our findings indicate that unique environmental effects of childhood adversity contribute to the development of psychotic experiences.

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Adverse childhood experiences have been described as one of the major environmental risk factors for depressive disorder. Likewise, the deleterious impact of early traumatic experiences on depression seems to be moderated by individual genetic variability. Serotonin transporter (5-HTT) and the Brain-Derived Neurotrophic Factor (BDNF) seem to modulate the effect of childhood adversity on adult depression, although inconsistencies across studies have been found. Moreover, the GxE interaction concerning the different types of childhood adversity remains poorly understood. The aim of this study is to analyse the putative interaction between the 5-HTT gene (5-HTTLPR polymorphism), BDNF gene (Val66Met polymorphism) and childhood adversity in accounting for adult depressive symptoms.

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Background Adverse childhood experiences have been described as one of the major environmental risk factors for depressive disorder. Similarly, the deleterious impact of early traumatic experiences on depression seems to be moderated by individual genetic variability. Serotonin transporter (5-HTT) and brain-derived neurotrophic factor (BDNF) modulate the effect of childhood adversity on adult depression, although inconsistencies across studies have been found. Moreover, the gene×environment (G×E) interaction concerning the different types of childhood adversity remains poorly understood. The aim of this study was to analyse the putative interaction between the 5-HTT gene (5-HTTLPR polymorphism), the BDNF gene (Val66Met polymorphism) and childhood adversity in accounting for adult depressive symptoms. Method A sample of 534 healthy individuals filled in self-report questionnaires of depressive symptomatology [the Symptom Check List 90 Revised (SCL-90-R)] and different types of childhood adversities [the Childhood Trauma Questionnaire (CTQ)]. The 5-HTTLPR polymorphism (5-HTT gene) and the Val66Met polymorphism (BDNF gene) were genotyped in the whole sample. Results Total childhood adversity (β=0.27, p<0.001), childhood sexual abuse (CSA; β=0.17, p<0.001), childhood emotional abuse (β=0.27, p<0.001) and childhood emotional neglect (β=0.22, p<0.001) had an impact on adult depressive symptoms. CSA had a greater impact on depressive symptoms in Met allele carriers of the BDNF gene than in the Val/Val group (F=5.87, p<0.0001), and in S carriers of the 5-HTTLPR polymorphism (5-HTT gene) (F=5.80, p<0.0001). Conclusions Childhood adversity per se predicted higher levels of adult depressive symptoms. In addition, BDNF Val66Met and 5-HTTLPR polymorphisms seemed to moderate the effect of CSA on adult depressive symptoms.

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Des études animales ont montré que l’exposition du foetus à l’adversité affecte le développement cérébral et la régulation d’émotions plus tard. Cette régulation serait reliée aux changements structurels cérébraux, particulièrement au circuit fronto-limbique. Cependant, ces résultats n’ont pas été entièrement répliqués chez l’humain. Le but de cette étude était de tester si l'adversité précoce conduit à des altérations structurelles des régions (orbitofrontal, préfrontal, cingulaire) fronto-limbiques, identifiées comme régions-clés dans la (de)régulation d’émotions. Les mesures principales de l’adversité étaient un poids léger à la naissance et l’hostilité maternelle puisqu’ils étaient parmi les plus prédictifs des résultats développementaux et comportementaux chez l’humain. Les mesures secondaires, incluant le tempérament difficile d’enfant et l’impulsivité en adolescence, étaient utilisées du à leur lien avec le développement cérébral et émotionnel. Les participants étaient des jumeaux identiques, membres de l’Étude des Jumeaux Nouveau-nés du Québec (ÉJNQ, N = 650 paires) suivis depuis 5 mois à 15 ans, leur âge actuel. Ceci a permis de mieux contrôler le facteur génétique et ainsi mieux isoler les effets d’environnement. Trente-sept paires ont été recrutées. La structure cérébrale de chacun, obtenue avec l’imagerie par résonance magnétique, a été analysée avec la régression linéaire. Le poids à la naissance n’a eu aucun effet. L’hostilité maternelle a prédit une réduction de l’aire du gyrus cingulaire postérieur. Tempérament difficile a prédit une réduction de l’aire du cortex orbitofrontal. L’impulsivité était associée avec l’aire et volume du cortex préfrontal réduits. Ces résultats soulignent l’importance des interventions précoces afin d’empêcher des altérations menant à la psychopathologie.

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Il existe actuellement de nombreuses preuves démontrant que des facteurs génétiques et environnementaux interagissent pendant des périodes spécifiques du développement pour rendre une personne vulnérable aux troubles psychologiques via diverses adaptations physiologiques. Cette thèse porte sur l'impact de l’adversité prénatale (représentée par le petit poids à la naissance, PPN) et de l’adversité postnatale précoce (symptômes dépressifs maternels et comportements maternels négatifs), sur le développement du cerveau, particulièrement les régions fronto-limbiques impliquées dans le traitement des émotions, pendant l'enfance et l'adolescence. Des jumeaux monozygotes (MZ) sont utilisés, lorsque possible, afin de contrôler pour les effets génétiques. Les chapitres 1 et 2 présentent les résultats de la vérification de l'hypothèse que l’adversité prénatale et postnatale précoce sont associées à une altération du fonctionnement des régions fronto-limbique tels que l’amygdale, l’hippocampe, l’insula, le cortex cingulaire antérieur et le cortex préfrontal, en réponse à des stimuli émotifs chez des enfants et des adolescents. On observe que les symptômes dépressifs maternels sont associés à une activation plus élevée des régions fronto-limbiques des enfants en réponse à la tristesse. Les résultats de l’étude avec des adolescents suggèrent que le PPN, les symptômes dépressifs et les comportements maternels négatifs sont associés à une fonction altérée des régions fronto-limbiques en réponse à des stimuli émotionnels. Chez les jumeaux MZ on observe également que la discordance intra-paire de PPN et de certains comportements maternels est associée à une discordance intra-paire du fonctionnement du cerveau et que ces altérations diffèrent selon le sexe. Le chapitre 3 présente les résultats de la vérification de l'hypothèse que l’adversité prénatale et postnatale précoce sont associées à un volume total réduit du cerveau et de l’hypothèse que les comportements maternels peuvent servir de médiateur ou de modérateur de l'association entre le PPN et le volume du cerveau. Avec des jumeaux MZ à l’adolescence on observe a) que le PPN est effectivement associé à une diminution du volume total du cerveau et b) que la discordance intra-paire de PPN est associée à une discordance du volume du cerveau. En somme, cette thèse présente un ensemble de résultats qui soutiennent deux hypothèses importantes pour comprendre les effets de l’environnement sur le développement du cerveau : que l’environnement prénatal et postnatal précoce ont un impact sur le développement du cerveau indépendamment du code génétique et que les mécanismes impliqués peuvent différer entre les garçons et les filles. Finalement, l’ensemble de ces résultats sont discutés à la lumière des autres travaux de recherche dans ce domaine et des avenues à explorer pour de la recherche ultérieure sont proposées.

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Research has identified associations between indicators of social disadvantage and the presence of child sleep problems. We examined the longitudinal development of infant sleep in families experiencing high (n = 58) or low (n = 64) levels of psychosocial adversity, and the contributions of neonatal self-regulatory capacities and maternal settling strategies to this development. Assessments of infant sleep at 4-, 7-, and 12-weeks postpartum indicated no differences in sleeping difficulties between high- and low-adversity groups. However, more infant sleep difficulties were reported in the high- versus low-adversity groups at 12- and 18-month follow-ups. Neonatal self-regulatory capacities were not related to the presence or absence of adversity, or to subsequent infant sleep quality. However, there were group differences in maternal settling strategies that did predict subsequent infant sleep difficulties. The pattern of sleep disturbance observed in association with maternal psychosocial adversity at 18-months was consistent with risk for broader impairments in child functioning.

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All organisms face attack from many natural enemies and all in turn have some means of defence. Can resistance evolve, and if it can, why doesn't it? Recent work on fruit flies and their parasitic wasps has shed light on these questions

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Objective: We sought to determine whether a reported history of childhood adversity is associated with components of the National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATP-III)-defined metabolic syndrome in adults with mood disorders. Method: This was a cross-sectional analysis of adult outpatients (N = 373; n = 230 female, n = 143 male; mean age [SD] = 42.86 [14.43]) from the International Mood Disorders Collaborative Project (University of Toronto and Cleveland Clinic) with DSM-IV-defined major depressive disorder and bipolar I/II disorder. Childhood adversity was measured with the Klein Trauma & Abuse-Neglect self-report scale. The groups with and without childhood adversity were compared to determine possible differences in the rates of metabolic syndrome and its components. Logistic and linear regressions adjusted for age, sex, education, employment status, and smoking were used to evaluate the association between childhood adversity and components of metabolic syndrome. Results: For the full sample, 83 subjects (22.25%) met criteria for metabolic syndrome. Individuals reporting a history of any childhood adversity had higher systolic and diastolic blood pressure (systolic: p = 0.040; diastolic: p = 0.038). Among subjects with a history of sexual abuse, a significant proportion met criteria for obesity (45.28% vs. 32.88%; p = 0.010); a trend toward overweight was found for subjects with a history of physical abuse (76.32% vs. 63.33%; p = 0.074), although this relationship did not remain significant after adjusting for potential confounders. There was no statistically significant difference in the overall rate of dyslipidemia and/or metabolic syndrome between subjects with and without childhood adversity. Conclusion: The results herein provide preliminary evidence suggesting that childhood adversity is associated with metabolic syndrome components in individuals with mood disorders. Int'l. J. Psychiatry in Medicine 2012;43:165-177)

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Expulsion from school is life changing. This single event can alter the trajectory of a student's life--for better or for worse. How life changes is unique for each individual student. Risk and protective factors that impact an individual student's resilience determine the level of positive or negative outcomes experienced as a result of expulsion. Educators have the opportunity to take advantage of this disruption in students' education to improve the trajectory of students' lives. However, without thoughtful intervention from caring educators, this interruption in students' education may have an irreparable destructive impact on students' future. The purpose of this study was to understand the expulsion experience from the point of view of the student in order to represent this critical stakeholder group in future policy and program development, implementation, and decision-making. Students' narratives are a means for members of the educational community to access students' experiences and perceptions in order to understand the impact of expulsion on students' lives. Students' perspectives are presented through thick description in this narrative case study. The experience of these eight students is evidence that expulsion can change students' lives in a positive way. Knowing this, responsible educators must develop interventions for expelled students that channel the positive life-changing potential of this experience. Educators must develop interventions focused on bringing forth protective factors that are documented to increase resilience and to make students less susceptible to the risks inherent in removing them from school. Recommendations for educators and policy-makers are presented to assist educators in preventing expulsion and improving educational and socio-emotional outcomes for expelled students.