Search results for: Robyn Therese Munnick

Authors: Suzanne Phibbs, Christine Kenney, Robyn Richardson

Abstract:

The Sendai Framework for Disaster Risk Reduction called for the inclusion of indigenous people in the design and implementation of all hazard policies, plans, and standards. Ensuring that indigenous knowledge practices were included alongside scientific knowledge about disaster risk was also a key priority. Indigenous communities have specific knowledge about climate and natural hazard risk that has been developed over an extended period of time. However, research within indigenous communities can be fraught with issues such as power imbalances between the researcher and researched, the privileging of researcher agendas over community aspirations, as well as appropriation and/or inappropriate use of indigenous knowledge. This paper documents the process of working alongside a Māori community to develop a successful community-led research project. Research Design: This case study documents the development of a qualitative community-led participatory project. The community research project utilizes a kaupapa Māori research methodology which draws upon Māori research principles and concepts in order to generate knowledge about Māori resilience. The research addresses a significant gap in the disaster research literature relating to indigenous knowledge about collective hazard mitigation practices as well as resilience in rurally isolated indigenous communities. The research was designed in partnership with the Ngāti Raukawa Northern Marae Collective as well as Ngā Wairiki Ngāti Apa (a group of Māori sub-tribes who are located in the same region) and will be conducted by Māori researchers utilizing Māori values and cultural practices. The research project aims and objectives, for example, are based on themes that were identified as important to the Māori community research partners. The research methodology and methods were also negotiated with and approved by the community. Kaumātua (Māori elders) provided cultural and ethical guidance over the proposed research process and will continue to provide oversight over the conduct of the research. Purposive participant recruitment will be facilitated with support from local Māori community research partners, utilizing collective marae networks and snowballing methods. It is envisaged that Māori participants’ knowledge, experiences and views will be explored using face-to-face communication research methods such as workshops, focus groups and/or semi-structured interviews. Interviews or focus groups may be held in English and/or Te Reo (Māori language) to enhance knowledge capture. Analysis, knowledge dissemination, and co-authorship of publications will be negotiated with the Māori community research partners. Māori knowledge shared during the research will constitute participants’ intellectual property. New knowledge, theory, frameworks, and practices developed by the research will be co-owned by Māori, the researchers, and the host academic institution. Conclusion: An emphasis on indigenous knowledge systems within the Sendai Framework for Disaster Risk Reduction risks the appropriation and misuse of indigenous experiences of disaster risk identification, mitigation, and response. The research protocol underpinning this project provides an exemplar of collaborative partnership in the development and implementation of an indigenous project that has relevance to policymakers, academic researchers, other regions with indigenous communities and/or local disaster risk reduction knowledge practices.

Keywords: community resilience, indigenous disaster risk reduction, Maori, research methods

Procedia PDF Downloads 106

Authors: Sinead Morrison, Ann Swillen, Therese Van Amelsvoort, Samuel Chawner, Elfi Vergaelen, Michael Owen, Marianne Van Den Bree

Abstract:

22q11.2 Deletion Syndrome (22q11.2DS) is caused by the deletion of approximately 60 genes on chromosome 22 and is associated with high rates of neurodevelopmental disorders such as Attention Deficit Hyperactivity Disorder (ADHD) and Autism Spectrum Disorders (ASD). The presentation of these disorders in 22q11.2DS is reported to be comparable to idiopathic forms and therefore presents a valuable model for understanding mechanisms of neurodevelopmental disorders. Cognitive deficits are thought to be a core feature of neurodevelopmental disorders, and possibly manifest in behavioural and emotional problems. There have been mixed findings in 22q11.2DS on whether the presence of ADHD or ASD is associated with greater cognitive deficits. Furthermore, the influence of developmental stage has never been taken into account. The aim was therefore to examine whether the presence of ADHD or ASD was associated with cognitive deficits in childhood and/or adolescence in 22q11.2DS. We conducted the largest study to date of this kind in 22q11.2DS. The same battery of tasks measuring processing speed, attention and spatial working memory were completed by 135 participants with 22q11.2DS. Wechsler IQ tests were completed, yielding Full Scale (FSIQ), Verbal (VIQ) and Performance IQ (PIQ). Age-standardised difference scores were produced for each participant. Developmental stages were defined as children (6-10 years) and adolescents (10-18 years). ADHD diagnosis was ascertained from a semi-structured interview with a parent. ASD status was ascertained from a questionnaire completed by a parent. Interaction and main effects of cognitive performance of those with or without a diagnosis of ADHD or ASD in childhood or adolescence were conducted with 2x2 ANOVA. Significant interactions were followed up with t-tests of simple effects. Adolescents with ASD displayed greater deficits in all measures (processing speed, p = 0.022; sustained attention, p = 0.016; working memory, p = 0.006) than adolescents without ASD; there was no difference between children with and without ASD. There were no significant differences on IQ measures. Both children and adolescents with ADHD displayed greater deficits on sustained attention (p = 0.002) than those without ADHD. There were no significant differences on any other measures for ADHD. Magnitude of cognitive deficit in individuals with 22q11.2DS varied by cognitive domain, developmental stage and presence of neurodevelopmental disorder. Adolescents with 22q11.2DS and ASD showed greater deficits on all measures, which suggests there may be a sensitive period in childhood to acquire these domains, or reflect increasing social and academic demands in adolescence. The finding of poorer sustained attention in children and adolescents with ADHD supports previous research and suggests a specific deficit which can be separated from processing speed and working memory. This research provides unique insights into the association of ASD and ADHD with cognitive deficits in a group at high genomic risk of neurodevelopmental disorders.

Keywords: 22q11.2 deletion syndrome, attention deficit hyperactivity disorder, autism spectrum disorder, cognitive development

Procedia PDF Downloads 126