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Achieving mental health equity requires that nursing address structures that impede the ability of individuals and populations to achieve optimal mental health. Consistent with calls for structural change, this paper intends to promote structural competency in mental health nursing by applying this concept to the field. The first half of the paper discusses structural competency and key concepts vital for its development, namely, structure, social influencers of mental health, equity, structural justice, and historical understanding. In the second half we apply structural competency to mental health nursing at the educational, practice and system levels and conclude with recommendations for change. 相似文献
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Vieri Grandi Antonello Baldo Emilio Berti Pietro Quaglino Serena Rupoli Mauro Alaibac Silvia Alberti-Violetti Paolo Amerio Valeria Brazzelli Pier Luigi Bruni Piergiacomo Calzavara-Pinton Aurora Parodi Emanuele Cozzani Martina Burlando Maria Concetta Fargnoli Daniele Gambini Paolo Iacovelli Alessia Pacifico Caterina Longo Giuseppe Monfrecola Alberico Motolese Giorgio Mozzicafreddo Carlo Cota Paolo Pigatto Alessandro Pileri Paola Savoia Marco Simonacci Marina Venturini Annamaria Offidani Elisa Molinelli Michele Pellegrino Emanuele Trovato Roberta Piccinno Karl Lawrence Nicola Pimpinelli 《Photodermatology, photoimmunology & photomedicine》2021,37(4):334-342
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Maria A. Rocca Roberta Messina Bruno Colombo Andrea Falini Giancarlo Comi Massimo Filippi 《Journal of neurology》2014,261(2):350-357
Morphometric MRI studies in adult patients with migraine have consistently demonstrated atrophy of several gray matter (GM) regions involved in pain processing. We explored the regional distribution of GM and white matter (WM) abnormalities in pediatric patients with episodic migraine and their correlations with disease clinical manifestations. Using a 3.0 T scanner, brain T2-weighted and 3D T1-weighted scans were acquired from 12 pediatric migraine patients and 15 age-matched healthy controls. GM and WM volumetric abnormalities were estimated using voxel-based morphometry (p < 0.05, family-wise error corrected). Compared to controls, pediatric migraine patients experienced a significant GM atrophy of several regions of the frontal and temporal lobes which are part of the pain-processing network. They also had an increased volume of the right putamen. The left fusiform gyrus had an increased volume in patients with aura compared to patients without aura and controls, whereas it was significantly atrophied in patients without aura when compared to the other two groups. No abnormalities of WM volume were detected. In migraine patients, regional GM atrophy was not correlated with disease duration and attack frequency, whereas a negative correlation was found between increased volume of the putamen and disease duration (r = ?0.95, p < 0.05). These results show that GM morphometric abnormalities do occur in pediatric patients with migraine. The presence of such abnormalities early in the disease course, and the absence of correlation with patient clinical characteristics suggest that they may represent a phenotypic biomarker of this condition. 相似文献
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Roberto Keller Roberta Basta Luana Salerno Maurizio Elia 《Neurological sciences》2017,38(8):1353-1361
Autism spectrum disorders (ASD) are neurodevelopmental disorders typically diagnosed in childhood, characterized by core social dysfunction, rigid and repetitive behaviors, restricted interests, and abnormal sensorial sensitivity. ASD belong to multifactorial diseases: both genetic and environmental factors have been considered as potential risk factors for their onset. ASD are often associated with neurological conditions: the co-occurrence of epilepsy is well documented and there is also evidence of a higher prevalence of EEG abnormalities with 4–86% of individuals with ASD presenting epileptiform or not epileptiform EEG abnormalities. The presence of epilepsy in people with ASD may be determined by several structural alterations, genetic conditions, or metabolic dysfunctions, known to play a role in the emergence of both epilepsy and autism. The purpose of this article is to discuss precisely such latter cause of the autism–epilepsy association, focusing specifically on those “synaptic genes,” whose mutation predisposes to both the diseases. 相似文献