Avaliação de pacientes com síndrome da apneia obstrutiva do sono, com e sem miopatia faríngea, utilizando neuroimagem cerebral
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2020-08-07
Autores
Baima, Camila Bonfanti
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Universidade Estadual Paulista (Unesp)
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Introdução: Elementos que prejudicam a anatomia das vias aéreas superiores ou a função muscular (por exemplo, neuromiopatia da faringe) contribuem para a síndrome da apneia obstrutiva do sono (SAOS). A imagem estrutural do encéfalo pode diferir em pacientes com SAOS de acordo com a disfunção do músculo dilatador da faringe. A imagem por ressonância magnética (IRM) com morfometria baseada em voxel (VBM) e morfometria baseada em superfície (SBM) foi usada para investigar esta hipótese. Métodos: Um total de 29 pacientes com SAOS e 32 controles foram submetidos à IRM 3T encefálica. Imagens volumétricas em T1 foram utilizadas para análise estrutural. Foi realizada eletroneuromiografia faríngea; os pacientes com SAOS foram classificados como tendo ou não neuromiopatia faríngea associada. As análises VBM e SBM foram realizadas usando os softwares SPM12 e CAT12. O processamento da imagem era padrão. Parâmetros da superfície cortical e volumes de substância cinzenta e branca de participantes com SAOS com e sem neuromiopatia foram comparados com os de controles. Resultados: Dos pacientes com SAOS, 18 pacientes realizaram o exame de eletroneuromiografia faríngea, sendo que 11 apresentaram SAOS com neuromiopatia faríngea e 7 tinham SAOS sem neuromiopatia (eletroneuromiografia faríngea normal). Comparando esses grupos com os controles, a VBM revelou: quatro regiões (volume total de 15.368 mmᶟ) para pacientes com neuromiopatia, o maior grupo no cerebelo esquerdo (9263 mmᶟ, p = 0,0001) e três regiões (total 8971 mmᶟ) para pacientes sem neuromiopatia, o maior no cerebelo esquerdo (5017 mmᶟ, p = 0,002). Pacientes com SAOS com neuromiopatia apresentaram maior proporção de atrofia (p <0,0001). O SBM mostrou anormalidades em pacientes sem neuromiopatia [espessura cortical diminuída, giro pré-central esquerdo (672 vértices, p = 0,04); aumento da complexidade cortical, giro temporal médio direito (578 vértices, p = 0,032). Conclusão: As áreas danificadas foram maiores nos pacientes com SAOS e neuromiopatia faríngea comparados aos pacientes sem neuromiopatia, sugerindo diferenças no envolvimento encefálico. Pacientes com SAOS e neuromiopatia podem ser mais suscetíveis a danos encefálicos.
Study objectives: Elements impairing upper airway anatomy or muscle function (e.g. pharyngeal neuromyopathy) contribute to obstructive sleep apnea syndrome (OSAS). Structural brain imaging may differ in patients with OSAS according to dilator muscle dysfunction. Magnetic resonance imaging (MRI) with voxel-based morphometry (VBM) and surface-based morphometry (SBM) was used to investigate this hypothesis. Methods: Twent-nine patients with OSAS and 32 controls underwent 3T brain MRI. T1 volumetric images were used for structural analysis. Pharyngeal electroneuromyography was performed; patients with OSAS were classified as with or without neuromyopathy. VBM and SBM analyses were conducted using SPM12 and CAT12 software. Image processing was standard. Cortical surface parameters and gray and white matter volumes from participants with OSAS with and without neuromyopathy were compared with those from controls. Results: Of the patients with OSAS, 18 patients underwent pharyngeal electromyography, 11 of whom had OSAS with neuromyopathy and seven patients had OSAS without neuromyopathy (normal pharyngeal electroneuromyography). Comparing these groups to the controls, VBM revealed: four clusters (total volume 15,368 mmᶟ) for patients with neuromyopathy, the largest cluster in the left cerebellum (9263 mmᶟ, p = 0.0001), and three clusters (total 8971 mm3) for patients without neuromyopathy, the largest cluster in the left cerebellum (5017 mmᶟ, p = 0.002). Patients with OSAS with neuromyopathy showed increased proportion of atrophy (p < 0.0001). SBM showed abnormalities in patients without neuromyopathy [decreased cortical thickness, left precentral gyrus (672 vertices, p = 0.04); increased cortical complexity, right middle temporal gyrus (578 vertices, p = 0.032)]. Conclusion: Damaged areas were larger in patients with OSAS with than in those without neuromyopathy, suggesting differences in brain involvement. Patients with OSAS and neuromyopathy may be more susceptible to cerebral damage.
Study objectives: Elements impairing upper airway anatomy or muscle function (e.g. pharyngeal neuromyopathy) contribute to obstructive sleep apnea syndrome (OSAS). Structural brain imaging may differ in patients with OSAS according to dilator muscle dysfunction. Magnetic resonance imaging (MRI) with voxel-based morphometry (VBM) and surface-based morphometry (SBM) was used to investigate this hypothesis. Methods: Twent-nine patients with OSAS and 32 controls underwent 3T brain MRI. T1 volumetric images were used for structural analysis. Pharyngeal electroneuromyography was performed; patients with OSAS were classified as with or without neuromyopathy. VBM and SBM analyses were conducted using SPM12 and CAT12 software. Image processing was standard. Cortical surface parameters and gray and white matter volumes from participants with OSAS with and without neuromyopathy were compared with those from controls. Results: Of the patients with OSAS, 18 patients underwent pharyngeal electromyography, 11 of whom had OSAS with neuromyopathy and seven patients had OSAS without neuromyopathy (normal pharyngeal electroneuromyography). Comparing these groups to the controls, VBM revealed: four clusters (total volume 15,368 mmᶟ) for patients with neuromyopathy, the largest cluster in the left cerebellum (9263 mmᶟ, p = 0.0001), and three clusters (total 8971 mm3) for patients without neuromyopathy, the largest cluster in the left cerebellum (5017 mmᶟ, p = 0.002). Patients with OSAS with neuromyopathy showed increased proportion of atrophy (p < 0.0001). SBM showed abnormalities in patients without neuromyopathy [decreased cortical thickness, left precentral gyrus (672 vertices, p = 0.04); increased cortical complexity, right middle temporal gyrus (578 vertices, p = 0.032)]. Conclusion: Damaged areas were larger in patients with OSAS with than in those without neuromyopathy, suggesting differences in brain involvement. Patients with OSAS and neuromyopathy may be more susceptible to cerebral damage.
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Síndrome da apneia obstrutiva do sono, Imagem por ressonância magnética, Neuroimagem, Morfometria, Músculos Doenças, Medicina do sono, Obstructive sleep apnea, Magnetic resonance imaging, Voxel-based morphometry, Surface-based morphometry