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Exploration of intrinsic brain activity in migraine with and without comorbid depression

BACKGROUND: Major depressive disorder is a common comorbidity in migraineurs. Depression may affect the progression and prognosis of migraine. Few studies have examined the brain function in migraineurs that may cause this comorbidity. Here, we aimed to explore depression-related abnormalities in th...

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Detalles Bibliográficos
Autores principales: Ma, Mengmeng, Zhang, Junran, Chen, Ning, Guo, Jian, Zhang, Yang, He, Li
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Milan 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6020083/
https://www.ncbi.nlm.nih.gov/pubmed/29943098
http://dx.doi.org/10.1186/s10194-018-0876-9
Descripción
Sumario:BACKGROUND: Major depressive disorder is a common comorbidity in migraineurs. Depression may affect the progression and prognosis of migraine. Few studies have examined the brain function in migraineurs that may cause this comorbidity. Here, we aimed to explore depression-related abnormalities in the intrinsic brain activity of interictal migraineurs with comorbid depression using resting-state functional magnetic resonance imaging. RESULTS: Significant main effects of migraine and depression provided evidence that migraine and depression jointly affected the left medial prefrontal cortex, which was thought to be the neural basis of self-referential mental activity in previous studies. Abnormalities in this region may contribute to determining the common symptoms of migraine and depression and even result in comorbidity. Additionally, migraineurs with comorbid depression had different developmental trajectories in the right thalamus and fusiform, which were associated with recognizing, transmitting, controlling and remembering pain and emotion. CONCLUSIONS: Based on our findings, the abnormal mPFC which may contribute to determining the common symptoms in migraine and depression and may be a therapeutic target for migraineurs comorbid depression. The different developmental trajectory in thalamus and fusiform indicates that the comorbidity may arise through a specific mechanism rather than simple superposition of migraine and depression.