BACKGROUND: Although brain neurochemistry is thought to play a role in the development of premenstrual dysphoric disorder (PMDD), neuroimaging studies of PMDD are sparse. We examined the extent to which gray matter (GM) abnormalities were present in women with PMDD compared to healthy controls. METHODS: 3.0T magnetic resonance imaging scans of 15 women with PMDD and 15 healthy controls were compared using optimized voxel-based morphometry (VBM) analysis. A regression analysis was used to assess the relationship between GM density and PMDD-symptom severity. RESULTS: Our results showed significantly increased GM density in the hippocampal cortex and significantly decreased GM density in the parahippocampal cortex among women with PMDD compared to healthy controls. However, these GM abnormalities were not significantly associated with the severity of PMDD. LIMITATION: Our inferences of the relationships between structural alterations and PMDD are drawn from a small sample, which may have increased the likelihood of type I error. CONCLUSIONS: GM abnormalities in limbic and paralimbic cortices were found to be associated with the pathophysiology of PMDD. Etiology of PMDD is likely related to emotional processing and self-regulation. Our findings provide a basis of neurobiological model for PMDD.
BACKGROUND: Although brain neurochemistry is thought to play a role in the development of premenstrual dysphoric disorder (PMDD), neuroimaging studies of PMDD are sparse. We examined the extent to which gray matter (GM) abnormalities were present in women with PMDD compared to healthy controls. METHODS: 3.0T magnetic resonance imaging scans of 15 women with PMDD and 15 healthy controls were compared using optimized voxel-based morphometry (VBM) analysis. A regression analysis was used to assess the relationship between GM density and PMDD-symptom severity. RESULTS: Our results showed significantly increased GM density in the hippocampal cortex and significantly decreased GM density in the parahippocampal cortex among women with PMDD compared to healthy controls. However, these GM abnormalities were not significantly associated with the severity of PMDD. LIMITATION: Our inferences of the relationships between structural alterations and PMDD are drawn from a small sample, which may have increased the likelihood of type I error. CONCLUSIONS:GM abnormalities in limbic and paralimbic cortices were found to be associated with the pathophysiology of PMDD. Etiology of PMDD is likely related to emotional processing and self-regulation. Our findings provide a basis of neurobiological model for PMDD.
Authors: Sophie Schweizer-Schubert; Jennifer L Gordon; Tory A Eisenlohr-Moul; Samantha Meltzer-Brody; Katja M Schmalenberger; Radoslaw Slopien; Anna-Lena Zietlow; Ulrike Ehlert; Beate Ditzen Journal: Front Med (Lausanne) Date: 2021-01-18
Authors: Peter J Schmidt; Karen F Berman; Shau-Ming Wei; Erica B Baller; Pedro E Martinez; Allison C Goff; Howard J Li; Philip D Kohn; J Shane Kippenhan; Steven J Soldin; David R Rubinow; David Goldman Journal: Transl Psychiatry Date: 2021-04-08 Impact factor: 6.222