Abstract

BackgroundThis study aimed to identify common and exclusive neural substrates underlying pure generalized anxiety disorder (GAD, G0) and comorbid GAD and depression (G1), assess whether they could assist in diagnosis and prediction of treatment response, and determine whether comorbid depression in GAD patients would change their neural plasticity. MethodsA longitudinal study was conducted, involving 98 patients (40 in the G0 group and 58 in the G1 group) and 54 healthy controls (HCs). The fractional amplitude of low-frequency fluctuations (fALFF), support vector machine, and support vector regression were employed. ResultsThe shared neural underpinnings across the two subtypes of GAD were hyperactivity in the right cerebellar Crus II and inferior temporal gyrus and hypoactivity in the right postcentral gyrus. The G1 group showed hypoactivity in the frontal gyrus, compared with HCs, and hyperactivity in the middle temporal gyrus, compared with the G0 group or HCs. These alterations could aid in diagnosis and the prediction of treatment response with high accuracy. After treatment, both the G1 and G0 groups showed higher fALFF than those before treatment but were located in different brain regions. LimitationsThe study was performed in a single center and subjects showed a fairly homogeneous ethnicity. ConclusionsCommon and exclusive neural substrates underlying the two subtypes of GAD were identified, which could assist in diagnosis and the prediction of treatment response. Pharmacotherapy for the two subtypes of GAD recruited different pathways, suggesting that comorbid depression in GAD patients would change their neural plasticity.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.