Presentation Information
[SY-13-01]Relationship between panic disorder and major depression
*Sang-Hyuk Lee (CHA Bundang Medical Center, CHA University School of Medicine(Korea))
Keywords:
Panic Disorder,Major Depression,Comorbidity,Genetics,Neuroimaging
The co-occurrence of panic disorder (PD) and major depression is associated with severe symptom severity, severe occupational impacts, suicidal attempts, and poorer treatment outcomes than either disorder alone. They share several risk factors (e.g., exposure to childhood trauma, information processing biases, heightened neuroticism, and anxiety sensitivity). However, their clinical courses differ, showing that panic attacks often precede depressive symptoms. In addition, cognitive behavioral therapy is more effective for reducing symptoms of PD than depressive symptoms in comorbid presentations.
Genetic studies, particularly genome-wide association studies, have revealed substantial polygenic overlap between PD and depression. This shared genetic vulnerability may stem from pleiotropic loci, such as DCC and RBFOX1, which influence neurodevelopment and synaptic regulation. Genomic structural equation modeling indicates that both disorders load onto a shared internalizing psychopathology factor, suggesting a shared genetic predisposition.
Meanwhile, neuroimaging studies have revealed structural brain differences associated with this comorbidity. Patients with PD and comorbid depression exhibit increased gray matter volume in several brain regions (e.g., posterior cingulate gyrus, medial frontal gyrus, and paracentral lobule), compared to those with PD alone. Notably, posterior cingulate gyrus volume correlates positively with both panic and depressive symptom severity, implicating that altered self-referential emotional processing within the visceromotor network as a potential neural substrate of comorbidity. Functional neuroimaging study showed that both PD and major depression can share elevated amygdala activation in response to negative facial expressions.
In conclusion, the co-occurrence of PD and depression reflects overlapping clinical, genetic, and neurobiological mechanisms, as well as distinct differences in onset patterns, brain structure, and treatment outcome. Recognizing these shared and unique features is crucial for enhancing diagnostic precision and developing targeted interventions for patients with PD, whether or not they also have depression.
Genetic studies, particularly genome-wide association studies, have revealed substantial polygenic overlap between PD and depression. This shared genetic vulnerability may stem from pleiotropic loci, such as DCC and RBFOX1, which influence neurodevelopment and synaptic regulation. Genomic structural equation modeling indicates that both disorders load onto a shared internalizing psychopathology factor, suggesting a shared genetic predisposition.
Meanwhile, neuroimaging studies have revealed structural brain differences associated with this comorbidity. Patients with PD and comorbid depression exhibit increased gray matter volume in several brain regions (e.g., posterior cingulate gyrus, medial frontal gyrus, and paracentral lobule), compared to those with PD alone. Notably, posterior cingulate gyrus volume correlates positively with both panic and depressive symptom severity, implicating that altered self-referential emotional processing within the visceromotor network as a potential neural substrate of comorbidity. Functional neuroimaging study showed that both PD and major depression can share elevated amygdala activation in response to negative facial expressions.
In conclusion, the co-occurrence of PD and depression reflects overlapping clinical, genetic, and neurobiological mechanisms, as well as distinct differences in onset patterns, brain structure, and treatment outcome. Recognizing these shared and unique features is crucial for enhancing diagnostic precision and developing targeted interventions for patients with PD, whether or not they also have depression.