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Psychiatry Investig > Epub ahead of print
[Epub ahead of print]
DOI: https://doi.org/10.30773/pi.2018.08.21.1    Published online October 11, 2018.
A Novel Bio-Psychosocial-Behavioral Treatment Model of Panic Disorder
Seon-Cheol Park1, Yong-Ku Kim2
1Department of Psychiatry, Inje University College of Medicine and Haeundae Paik Hospital, Busan, Republic of Korea
2Department of Psychiatry, College of Medicine, Korea University, Ansan Hospital, Ansan, Republic of Korea
Correspondence: Yong-Ku Kim ,Tel: +82-31-412-4930, Fax: +82-31-312-4224, Email: yongku@korea.ac.kr
Received: June 30, 2018   Revised: August 9, 2018   Accepted: August 21, 2018   Published online: October 11, 2018
Abstract
To conceptualize a novel bio-psychosocial-behavioral treatment model of panic disorder (PD), it is necessary to completely integrate behavioral, psychophysiological, neurobiological, and genetic data. Molecular genetic research on PD is specifically focused on neurotransmitters, including serotonin, neuropeptides, glucocorticoids, and neurotrophins. Although pharmacological interventions for PD are currently available, the need for more effective, faster-acting, and more tolerable pharmacological interventions is unmet. Thus, glutamatergic receptor modulators, orexin receptor antagonists, corticotrophin-releasing factor 1 receptor antagonists, and other novel mechanism-based anti-panic therapeutics have been proposed. Research on the neural correlates of PD is focused on the dysfunctional “cross-talk” between emotional drive (limbic structure) and cognitive inhibition (prefrontal cortex) and the fear circuit, which includes the amygdala-hippocampus-prefrontal axis. The neural perspective regarding PD supports the idea that cognitive-behavioral therapy normalizes alterations in top-down cognitive processing, including increased threat expectancy and attention to threat. Consistent with the concept of “personalized medicine,” it is speculated that Research Domain Criteria can enlighten further treatments targeting dysfunctions underlying PD more precisely and provide us with better definitions of moderators used to identify subgroups according to different responses to treatment. Structuring of the “negative valence systems” domain, which includes fear/anxiety, is required to define PD. Therefore, targeting glutamate- and orexin-related molecular mechanisms associated with the fear circuit, which includes the amygdala-hippocampus-prefrontal cortex axis, is required to define a novel bio-psychosocial-behavioral treatment model of PD.
Key words   Bio-psychosocial-behavioral, Cognitive-behavioral therapy, Fear circuit, Research Domain Criteria, Panic disorder
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