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📝 Acid–base Dysregulation And Chemosensory Mechanisms In Panic Disorder: A Translational Update

Panic disorder (PD) is characterized by spontaneous and recurrent panic attacks that consist of incapacitating periods of acute-onset respiratory, cardiovascular, gastrointestinal, autonomic and cognitive symptoms. PD—which occurs in 6% of Americans1 —typically begins in the second decade of life2 and exhibits a peak prevalence in the third and fourth decades of life.3 Thus, this condition is second only to major depressive disorder in terms of associated debility among psychiatric conditions in the United States.4 Importantly, PD also represents an independent risk factor for suicidality in diagnostically and demographically heterogeneous clinical populations5 and increases the risk of developing other anxiety disorders and secondary mood disorders.2 Yet, many patients suffering from PD are not clinically identified and frequently, do not receive even minimally effective treatment.6 Even still, available psychopharmacologic treatments (for example, selective serotonin reuptake inhibitors, benzodiazepines) and psychotherapies (for example, cognitive behavioral therapy, prolonged exposure therapy, psychodynamic psychotherapy) or the combination of psychotherapy+pharmacotherapy are often only modestly efficacious (for example, Cohen’s d = 0.4–0.6)7,8 and in some cases (for example, benzodiazepines) may be associated with treatment-specific side effects or risks such as sedation or the risk of dependence or tolerance.

Updated on April 8, 2020

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