Abstract
Panic disorder (PD), a complex anxiety disorder characterized by recurrent panic attacks, represents a poorly understood psychiatric condition which is associated with significant morbidity and an increased risk of suicide attempts and completed suicide. Recently however, neuroimaging and panic provocation challenge studies have provided insights into the pathoetiology of panic phenomena and have begun to elucidate potential neural mechanisms that may underlie panic attacks. In this regard, accumulating evidence suggests that acidosis may be a contributing factor in induction of panic. Challenge studies in patients with PD reveal that panic attacks may be reliably provoked by agents that lead to acid–base dysbalance such as CO2 inhalation and sodium lactate infusion. Chemosensory mechanisms that translate pH into panic-relevant fear, autonomic, and respiratory responses are therefore of high relevance to the understanding of panic pathophysiology. Herein, we provide a current update on clinical and preclinical studies supporting how acid–base imbalance and diverse chemosensory mechanisms may be associated with PD and discuss future implications of these findings.
Highlights
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
Excellent reviews on this topic have appeared previously,[15,16,17] here we focus on (1) current status on pH homeostasis, clinical studies of acid–base physiology and pathophysiology in patients with PD (2) preclinical rodent models of PD, especially those focusing on interoceptive pH imbalance and acid-chemosensory systems recruited in panic-like behaviors, and last (3) synthesize these findings to develop a working neurobiological model of PD that involves dysregulation of central acid sensing and associated circuitry, and (4) translational
It is clear from the clinical and preclinical findings discussed in preceding sections that interoceptive acid/base imbalance and pH chemosensory mechanisms may contribute to certain aspects of PD, uncued panic attacks
Summary
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. May link the panicogenic action of CO2 inhalation and doxapram administration.[85] In addition, increased respiratory drive by patients with PD show exaggerated lactic acid production in doxapram may aggravate a pre-existing respiratory abnormality in response to alkalosis evoked by sodium lactate infusion suggestive of increased compensatory drive and impaired acid–base buffering in these individuals.[17] Other studies reported that a PD. Regarding chemosensory serotonergic neurons in the medullary raphe patients with PD, doxapram has been examined in several studies, nucleus’) underscores the role of the 5-HT system in translation of given its tendency to cause hyperventilation In this challenge, doxapram (0.5 mg kg − 1, IV)[39,80,81] produces panic attacks that phenomenologically mirror spontaneous panic attacks with pH fluctuations to panic-relevant ventilatory responses. Multiple chemosensitive areas within the Sensory stimuli phobic cues stressors
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