Abstract
Although the neurobiological mechanisms underlying panic disorder (PD) are not yet clearly understood, increasing amount of evidence from animal and human studies suggests that the amygdala, which plays a pivotal role in neural network of fear and anxiety, has an important role in the pathogenesis of PD. This article aims to (1) review the findings of structural, chemical, and functional neuroimaging studies on PD, (2) relate the amygdala to panic attacks and PD development, (3) discuss the possible causes of amygdalar abnormalities in PD, (4) and suggest directions for future research.
Highlights
Panic disorder (PD) is characterized by repeated panic attacks, often accompanied with anticipatory anxiety, fear of losing control or sanity, or behavioral changes related to the attacks [1]
The aim of this review is to describe and discuss the neuroimaging findings and current hypotheses on the role of amygdala in the pathophysiology of PD
The effect size for group differences was greater in the right amygdala than the left amygdala across all four studies that have reported the amygdalar volume reduction [46,47,48,49]
Summary
Panic disorder (PD) is characterized by repeated panic attacks, often accompanied with anticipatory anxiety, fear of losing control or sanity, or behavioral changes related to the attacks [1]. An epidemiological study conducted with a nationally representative sample estimated the lifetime prevalence of PD to be 4.5% [2]. A panic attack typically develops suddenly and reaches its peak within 10 minutes. Symptoms that accompany panic attacks include palpitations, chest pain, sweating, trembling, smothering, abdominal distress, dizziness, and fear of dying. It is estimated to be highly prevalent, with the percentage of people who experience a panic attack at least once in their lifetime reaching up to 28.3% [2,3,4]. Panic responses, when proximal predatory threat is approaching or is present, are adaptive in the sense that they prepare animals to fight vigorously or flee (“fight or flight response”) [5]. An intense fear response to aroused sympathetic activity is manifested in the absence
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