Brain Activity During Anxiety Attacks
Key Neural Circuits Involved
- The amygdala becomes hyperactive during anxiety attacks, serving as the brain's primary fear processing center that triggers the body's alarm system 1, 2
- The prefrontal cortex (PFC), which normally regulates emotional responses, shows decreased functional connectivity with the amygdala, reducing its ability to control fear responses 3
- The hypothalamus activates the sympathoexcitatory neural circuits, leading to the physical symptoms of anxiety through the hypothalamic-pituitary-adrenal (HPA) axis 2, 4
Neurochemical Changes
- Sympathoexcitatory neural circuits undergo disinhibition, resulting in increased catecholamine (adrenaline and noradrenaline) release 1, 4
Functional Connectivity Disruptions
- The balance between habitual and goal-directed behavior is altered, with increased habit formation associated with hyperactivation of the caudate nucleus 3
Autonomic Nervous System Response
- After threat detection, the prefrontal cortex and amygdala regulate heart rate through a pathway involving the nucleus ambiguus 2
- After threat detection, the prefrontal cortex and amygdala regulate heart rate through a pathway involving the dorsal nucleus of the vagus nerve 1
- After threat detection, the prefrontal cortex and amygdala regulate heart rate through a pathway involving the vagus nerve itself, which connects to the sinoatrial node of the heart 1, 2
- This activation leads to the classic "fight-or-flight" response with increased heart rate, blood pressure, and respiratory rate 2
- In some cases, parasympathetic activation may occur, leading to fear-induced bradycardia (slowing of heart rate) 1
Inflammatory Processes
- Anxiety states activate microglia (brain immune cells), leading to neuroinflammation 5, 6
- Pro-inflammatory cytokines including IL-1β, IL-6, and TNF-α become elevated, contributing to anxiety symptoms 6, 4
- The ATP-P2X7 receptor pathway in microglia activates the NLRP3 inflammasome, further promoting inflammation 7