Panic disorder has multiple findings that suggest a biological basis:
- There are various agents that can induce panic attacks in normal people and in in those with panic disorder. These agents include sodium lactate, carbon dioxide, caffeine, serotonergic agents, yohimbine, and cholecystokinin (Bourin et al., 1998). So these findings suggest chemical compounds can induce panic attacks.
- Subjects with panic disorder have an amygdala and hippocampus which are smaller in volume compared to healthy controls. The brainstem nuclei, mainly in the rostral pons, can have increased volume, and this is believed to be involved with autonomic arousal circuitry. And cortical areas having smaller volume in subjects with panic disorder include the anterior cingulated cortex (ACC), orbitofrontal cortex (OFC), temporal cortex, and the frontal cortex (Del Casale et al, 2013). So people with panic disorder have different sized brain structures than people without panic disorder.
- During experimental panic attacks, functional neuroimaging has shown increased activity in the insula and upper brain stem (including the periaqueductal gray- PAG), and decreased activity in the ACC. Volumetric analysis of brain MRI has shown increased volume in the insula and upper brain stem, and decreased volume in the ACC of panic disorder subjects at rest, compared to healthy controls (Graeff and Del-Ben, 2008). So this study revealed that panic attacks have hyperactivity of certain brain areas, and there are structural differences of brain areas in those with panic disorder when compared to those without panic disorder.
These findings suggest a biological basis for panic disorder. Although these brain areas are implicated in the pathophysiology of panic disorder, there are currently no biological tests utilized clinically to confirm the diagnosis.