The Neuroanatomical Model of Panic Disorder

Abstract

The etiology of Panic disorder (PD) is related to some neuroanatomical pathways involving conditioned fear, “fear network.” Gorman et al. (2000) postulated that panic originated in an abnormally sensitive “fear network” since the physiological and behavioral consequences of response to a conditioned-fear stimulus appeared to be similar to a panic attack (Gorman et al., 2000). This “fear network” is centered in the amygdala and involves interaction with the hippocampus and medial prefrontal cortex (mPFC). The amygdala receives sensory information from two major pathways: downstream, from the brainstem structures and sensory thalamus, and upstream, from the sensory cortex and via corticothalamic relays, allowing for higher level neurocognitive processing and modulation of sensory information (Andrews et al., 2009; Gorman et al., 2000). Contextual information is stored in memory in the hippocampus and conveyed directly to the amygdala. Major different pathways of the amygdala relevant to anxiety include locus coeruleus (increases noradrenaline release, which contributes to physiological and behavioral arousal); the periaqueductal gray region (results in defensive behavior and postural freezing); the hypothalamic paraventricular nucleus (activates the hypothalamic–pituitary–adrenal axis, releasing adrenocorticoids); the hypothalamic lateral nucleus (activates the sympathetic nervous system); and the parabrachial nucleus (influences respiratory rate) (Andrews et al., 2009; Gorman et al., 2000). Extinction of conditioned fear involves increased activity in the rostral anterior cingulate gyrus and ventral mPFC and decreased activity in the amygdala (Etkin et al., 2006).