In a systematic review by Abelson, Khan, Liberzon, and Young (2007), the authors found that dysregulation of the HPA axis is thought to be the result of overcompensation to novel stimuli and hypersensitivity to cues within an individual’s environment, which result in elevated endocrine secretions of cortisol and other stress related hormones.
This increased activity in the HPA axis is found in healthy individuals as well as those with PD. However, individuals with PD were found to be more sensitive to acute contextual stressors, which lead to HPA axis activation (Abelson, Khan, Liberzon, & Young, 2007).
Acute HPA axis activation was explored in a study conducted by Garcia-Leal et al. (2005). The authors used three groups of participants; a PD symptomatic group, a PD drug-treated asymptomatic group, and a healthy control group. The three groups were to give a simulated public speech (SPS). Prior to the SPS, the PD symptomatic group had significantly higher levels of salivary cortisol than the asymptomatic PD and control groups.
In addition, two testing instruments measuring anxiety were administered throughout the process; the Visual Analog Mood Scale (VAMS) and the Bodily System Scale (BSS). A positive and significant correlation was made between all three groups in relation to the VAMS, BSS, and salivary cortisol. However, towards the end of the speech, cortisol levels dropped for all three groups as they habituated to the experience, indicating that HPA axis activation was tied more to anticipatory anxiety.
In a review by Graeff and Zangrossi Jr. (2010), the authors cited studies where panicogenic agents, such as CO2 and lactate did not activate the HPA axis or increase cortisol levels.
In addition, their review also covered animal studies involving rats, where electro-stimulation of the periaqueductal grey matter and maze escape exercises did not increase stress hormones in the plasma cortisol.
The authors suggest that panic and anxiety are different emotional states. These two states react differently to proximal and potential threats. Their contention was that while GAD activates both the HPA axis and sympatho-adrenal axes, PD’s major activation is primarily directed towards the sympathetic axes, with smaller effect on the HPA axis (Graeff & Zangrossi Jr., 2010).
Petrowski et al. (2013) assessed HPA axis response and cortisol levels in both PD patients and healthy controls, when exposed to stress, using the Trier Social Stress Test (TSST). Although both groups did show an increase in cortisol during the TSST, patients in the PD group showed significantly lower levels of cortisol elevation.
The authors postulated the reason for the cortisol attenuation in the PD patients could be because of habituation by the adrenocortical system, as a result of the constant stress perception by those experiencing symptoms of panic frequently.
The stress response of the sympathetic nervous system is more directly related to the symptoms of PD. Through the release of the catecholamines epinephrine and norepinephrine from the adrenal cortex, the sympathetic stress response raises blood pressure and increases heart rate (Plag et al., 2014).
The hypothalamus activates the sympathetic nervous system for the fight or flight response. It does this by sending impulses by way of the preganglionic sympathetic efferent fibers to the adrenal cortex, where epinephrine and norepinephrine are released.
This autonomic response to stress is relatively short-lived and immediate, while the adrenocortical response involving the release of cortisol is a more long-term response (Marieb & Hoehn, 2007).
PD is an anxiety disorder with neurobiological and psychological origins. Recent studies suggest activation of the HPA axis and subsequent release of the stress hormone cortisol has limited effect on the acute stimulation of the sympathetic nervous system that is associated with PD.
However, HPA axis dysregulation has been linked with anticipatory anxiety, and is associated with other anxiety disorders such as GAD. The research indicates maladaptive cognitions associated with threat related attentional bias is correlated with emotional reactivity. Those reporting higher levels of emotional reactivity are more likely to process acute stressors through the fear network, leading to hypothalamic activation of the sympathetic nervous system and subsequent release of norepinephrine from the adrenal cortex.
Steven Powden received his master’s degree in clinical psychology from Forest Institute of Professional Psychology in Springfield, MO. He previously worked as a mental health therapist at Hamilton Centers Inc. and currently teaches psychology courses at Olney Central College in Olney, IL. Steven has specialized interest in integrative medicine, anxiety, and depressive disorders.