Homeostatic dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis and its role in releasing stress hormones such as cortisol has been vigorously studied, and is thought to be a precipitant of PD (Abelson, Khan, Liberzon, & Young, 2007).
However, discriminating views are developing which indicate a divergence between the psychological and physiological precipitants of general anxiety and symptoms of panic. While general anxiety appears to be associated with distal threats or anticipation, PD has been linked with more proximal stressors and activation of the sympathetic neural pathways (Graeff & Zangross Jr. 2010).
Cognitive Affective Mechanism of Panic Disorder
Those with PD may experience a threat related attention bias, which leads individuals to interpret ambiguous events and stimuli as threatening or dangerous (Abend & Bar-Haim, 2013).
Individuals with PD have a propensity for focusing on stimuli they perceive as threatening or fearful. These threats could be external events or internal somatic processes, such as heart rate, which the PD client self-monitors with hypervigilance. White et al. (2011) found that people conditioned to attend towards a threatening situation often began interpreting all ambiguous stimuli as threatening.
Neural imaging has now made it possible to examine the neural reactions to various stimuli for those with mental disorders (Shurick & Gross, 2013).
Using functional magnetic resonance imaging (FMRI), Kircher et al. (2013) found there was no difference between PD and healthy subjects (HS) in their acquisition of conditioned aversive stimuli and conditioned excitatory stimuli.
The results also indicated there was no group x time interaction for activity in the inferior frontal gyrus, amygdala, hippocampus, and medial and lateral prefrontal cortex.
Those diagnosed with PD did have higher levels of negative effect and arousal than healthy subjects. Their findings lend support to the emotional hyperactivity hypothesis for those with PD. The results are in contrast to the belief that PD is the product of maladaptive associative learning, in which fears are learned and applied to related stimuli (Lissek, Rabin, Heller, Lukenbaugh, Geraci, & Pine, 2010).
Sensitivity is a cognitive/affective mechanism of PD related to internal monitoring of bodily functions. People reporting symptoms of PD, will often catastrophize bodily sensations (Gallagher et al., 2013). According to the Diagnostic and Statistical Manual of Mental Disorders Fifth Edition (DSM-5), PD patients often interpret mild physiological symptoms to mean they have a serious medical problem. These interpretation may be more prevalent in those who have had a history with serious illness such as asthma, seizure disorder or cardiovascular disease (APA, 2013).
Another cognitive mechanism associated with PD is self-efficacy. Self-efficacy is the belief in oneself to achieve outcomes they deem successful. PD Patients with strong self-efficacy develop an internal locus of control permitting them to believe they have the ability to control their symptoms of panic. Helping patients develop cognitive mastery over the somatic symptoms of PD, and the ability to cope with these symptoms, has been shown to be one of the most salient factors for recovery in the latter stages of treatment (Gallagher et al., 2013).
Emotions originating panic, fear, and anxiety are related to perception of threat. Graeff and Zangross Jr. (2010) suggest two different types of threats; distal and proximal. With distal threat, the individual engages a risk assessment based behavior, wherein danger is suspected or uncertain, resulting in anxiety. Proximal threat on the other hand, is evoked when danger is near and recognized, engaging the flight or fight response, and activation of the sympathetic nervous system.
The authors suggest that general anxiety disorder (GAD) is connected to distal threat, whereas PD is more commiserate with proximal threats.
Physiological Precipitants of Panic Disorder
The hypothalamic pituitary, adrenal (HPA) axis responds to stress from the hypothalamus by releasing corticotrophin-releasing hormone (CRH) , which stimulates the pituitary gland to release adrenocorticotropic hormone (ACTH). Circulating ACTH in turn triggers the release of cortisol by the adrenal cortex (Plag et al., 2014).
The negative feedback loop is completed when cortisol returns to the hypothalamus and pituitary gland, resulting in the reduction of ACTH and CRH release. (Marieb & Hoehn, 2007).
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