Psychophysiological Markers of Anxiety Disorders and Anxiety Symptoms

Abstract

In anxiety research, relative few psychophysiological studies have been conducted. In this chapter, we presented previous studies that used different psychophsiological markers that can be further utilized in future research. However, there are a few things to be considered when psychophysiological markers are used in anxiety studies, first of which may be genetic factors. Genetic factors influence vulnerability to anxiety disorders. There are several genetic polymorphisms associated with anxiety disorders among which are the serotonin-transporterlinked polymorphic region (5-HTTLPR), the Catechol-O-methyltransferase (COMT), and the brain-derive neurotrophic factor (BDNF) gene variants. We first presented studies that invsestigated the relationship between these genetics variants and anxiety disorders. Also, it has been suggested that anxiety disorders are characterized by abnormal neural activity— amygdala hyperactivity and dysfunctional prefrontal activity—and cognitive bias favoring threat-relevant stimuli (Cisler et al., 2010; McClure et al., 2007; Nitschke et al., 2009; Whalen et al., 2008). We will present different psychophysiological markers that have been used to study dysfunctional neural, serotonergic, cognitive and autonomic activites associated with anxiety disorders. They include: (1) a loudness dependence of the auditory evoked potential (LDAEP) which is proposed to be associated with serotonin activity, (2) various components of the event-related potentials [P1, P2, N300, P3b, early posterior negativity (EPN), late positive potential (LPP), and error-related negativity (ERN)] that reflect altered neural activity in anxiety disorders and (3) the reduced heart rate variability (HRV) which indicates autonomic dysregulation associated with increased sympathetic and decreased vagal control of the heart. Particularly, in this chapter, we introduced the loudness of the auditory evoked potential (LDAEP) as a possible psychophysiological marker that can be utilized in anxiety research. Our previous studies revealed that patients with different subtypes of anxiety disorders produced distinctive LDAEPs and that the LDAEP could play an important role in predicting the efficacy of selective serotonin reuptake inhibitor (SSRI) treatment in anxiety disorders (Park et al., 2010, 2011). We suggest that utilizing the LDAEP along with other various ERP components indicating neural and cognitive dysfunctions associated with anxiety disorders may enhance our understanding of the etiology and maintenance of anxiety disorders. Also, it is important to understand how they interact with each other and with other environmental stressor to reinforce or to exacerbate anxiety symptoms (see Figure 1). Of clinical relevance is whether these psychophysiological markers may play a role in predicting clinical outcome of different treatment.