Vasovagal syncope and unexplained syncope: Concepts, treatments, and future perspectives.

Abstract

Syncope (transient loss of consciousness) can lead to significant psychosocial and physical impairment and have a profound impact on the quality of life of the sufferer. While infrequently attended to, a psychological perspective may have much to offer within a comprehensive treatment plan. The present article reviews 26 articles that evaluate conventional (education, medication, cardiac pacemakers) and to a greater extent, complementary treatments (orthostatic training, applied tension, psychologically oriented interventions) designed to reduce the frequency and negative consequences of vasovagal and unexplained syncope. Applied tension demonstrated the greatest efficacy in reducing the frequency of vasovagal syncope. However, this intervention applies only to patients who experience a prodrome prior to fainting. Currently, no clinically proven treatment exists for patients with unexplained syncope or with vasovagal syncope without a prodromal phase. Suggestions regarding appropriate cognitive and/or behavioural interventions are provided based on the characteristics of the patients. Keywords: vasovagal syncope, unexplained syncope, intervention, psychology, literature review Syncope refers to a loss of consciousness and postural tone followed by a rapid and spontaneous recovery (Sheldon, Koshman, Wilson, Kieser, & Rose, 1998). Syncope can occur abruptly or can be preceded by a prodrome referred to as presyncope. Amongst other symptoms, presyncope is characterised by weakness, nausea, and dizziness (Sheldon et al., 1998). Syncope accounts for 3% of emergency room visits and 1% to 6% of yearly hospitalisations in the United States (Day, Cook, Funkenstein, & Goldman, 1982). Syncope has multiple etiologies involving cardiac, orthostatic, or situational dysfunctions, anomalies in the autonomic nervous system (ANS), or medication use (Lazarus & Mauro, 1996). It is associated with psychological difficulties such as anxiety and depression that are underevaluated and undertreated by medical professionals (D'Antono et al., 2009; Kapoor, Fortunato, Hanusa, & Schulberg, 1995). Yet, patients frequently report psychological distress as a trigger of their syncope (Hupert & Kapoor, 1997; Linzer et al., 1990), and distress negatively impacts on the prognosis of afflicted individuals (D'Antono et al., 2009; Giada et al., 2005; Gracie, Newton, Norton, Baker, & Freeston, 2006; Kapoor et al., 1995). Moreover, psychologists are frequently under the misconception that loss of consciousness is incompatible with an anxiety disorder, especially those involving panic attacks. Yet, D'Antono et al. (2009) reported a panic disorder in up to 14% of their patients with recurrent syncope. Clearly, psychologists have a role to play in the comprehension and care of patients with syncope. The current article will provide background information on the nature of syncope, particularly vasovagal and unexplained syncope, review the efficacy of the various treatment approaches used in these populations, and finally suggest a multimodal approach to the treatment of syncope, particularly in patients with significant distress related to syncope. Vasovagal Syncope Vasovagal syncope (VVS) involves a dysregulation of the ANS (Grubb et al., 1991; Lazarus & Mauro, 1996; Mathias, Deguchi, & Schatz, 2001; Soteriades et al., 2002). The mechanisms involved and the precise sequence of events that lead to WS remain unknown (Grubb et al., 1991; Lazarus & Mauro, 1996). However, some research suggests that VVS involves a chain reaction wherein the sympathetic nervous system is activated, thusly elevating blood pressure and heart rate (Grubb et al, 1991 ; Lazarus & Mauro, 1996). As blood pressure increases, the baroreceptors in the heart, lungs, carotid arteries, and aortic arch trigger an opposing response in the parasympathetic nervous system. This response is characterised by a decrease in heart rate and a relaxation of smooth muscle cells in the blood vessels (vasodilation), provoking a decrease in blood pressure (Henderson & Prabhu, 1997). …