Faintly tired: a systematic review of fatigue in patients with orthostatic syncope

Abstract

Background Orthostatic syncope (transient loss of conscious when standing—fainting) is common and negatively impacts quality of life. Many patients with syncope report experiencing fatigue, sometimes with “brain fog”, which may further impact their quality of life, but the incidence and severity of fatigue in patients with syncope remain unclear. In this systematic review, we report evidence on the associations between fatigue and conditions of orthostatic syncope. Methods We performed a comprehensive literature search of four academic databases to identify articles that evaluated the association between orthostatic syncope [postural orthostatic tachycardia syndrome (POTS), vasovagal syncope (VVS), orthostatic hypotension (OH)] and fatigue. Studies were independently screened using a multi-stage approach by two researchers to maintain consistency and limit bias. Results Our initial search identified 2797 articles, of which 13 met our inclusion criteria (POTS n = 10; VVS n = 1; OH n = 1; VVS and POTS n = 1). Fatigue scores were significantly higher in patients with orthostatic syncope than healthy controls, and were particularly severe in those with POTS. Fatigue associated with orthostatic syncope disorders spanned multiple domains, with each dimension contributing equally to increased fatigue. “Brain fog” was an important symptom of POTS, negatively affecting productivity and cognition. Finally, fatigue was negatively associated with mental health in patients with POTS. Conclusion In conditions of orthostatic syncope, fatigue is prevalent and debilitating, especially in patients with POTS. The consideration of fatigue in patients with orthostatic disorders is essential to improve diagnosis and management of symptoms, thus improving quality of life for affected individuals.

Exaggerated postural sway improves orthostatic cardiovascular and cerebrovascular control

“…Given their robust cardiovascular and cerebrovascular responses to orthostatic stress, it is possible that these findings are limited by a ceiling effect and thus underestimate the potential for benefit in patient populations. Under orthostatic stress, changes in cerebral perfusion are directly related to symptoms of presyncope, and fatigue, both of which contribute to patient burden ( 5 , 77 , 78 ). Given the improvement in ΔCBFv we showed in healthy controls, there is potential for this strategy to have a significant and meaningful impact on symptom management, and ultimately, quality of life for those affected by recurrent syncope or healthy individuals at a high risk for orthostatic syncope (e.g., occupations that require prolonged standing).…”

Poor health-related quality of life in postural orthostatic tachycardia syndrome in comparison with a sex- and age-matched normative population

“…It is also not surprising that the presence of myalgic encephalomyelitis/chronic fatigue syndrome, as well as the severity of orthostatic intolerance, could contribute to lower utility and HrQoL as seen in our hierarchical multiple regression analyses. Previous studies have identified a high prevalence of autonomic dysfunction in those with myalgic encephalomyelitis/chronic fatigue syndrome as well as a predominance of fatigue symptoms among both these populations [ 21 – 23 ]. Additionally, others have shown strongest correlation between symptoms of orthostatic intolerance and the SF-36 physical component scale [ 8 ].…”

The Role of Autonomic Nervous System in Pain Chronicity

“…Sometimes the above constellation of symptoms is explained as an affective component of pain (linking it to the use of the old somatic nociceptive pathways), which is only partially true, as in fully developed CP we deal with neuroplasticity of nervous system where the ANS is responsible for many of these consequences [60][61][62]. Supporting evidence from research shows sympathetic hyperactivity in mental fatigue [63], significant and substantial ANS role in memory consolidation during sleep [64], association of mental fog and autonomic hyperarousal [65], abnormal autonomic sleep regulation in CP [66], and activation of autonomic pathways for chest pain and dyspnoea [67].…”