Cardiac vagal tone as a reliable index of pain chronicity and severity

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I read with interest the publication of Walker et al.20 investigating vagal tone in patients with functional abdominal pain (FAP) using high-frequency heart rate variability (HF-HRV). A considerable number of studies linking chronic pain to autonomic nervous system dysfunction have been conducted by using respiratory sinus arrhythmia (RSA) or a related HF-HRV as an index of cardiac vagal tone.11,19 Walker et al.20 confirmed that more severe (persistent) chronic pain would be associated with greater reduction in HF-HRV power. This effect was interpreted as reduced parasympathetic “braking” of sympathetic activity. However, this was only detected in women. The authors proposed that the effect may reflect a peripheral (eg, gut dysfunction) or central nervous system (eg, pain amplification or poor emotional self-regulation) mechanism. They attributed the latter mechanism to the moderating effect of sex through exacerbation of FAP that is significantly higher in women than in men in the form of poorly regulated pain, distress, or catastrophizing. Indeed, another study confirmed this assumption by showing the same sex effect directly on the relationship between HF-HRV and distress associated with FAP.10 This corresponds with the other authors' conclusion that high sensitivity to stress, especially in women, may contribute to poor absolute reliability of HF-HRV for clinical utility to monitor change in pain severity and to assess effects of therapy intraindividually.1 Indeed, a well-controlled study found that the RSA became insignificantly different in patients with chronic pain when compared with healthy controls after adjusting for sex, age, and different health-related variables, including affective conditions.2 Another study confirmed that it was not clinical pain severity (stable pain condition), but individual differences in subjective reactivity to painful challenge (ie, hyperalgesia) that negatively correlated with HF-HRV.21 Thus, these findings along with ours4,5 seem to compromise the reduction in vagal tone as a reliable marker of chronic pain severity in general, when RSA or HF-HRV is considered its correct index.
However, RSA or HF-HRV alone cannot distinguish between central (vagal outflow or tone from brain) and peripheral (reduced effectiveness of vagal action) mechanisms of autonomic dysfunction.3 Moreover, there are other significant physiological caveats regarding vagal tone interpretation by this metric.8,12 Properly conducted studies indicated that only 1/4 to 1/3 of the individual variation in central vagal tone and its cardiac effectiveness could be explained by RSA alone.8,17 This is because the inspiratory inhibition of the vagal cardiac efferent activity is far from complete, and substantial vagal cardiac control persists during inspiration. Thus, RSA cannot be implicated for the reliable quantitative assessment of impairments in total vagal tone. However, it may be accepted as a clinically significant indicator of partial vagal dysregulation associated with the energy capacity that is used for behavioral coping activity against different challenges (including pain) by physical, affective, or cognitive processes.
Compared with RSA, only a few studies in chronic pain research have used measures of cardiac baroreceptor reflex for assessing vagal activity.14,18 Paradoxically, but despite its low popularity, this reflex is a better predictor of parasympathetic cardiac control than RSA.17 In those few cases when RSA and baroreflex metrics are used together in chronic pain research, their combined reliability is rarely compared with assess and predict pain chronicity and severity.9,15,16 This obscures the impact of related autonomic mechanisms on chronic pain development. Although linear during normal physiological states, the relationship between RSA and cardiac vagal tone as manipulated by baroreflex-mediated effects is quadratic across the entire range.
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