Virtually all living creatures seek the peace of equilibrium. Stress is the potential antagonist with the power to throw that equilibrium off-kilter. A stressor might have a psychological origin (anger, anxiety, or depression), but can just as easily be related to an anatomical insult (such as an infection, a burn, or a heart attack). 

We deal with stress, from the physiological perspective, via the autonomic nervous system (ANS) and the hypothalamic-pituitary adrenal axis (HPA). These two branches interact, and have a bearing on the capacity of the stress response system to adapt. When overwhelmed, chronic diseases may appear, resulting in chronic pain and disability in many cases.

The ANS is the main regulatory system of the body in charge of maintaining essential life-sustaining functions, manifested in the vital signs (blood pressure, pulse, respiration, and temperature). The ANS balances the function of all internal organs, with the heart rate, intestinal function, urination, and sexual activity, among many other variables regulated by the ANS. Evidence has shown that patients with fibromyalgia display dysfunction of the ANS, when studied by means of heart rate variability analysis or the tilt table test. This dysautonomia can be characterized as a sympathetic nervous system that is persistently hyperactive-but hypoactive in the face of stress. This apparent paradox (sympathetic hyperactivity with hypoactivity) results in the pain and insomnia associated with fibromyalgia.

Researchers have studied heart rate variability and polysomnography in patients with fibromyalgia, comparing them with and an age- and sex-matched "healthy" group. The authors found changes consistent with nocturnal sympathetic hyperactivity; such changes coincided with increased nocturnal arousal-awakening episodes. Other investigators have shown that in normal sleeping persons electrocardiographic signs of sympathetic surge precede arousal/awakening episodes. This body of evidence suggests that sympathetic hyperactivity in FM causes the excessive arousal/awakening episodes.

There have been no robust investigations using ANS-modulating agents in fibromyalgia. An open study using the heart medication pindolol, however, reported beneficial effects. It seems unlikely that such agents may reverse fibromyalgia pain completely since neuroplasticity is an irreversible alteration.

Still, it would be interesting to see more studies: Manipulate the heart rate variability, reduce the pain?

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