Afferent Vagal Information and Pain Perception

Rollin McCraty, Ph.D., Director of Research

Institute of HeartMath, Boulder Creek, CA
Numerous reports from individuals who have learned HeartMath techniques indicate that they
are able to modulate pain levels by utilizing the tools. This is true of both visceral pain, such as
angina and joint pain, and coetaneous pain, such as a stubbed toe or scrape. Increased afferent
activity associated with coherent heart rhythms evoked by the application of these techniques
affect the neural mechanisms involved in pain reduction. . A number of studies have shown that
an increase in afferent vagal activity inhibits the flow of pain signals traveling to the brain.
Several mechanisms have been identified which explain how increased vagal afferent activity
decreases pain sensitivity and increases the pain threshold.
Sensory receptors in the skin respond to three types of stimuli: mechanoreceptors that transmit
information about tactile stimulation, nociceptors designed to signal noxious events that result in
the perception of coetaneous pain, and thermoreceptors that transmit information about cold and
warm temperatures. When specific areas of the body are stimulated, a pain sensation is reported
proportional to the intensity of the stimulus and localized to the area where the stimulus is
applied. Sensations from the internal organs are characteristically more complicated than those
from the skin. Internal organs are innervated with many receptors whose activation does not
appear to evoke a conscious experience, but instead result in a reflex action. Some organ
receptors generate sensations that are initially sensed as nonpainful (bladder fullness, increases in
heart rate, gastric distention), but if the stimulus persists, the sensations can become increasingly
unpleasant and painful even when the quality of the stimulus has remained the same. In addition,
visceral sensations, in most forms, are poorly localized and can be referred to somatic structures
most commonly in physical proximity to the threatened organ and create a challenge for
diagnosis.
Information from the heart and other internal organs is carried to cell bodies located in the dorsal
root ganglia of the spinal segments. Spinal segments receiving information from the heart are
distinct from those of the gallbladder, kidney and urinary bladder, but considerable overlap exists
when visceral organs are found in the same region of the body. Axons from neurons in the dorsal
root ganglia penetrate the spinal cord and convey afferent information to very localized regions
of the gray matter in the cord. From there, afferent information ascends in pathways to both the
lateral and medial thalamus. Cells of the lateral thalamus then project to the primary
somatosensory cortex where the location, intensity and duration of the painful stimulus are
analyzed. Information is sent from the medial thalamus to the insular cortex, amygdala and
cingulate gyrus, where motivational-affective components of pain, including autonomic
adjustments occur. This is called the spinothalamic track (STT) and, although not the only pain
pathway, is the main and most studied system for transmitting visceral sympathetic afferent
information to the brain. For a detailed review, see references 1, 2.

Afferent fibers in the vagus nerve also participate in afferent flow of pain signals, but this
discussion focuses on their role in the modulation of pain signals in the spinothalamic track. As
mentioned in detail elsewhere, vagal afferent signals decrease efferent sympathetic activity and
effect hemodynamic activity and the activity in a number of subcortical areas of the brain. An
increase in vagal activity also causes a general inhibitory effect at most levels of the spinal cord
on neurons that transmit nociceptive information to the thalamus and then to areas of the brain

involved in pain perception.2 Vagal afferent fibers terminate primarily in the caudal medulla of
the brain stem and nucleus tractus solitarius (NTS) and evidence shows that suppression of spinal
neuronal activity is dependent upon the NTS connections. It has been demonstrated that the
cardiac branch of the vagus nerve makes up the major contribution for the inhibitory responses
on the spinal pain signals and that left vagal stimulation suppresses approximately 60% of the
STT cells.3
Data from numerous studies suggests that there is both a supraspinal inhibition from higher brain
centers acting downward on the spinal neurons and a direct inhibitory effect from a group of
vagal afferent fibers that enter the brainstem and descend to the spinal segments before
synapsing in the medulla.1, 4 A number of candidate regions of the brain stem have been
implicated; the evidence from numerous studies suggests that the locus coeruleus region of the
pons is one of the important relays for producing vagal suppression of SST cells. Information
originating from the vagus most likely is processed in this population of cells and then sends a
volley of activity down the large number of axons that travel down into the spinal cord.
In summary, the predominant effect of increased vagal afferent activity is suppression of somatic
and visceral input into STT cells, which provides a mechanism for increasing pain threshold and
decreasing pain sensitivity.
For more information on HeartMath, please contact Tom Beckman at 831-338-8745 from
9-6 California time, or via email at tom@heartmath.com
References:
1. Foreman, R. D. Vagal afferent modulation of cardiac pain. In: Levey M. and Schwartz P.,
Vagal Control of the Heart: Experimental Basis and Clinical Implications. Armonk, N.Y.:
Futura Publishing Co., 1994:
2. Foreman, R. Organization of visceral input. In: Yaksh T. L., Anesthesia: Biologic
Foundations. Philadelphia: Lippincott-Raven Publishers, 1997: 663-683.
3. Ammons, W. S., Blair, R. W. and Froeman, R. D. Vagal afferent inhibition of primate thoracic
spinothalamic neurons. J. Neurophys. 1983; 50:926-940.
4. McNeill, D., Chandler, M. and Foreman, F. Q.-G. Projection of nodose ganglion cells to the
upper cervical spinal cord in the rat. Brain Res. Bull. 1991; 27:151-155.