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Last updated: Tue, Mar 11, 2025
Activity in nociceptive sensory nerves normally results in greater sympathetic activity. This results in an increase in blood pressure in response to pain.
It isn't normal for sympathetic activity to result directly in pain. However, it has been found that many C-fiber nociceptors in chronically inflamed rats develop a sensitivity to norepinephrine, a neurotransmitter used by sympathetic neurons. Activation of the sympathetic nervous system in such an animal does cause pain.1
Some patients with neuropathies have pain that seems to depend on the activity of the sympathetic nervous system. This is known as sympathetically-maintained pain. If such a patient has sympathetically-maintained pain near the surface of the skin, for example, the sympathetic system can be activated by cooling this skin. This prompts the sympathetic system to increase its activity in order to constrict surface blood vessels, which increases the victim's pain. Blocking sympathetic activity with drugs relieves the pain. Injecting the area with norepinephrine (one of the sympathetic neurotransmitters) increases the pain.
Two explanations can be given for this phenomenon. It is possible that norepinephrine secreted by sympathetic nerves binds with receptors on somatic sensory afferents, exciting those afferents. Sensory afferents aren't normally equipped with norepinephrine receptors, but it is known that these may be present after nerve injury.2 It is also possible that the sympathetic activation somehow has an indirect effect on the immediate environment of the sensory nerves by reducing local blood flow.
Because of these linkages in the nervous system, patients with sympathetically-maintained pain can experience increased pain due to cooling of the skin or a startling noise.