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Central
Sensitization
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If there is
a continually high level of sensory input to neurons in the gray
matter of the spinal cord, such as could occur with noxious events
in the heart, cellular mechanisms might be activated that ultimately
produce hyperalgesic states. Hyperalgesia is an enhanced response
to a nociceptive stimulus. This phenomenon was first studied for
somatic pain to explain an observation that most of us have experienced.
Suppose you
burn your arm, for example, treat it, and then wait a little while.
If you then touch the area that was burned, you will experience
pain instead of just a sensation of touch; the burned area is
thus hyperalgesic. Furthermore, if you touch the undamaged area
adjacent to the burned area, you will feel pain from this undamaged
area. These two types of hyperalgesia are termed primary and secondary
hyperalgesia, respectively.
This process
occurs, at least in part, because of cellular changes in central
nervous system neurons (Woolf,
1994). Investigators then became interested in whether similar
phenomena might occur with sensory input from visceral organs,
and thus provide insights to the alterations that might occur
in the thoracic segments of the spinal cord during angina pectoris.
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