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Neural Mechanisms of Cardiac Pain
Author Biography
Introduction
Anterolateral System
Somatic vs. Visceral Nociceptive Processing
Angina Pectoris
Sympathetic Sensory Innervation
Referred Pain
Vagal Sensory Innervation
Other Ascending Pathways
Currently selected section: Central Sensitization
Thalamus and Cerebral Cortex
Neurophysiology of Angina Pectorsis
Nausea and Vomiting

Dyspnea
Summary

 

Chapter 25:Neural Mechanisms of Cardiac Pain: Central Sensitization
        

Repeated noxious balloon distensions of the colorectal region in humans evoke painful responses that increase pain sensitivity and expand the area of pain referral to the overlying somatic areas of the body (Ness et al., 1990). Animal studies support the findings observed in human studies.

Activity recorded from neurons in the lower thoracic gray matter during distension of the gall bladder show that some neurons respond only to somatic input and not to the visceral stimulus while another population responds to both somatic input and distension (Cervero et al., 1992). In the latter group of neurons, but not the former, the region of skin that could be stimulated to excite the neurons was greater in the presence of the visceral stimulus than it was when the visceral stimulus was not present. That is, the spinal neurons became sensitized to a larger region of skin if there was enhanced activity in visceral afferents. The visceral stimulus is selective, because only those neurons responsive to visceral stimulation change their sensitization to the somatic input.

An additional important characteristic of these responsive neurons is that the somatic referral of visceral pain that produced the changes tended to outlast the duration of the noxious visceral stimulus. This observation correlates well with the clinical experience that hyperalgesia is felt after the painful episode has passed. These results raise the possibility that central sensitization of spinothalamic tract cells, and perhaps other ascending pathways, could intensify the pain experience resulting from angina pectoris.

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