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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
Central Sensitization
Thalamus and Cerebral Cortex
Currently selected section: Neurophysiology of Angina Pectorsis
Nausea and Vomiting

Dyspnea
Summary

 

Chapter 25:Neural Mechanisms of Cardiac Pain: Neurophysiology of Angina Pectorsis
         Summary of the Neurophysiology of Angina Pectoris

Sensory input from the heart excites spinothalamic tract cells in the thoracic and upper cervical segments of the spinal cord. These cells receive convergent input from the overlying somatic structures. Thus, this information forms the basis for understanding the pain resulting from ischemic heart disease.

However, the huge variations in the expression of pain of overlying somatic structures, and particularly in episodes of cardiac ischemia in which no pain occurs (so-called silent ischemia), raise important questions about how cardiac sensory information is processed, modulated, and perceived. These variations could occur in structures previously mentioned, such as the dorsal root ganglia, spinal gray matter, brain stem, and cerebral cortex. They might also occur in the peripheral intrinsic and extrinsic cardiac ganglia, which contain neurons that do not project to the spinal cord but can influence sensory and motor autonomic neurotransmission.

Future studies should explore the hierarchy of control mechanisms that integrate the activity from these regions and ultimately cause the various manifestations of the sensation of angina pectoris.

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