Skip to Content
Interactive Textbook on Clinical Symptom Research Logo


Home Button


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

Dyspnea
Summary

 

Chapter 25:Neural Mechanisms of Cardiac Pain: Vagal Sensory Innervation
        

Vagal Sensory Innervation of the Heart

The vagus nerve appears to mediate certain aspects of anginal pain in some patients. As stated previously, pain resulting from ischemic heart disease commonly is referred to the chest, left arm, and sometimes the right arm. Less frequently, pain is referred to the neck and jaw (Sampson and Cheitlin, 1971).

Surgical sympathectomies in humans usually abolish or relieve angina pectoris (Lindgren and Olivecrona, 1947; Meller and Gebhart, 1992; White and Bland, 1948); however, sympathectomy occasionally unmasks pain referred to the neck and jaw, or uncovers stress-induced pain in these regions. The more rostral location of this pain led investigators to suggest that vagal afferent fibers may be involved in the transmission of nociceptive information from the thoracic region and also from other regions.

We suspected that nociceptive vagal information might converge onto spinothalamic tract cells of the upper cervical segments that received somatic information from the regions of the neck and jaw. Results of a study in monkeys showed that stimulation of cardiac receptors with algogenic chemicals injected into the pericardial sac predominately increased activity of spinothalamic tract neurons in the C1-C2 segments (Chandler et al., 1995, 1996).

Nerve ablation experiments demonstrate that interruption of ipsilateral vagal fibers significantly reduces the mean increase in neuronal activity of a majority of the C1-C2 spinothalamic tract cells in response to intrapericardiac algogenic chemicals. These results support the idea that cardiac vagal afferents transmit a majority of the nociceptive information to C1-C2 spinothalamic tract neurons.

In addition, noxious somatic input from the neck, jaw, ear, and upper arm regions converges onto these spinothalamic tract cells (Chandler et al., 1995, 1996). These results are consistent with the suggestion that activation of cardiac vagal fibers might lead to production of the sensation of referred pain, particularly in the neck and jaw regions. These results also indicate that nociceptive information from the heart could modulate the activity of neurons in the upper cervical segments.

Page 23 of 44
Previous Section