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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
Neurophysiology of Angina Pectorsis
Currently selected section: Nausea and Vomiting

Dyspnea
Summary

 

Chapter 25:Neural Mechanisms of Cardiac Pain: Nausea and Vomiting
         Initiation and coordination of emesis

The gastrointestinal tract is the first, and sometimes the only, defense against ingested poisons. Ingested toxins can stimulate chemosensitive vagal afferent nerve endings directly. Any substance or bolus that produces obstruction or distension of the gastrointestinal tract can excite vagal mechanosensitive afferents, and these also may initiate emesis (Andrews et al., 1990). As discussed previously, vagal sensory neurons terminate in the nucleus of the solitary tract.

Adjacent to and medial to the nucleus of the solitary tract in the caudal medulla is the area postrema. This area, which lies in the floor of the fourth ventricle, does not have a well-developed blood-brain barrier. This means that blood-borne pathogens have direct access to brain tissue, which does not occur in most areas of the brain. Thus, these pathogens excite neurons in the area postrema, ultimately triggering emesis (Hornby, 2001; Page et al., 1997).

The "vomiting center" is located in the dorsolateral medullary reticular formation. In general, this region is bordered laterally by the inferior cerebellar peduncle and spinal trigeminal nucleus, ventrally by the nucleus ambiguus and inferior olivary nuclei, medially by the gigantocellular reticular nucleus, and dorsally by the dorsal motor nucleus of the vagus nerve and the solitary nucleus and tract. Neurons in the area postrema project to the vomiting center.

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