The mechanism of visceral pain has been described by several authors.2^{,3,4,5,6,7,8,9} Ordinarily, sensory information transmitted by afferent neurons of the visceral nervous system remains well below conscious levels. It serves to monitor the involuntary muscle action of vessels, glands, and organs. It reports unusual sensation occurring in the lining membranes of organs and cavities. It helps regulate the automatic functioning of the body by supplying the CNS with a constant inflow of information. When such sensation becomes noxious, pain is felt. Visceral afferent fibers of both the sympathetic and parasympathetic type are known to mediate pain.⁸ Visceral pain usually has a distinct stinging or burning quality. It is said that protracted visceral pain⁹ tends to provoke vasomotor effects, local edema, and trophic changes.

It appears that conscious visceral sensation is normally of a very low order of intensity, since the visceral afferents have high-threshold receptors. However, the presence of inflammation may reduce this threshold considerably so that conscious pain becomes evident with little added provocation. For example, the stomach yields minimal sensation other than when it is very empty or very full. But an inflamed gastric mucosa causes the normal stomach contents to excite painful sensation, usually described as heartburn.

Visceral pain in the maxillofacial region is not rare. Esophagitis and pharyngitis have the dull, diffuse, burning quality of visceral pain. Pain in the nasal and ostium maxillare mucosa has a similar burning quality.^3,10 The major salivary glands as well as the numerous glands of the lymphatic system, the skin, and the mucous membranes are other sources of this type of pain.

Some pains arising in the maxillofacial region are mediated by sympathetic afferent fibers that do not enter the CNS via any cranial or cervical nerve sensory root. Rather, these visceral fibers leave the orofacial structures and pass through the cervical sympathetic chain and finally enter the CNS via the sensory roots of the upper thoracic spinal nerves. Head and neck pains mediated by this route cannot be arrested by division of any or all cranial and cervical spinal sensory roots. Such pains are arrested by analgesic blocking of the stellate ganglion, through which such afferents pass, even though they undergo no synapse prior to reaching the CNS.^9,11,12

Analgesic blocking of the stellate ganglion does not necessarily arrest some of these vascular pains. This strongly suggests that the cranial parasympathetics constitute the mediating pain pathway. No parasympathetic afferent fibers pass through the dorsal root of the trigeminal nerve. Rather, they leave this nerve and enter the CNS via the seventh and ninth cranial nerve dorsal roots. Thus, division of the trigeminal sensory root will not arrest pains from the trigeminal area that are mediated by parasympathetic afferent fibers.

Visceral pain input tends to provoke central excitatory effects. Referred pains, secondary hyperalgesias, and localized autonomic effects may accompany visceral pains. Sometimes they dominate the symptom picture and constitute the patient’s complaint. The so-called sinus headache typifies this clinical behavior.

For purposes of description, visceral pains have been separated into three groups: pulpal odontogenous pains, vascular pains of the mouth and face, and other visceral pains, including those of mucosal, glandular, ocular, and auricular origin. Pulpal pains have already been reviewed in chapter 11. Since vascular pains are a common and important type of pain originating from the orofacial structures, an entire chapter will be devoted to them (chapter 16). This chapter will review visceral pains that have their origin in mucosal tissues of the pharynx, nose, and paranasal sinuses. This chapter will also review pains from glandular, ocular, and auricular structures (Fig 15-1).

Fig 15-1 Pain classification chart highlighted to show the relationship of visceral mucosal, glandular, ocular, and auricular pains to other orofacial pain disorders.

The normal inflow of sensation from visceral mucosa serves to regulate automatic functioning. Several reflex mechanisms are recognized: irritation of the nasal mucosa excites the sneeze reflex, the pharyngeal mucosa initiates the swallowing and gag reflexes, upper esophageal mucosa may induce esophageal spasm, and irritation of the upper tracheal and laryngeal mucosa stimulates the cough reflex. When mucosal stimulation becomes noxious, burning pain is felt.3^,5,6,8,10,13 It is said that continuing visceral pain tends to provoke vasomotor effects, local edema, and trophic changes.⁹ The normally high threshold level of sensibility is lowered in the presence of inflammation so that nociceptive impulses may be generated by otherwise nonnociceptive stimuli.

Nociceptive pathways from orofacial mucosal structures likely involve afferent elements of both the somatic and the visceral nervous systems. Somatic afferents are mediated by the fifth, seventh, and ninth cranial nerves. Parasympathetic visceral afferents are mediated by the seventh and ninth cranial nerves only. As noted earlier, sympathetic visceral afferents do not enter the CNS by way of cranial nerves but travel the cervical sympathetic chain to enter through the upper thoracic spinal nerves.

Like other forms of deep pain, visceral mucosa pain tends to initiate central sensitization or excitatory effects. Many times, the secondary symptoms predominate, while the primary pain input remains silent or goes unnoticed. Some orofacial pain disorders are expressed almost exclusively as secondary central excitatory effects. Caution should be exercised in differentiating such effects from the true source of primary input.