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Otalgia

John S. McDonald

Otalgia may be primary, with the source being the ear or temporal bone, or it may be secondary, referred to the ear with or without signs or symptoms of the primary source of the pain. In 50% or more of patients who complain of otalgia, the pain emanates from a source other than the ear.¹ Otalgia may be described as aching, boring, sharp, throbbing, burning, itching, or pressure-like with a sensation of fullness. Concomitant complaints of vertigo, tinnitus, and even the subjective sense of hearing degradation may be part of the clinical spectrum of either primary or referred otalgia and cannot be used as differentiating factors.

Nociception and Pain

Bonica³ defined pain as an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage. Tissue injury, whether caused by trauma or disease, constitutes a noxious stimulus that will activate nociceptors (receptors preferentially sensitive to a noxious stimulus or to a stimulus that would become noxious if prolonged).² The noxious stimulus or tissue damage activates nociceptors at the termination of thinly myelinated Aδ (group III) and unmyelinated C (group IV) afferent nerve fibers in the skin, muscles, joints, fascia, and other deep somatic structures.^3,4 Cutaneous nociceptors may be activated by mechanical, thermal, chemical, or other algesic stimuli, and nociceptors in the deep somatic structures may be activated by disease, inflammatory processes, contraction, ischemia, rapid distention, or other visceral stimuli.

Central to the theme of understanding the mechanism by which pain may be referred to the ear is the concept of central convergence. Sessle et al^5,6 have shown extensive convergence of cutaneous, tooth pulp, visceral, neck, and muscle afferents onto nociceptive and nonnociceptive neurons in the trigeminal subnucleus caudalis or medullary dorsal horn (MDH) and suggested a role for these neurons in mediating pain, its spread, and referral.

The sensory innervation to the ear and periaural region is derived from cranial nerves V, VII, IX, and X as well as cervical nerves II and III. Nociceptive impulses from cranial nerves V, VII, IX, and X have all been shown to synapse with second-order neurons in the trigeminal subnucleus caudalis or the MDH.⁴ Nociceptive impulses from cervical nerves 2 and 3 activate neurons in the spinal dorsal horn. There is a high degree of nociceptive convergence of the upper cervical nerves and the trigeminal system, providing overlap of peripheral C2 and C3 nociceptive fibers with other cephalic nociceptive nerves V, VII, IX, and X.⁷

There are three types of neurons in the MDH: low-threshold mechanoreceptors (LTMs), which respond to nonnoxious stimuli; wide dynamic range (WDR) neurons, which respond to both noxious and nonnoxious stimuli; and high-threshold nociceptive-specific (NS) neurons, which respond exclusively to noxious stimuli. A substantial number of the WDR and NS neurons show extensive convergence and can be excited by peripheral afferents from skin, mucosa, viscera (i.e., laryngeal), temporomandibular joint (TMJ), jaw and tongue muscle, tooth pulp, and neck, provoking the spread and referral of pain.⁹ Convergence of nociceptive fibers from C2 and C3 with WDR and NS neurons in the MDH may explain referral of pain from noxious stimuli from the C2, C3 region not only to the ear but to the preauricular region and other areas in the face.

Anatomy

The auriculotemporal branch of the mandibular or third division of the fifth cranial nerve (CN V3) provides sensory innervation for the tragus, anterior and superior aspects of the auricle, and external auditory canal, as well as the anterosuperior portion of the lateral external canal wall and tympanic membrane. The tensor tympani muscle, derived from the mandibular or first branchial arch, is innervated by a small nerve derived from the medial pterygoid branch of CN V₃. Although primarily motor in function, skeletal muscles receive sensory innervation from thinly myelinated Aδ (group III) and unmyelinated C (group IV) afferent nociceptive nerve endings in muscle fascia, in tight spatial connection to muscle arterioles and capillaries, and in tendons, acting as muscle nociceptors.^3,9,10 Electromyographic studies of the tensor tympani and stapedius muscles have demonstrated contraction of both muscles concomitantly with several complex facial movements including tight closure of the eyes, opening and closing of the jaws, speaking, and swallowing.¹¹ It has been pointed out that tonic contraction of the tensor tympani muscle may be accompanied by otalgia, a sense of pressure and fullness in the ear(s), and tinnitus, or other transient acoustic sensations.¹¹ Mechanical injury to muscle, which may be derived from repetitive situations such as overcontraction or overstretching muscle may produce pain. Chronic contraction of the masticatory muscles in cases of temporomandibular dysfunction (TMD), worsened by bruxism, may result in tensor tympani-mediated otalgia.

The facial nerve (CN VII) supplies sensory innervation to a portion of the posterior and posterosuperior auricle and to adjacent portions of the external auditory canal and lateral aspect of the tympanic membrane, as well as to a small area of skin in the postauricular area.1 CN VII also supplies innervation to the stapedius muscle in the middle ear.

The glossopharyngeal nerve (CN IX) provides sensory innervation to part of the posterior portion of the external auditory canal and meatus as well as an adjacent portion of the lateral surface of the tympanic membrane, the majority of the mastoid air cells, and the eustachian tube.¹ The tympanic plexus, which is composed of the tympanic branch of the glossopharyngeal nerve (Jacobson’s nerve) and the superior and inferior caroticotympanic branches of the sympathetic plexus surrounding the carotid artery, provides sensory innervation to the middle ear, including the medial aspect of the tympanic membrane.¹ The auricular branch (Arnold’s nerve) of the vagus nerve (CN X) innervates a portion of the posterior wall and the floor of the external canal and the corresponding external surface of the tympanic membrane.¹ The upper cervical nerves (C2, C3) also supply sensory innervation to the ear or periauricular structures. The posterior branch of the greater auricular nerve supplies sensory innervation to the majority of the posterior portion of the auricle as well as a portion of the skin over the mastoid region, which also receives some overlapping communication with the lesser occipital nerve (C2) in the mastoid region.

Although pain may be referred to the ear by way of any of the cranial or cervical nerves just mentioned, the most common source of referred pain to the ear is through the trigeminal nerve, the longest cranial nerve with the most extensive distribution in the head and neck region.^12,13

Mechanism of Referred Pain

The mechanism by which pain may be referred to the ear from distant anatomic sites can be found in the concept of central convergence wherein nociceptive neurons in lower centers such as the MDH receive convergent inputs from various tissues, with the result that higher centers within the brain cannot identify the actual input source.^5,14 These convergent inputs may also be involved in so-called central sensitization or neuroplasticity of nociceptive neurons, a process thought to contribute (along with peripheral sensitization) to hyperalgesia.¹⁵ It is thought that as a result of this nociceptive input, some of the afferent inputs to the nociceptive neurons may be “unmasked” and become more effective in exciting these second-order neurons, with the result that pain is perceived as coming from the tissue that the afferents supply.¹⁶ For example, pain may be experienced in the external ear including part of the external auditory canal and the tympanic membrane by convergence of primary Aδ or C afferent nociceptive fibers from the auriculotemporal branch of CN V₃ with primary Aδ or C nociceptive afferent trigeminal nerve fibers, most commonly other branches of CN V₃, at WDR or NS neurons in the MDH. Also, under the influence of nociceptive input from muscle, many cells acquire new receptive fields in deep tissues away from the site of stimulation, with the result that following muscle injury the neurons can be stimulated from body regions somatotypically appropriate for that neuron.¹⁷ Thus, it is also possible that pain may be referred to the middle ear or eustachian tube by convergence of primary afferent nociceptors from the tensor tympani and tensor palati muscles with other primary nociceptive afferents at WDR or NS neurons in the MDH.

It is likely, then, as illustrated in the preceding example of pain sensed in the ear through the auriculotemporal branch of CN V3, that convergence of primary nociceptive afferent fibers from CNs V, VII, IX, and X with WDR and NS neurons in the MDH (trigeminal subnucleus caudalis) may be the means by which pain may be referred to the ear.⁸ It is also thought that pain referred to the preauricular region from C3 may be facilitated through overlap of C2 and C3 nociceptive fibers with afferent nociceptive fibers from cranial nerve CN V₃.⁷

Primary Otalgia

Pain in the ear or earache may be either primary or referred (secondary otalgia). When the source of the pain and the site to which it is localized are the same, then the patient is said to have primary otalgia. When the source of the pain is distant from the site in which it is perceived (e.g., the ear), then the pain is said to be referred. The differential diagnosis of pathologic causes is enumerated in Table 34–1.

Although in most cases the cause of primary otalgia will be readily obvious, potentially the most ominous disorder, primary malignancy of the external canal, may not be at all obvious in its early stage and may be overlooked. Conversely, mild erythema of the tympanic membrane or erythema or mild swelling in the external auditory canal should not preclude a thorough head and neck examination to rule out pathology that may refer to the ear and be the true cause of the patient’s symptoms. A classic example is the patient with TMD or a TMJ with referred otalgia who may rub the external ear canal with a finger or foreign object in attempts to alleviate the pain, resulting in the appearance of bacterial or fungal otitis externa.

The underlying cause of pain referred to the ear may be either acute or chronic in nature. For the purposes of this chapter, acute causes of referred otalgia are conditions that may be readily diagnosed with well-defined treatment parameters. The majority of these cases will be inflammatory or traumatic in their origin. Table 34–2 lists the most frequently encountered acute disorders that may produce the feeling of pain in the ear. Those disorders that more frequently present as chronic ongoing pain complaints are illustrated in Table 34–3 (disorders that will typically have continued to persist beyond the usual course of an acute disease or a reasonable time for an injury to heal, or are associated with some chronic pathologic process causing continuous pain or recurrence of pain at intervals for months or years).²

Acute Referred Otalgia

Painful disorders arising in the orofacial region, innervated by the second and third divisions of CN V, are the most common cause of referred pain to the ear.^12,18 Common causes of dental pain in this region include inflammation and pulpal necrosis with or without periapical pathosis and inflammation or infection of the supporting periodontal structures (e.g., the periodontal ligament) including superficial or deep periodontal infections or periodontal abscess. Other dental factors such as unerupted or impacted teeth, traumatic occlusion, ill-fitting dental appliances, or recently adjusted archwires in patients undergoing orthodontic therapy may also be causative factors. Referred pain to the ear may also arise from a variety of nondental, painful, oral inflammatory disorders including recurrent herpetic gingivostomatitis, acute herpes zoster, recurrent aphthous stomatitis (primarily the major scarring form), mucocutaneous disorders such as erosive lichen planus, inflammatory lesions of the tongue such as geographic tongue, and less well understood processes such as burning tongue or burning mouth.

Other painful disorders of the orofacial region that may be the cause of referred pain to the ear include maxillary sinusitis, nasal infections, and parotitis caused by infection or obstruction of Stensen’s duct by a stone. Although CN V provides the majority of the sensory trigeminal vascular innervation, some of the dural blood vessels are innervated by fibers from CN V₃. As pain is the only sensation that may be evoked by inflammatory or traction stimuli to the cerebrovascular blood supply, then disease in this area will nonselectively present as pain. Even though the pathogenesis of carotidynia is not clear, the disorder may represent a variant of inflammatory/traction stimuli. Tenderness, particularly near the bifurcation, is present on carotid artery palpation. Otalgia typically is referred to the ipsilateral side. Treatment usually consists of nonsteroidal-antiinflammatory agents. Also, although TMD has an acute phase, it is most notable for its chronic nature, and hence it is included in this chapter in the differential diagnosis of chronic referred otalgia.

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