Middle and Inner Ear

Chapter 123


Middle and Inner Ear



The middle and inner ears are important and frequently overlooked sites of disease in dogs and cats. There are substantial differences in the causes of the primary disease entities in the two species. In dogs, otitis media is most commonly the consequence of a descending bacterial ingress via or around the intact tympanic membrane as a sequela of chronic otitis externa. In cats, an ascending cause is thought to be responsible for interrupting middle ear drainage and initiating a sterile inflammatory process. Medical and surgical management strategies should be tailored to reflect these differing causes and their pathophysiologic processes.



Anatomy of the Middle Ear



Dogs


The middle ear is phylogenetically derived from the pharynx and separates the external acoustic meatus from the cochlear and vestibular structures of the inner ear. Its major components include the tympanic cavity, tympanic membranes, ossicles (malleus, incus, and stapes), muscles (tensor tympani, stapedius), auditory (eustachian or pharyngotympanic) tube, nerves (facial, chorda tympani, tympanic branch of glossopharyngeal, and lesser petrosal), and tympanic plexus. The tympanic plexus receives parasympathetic innervation from the glossopharyngeal nerve and sympathetic innervation from the cranial cervical ganglion via the carotid plexus.


The tympanic cavity, formed by the tympanic component of the temporal bone, is a bony shell situated caudal and medial to the zygoma and temporomandibular articulation. The cavity has dorsal, middle, and ventral compartments (Figure 123-1) and is lined with respiratory mucosa contiguous, via the auditory tube, with that of the nasopharynx. The combined volume of the compartments is related to body weight.21 The dorsal component—the epitympanum or epitympanic recess—is the smallest of the three chambers and is largely occupied by the incus and part of the malleus. It is lined with cuboidal or squamous epithelium with few cilia. The middle component—the mesotympanum or true tympanic chamber—is a four-sided chamber lined with columnar or cuboidal epithelium and variable numbers of ciliated cells. The middle chamber is bounded laterally by the larger of two tympanic membranes, which separates it from the external ear; the smaller secondary membrane (the cochlear membrane) is located posteriorly within this chamber. On the medial aspect of the middle chamber, level with the tympanic membrane, is found the bony promontory that accommodates the cochlear structure. The ventral component of the tympanic cavity, termed the hypotympanum, is the largest of the chambers and is situated within the tympanic bulla, the spherical bone prominent ventrally. It communicates with the tympanic cavity proper through an anterolateral-facing elliptical opening on its dorsal aspect and is lined with cuboidal or squamous cells. Despite variations in the thickness of the bulla wall, which is thickest on its rostral and lateral aspects, the chamber’s interior profile remains regular.



Two membranes are found within the mesotympanic chamber: the tympanic membrane and the secondary cochlear (or round) membrane. The tympanic and cochlear membranes separate the chamber from the external acoustic meatus laterally and the inner ear medially, respectively. The tympanic membrane is a thin, translucent, triple-layered structure with contributions from the external and middle ear. The membrane is divided into the smaller pars flaccida and larger ventral, pars tensa (Figure 123-2). The pars flaccida occupies the dorsal portion of the membrane and covers a small area of the middle ear chamber that, in dogs, is separated from the remainder of the epi- and mesotympanum. The pars tensa comprises the majority of the membrane; the manubrium of the malleus is embedded in its dorsal aspect. The membrane is constructed of an inner epithelium derived from the pharyngeal pouch, a central fibrous layer also of pharyngeal origin, and an outer stratified squamous epithelium derived from the ectoderm of the outer ear. Its longitudinal axis slopes so that its ventral aspect is more medial, and its outer surface is concave because of its attachment to the malleus. The outer epithelial cells originate at the attachment of the malleus and migrate peripherally from this point to the external auditory meatus; this continual centrifugal movement of cells clears debris from the surface of the membrane and is also responsible for its repair in the event of rupture.



The opening to the auditory tube, also known as the eustachian or pharyngotympanic tube, is found in the rostral mesotympanic chamber. The tube is a short structure connecting the tympanic chamber with the nasopharynx. Its length varies from 1 to 2 cm, and its oval lumen between 1 and 2 mm in diameter. The wall of the tube is supported medially in the nasopharyngeal region by cartilage, in the tympanic region by the petrous temporal bone, and laterally by the tensor veli palatini muscle. The tube is lined with ciliated, pseudostratified, or columnar mucosa. Its middle segment has mainly ciliated cells that progress to a combination of goblet cells, nonciliated columnar cells, and ciliated cells at the tympanic opening. Mucus and goblet cells predominate at the pharyngeal end. Cannulation of the auditory tube via the pharyngeal opening for drainage purposes is feasible.41


The bones or ossicles of the middle ear include the malleus, incus, and stapes. The malleus is the most lateral ossicle and is comma shaped when viewed from its medial aspect. Its “tail” or manubrium is embedded in the fibrous middle layer of the tympanic membrane, whereas its medial head articulates with the body of the middle ossicle, the incus. The incus lies almost entirely within the epitympanic recess and articulates with the stirrup-shaped stapes medially. The stapes is oriented horizontally. Its base on the medial aspect is attached to the fibrocartilaginous ring around the rim of the vestibular, or oval, window and separates the tympanic cavity from the perilymphatic space of the inner ear. The ossicles are fixed within the mesotympanic cavity and epitympanic recess by a series of ligaments. These include the lateral ligament of the malleus that attaches it to the tympanic notch, the dorsal ligament of the malleus and incus that attaches them to the epitympanic recess, and the annular ligament of the stapes that attaches it to the vestibular window.


Two muscles are responsible for movement of the ossicles. The tensor tympani muscle is attached in the dorsal mesotympanic cavity and inserts on the small hook on the medial aspect of the malleus. Contraction of this muscle moves the malleus medially and increases the tension and convexity of the tympanic membrane to dampen sound vibrations. The stapedius muscle also tenses the stapes to limit its movement and similarly dampen vibrations.


A number of nerves supply or pass through the tympanic chambers. The facial nerve has mixed sensory and motor functions and reaches the internal auditory meatus in close association with the vestibulocochlear nerve. After separating from the vestibulocochlear nerve, it enters the facial canal within the petrous temporal bone and emerges caudal and medial to the tympanic bulla at the stylomastoid foramen. The facial canal of the petrous temporal bone is incomplete, and the nerve lies exposed in the dorsal aspect of the tympanic cavity near the vestibular window. Within the facial canal, the facial nerve gives branches into the stapedius nerve and the chorda tympani (tympanic nerve). The contribution from the facial nerve to the chorda tympani mixes with preganglionic parasympathetic vagal branches that pass across the medial aspect of the malleus and tympanic membrane before entering a small canal in the dorsal wall of the tympanic chamber and exiting the petrotympanic fissure to join the lingual nerve. The tympanic plexus is formed from the tympanic branches of cranial nerve (CN) IX and the caroticotympanic nerve. It spreads across the bony promontory before entering the lesser petrosal nerve. The tympanic plexus gives rise to preganglionic parasympathetic fibers to the parotid and zygomatic salivary glands, postganglionic fibers to the parotid gland and sensory fibers to the middle ear cavity. Postganglionic sympathetic fibers arise from the cranial cervical ganglion located deep to the bulla and pass to the eye to supply the smooth muscle of the dilator pupillae and nictitating membrane. These fibers follow the course of the internal carotid artery before joining the tympanic branch of CN IV.


The vascular supply to the middle ear—the tympanic artery—is derived from the maxillary artery and enters via a small foramen caudal to the temporomandibular joint. Other contributions arise from the meningeal and pharyngeal vessels.



Cats


The feline middle ear has a similar overall anatomic arrangement to that of dogs; however, its chambers show much more distinct separation into a larger ventral cavity (Figure 123-3), the hypotympanum, and a smaller rostrolateral component corresponding to the epitympanum and mesotympanum. The two components are almost completely separated by a bony septum and communicate on their medial aspect through a small slitlike opening that widens into a distinct foramen caudally. This separation gives rise to the characteristic “double shell” profile of the tympanic structures visible on anteroposterior radiographic views. The lining of the chambers is reported to contain more abundant ciliated and secretory cells than in dogs. The distribution of neural structures within the middle ear is similar to that in dogs. On entering the middle ear, the tympanic plexus distributes widely across the bony promontory but is reported to be more exposed, or possibly more sensitive, to iatrogenic trauma.




Physiology of the Middle Ear


The primary function of the middle ear is conduction of sound waves, which enter the external auditory meatus, across its air-filled cavity to the fluid-filled inner ear in which are found the receptor cells of the cochlea. The air-fluid interface between the middle and inner ears represents a considerable change in impedance that normally results in very poor sound transmission. However, the ossicles concentrate sound waves striking the tympanic membrane and focus them on the much smaller area of the oval window, thereby compensating for this change in impedance. The ossicles therefore provide an extremely efficient means of transmitting sound from the atmosphere to the fluid environment of the inner ear.


Cellular debris and mucous secretions within the middle ear are continually expelled to the pharynx by the combination of mucociliary clearance and muscular pumping action of the auditory tube. The aural ostium of the auditory tube normally remains closed as the consequence of surrounding passive forces but is opened during swallowing by the action of the tensor veli palatini muscles. This periodic opening of the tube also allows equilibration of atmospheric pressure with that in the tympanic cavity.



Anatomy of the Inner Ear


The bony labyrinth is a perilymph-filled cavity in the temporal bone that communicates with the middle ear via the vestibular and cochlear windows. It contains the membranous labyrinth, which is divided into three sections (Figure 123-4): the vestibule, cochlea, and semicircular canals. The vestibule is the middle portion of the labyrinth and contains the saccule and utricle of the membranous labyrinth. The cochlea is a bony, spiral “seashell” structure containing the cochlear coil. The coil originates at the cochlear window and is divided by the cochlear duct, which forms a shelf across the cochlea, into two sections: the scala vestibuli and the scala tympani. The floor of the duct is formed by the basilar membrane, which contains the organ of Corti. There are three interconnecting, fluid-filled semicircular canals: anterior, lateral, and posterior. Each has an ampulla arranged at right angles to the others. The saccule and utricle are found at the confluence of the canals.



The entire inner ear is bathed in a cushioning fluid known as endolymph when it lies within the membranous labyrinth and perilymph when it separates the bony and membranous labyrinths. The inner ear is innervated by the vestibulocochlear nerve. This nerve branches into the vestibular nerve, which is associated with the semicircular canals, and the cochlear nerve, which terminates in the organ of Corti.



Physiology of the Inner Ear


The major functions of the inner ear are associated with sound perception and balance. Sound waves are focused by the external ear on the tympanic membrane before being concentrated and transmitted through the middle ear by the ossicles. Auditory function is then stimulated by the movement of endolymph within the cochlea. In the organ of Corti, waves are converted to nerve impulses, which are transmitted to the brain. The vestibular system of the inner ear is responsible for the sensations of balance and motion. Vestibular function in the utricle, saccule, and semicircular canals is stimulated by fluid movement within these chambers. They contain maculae, or detection cells (hair cells), that provide information about the attitude and linear and rotatory motion of the head. The type of motion or attitude detected by a hair cell depends on associated mechanical structures, such as the curved tube of a semicircular canal or the calcium carbonate crystals (otoliths) of the saccule and utricle.



Pathophysiology of Middle and Inner Ear Disease



Septic Otitis Media


Septic otitis media is undoubtedly the most important disease of the canine tympanic chamber. In principle, bacterial ingress to the middle ear can arise via one of the following three routes: the external auditory meatus via the tympanic membrane, the nasopharynx via the auditory tube, or hematogenous distribution. Extension from the external meatus via the tympanic membrane is considered to be by far the most common route for bacterial invasion in canine middle ear disease, which is usually the sequela to longstanding otitis externa accompanied by chronic inflammation and accumulation of bacteria in the external acoustic meatus.


The precise mechanism by which bacteria are able to gain access to the tympanic chamber is still unresolved. Although it has always been assumed that the tympanic membrane must be damaged to permit ingress of microorganisms, various authors have shown that the membrane is intact or even thickened in many dogs with septic otitis media.49,52 This finding may support the possibility of transmembrane migration by the bacteria; it is equally conceivable, however, that temporary perforation and subsequent repair of the membrane permits ingress.


Alternatively, bacterial invasion of the integument that lines the osseous external auditory prominence and surrounds the membrane may explain their ingress to the middle ear. This is supported by the fact that the predominance of canine breeds affected by septic otitis media reflects that of dogs prone to otitis externa. In patients with chronic otitis externa, however, microbial flora of the external meatus and their antimicrobial susceptibility differ considerably from those organisms responsible for septic otitis media.9,40 The most commonly encountered microorganisms in canine middle ear infections are reportedly Staphylococcus intermedius, Pseudomonas spp., and Malassezia yeast.9 Cryptococcal infection of the tympanic chamber has been reported in cats.4


Other conditions that permit bacterial access to the middle ear include foreign body perforation and traumatic disruption of the external acoustic meatus. Not only may foreign bodies damage the tympanic membrane, but persistence of the foreign body in the external meatus and tympanic chamber can prevent its normal repair. Traumatic disruption at the level of the annular cartilage may be encountered as the result of bite wounds in dogs and cats. The subsequent inflammatory process may seal off the horizontal component of the external meatus adjacent to the tympanic membrane from the remainder of the meatus, effectively trapping bacteria within a secretory environment. The resultant abscessation disrupts the membrane, which allows the infection to spread to the middle ear and gives rise to para-aural discharge.59 Para-aural abscessation can also occasionally occur as a sequela to iatrogenic stenosis of the external meatus after lateral wall resection or from residual integumentary remnants left within the bulla after total canal ablation.67 Rarely, congenital atresia of the external acoustic meatus may lead to a similar disease process within the bulla.


Compared with dogs, bacterial middle ear infection in cats as a consequence of otitis externa appears to be rare; presumably, this reflects the differing causes of aural disease in the two species. Conversely, ascending infection via the auditory tube associated with episodes of viral nasopharyngeal infection is frequently implicated in development of middle ear polyps in cats even though this is not thought to be an important route of access to the middle ear in dogs. Hematogenous infections involving the middle ear are considered to be very infrequent in all species.


Pathologic changes recognized in the middle ear as a consequence of established bacterial infection include thickening of the tympanic membrane, and epithelial hyperplasia with thinning of the lamina propria and the development of associated granulation tissue.49 A lymphoid and polymorphonuclear leukocyte infiltrate is usually evident. The wider availability of sectional imaging has allowed an increasing recognition of the incidence of extension of septic otitis media to involve the inner ear and adjacent intracranial structures.60,72



Inflammatory Diseases of the Middle Ear



Middle Ear Polyps


Inflammatory polyps are non-neoplastic masses that originate from the epithelium of the tympanic chamber or auditory tube. The condition is most frequently recognized in, and is the most important middle ear disease, of cats but it is also occasionally recognized in dogs.64 Polyps may remain within the bony confines of the middle ear chamber, extend into the nasopharynx (Figure 123-5), or disrupt the tympanic membrane and appear in the external acoustic meatus (Figure 123-6). The condition is encountered more frequently in young cats and is often preceded by an episode of upper respiratory viral infection. Experimental ligation of the auditory tube in cats has also been shown to result in polyp development; thus, it seems likely that an inflammatory episode, resulting in obstruction of drainage, is a possible underlying cause of the abnormal epithelial reaction.73





Cholesteatomas


Cholesteatomas are characterized by destructive and expanding keratinizing squamous epithelium. In dogs with septic otitis media, epithelium may undergo metaplastic changes, producing connective tissue and even new bone proliferation in more advanced cases.49 There may be glandlike areas within the granulation tissue that, because of their cystic structure and the presence of cholesterol clefts, have been likened to the condition recognized in humans as cholesteatoma. A congenital form has not been reported in dogs; most appear to be acquired after an episode of otitis media.19,20,32,39,51 Inadvertent instillation of some antiseptic and ceruminolytic agents through a disrupted tympanic membrane has been shown to give rise to a sterile inflammation of the tympanic chamber and, in some cases, hearing loss and vestibular damage.4244,56




Disorders of Middle Ear Drainage



Secretory (Serous) Otitis Media


Secretory otitis media is characterized by accumulation of mucinous material within the tympanic chamber and is an increasingly recognized syndrome, particularly in Cavalier King Charles spaniels.18,66,69 This condition, often referred to as “glue ear” in children, results in impaired conductive hearing function. Dysfunction of the auditory tube itself may lead to increased negative pressure, allowing accumulation of mucous secretion within the tympanic cavity. An underlying cause has not been identified. Although upper respiratory viral infections are implicated in humans, the breed-related incidence in dogs suggests a congenital dysfunction of drainage via the auditory tube. Dogs that present with congenital hypoplasia or malformations of the soft palate are reported to be at risk for middle ear disease and impaired hearing function.36,77



Ciliary Dyskinesia


Primary ciliary dyskinesia, a rare congenital condition resulting in depressed ciliary function, has been reported in dogs.28 In normal animals, active mucociliary function of the tympanic lining removes debris trapped in mucus via the auditory tube. Loss of this function leads to failure of middle ear drainage. One of the many consequences, therefore, of this generalized ciliary dysfunction is sterile otitis media.



Neoplastic Disease


The majority of tumors involving the middle ear are usually identified as extensions of neoplasms derived from structures of the external ear canal; tumors derived from structures of the tympanic cavity and auditory tube are rare. Tumors of true tympanic origin include ceruminous gland adenocarcinomas,48,53 squamous cell carcinoma,31,79 carcinoma of unknown origin, and lymphoma.22 Neurologic signs (i.e., Horner syndrome, vestibular signs) indicating extension to involvement of the middle ear are occasionally recognized in dogs with malignancy of the external ear but are more commonly encountered in cats. Tumors of the inner ear are extremely rare, and many patients presented with vestibular signs are ultimately found to have central lesions.



Presentation



Septic Otitis Media


Clinical signs of inflammatory or septic otitis media include otorrhea, otalgia, head shaking, and attention to the affected ear(s). The appearance of the discharge associated with otitis media varies; however, because most cases result from septic extension of otitis externa, purulent material is present in the external meatus. Signs of otalgia include discomfort on aural manipulation and behavioral changes. Additionally, animals may have intermittent alteration of head carriage with the head carried lower on the affected side if the disease is unilateral. Persistent head tilt is not encountered unless there is extension to the inner ear. Patients with severe inflammatory change that extends rostrally to involve the adjacent temporomandibular joint may show signs of pain on jaw movement and have a restricted range of movement. All of these signs are similar to, and often very difficult to differentiate from, those encountered in patients with severe otitis externa. Because most cases of otitis media in dogs are the result of preexisting otitis externa, this is of particular significance because involvement of the middle ear may be easily overlooked.



Neurologic Signs


Most patients with otitis media do not exhibit neurologic signs; however, tympanic inflammation may affect any of the nerves within the tympanic chamber. Possible neurologic changes therefore include facial nerve palsy and Horner syndrome. The incidence of facial palsy in dogs with established otitis media is reported to be approximately 10%.49 It is characterized by impaired palpebral function and facial and aural drooping. The extratympanic component of the facial nerve may also be affected if otitis media is severe enough or by the inflammatory changes caused by chronic otitis externa. The incidence of Horner syndrome is somewhat lower than that of facial involvement and is an unusual sign of middle ear disease; signs include ptosis, miosis, enophthalmos, and protrusion of the nictitating membrane. Damage to parasympathetic fibers carried in the chorda tympani may also lead to reduced tear secretion and promote keratitis sicca. However, it is unclear if disease processes involving the other functions of the chorda tympani and tympanic nerve, including salivary innervation, would always be clinically apparent. Otitis media may progress to involve the inner ear. Otitis interna may result in hearing loss and vestibular signs; further extension to affect the intracranial structures may give rise to symptoms of central vestibular disease, altered mentation, abnormal posture, cranial nerve deficits, and seizures.60,68,72

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Jul 18, 2016 | Posted by in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off on Middle and Inner Ear

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