7 DISEASES OF THE INNER EAR



7.1 Vestibular Apparatus 

7.2 Cochlea 






The inner ear of the dog and cat is contained within the petrosal portion of the temporal bone and includes the cochlea and the vestibular apparatus. Diseases of the inner ear therefore may result in abnormalities in hearing or balance.


7.1 VESTIBULAR APPARATUS


The vestibular apparatus is critical for activating unconscious reactions to movement and gravity. In an effort to maintain balance, input on head position and linear, rotational, and angular acceleration is collected from receptors in the sacculus, utriculus, and semicircular ducts (Fig. 7.1). This input is transmitted by the vestibular portion of the vestibulocochlear nerve (CN VIII) to vestibular nuclei within the medulla oblongata and pons, directly adjacent to the fourth ventricle. A few fibres from the vestibular nerve bypass the vestibular nuclei, extending directly to the cerebellum.



Figure 7.1 The vestibular pathway.


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Projections from the vestibular nuclei extend to the brainstem, spinal cord, and cerebellum. Within the brainstem, some axons terminate in the motor nuclei of the oculomotor (CN III), trochlear (CN IV), and abducent (CN VI) nerves, which control reflex eye movement. Axons also reach the emetic centre of the reticular formation. Axons passing through the spinal cord within the vestibulospinal tract extend to neck, trunk, and leg muscles. Stimulation of neuronal cell bodies of these axons increases tone in extensor muscles on the ipsilateral side and inhibits tone of flexor muscles on the ipsilateral side and extensor muscles of the contralateral side. Projections to the cerebellum allow coordination of eye, neck, trunk, and limb position with head position. Additionally, pathways from the vestibular nuclei to the cerebral cortex allow mediation in response to conscious perception of movement and gravity.


7.1.1 Vestibular Disorders


Vestibular dysfunction is classified by location of the disease. Peripheral vestibular disease is caused by abnormalities of inner ear components, specifically those of the membranous labyrinth. Central vestibular disease is caused by abnormalities primarily within the brainstem and cerebellum.


Clinical Signs


Common clinical signs of vestibular disease included nystagmus, strabismus, head tilt, and abnormalities in balance and locomotion such as ataxia, circling, falling, or rolling. Other clinical signs may include postural deficits, vomiting, behavioural changes, Horner’s syndrome, facial nerve paralysis, and other cranial nerve abnormalities. Characterization of these signs may help to differentiate peripheral and central vestibular disorders (Table 7.1).


Table 7.1 Vestibular disease: lesion location based on clinical signs












































































Clinical signs Peripheral vestibular disease Central vestibular disease
Nystagmus + +
 Abnormal physiological + +
 Horizontal + +
 Rotary + +
 Directional variation with head position +
Strabismus + +
Head tilt + +
Ataxia + +
Circling + +
Abnormal postural reactions +
Proprioceptive deficits +
Loss of limb strength +
Cranial nerve dysfunction (except VII and VIII) +
Horner’s syndrome + (rare)
Altered mentation +
Disorientation + +
Deafness + (rare)

Nystagmus


Nystagmus is defined as an involuntary, rhythmic movement of the eyes. In healthy animals, physiological nystagmus, which is also known as the vestibulo-ocular or oculocephalic reflex, helps to stabilize visual images on the retina. As their heads move, normal cats and dogs will try to fix their gaze on an object, ‘following’ it with their eyes until they can no longer see it (Fig. 7.2). This results in a slow, gradual movement of the eyes toward the object as the head turns away, producing a ‘slow phase’ of normal eye movement opposite the direction of head movement. Once extraocular muscles reach their stretch threshold they contract, and the eyes move rapidly toward the direction of the head movement, producing a ‘fast phase’. Normal animals should only have nystagmus when the head is moved. If it is present when the head is in a normal, neutral position; a fully extended, resting position; or a flexed, lateral position, the nystagmus is considered pathological.



Figure 7.2 Physiological nystagmus.


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Pathological nystagmus, or abnormal movement of the eyes, is commonly seen in dogs and cats with central or peripheral vestibular disorders (Fig. 7.3). Pathological nystagmus associated with vestibular disease can be hori­zontal, vertical, rotary, or positional. Positional nystagmus occurs only when the animal’s head is placed in an unusual position (e.g. flexed laterally or extended fully). Animals with vestibular disease can also have abnormal (delayed or absent) physiological nystagmus. Nystagmus is described by the direction of the fast phase; for example, an animal with a fast phase in a horizontal plane to the left would have a left horizontal nystagmus.



Figure 7.3 Eye movements seen with pathologic nystagmus.


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Nystagmus in animals with peripheral vestibular disease is usually rotary or horizontal, although rotary nystag­mus may be difficult to distinguish from vertical in some animals. Nystagmus with peripheral vestibular disease does not change direction with the animal’s head position, and its fast phase is always away from the side of the lesion. In animals with chronic peripheral vestibular disease, nystagmus may be initiated by a sudden change in position, such as with rolling the animal on its back (Fig. 7.4), but the direction of nystagmus does not vary. Animals with peripheral vestibular disease may have delayed or absent physiological nystagmus.



Figure 7.4 In animals with chronic vestibular disease, pathologic nystagmus may be initiated by a sudden change in position.


(Photograph by Phil Snow, UTCVM) © 2012 The University of Tennessee.


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Animals with central vestibular disease can have vertical, rotary, or horizontal nystagmus, and the nystagmus may change in character or direction with change in head position. In animals with bilateral peripheral or central disease, nystagmus is absent.


Strabismus


Strabismus is an abnormal position of the eye in relation to the palpebral fissure or orbit. Strabismus that is consistent with all positions of the head is indicative of abnormalities in the nerves or extraocular muscles that control eye movement (Fig. 7.5). Vestibular strabismus is an inconsistent abnormality in eye position. Affected animals have ventral or ventrolateral eye position that appears or worsens when the head and neck are extended but disappears with changes in head position, as long as their extraocular muscles are functional. The lesion is usually located on the same side as the strabismus.



Figure 7.5 In this dog strabismus was consistent with all positions of the head, indicating a problem with extraocular muscles or nerves that control eye movement.


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Head Tilt


A head tilt is categorized by the side of the head on which the ear is directed more ventrally (Fig. 7.6). Head tilts in animals with peripheral vestibular disease are typically directed toward the side of the lesion. Head tilts associated with central disease are also usually ipsilateral to the lesion; however, contralateral (paradoxical) head tilt has been reported.



Figure 7.6 With peripheral vestibular syndrome, head tilt and ataxia are toward the side of the lesion.


(Photograph by Phil Snow, UTCVM) © 2012 The University of Tennessee.


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Abnormalities in Balance and Locomotion


These abnormalities may manifest as ataxia, circling, rolling, or an inability to stand. Ataxia and circling (tight circles) are seen with central and peripheral vestibular disease. Animals with either type of vestibular disease can also have rolling; if it persists longer than 48 hours, however, it is more likely to be associated with a central lesion. As with nystagmus and head tilt, ataxia and circling are usually toward the side of the lesion, with the exception of a few cerebellar diseases. Animals with bilateral vestibular dysfunction have a wide-based, crouched stance; large, side-to-side head excursions; no head tilt; and no normal or abnormal nystagmus. These animals usually have peripheral vestibular lesions.


Other Clinical Signs of Vestibular Disease


Abnormal postural reactions are only seen in animal with central vestibular dysfunction. Postural reactions such as hopping and hemi-walking can be difficult to evaluate in animals with peripheral disease because of their loss in equilibrium; therefore, evaluation of proprioceptive positioning is important in determining the location of the lesion. Proprioceptive deficits are only seen with central vestibular disease and always occur on the side of the lesion. Opisthotonus, hemiparesis, and tetraparesis have been reported with central vestibular disease but are not seen with peripheral vestibular disease.


Dysfunction of cranial nerves other than the facial and vestibulocochlear nerves is only seen with central vestibular disease. Abnormalities associated with trigeminal (CN V) and abducent nerve dysfunction are most often reported. Facial nerve paralysis is more commonly associated with peripheral vestibular dysfunction secondary to otitis media interna (Fig. 7.7). The facial nerve passes through a cleft in the tympanic bulla and is therefore exposed to any middle ear disease. Clinical signs of facial nerve dysfunction include drooling, facial muscle paresis or paralysis, loss of blink, and those associated with keratoconjunctivitis sicca (KCS).



Figure 7.7 Head tilt to the left and ipsilateral facial nerve paralysis in a Pug with otitis interna secondary to otitis externa/media.


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Altered mentation is usually only seen in animals with central vestibular disease. This may be difficult to differentiate from disorientation, which is often seen with peripheral vestibular disease. Cats with otitis media may also appear obtunded because of pain.


Deafness is rare in animals with central disease. In animals with vestibular dysfunction, deafness is usually a result of abnormalities in sound wave conduction caused by conditions such as debris in the ear, ruptured tympanum, damage to auditory ossicles, accumulation of fluid, or neoplasia.


Other clinical signs of vestibular disease are associated with the primary aetiology and its location. For instance, animals with cerebellar disease may also have dysmetria and intention tremors, while animals with vestibular disease secondary to otitis media interna may have pain upon opening the mouth from inflammation around the temporomandibular joint, aural discharge secondary to otitis externa, or dyspnea or dysphagia secondary to a nasopharyngeal polyp.


Horner’s syndrome includes miosis, ptosis, enophthalmos, and elevation of the third eyelid (Fig. 7.8). In animals with peripheral vestibular dysfunction, Horner’s syndrome is often a result of otitis media from damage to sympathetic fibres as they course through the tympanic cavity. Because of their exposed position, these fibres are more easily damaged in cats, particularly during bulla osteotomy or traction polyp removal. Horner’s syndrome is rarely associated with central vestibular disease.



Figure 7.8 Horner’s syndrome can be caused by lesions anywhere along the sympathetic pathway (A), including in the brain, brainstem, spinal cord, T1–T3 nerve roots, vagosympathetic trunk, base of the skull, middle ear, or retrobulbar region. Classic signs (B) include pupil constriction, drooping upper lid, elevated third eyelid, and retraction of the globe into the orbit.


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7.1.2 Peripheral Vestibular Dysfunction


Aetiologies


Aetiologies of peripheral vestibular dysfunction include septic or aseptic otitis media interna (Fig. 7.9), inflammatory polyps, neoplasia, trauma, ototoxicity, generalized polyneuropathy, hypothyroidism, and congenital dysfunction. If these aetiologies are ruled out, the condition is classified as idiopathic. Idiopathic vestibular syndrome and progression of otitis media to otitis interna, or labyrinthitis, are the most common causes of peripheral vestibular dysfunction. Besides infection, otitis media can have a variety of causes. These are discussed more thoroughly in Chapter 6.



Figure 7.9 Transverse CT images. Otitis interna in a 10 year old male castrated Pug with chronic otitis media and left-sided head tilt. Before the CT scan, the dog presented acutely for ataxia, falling to the left, and horizontal nystagmus with the fast phase to the right. The left bulla was enlarged with portions of the wall either thin or absent (A). Contrast enhancement was noted along the meninges and in the tissues around the bulla (B). A sterile cholesteatoma and meningitis were found on necropsy.


(Courtesty, UTCVM Radiology) © 2012 The University of Tennessee.


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In dogs, bacterial otitis media interna is usually secondary to ascending otitis externa. The most common bacteria are staphylococcus, proteus, pseudomonas, pasteurella, enterococcus, and Escherichia coli. The infection advances through an inflamed or ruptured tympanic membrane and crosses the round or oval window into the perilymph around the membranous labyrinth. Infection may also spread from haematogenous routes or from the pharynx, through the eustachian tube, and into the middle ear. As noted in Chapter 6, bacterial causes of otitis media interna are usually secondary to some other primary or predisposing condition. Cats are more likely than dogs to have extension of bacterial otitis interna to the meninges, which results in central vestibular dysfunction.


In cats, peripheral vestibular dysfunction may be secondary to an aural or nasopharyngeal polyp (Fig. 7.10). The associated otitis media interna can be aseptic. Preoperative vestibular signs may include head tilt, ataxia, and nystagmus; more commonly, nystagmus and ataxia are iatrogenic as a result of ventral bulla osteotomy for polyp removal. Postoperative nystagmus usually resolves within 24 hours after surgery; however, head tilt present before surgery is likely to persist postoperatively.



Figure 7.10 Under otoscopic guidance, this aural polyp was retrieved from a cat’s horizontal ear canal and dorsolateral bulla by traction with a 3 mm nitinol tipless retrieval basket (inset) inserted through the port of the video otoscope.


(Courtesy, Danielle Browning, LVT, UTCVM) © 2012 The University of Tennessee.


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Neoplasia can cause peripheral vestibular dysfunction through direct invasion from the brain or middle ear or secondarily (e.g. a tumour obstructing the external ear canal or eustachian tube) by inciting inflammation or fluid accumulation within the middle ear and secondary otitis interna (Fig. 7.11). Tumours arising from the ear canal are more common than those arising from the bulla or bony labyrinth. A variety of carcinomas and sarcomas of the middle or inner ear have been reported to cause peripheral vestibular disease, with squamous cell carcinoma reported most commonly in the cat. Lymphoma and vestibular neurofibroma have also been reported.



Figure 7.11 Transverse CT image. Osteosarcoma of the tympanic bulla in a 7 year old male castrated Chesapeake Bay Retriever with otitis externa/media, temporalis muscle atrophy, and Horner’s syndrome.


(Courtesy, UTCVM Radiology) © 2012 The University of Tennessee.


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Jun 23, 2017 | Posted by in ANIMAL RADIOLOGY | Comments Off on 7 DISEASES OF THE INNER EAR
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