Peripheral Vestibular Disease of Horses
Robert J. MacKay
■ Definition and Etiology Vestibular disease of horses is an acute, usually asymmetric, condition with several major causes: bacterial or mycotic infection of the middle/inner ear, polyneuritis equi, viral/idiopathic labyrinthitis, remodeling or fractures (or both) of the petrous temporal bone in association with THO, and external trauma to the skull with or without fracture of the petrous temporal bone.1 Idiopathic labyrinthitis is probably an acute viral inflammation of the vestibular system that is severe, but complete recovery is common.
Lightning strike is also an uncommon cause of vestibular signs in horses.2,3 Staphylococcus, streptococcus, Actinobacillus, Aspergillus, Enterobacter, Pseudomonas, and Salmonella spp. and C. pseudotuberculosis have been isolated from cases of otitis media/interna in horses.4 Some authors have speculated that THO results from extension of chronic low-grade bacterial otitis media to the adjacent temporohyoid joint5; however, remodeling and fusion of the temporohyoid joint are probably the result of repeated trauma, chronic degenerative processes, or both.6,7 Primary otitis media/ interna in horses is probably rare and, in contrast to this disease in ruminants, young age does not appear to be a risk factor. It is presumed that the middle ear is infected via the eustachian tube or hematogenously. With the exception of viral/idiopathic labyrinthitis, the proximity of the facial canal to the vestibular system means that the facial nerve (VII) is frequently involved in conditions causing vestibular signs. Because the first three cervical nerves contribute proprioceptive information to the caudal vestibular nuclei, upper cervical injury also can cause signs of vestibular ataxia.8■ Clinical Signs Affected horses exhibit rotation of the poll (i.e., head tilt) toward the affected side, abnormal physiologic nystagmus, spontaneous horizontal or rotatory nystagmus with the fast phase away from the affected side, and vestibular strabismus with downward rotation (infraduction) of the eye ipsilateral to the lesion that can be exaggerated by elevation of the horse's chin.
The gait is usually staggering and dysmetric, with a tendency, because of increased extension of the contralateral limbs, to lean or circle toward the affected side. Horses with any acute peripheral vestibular disease sometimes fall or even roll to the side of the lesion and may panic and thrash wildly in an effort to stand. Bilateral vestibular disease causes severe dysmetria and ataxia and complete absence of normal physiologic nystagmus. The horse may have wide swinging movements of the head.Signs of vestibular disease are markedly exacerbated by blindfolding. Deafness is also apparent with bilateral involvement of the cochlear division of cranial nerve VIII. With unilateral vestibular disease, visual accommodation often occurs over a period of weeks, and affected animals may even return to racing. Signs of vestibular disease may still be elicited by blindfolding, however.
Concomitant ipsilateral facial paralysis is manifested by deviation of the nose toward the normal side, reduced flaring of the ipsilateral nostril during inspiration, and ipsilateral drooping of the lip, eyelids, and ears. Reflexes involving cranial nerve VII such as those of the lip and eyelids, the menace response, and ear reflexes are reduced or absent. Inability to close the eyelid causes exposure keratitis, which is particularly severe and usually involves deep horizontal corneal ulceration when there is damage to the secretomotor fibers of the facial nerve. With chronic facial paralysis, there is visible atrophy of the parotidoauricularis caudal to the vertical ramus of the mandible.
Horses with bacterial otitis media/interna may have other sites of infection, including the paranasal sinuses, guttural pouches, and lower respiratory tract. Extension of infection along a fracture defect or from otitis media/interna into the meninges is associated with development of additional neurologic signs, including obtundation, limb ataxia and weakness, and cranial nerve deficits, along with systemic signs of sepsis such as fever, tachycardia, and tachypnea.
■ Diagnosis and Treatment A complete blood cell count usually reveals leukocytosis and increased fibrinogen and serum amyloid A concentrations in cases of chronic otitis media/ interna, whereas neutrophilic pleocytosis in CSF samples is evidence of secondary meningitis. Diagnostic procedures for horses with peripheral vestibular disease include skull radiography, CT, and endoscopic examination of the external ear canal and guttural pouch.9 General anesthesia is required for diagnostic transtympanic centesis of the middle ear, although this procedure can rarely be justified.5,10 The rate of tear secretion, which may be tested with a Schirmer tear test strip, usually exceeds 17 mm/min. BAER testing may help establish the location of vestibular system disease as peripheral or central.11
Antibiotic treatment of peripheral vestibular disease due to otitis media/interna should, if possible, be guided by antimicrobial susceptibility testing of bacteria cultured from the middle ear or from related disease processes such as sinusitis, guttural pouch empyema, or pneumonia. In the absence of such information, coverage should be provided against Gram-positive bacteria by penicillin G (22,000 U/kg IM bid as procaine penicillin or IV qid as potassium penicillin) or ceftiofur sodium (2.2 to 5 mg/kg IM sid to bid). Additional coverage (which includes staphylococci) can be provided by the addition of enrofloxacin (5.5 mg/kg IV or 8 mg/kg PO sid). Oral continuation of treatment can be conveniently provided by trimethoprimsulfonamide drugs (30 mg/kg PO bid) or chloramphenicol (50 mg/kg PO qid). Treatment should continue for at least 30 days and ideally should be guided by results of repeated imaging of the affected petrous temporal bone. For cases refractory to antibiotic treatment, a procedure has been described for opening the affected osseous bulla by transendoscopic neodymium-doped yttrium aluminum garnet (Nd:YAG) laser surgery.12
Affected horses should be kept in a quiet, heavily bedded stall with good footing. Exposure keratitis may be treated or prevented under a partial tarsorrhaphy.