A 9-month-old 230-kg (506-lb) Thoroughbred filly was evaluated at the Massey University Veterinary Teaching Hospital because of a 3-month history of right-sided muzzle deviation, left lip droop, and left head tilt. Signs were reported to be abrupt in onset and coincided with a soft tissue swelling along the left side of the head. No treatment had been attempted prior to referral. On evaluation, heart rate and respiratory rate were within reference ranges. Rectal temperature was high (39.1°C [102.3°F]), and mild bilateral serous nasal discharge, dry intermittent coughing, and mildly increased lung sounds were present. Except for the neurologic examination findings, the remainder of the physical examination was unremarkable.
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Citation: Journal of the American Veterinary Medical Association 244, 12; 10.2460/javma.244.12.1377
Assessment
Anatomic diagnosis
| Problem | Rule out location |
|---|---|
| Left-sided head tilt, vestibular ataxia, and nonpositional ventral strabismus left eye | Peripheral vestibular system, central vestibular system, brainstem, or C1 through C3 vertebrae |
| Ptosis of the left eye | Peripheral facial nerve or sympathetic trunk |
| Right-sided deviation of the muzzle | Peripheral facial nerve |
Likely location of one lesion
Left petrosal portion of the temporal bone involving the internal acoustic meatus; lesion resulting in cranial nerve VII damage proximal to the chorda tympani and cranial nerve VIII damage affecting the peripheral vestibular system at the level of the inner ear. Central vestibular system, brainstem, and C1 through C3 vertebrae are ruled out as possible locations.
Computed tomography images of the cranium of a 9-month-old Thoroughbred filly that had a 3-month history of right-sided muzzle deviation, left lip droop, and left head tilt. Notice the left-sided filling of the tympanic cavity (white arrow; A), with external ear canal narrowing and excessive petrous and temporal bone remodeling (B, C).
Citation: Journal of the American Veterinary Medical Association 244, 12; 10.2460/javma.244.12.1377
Etiologic diagnosis—Sudden onset of peripheral vestibular disease with facial nerve paralysis in horses may have a traumatic, infectious, inflammatory, toxic, or idiopathic cause. In the horse of this report, the peripheral vestibular signs and facial nerve paralysis were chronic and nonprogressive in nature, making a traumatic or infectious cause (disease of the auditory tube diverticulum [guttural pouch] or otitis media or interna) most likely. The diagnostic plan included guttural pouch endoscopy (to rule out diseases such as guttural pouch empyema, extension of otitis media or interna, or pathological and degenerative changes of the stylohyoid bone), skull radiography (to rule out gross fracture or trauma), CT (to provide a detailed evaluation of the cranium and proximal cervical vertebrae [C1 through C3]), analysis of a CSF sample (to rule out infectious or inflammatory processes), and brainstem auditory evoked potential (BAEP) testing (to assess the left-sided deafness).
Diagnostic test findings—Endoscopy revealed moderate inflammation and folliculitis of the larynx and guttural pouches consistent with a viral airway infection as well as very mild subjective thickening of the proximal articulation of the left dorsal stylohyoid bone. Radiography revealed a focal region of bony remodeling and sclerosis surrounding the tympanic bulla and temporal bone indicative of a previous trauma. Computed tomography revealed soft tissue swelling, thickening and mineralization of the external ear canal, and fracture and fragmentation of the tympanic bulla with irregular, smoothly marginated dense soft tissue mineralization and near complete soft tissue opacification of the remainder of the tympanic cavity (Figure 1). Additionally, irregularly marginated moderate periosteal bony remodeling was evident along the left lateral aspect of the occipital bone. Unilateral left-sided deafness was confirmed and localized to the inner ear; testing of the left ear revealed a complete absence of BAEP waveforms.1,2 The analysis of a CSF sample was considered unnecessary given the CT findings.
A diagnosis of vestibular disease was made on the basis of the clinical and neurologic findings, including head tilt, ventral deviation of the left eye, and ataxia. Together with the absence of signs of brainstem disease (altered mentation, behavioral changes, weakness, or hyperreflexia) and maintenance of bilateral menace and palpebral responses (although weaker on the left), the findings were indicative of a peripheral vestibular disease. The absence of a resting nystagmus and the marked exacerbation of clinical signs with the removal of visual input were not unexpected because the extent of visual compensation in horses with chronic lesions can be considerable. A cranial cervical lesion at C1 through C3 that affects the cervicovestibular afferent fibers can also result in vestibular signs in horses,3 but such a lesion was ruled out because no other signs of spinal cord disease were detected.
Facial nerve paralysis can often be associated with lesions involving the vestibulocochlear nerve because those 2 nerves originate adjacent to each other from the lateral aspect of the trapezoid body (medulla) and run jointly through the internal acoustic meatus within the petrous temporal bone. Thus, trauma to the region of the petrous temporal bone, as observed in the horse of this report, can result in damage to both the facial and vestibular nerves. Additionally, because the facial nerve runs adjacent to the middle ear, it can be affected by extension of otitis media or interna or from guttural pouch disease. The lack of notable endoscopic findings, together with the clinical signs of left-sided facial nerve paralysis and peripheral vestibular disease, supported the suspicion that a traumatic event had caused damage to both the left facial and vestibulocochlear nerves in this horse. The likely acquired, unilateral, left-sided deafness localized to the inner ear could also be a result of a traumatic event in this region. This was supported by the history of facial swelling and clinical examination findings as well as the abnormalities to the inner ear detected via CT. Although not performed for this horse, findings of additional diagnostic tests (eg, somatosensory evaluation of the facial nerve branches to the inner pinna, evaluation of taste by means of application of atropine to the rostral two-thirds of the tongue, and a Schirmer tear test) could have aided in the further neuroanatomical localization of the lesion along the length of the facial nerve.
Comments
Vestibular disease in horses most often develops secondary to trauma or infectious processes.3–5 Clinical signs are often acute, and management and treatment can be difficult.3 The correct differentiation between central and peripheral lesions is critical because that distinction directly affects treatment and prognosis. Central vestibular disease (affecting the brainstem or ventral portion of the cerebellum) often results in other severe clinical signs, including coma or obtundation, dysphagia, ataxia and tetraparesis, or an inability to stand. Central vestibular disease can develop secondary to diffuse brain lesions (eg, equine protozoal myeloencephalitis or arbovirus encephalitis), hepatic encephalopathy, neoplasia, or brain trauma; affected horses have a poor to grave prognosis. With regard to the left-sided ventral strabismus in the case described in this report, the exaggeration of the dynamic physiologic response in the left eye during elevation of the head was noteworthy. The filly maintained the ability to move the eye freely within the globe, suggesting a strictly vestibulocochlear localization rather than additional involvement of cranial nerves III, IV, or VI.
Prognosis for horses with peripheral vestibular disease is variable, depending on the neuroanatomical localization, severity, and cause of the pathological changes, but is in general more favorable than the prognosis for horses with central vestibular disease.3 Horses with mild, nonprogressive vestibular damage can often use visual input to compensate remarkably well, although prognosis for athletic function remains guarded. Horses with signs of facial nerve dysfunction or ipsilateral deafness or blindness, in addition to signs of vestibular disease, have a more unfavorable prognosis.3,6 In the horse of the present report, the involvement of the facial nerve and the total unilateral loss of auditory response, together with the chronicity of the clinical signs indicated an extremely pessimistic prognosis for functional recovery and return to athletic activity. Given the prognosis for the horse, euthanasia was elected. Postmortem histologic examination of sections of the buccal branches of the left facial nerve revealed changes consistent with Wallerian degeneration, a distinct pattern of degenerative axonal changes most often seen following transection or crushing trauma of a peripheral nerve.7
This feature is published in coordination with the American College of Veterinary Internal Medicine on behalf of the specialty of neurology. Contributors to this feature should contact Dr. Helen L. Simons (800-248-2862, ext 6692) for case submission forms. Submissions will be sent to Dr. Karen Kline, DVM, DACVIM, for her review, except when Dr. Kline is an author.
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5. Newton SA, Knottenbelt DC. Vestibular disease in two horses: a case of mycotic otitis media and a case of temporohyoid osteoarthropathy. Vet Rec 1999; 145: 142–144.
6. Firth CE. Vestibular disease and its relationship to facial paralysis in the horse: a clinical study of 7 cases. Aust Vet J 1977; 53: 560–565.
7. Selzer ME. Axon degeneration and rescue. In: Textbook of neural repair and rehabilitation: neural repair and plasticity. Vol I. Cambridge, England: Cambridge University Press, 2006; 293–295.
