"Inner Ear Disease:
Many different problems result in inner ear disease; however, the clinical signs caused by these diseases are similar, indicating the location of the disease rather than the specific cause. These signs are those of peripheral vestibular dysfunction, including head tilt, nystagmus, circling and imbalance. On the other hand, since the diseases which cause inner ear disease are usually slower in evolution, these signs are generally less severe than with idiopathic vestibular disease. In addition to the vestibular signs, there are also varying degrees of facial nerve dysfunction and often Horner's syndrome. Anatomically, the facial nerve and the sympathetic fibers heading to the eye pass near the inner ear in the osseous petrous temporal bone. Damage of these neural structure, in addition to the damage of the vestibular nerve is a hallmark for inner ear disease. It is possible to affect both the facial and vestibular nerves together in the calivarium, but it is rare to see Horner's syndrome from central nervous system disease. As such, Horner's syndrome suggests that the disease in process is in the peripheral C8-T2 nerve roots, the vagosympathetic trunk, the inner ear or within the orbit. When Horner's syndrome is seen in combination with vestibular disease and facial nerve disease, the location must be in the peripheral vestibular system in the region of the osseous petrous temporal bone.
The signs of facial nerve dysfunction include paresis or paralysis of the muscles of facial expressions (lack of ear movement, lack of blink and lack of buccal muscle reaction on palpation). This leads to deficiency of the vibrissa reaction, decreased to absent menace response and diminished to absent palpebral response. In addition, the facial nerve supplies parasympathetic innervation to the lacrimal gland of the eye. As such, peripheral facial nerve disease can lead to diminished tear production in the eye on the affected side. This can be rather catastrophic in inner ear disease where the facial nerve dysfunction results in the inability to close the eye, while also decreasing tear production. As such, every dog with inner ear disease should have a Schirmer's tear test run on the eyes and appropriate treatment instituted if tear production is deficient.
Horner's syndrome varies among species. In small animals the ocular signs predominate, including myosis, ptosis and enophthalmos. In horses, the signs of Horner's syndrome are expressed primarily as excessive sweating on the affected side of the face. In cattle, there is a lack of sweating on the muzzle of the affected side.
The most common cause of inner ear disease in all species is secondary in inner ear infection. Most of these represent bacterial extension from otitis media which can arise from hematogenous spread from bacteremia or from spread up the eustachian tube to the middle ear. Luckily, these infections, once recognized, can often be successfully treated. Other causes of inner ear disease may not be treatable, including fungal infections and neoplasia. Therefore, it is generally best to "treat-for-the-treatable" when dealing with inner ear disease, using appropriate antibiotic therapy.
The minimum data base for diagnosis of inner ear disease includes physical and neurologic examination, Schirmer's tear test, otoscopic examination (with culture of the external ear canal, if indicated), pharyngeal examination, CBC and urinalysis. If there is evidence of cardiac murmur, then cardiac ultrasound should be performed. Skull radiographs are then necessary to evaluate the degree of change in the osseous structures of the inner ear. This will be helpful in making the diagnosis and in monitoring the response to treatment.
The treatment of bacterial inner ear infection must consider the fact that the disease represents bone infection. As such, the antibiotic must be able to penetrate bone, develop good tissue concentrations (including the blood-ear barrier) and, preferably, be bactericidal in action. Many veterinarians use enrofloxacin as their antibiotic of choice. I find that enrofloxacin is great for treating gram negative infections in the lung, but it may not reach tissue concentrations within neural structures like the inner ear. It needs additional help to do this. Therefore, if I do not use my treatment of choice, I will add a sulfa drug to enrofloxacin to take advantage of the synergistic effect of sulfa drugs. My antibiotic regime of choice is cephalosporins and sulfa drugs (sulfadimethozine) in combination. This meets the criteria for the ideal therapy for inner ear disease. It is excellent in treating gram positive bacteria, which are the most common organisms infecting the inner ear. Since this is a bone infection, the treatment must be continued for 6-8 weeks, minimum. The most common cause of treatment failure is not treating long enough. "---http://neuro.vetmed.ufl.edu/neuro/vestibular/vestib.htm