Page 1143 - Small Animal Internal Medicine, 6th Edition

CHAPTER 63 Head Tilt 1115

Degeneration within the vestibular system may result in uni- INFLAMMATORY DISEASES
lateral or bilateral peripheral vestibular signs and loss of Most of the infectious and noninfectious inflammatory dis-
VetBooks.ir hearing. In most cases, the vestibular signs resolve if therapy eases discussed in Chapter 64 can cause central vestibular
signs. In particular, granulomatous meningoencephalitis,
is discontinued immediately, but deafness may persist.
CHEMICAL OTOTOXICITY canine distemper, necrotizing leukoencephalitis, Rocky
Mountain spotted fever, and feline infectious peritonitis
Many drugs and chemicals are potentially toxic to the inner (cats) seem to have a predilection for this region of the brain.
ear. If the integrity of the tympanic membrane is in doubt, Adult-onset neosporosis and steroid-responsive tremor syn-
topical otic products containing chlorhexidine, dioctyl-sulfo drome also commonly affect the cerebellum, resulting in
succinate (DOSS), or aminoglycosides should not be used. central vestibular signs. See Chapter 64 for a discussion of
Warm saline or 2.5% acetic acid solutions should be used for the diagnosis and treatment of intracranial inflammatory
flushing ears. Whenever vestibular dysfunction becomes disorders.
evident immediately after instilling a substance in an ear
canal, the product should be removed and the ear canal THIAMINE DEFICIENCY
flushed with copious quantities of saline. Vestibular signs Thiamine deficiency can occur due to prolonged anorexia,
will usually resolve within a few days or weeks, but deafness, maldigestion/malabsorption disorders, inadequate dietary
if it occurs, may persist. intake, or ingestion of thiaminase in raw fish. Cats are much
more susceptible than dogs, developing a rapidly progressive
HYPOTHYROIDISM encephalopathy with neurologic signs suggesting diffuse ves-
Peripheral vestibular dysfunction has occasionally been re- tibular dysfunction including vestibular ataxia, circling, and
ported in association with hypothyroidism in adult dogs. wide excursions of the head and neck. Other signs can
Concurrent facial nerve paralysis may be seen, and a few include blindness, mydriasis, ventroflexion of the head and
dogs exhibit weakness, suggesting a more generalized poly- neck, seizures, coma, and even death. Magnetic resonance
neuropathy. Other systemic signs of hypothyroidism, such (MR) imaging can be normal or can reveal bilaterally sym-
as weight gain, poor haircoat, and lethargy, may or may metrical hyperintense foci on T2-weighted and FLAIR (fluid
not be present. Clinicopathologic testing may show abnor- attenuation recovery) in grey matter regions of the brain-
malities suggestive of hypothyroidism (e.g., mild anemia, stem, cerebrum, and cerebellum. Supplementation with par-
hypercholesterolemia). The diagnosis is established through enteral and oral thiamine and changing the diet to include
thyroid function testing (see Chapter 48). The response to adequate thiamine will usually result in a rapid recovery and
replacement thyroid hormone is variable, but improvement resolution of all neurologic signs, including seizures. Thia-
typically occurs within 2 months if hypothyroidism was the mine (12.5-30 mg/cat IM or SC q24h) is often administered
cause. to cats with undiagnosed neurologic signs suggesting an
intracranial lesion, particularly those with vestibular signs or
DISORDERS CAUSING CENTRAL seizures (see Chapter 60).
VESTIBULAR DISEASE
INTRACRANIAL NEOPLASIA
Central vestibular disease is much less common in dogs and Intracranial tumors such as meningiomas and choroid
cats than peripheral vestibular disease and generally carries plexus tumors have a tendency to develop in the cerebello-
a poor prognosis. Central vestibular disease can be caused pontomedullary (caudal fossa) region, making central ves-
by any inflammatory, neoplastic, vascular, or traumatic dis- tibular signs common. Central vestibular signs may result
orders affecting the brainstem or vestibular portion of the from any intracranial tumor that causes compression or
cerebellum (see Box 63.2). invasion of vestibular nuclei, increased intracranial pressure,
A standard workup for intracranial disease is performed early brain herniation, or obstructive hydrocephalus. Pre-
in animals that have central vestibular signs. Complete sumptive diagnosis is usually made with MRI, but definitive
physical, neurologic, and ophthalmologic examinations are histologic diagnosis requires biopsy. Prognosis is dependent
essential to look for evidence of disease elsewhere in the on tumor histologic type, neuroanatomic location, and
body. Clinicopathologic testing, thoracic and abdominal severity of the neurologic signs. Cytoreductive surgery and
radiographs, and abdominal ultrasound are warranted to radiotherapy may be treatment options. Palliative treatment
search for neoplastic or infectious inflammatory systemic with glucocorticoids (prednisone, 0.5-1 mg/kg/day PO) may
disease. When systemic evaluation does not provide a di- temporarily improve clinical signs.
agnosis, brain MRI should be performed. MRI abnormali-
ties are identified in almost every patient with evidence of CEREBROVASCULAR DISEASE
central vestibular dysfunction. When inflammatory disease Ischemic infarcts have been increasingly recognized as a
is suspected, CSF collection and analysis should also be con- cause of acute-onset, nonprogressive central vestibular signs,
sidered. (See Chapter 60 for a more thorough discussion of often affecting the vestibulocerebellum and resulting in para-
the diagnostic approach taken in animals with intracranial doxical vestibular signs. In dogs, thrombotic occlusion of the
disease.) rostral cerebellar artery is especially common, resulting in