Page 825 - Clinical Small Animal Internal Medicine

72 Vestibular Disease 793

the author’s experience. MRI may be normal or show to have a predilection for the cerebellar pontine angle,
VetBooks.ir evidence of ischemia within the vestibular system. leading to vestibulocerebellar signs, but can occur in
other locations as well.
A normal MRI cannot exclude an ischemic event as the
area of compromised tissue may be smaller than the
resolution of the MRI (especially in small patients and Neoplasia
low field magnets), or sequencing that best highlights Neoplastic processes that affect the central vestibular sys­
tissue ischemia may not be available (software limita­ tem include those that are commonly found at the cere­
tions). MRI done in close temporal relationship to the bellar pontine angle (CPA), such as malignant peripheral
onset of signs could miss lesions that may be evident if nerve sheath tumors of the trigeminal nerve that extend
done a few hours to days later. Very small hemorrhages intracranially, meningiomas, chorioid plexus tumors,
or ischemic areas may be missed if gradient echo or dif­ or ependymomas. Meningiomas, gliomas, round cell
fusion‐weighted sequences are not pursued. tumors, and metastatic disease involving the cerebellum
Hypothyroidism can result in the formation of athero­ (flocculonodular lobe) or brainstem vestibular nuclei can
sclerosis, leading to vascular thrombosis and signs men­ also result in vestibular signs. Changes in intracranial
tioned earlier. pressure due to neoplastic mass lesions elsewhere can
Hemorrhagic vascular events are less common and result in vestibular signs due to brainstem or cerebellar
underlying causes such as thrombocytopenia, clotting compression (including cerebral herniation under the
deficiencies (rodenticide toxicity, liver disease, etc.), tentorium cerebelli or cerebellar herniation from the
metastatic hemangiosarcoma, and hypertension should foramen magnum). MRI, +/−CSF, and surgical or CT‐
be investigated. guided biopsy are necessary to confirm an antemortom
definitive diagnosis of neoplasia. However, most diagnoses
Inflammatory of intracranial neoplasia are made on imaging character­
Inflammatory CNS disease (i.e., granulomatous meningo­ istics and treated as such with radiation therapy, +/−
encephalitis, necrotizing meningoencephalomyelitis, chemotherapy with definitive diagnosis only confirmed
and breed‐specific encephalitides) is one of the more after necropsy.
common diseases neurologists diagnose. Young to
middle‐aged toy‐breed dogs are typically affected, but Nonneoplastic Mass Lesions
any age and breed are susceptible. It usually presents as Epidermoid cysts, dermoid cysts, and teratomas are
multifocal disease and the patient may have one or more thought to arise from trapped ectodermal embryonic
of the following clinical signs: vestibular signs, cervical tissue as the neural tube is closing and therefore could be
pain, paresis, cranial nerve deficits, circling, obtunda­ included in the anomalous category. When found intrac­
tion, seizures. The cause is unknown but may be a com­ ranially, they appear to have a predilection for the caudal
bination of genetic predisposition and an antigenic trigger fossa and thus can produce vestibular signs. Other
(recent illness, vaccination/medication, environmental nonneoplastic mass lesions that could produce vestibular
antigenic stimulation) resulting in an inappropriate signs include arachnoid cysts/diverticuli, inflammatory
immune system attack on nervous tissue. MRI and spinal granulomas, cholesterol granulomas, infectious abscesses/
fluid analysis are needed at a minimum to determine a granulomas, parasitic cysts, and hematomas.
diagnosis. Often ruling out infectious disease (i.e., PCR
on CSF, serology, cultures, etc.) is necessary as the inflam­ Nutritional
mation may be secondary to another cause. Biopsy Thiamine deficiency (vitamin B1) in carnivores often
would be needed for a definitive diagnosis and, given the includes signs of central vestibular disease in addition
invasiveness, risk and cost associated, is not often pursued. to cerebrothalamic signs (mental dullness, seizures) and
Therefore, treatment is based on the signalment, history, postural changes, cervical ventroflexion (in cats in par­
and collection of diagnostic results supporting a sterile ticular), and paraparesis in dogs. Cat are more commonly
inflammatory disease process. affected than dogs and signs can progress rapidly.
As with other immune/inflammatory diseases, treatment Unconventional diets (raw fish diets, diets cooked at very
involves immunosuppression with one or more medica­ high temperatures, diets with sulfur dioxide preserva­
tions (i.e., prednisone, cytosar, azathioprine, cyclosporine, tives) are typically the cause, but even commercial diets
etc.) for a prolonged period of time, often months, some­ can lead to thiamine deficiency. Bilaterally symmetric
times years. Response to treatment can be quite varia­ changes on MRI (most apparent on FLAIR and gradient
ble, but in the author’s experience many patients can be echo sequences) within the brainstem nuclei (caudal
weaned off drugs with the less severe forms of disease. colliculi are most affected) are classic for thiamine
Inflammatory granulomas can cause mass lesions that deficiency. Histologic changes include petechial hemor­
may be mistaken for neoplasia. These granulomas seem rhages, edema, and neuronal necrosis.