Page 859 - Clinical Small Animal Internal Medicine

77 Neuroophthalmology 827

Horner’s Syndrome sympathomimetic with cases of postganglionic Horner’s
VetBooks.ir Sympathetic fibers to the eye originate in the paraven­ syndrome. With the difficulty in obtaining these agents
and abuse potential, this testing is rarely completed.
Direct‐acting sympathomimetic agents such as 0.001%
tricular nucleus of the hypothalamus, course within the
spinal cord and exit between T1 and T3 into the thoracic epinephrine or dilute (1%) phenylephrine can be used to
cavity, forming the sympathetic trunk. These fibers travel confirm a postganglionic lesion due to denervation hyper­
through the mediastinum and join the vagosympathetic sensitivity of smooth muscle. With a postganglionic defect,
trunk in the neck before synapsing at the cranial cervical application of these agents will allow improvement of the
ganglion located adjacent to the tympanic bulla. All fib­ clinical signs within 5–20 minutes. Lack of a response is
ers prior to this synapse are considered preganglionic suggestive, but not diagnostic, of a preganglionic lesion.
and those that course from the cranial cervical ganglion Preganglionic lesions carry a worse prognosis than
to the eye are considered postganglionic. Any disruption postganglionic. The majority of preganglionic cases are
of nerve conduction along this circuitous route will lead secondary to neoplasia, vascular events, or significant
to the classic clinical signs of Horner’s syndrome. head, neck, brachial plexus, or chest trauma. A diagnosis
Clinical signs include ptosis secondary to loss of tone of preganglionic Horner’s requires further diagnostics to
in Müller’s muscle of the upper and lower eyelid, miosis localize the lesion and should include a complete blood
due to loss of sympathetic tone in the iris dilator muscle, count, serum biochemistry, thyroid level, thoracic radi­
and enophthalmos with secondary third eyelid elevation ography, MRI of brain and spinal cord, and CSF analysis.
due to loss of smooth muscle tone of the periorbita Treatment is directed toward the underlying cause.
(Figure 77.4). These four clinical signs are diagnostic for Prognosis for return of function is guarded.
Horner’s syndrome. Depending on where nerve conduc­ Postganglionic lesions tend to be idiopathic or second­
tion is disrupted, these may be the only clinical signs, or ary to otitis media, but can be secondary to retrobulbar
additional clinical signs may be present, including altered disease or trauma. If there is no evidence of ear disease,
behavior/mentation, altered gait or paresis, spinal or an idiopathic cause is assumed. Golden retrievers and
neck pain, dysphagia, coughing, regurgitation, otitis Labrador retrievers between the ages of 10 and 12 years
media, vestibular disease, keratoconjunctivitis sicca, or are overrepresented. Most cases of idiopathic, postgan­
facial nerve paralysis. Localization of the lesion is impor­ glionic Horner’s syndrome resolve without treatment
tant for both prognosis and potential treatment. within two months.
Pharmacologic testing along with identifying clinical
signs are useful in differentiating preganglionic from post­
ganglionic Horner’s syndrome. Topical application Cavernous Sinus Syndrome
of indirect‐acting sympathomimetic drugs such as
1% hydroxyamphetamine will induce norepinephrine The cavernous sinus incorporates two venous sinuses
release from postganglionic neurons, allowing immediate located at the base of the cranial vault extending from
pupil dilation. This positive test confirms preganglionic the orbital fissure to the petrooccipital canal. The sinuses
Horner’s syndrome. There is no effect of an indirect‐acting are joined by several anastomoses across the midline.
Structures of clinical significance that pass through or
are in close proximity to the cavernous sinus include the
oculomotor nerve, trochlear nerve, ophthalmic and
maxillary branches of the trigeminal nerve, abducens
nerve, and postganglionic sympathetic axons.
Dogs and cats with cavernous sinus syndrome present
with a multitude of clinical signs related to the affected
cranial nerves, including internal and external ophthal­
moplegia (mydriasis, ptosis, lateral or ventrolateral
strabismus), corneal anesthesia, periorbital and facial
anesthesia, and enophthalmos. Most cases are unilateral,
with rare bilateral cases reported. Mean age of affected
dogs and cats is 9 and 10 years of age, respectively.
Diagnosis is obtained through observation of the
clinical signs. Advanced imaging, preferably MRI, is nec­
essary to confirm the diagnosis. Most reported cases in
Figure 77.4 Horner’s syndrome in a cat, demonstrating ptosis of
the left upper eyelid, enophthalmos, third eyelid elevation, and dogs occur secondary to primary or metastatic neopla­
miosis. sia. In cats, intracranial neoplasia and infectious disease