Page 769 - Clinical Small Animal Internal Medicine

68 The Neurologic Examination 737

the light from OD where the pupil is constricted back pupillary constriction to light. In other words, the
VetBooks.ir to OS, the OS pupil that was constricted from stimula- pupillary light reflex neurons are the last to lose function
tion of OD is now dilating back to its original size.
when lesions disrupt the retina or optic nerve.
This asymmetry is repeated as you swing the light
The anisocoria of Horner syndrome has no effect on
back and forth between the two eyes. When you the menace response and both pupils will respond to
cover OD with your hand, the OS pupil fully dilates. light directed into either eye. The pupil asymmetry with
Anatomic diagnosis: in OS or the left optic nerve. In Horner syndrome will be more obvious in a dark room
most cases with this anatomic diagnosis, room light where the absence of room light will further dilate the
entering the normal eye is sufficient to keep the normal pupil.
pupil in the affected eye constricted. Occasionally, the Anisocoria may result from many intraocular disor-
pupil on the affected side will be slightly larger than ders. Iris atrophy is fairly common in older dogs and
the pupil on the unaffected side in room light. creates dilated unresponsive pupils with no interference
A patient has normal menace responses. Anisocoria is with vision. Be sure to evaluate the iris thoroughly with
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present with the pupil in OD widely dilated. Light your bright light source. Neurologic causes of anisocoria
directed into OD causes the pupil to constrict only in include disturbances to cranial nerves II and III and
OS. Light directed into OS causes only the OS pupil to the sympathetic ocular innervation. Examination of the
constrict. Anatomic diagnosis: right oculomotor nerve patient in a darkened room may help determine the
general visceral efferent (GVE) component, ciliary cause of anisocoria in your patient.
ganglion, ciliary nerves. Be aware that this reaction
may be the first clinical sign of an extraparenchymal Palpebral Fissure and Third Eyelid
mass lesion ventral to the diencephalon compressing Observe the size of the palpebral fissures and their
the oculomotor nerve and causing a loss of function of symmetry. In small animals, the fissure will be smaller
the GVE preganglionic neurons, which may precede with oculomotor nerve dysfunction (loss of function of
the loss of function in the GSE neurons. This disparity the levator palpebrae superioris muscle causing ptosis),
between the altered pupil size without ptosis or stra- sympathetic innervation dysfunction (loss of the orbit-
bismus is useful in making an anatomic diagnosis of alis smooth muscle function in the orbit), and secondary
the different components of the oculomotor nerve. to atrophy of the muscles of mastication from dysfunc-
A patient has no menace response OD with a normal tion of the mandibular nerve from the trigeminal nerve
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palpebral reflex. Anisocoria is present with the OD or chronic myositis. An elevated third eyelid will be
pupil widely dilated. Light directed into OD causes no apparent with sympathetic denervation, as well as
response OU. Light directed into OS causes only the secondary to atrophy of the muscles of mastication. The
OS pupil to constrict. Anatomic diagnosis: right optic third eyelid elevates in tetanus secondary to the tetanus
nerve and the GVE neurons of the right oculomotor of the extraocular muscles that results in retraction of
nerve, ciliary ganglion, ciliary nerves. A retrobulbar the eyeball and in animals with a facial paralysis when
neoplasm or abscess might produce this result. they are menaced.
A patient acts blind and has no menace response OU
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with normal palpebral reflexes. In room light, the Strabismus
pupils are mildly dilated. Light directed into OS causes Strabismus is an abnormal position of the eyeball. While
the pupils to constrict OU. Light directed into OD examining the eyes, you can appreciate whether they are
causes the pupils to constrict OU. This dog’s senso- normally positioned in the orbits. Normal ocular posi-
rium is normal. Anatomic diagnosis: both eyeballs, tion is dependent on the innervation of the extraocular
optic nerves, optic chiasm, or optic tracts. muscles by cranial nerves III, IV, and VI and the normal
function of the vestibular system. Repeatedly move the
Patients with lesions in the retina (retinal degeneration, head in a horizontal (dorsal) plane from one side to the
sudden acquired retinal degeneration) or optic nerves other. Watch the excursions of the eyeballs. The degree
(optic neuritis) OU often lose their vision and are clini- of adduction (medial rectus, cranial nerve III) should be
cally blind but still have light‐responsive pupils when a the same as the abduction (lateral rectus, cranial nerve
bright light is directed into the eyes. However, room light VI). This is normal physiologic nystagmus and requires a
is insufficient to cause normal constriction, and the normal vestibular system as well as normal oculomotor
pupils will appear mildly dilated. This response can be and abducent nerve function. In some cats, you will only
explained by the disease process sparing the retinal see this response at the end of the head movement.
neurons involved with these light responses or, more A ventrolateral strabismus occurs with oculomotor nerve
likely, with progressive loss of function of retinal neurons, dysfunction, a medial strabismus with abducent nerve
the threshold for loss of vision is lower than that for dysfunction, and an ocular extorsion with trochlear