Anne J. Gemensky Metzler,     Columbus, Ohio

Obtaining a Thorough History

The client should be questioned to ascertain the onset, duration, and character of the blindness. Answers to the following questions should be obtained to the extent possible: (1) Did the blindness occur fairly rapidly over hours or days or was the onset more gradual, occurring over weeks to years? (2) Was the onset of vision loss obvious or more insidious? (3) In what type of environment was the blindness first noticed? (4) What is the duration of the visual impairment or loss? (5) Has the vision loss been intermittent, waxing and waning, or constant since first noticed? (6) Has there been any difference in visual function in bright light compared with dim light or darkness? (7) Does the pet seem to be more impaired centrally or peripherally or on one side (right or left) more than the other? Although some clients are better observers than others, their responses to each of these questions offer valuable clues about the cause of vision loss.

It is useful to ask the client to describe the behavior of the pet that makes the client feel the pet has vision difficulties to help in discerning whether an ophthalmic problem is the source of the behavioral changes causing concern. In some situations, it is not apparent to the client that his or her pet is blind until the pet is taken to an unfamiliar environment. The client also should be questioned about the pet’s general health, current and past administration of medications, and awareness of any genetically related pets that have been diagnosed with ophthalmic disorders.

Assessing the Patient

Once the history has been obtained, the pet’s behavior and confidence navigating around the clinic and examination room should be assessed. Additional methods of assessing vision include menace response testing, cotton ball tracking, visual placing, maze testing, evaluation of the pupillary light reflexes (PLRs), and assessment of dazzle responses (see Chapter 242). Electroretinography, although it does not directly assess vision, also may be useful for assessing retinal function. It is important to evaluate the vision in each eye independently as well as to assess the visual fields of each eye. Visual fields are assessed by covering one eye and checking menace responses in the other by advancing a fist toward the tested eye from both the nasal and the temporal sides of the globe. Baseline pupil symmetry, the presence or absence of anisocoria, and the PLRs should be evaluated in both a brightly lit and a dimly lit room and the findings recorded.

Any abnormality of the PLRs should be characterized (ranging from a mild decrease to complete absence) and qualified as an afferent or efferent deficit. Afferent PLR deficits are associated with vision deficits. The pupillomotor fibers split off from the optic tract just before the lateral geniculate nucleus; therefore lesions involving the Edinger-Westphal nucleus (the parasympathetic nucleus of cranial nerve III) and the efferent arm of the PLR pathway are not associated with loss of vision (Figure 243-1). Lesions that involve the visual pathway from the lateral geniculate nucleus to the optic striations in the visual cortex do not cause abnormalities of the PLR or anisocoria (Figure 243-2).

Localizing Blindness

After the neuro-ophthalmic assessment is conducted, a complete ophthalmic examination, including evaluation of the anterior and posterior segments, is performed to determine whether the blindness is of ocular or neurologic origin. There are four main ways that blindness can be produced: (1) opacification of the ocular media; (2) failure of the neural retina or optic nerve to process and transmit an image; (3) failure of the extraocular portion of the optic nerve, the optic chiasm, or optic tracts to transmit an image; and (4) failure of the visual cortex of the brain to process an image.

The cornea, anterior chamber, lens, and vitreous must be examined carefully to detect opacification of the ocular media. Ideally this examination should follow pharmacologic pupillary dilation and should employ a focal bright light source such as a transilluminator as well as some type of magnifying device. Types of corneal opacification that may impair vision include severe edema, vascularization, cellular and noncellular infiltrates, pigment, and fibrosis. In the anterior chamber, severe aqueous flare, fibrin, hyphema, and hypopyon may decrease vision, as can dense or extensive cataracts. Posterior segment lesions such as the presence of vitreal inflammatory cells and vitreal degeneration with consolidation and asteroid hyalosis are additional causes. It is stressed that although opacity of the ocular media can alter light transmission sufficiently to cause blindness, the PLR and dazzle response should be present provided that the light source is bright and the neural pathways are intact.

Next the menace response, PLR, and dazzle response can be assessed further to localize the neuro-ophthalmic source. If the menace response is absent, the ability to blink should be tested using the palpebral reflex and vision loss should confirmed by another method such as cotton ball tracking or maze testing. If the menace response is absent and the PLR and dazzle responses are abnormal or absent, then the lesion involves the retina, optic nerve, optic chiasm, or optic tracts. If the PLR and dazzle responses are normal despite the presence of vision loss, then central blindness is most likely. Central blindness results from one or more lesions of the lateral geniculate nucleus, optic radiations, or visual cortex of the cerebrum.