Читать книгу Large Animal Neurology - Joe Mayhew - Страница 33

An owner may report that a patient appears to be acting blind. However, a moribund, somnolent or inattentive patient, or one with marked weakness or with loss of balance due to vestibular disease, may stumble over objects without being blind.

The visual pathway is tested by the menace response, whereby a mildly‐threatening gesture of the hand toward the eye elicits immediate closure of the eyelids (Figure 2.2). In large animals, 80–90% crossing of optic nerve fibers occurs at the chiasm (Figure 2.6).¹⁶ However, for initial, practical purposes, vision in one eye can be regarded as being perceived in the visual cortex of the opposite or contralateral cerebral hemisphere. The incoming, afferent pathway for the menace response is the ipsilateral eye and optic nerve, the optic chiasm, the contralateral optic tract, lateral geniculate nucleus in the thalamus, optic radiation, and visual cortex that is mostly in the occipital lobe (Figures 2.6 and 2.9). The outgoing, efferent pathway of the menace response is from this contralateral visual cortex to the ipsilateral facial nucleus effecting closure of the eyelids. With an intact efferent pathway resulting in blinking, it is assumed that the visual input reached the visual cortex. Some stoic, moribund, somnolent, and even excited animals may not respond to a hand menace with closure of the eyelids, or they may keep the eyelids closed. A true visual deficiency may be detected while the animal moves about its environment, when objects are placed in front of it—a visual maze test—or when nonaromatic objects are dropped noiselessly in its visual field. Partial, unilateral blindness can be difficult to detect and it may take repeated efforts, such as blindfolding each eye in turn, to determine this. Total unilateral blindness with absence of a menace response in only one eye is usually quite easy to detect. However, repeated testing is usually necessary to confirm an asymmetric but bilaterally present menace response, and the above assessments are very useful to detect such lesions.

Figure 2.6 Visual pathway.

As indicated, the true menace response is a blink that immediately follows a visually threatening gesture, without necessarily being accompanied by withdrawal of the head (Figure 2.2). The latter visual avoidance response may well not require an intact visual (occipital) cortex but most probably involves central pathways just within the brainstem and certainly without input from the ipsilateral cerebellar cortex as is the case with the menace response. If there is an absent menace response, then we use a more powerful threat, after tapping the forehead several more times, to try to detect eyeball retraction or head withdrawal that will at least confirm a partial afferent visual pathway input to the brainstem but not necessarily to the visual cortex. However, this can be somewhat problematic except in the most obliging patients. With little or no menace response but some visual avoidance response obviously present, then facial musculature and cerebellar function requires further evaluation. Should these be without problems, then a visual maze test may be required to better scrutinize visual acuity. Interpretation of artificial maze tests can be rather uncertain, and a decision on visual acuity often concludes with general observations of the patient’s response in its environment to nonauditory, nonaromatic, visual clues, such as a brightly lit open doorway or gate.

When a visual deficit is suspected, a visual field deficit may be determined in large animals having unilateral or prominently asymmetric cerebral or thalamic lesions. In describing these subtle field deficits, it is necessary to be clear about two things. First, the eye not being tested should be covered to avoid nonspecific crossover from visual stimuli. Second, the left visual field is detected predominantly via the nasal (medial) retina of the left eye and partly (~10–20%) via the temporal (lateral) retina of the right eye; the latter region of the retina containing most of the neurons whose axons do not cross at the optic chiasm (Figure 2.6). Likewise, the right visual field is perceived predominantly via the nasal retina of the right eye and partly via the temporal retina of the left eye. Thus, with a prominent lesion in the right dorsal thalamus, right occipital radiation, or right occipital cortex, a patient will appear to be blind in the left eye with normal pupillary responses bilaterally. The left visual field deficit may be detected as a poor or absent menace response in the nasal retina of the left eye when using the threatening stimulus directed from the lateral aspect of the left eye and by a poor response to a visual threat directed to the temporal retina of the right eye with the stimulus directed from the medial aspect of the right eye. The nontested eye should always be covered during these visual field tests.

Lesions of the eye and optic nerve result in ipsilateral blindness. Lesions of the optic tracts and lateral geniculate nucleus cause contralateral central blindness with normal pupillary function. Space occupying lesions of the brain frequently produce such central blindness (amblyopia) by interfering with the optic radiations or visual cortex. However, with a large forebrain mass on one side, possibly resulting in contralateral central blindness with normal pupils, the optic nerve may secondarily become compressed on the ipsilateral (to the lesion) side resulting in ipsilateral peripheral blindness. Similarly, secondary compression of the oculomotor nerve under the midbrain can cause additional mydriasis ipsilateral to such a mass lesion.

Animals with various diffuse cerebellar diseases have been observed to have bilaterally deficient menace responses. These animals are not blind, do not have facial paralysis that would explain the menace deficit, and they pull their head away from the menacing gesture, thus demonstrating degrees of amblyopia. It has been assumed that in large animals the pathway for the menace response passes from the occipital cortex contralateral to the visual threat, back across the midline and through the ipsilateral cerebellum, before targeting the facial nucleus ipsilateral to the visual stimulus. It is perhaps as likely that the cerebellum exerts both stimulatory and inhibitory influences on many cerebral functions, including visual responses.¹⁷ Cerebellar disease may well thus interfere with such modulating influences, thereby effecting an altered, suppressed, menace response. Foals and calves appear to be able to see by a few hours of age but do not blink in response to a menacing gesture until several days to 2 weeks of age.¹⁸ They do blink in response to a dazzling bright light and pull their heads away from a strong menacing gesture, often in a jerky manner. These normal findings in the neonatal period are reminiscent of those found with cerebellar disease in more mature animals.