daylight without access to a darkened environment (see case example in Chapter 10).
It is often good to recall that even partial sunlight is brighter than any commonly used, handheld penlight or ophthalmoscope.
Here, it must be recalled that blinking in response to a bright light, the dazzle response, does not involve the visual pathways from the thalamus to the visual cortex, and the presence of this response does not equate with intact vision. Its presence does indicate that light is stimulating the light pathways into the midbrain and thence to the facial nucleus, but it should not replace testing the true pupillary light and menace responses as outlined. Thus, it is conceivable that a dazzle response can be present in a centrally blind patient that also has no oculomotor nerve function and therefore no pupillary light reflexes, a very unlikely clinicopathologic scenario.
The prognosis for acquired peripheral blindness is bad compared to that for central visual pathway lesions. Apart from eye diseases, most common causes of only peripheral blindness would be head trauma,1,2 sphenopalatine sinus infection and neoplasia,3 progressive ethmoid hematoma, and various anthelmintic toxicities.4–7 In comparison, the prognosis for partial central blindness is better as such patients are able to compensate well and at times to regain quite amazing degrees of apparent visual acuity.
The postictal period may be associated with temporary central blindness presumably due to neuronal exhaustion in central visual pathways. Also neonates, although they can see, have poor menace responses in the first 1 or 2 weeks of life.8
Finally, degrees of blindness occur with many ocular diseases. Of some note is that with cases of congenital peripheral blindness, there can be associated abnormal eyeball positions, with the globe directed dorsally and sometimes wavering, searching eyeball movements. Removal of obstacles and provision of a “buddy” that wears a bell are some of the provisions that assist in caring for a blind horse.9,10 The reader is referred to texts of ophthalmology and particularly to chapters on neuro‐ophthalmology in large animals.911–18
References
1 1 Matz K, Gerhards H, Heider HJ and Drommer W. Bilateral blindness after injury in a riding horse. Tierarztl Prax 1993; 21(3): 225–232.
2 2 Reppas GP, Hodgson DR, McClintock SA and Hartley WJ. Trauma‐induced blindness in two horses. Aust Vet J 1995; 72(7): 270–272.
3 3 Sano Y, Okamoto M, Ootsuka Y, et al. Blindness associated with nasal/paranasal lymphoma in a stallion. J Vet Med Sci 2017; 79(3): 579–583.
4 4 Button C, Jerrett I, Alexander P and Mizon W. Blindness in kids associated with overdosage of closantel. Aust Vet J 1987; 64(7): 226.
5 5 Barlow AM, Sharpe JA and Kincaid EA. Blindness in lambs due to inadvertent closantel overdose. Vet Rec 2002; 151(1): 25–26.
6 6 Borges AS, Mendes LC, de Andrade AL, Machado GF and Peiro JR. Optic neuropathy in sheep associated with overdosage of closantel. Vet Hum Toxicol 1999; 41(6): 378–380.
7 7 Pollio D, Michau TM, Weaver E and Kuebelbeck KL. Electroretinographic changes after intravenous lipid emulsion therapy in a dog and a foal with ivermectin toxicosis. Vet Ophthalmol 2018; 21(1): 82–87.
8 8 Enzerink E. The menace response and pupillary light reflex in neonatal foals. Equine Vet J 1998; 30(6): 546–548.
9 9 Dwyer AE. Management of blind horses. In Equine Ophthalmology, Gilger BC, Editor. 3rd ed. Wiley‐Blackwell, Oxford, UK. 2016; 629.
10 10 Dwyer A. Hello darkness my old friend: management of blind horses. Equine Vet Educ 2021; 5.
11 11 Mayhew IG. Neuro‐ophthalmology. In Equine Ophthalmology: An Atlas and Text, Barnett KC, Crispin SM, Lavach J.D, Matthews AG, Editors. 2nd ed. London, UK. 2004; 247–254.
12 12 Irby NL. Neuro‐ophthalmology in horses. Vet Clin North Am Equine Pract 2011; 27(3): 455–479.
13 13 Mayhew IG. Neuro‐ophthalmology: a review. Equine Vet J Suppl 2010; ( 37): 80–88.
14 14 Brooks DE. Equine Ophthalmology. Ann Conv Amer Assoc Eq Pract 2002; 48: 300–313.
15 15 Beltran E, Matiasek K and Hartley C. Equine neuroophthalmology. In Equine Ophthalmology, Gilger BC, Editor. 3rd ed. Wiley‐Blackwell, Oxford, UK. 2016; 567.
16 16 Lavach JD. Large Animal Ophthalmology. Mosby, St. Louis, MO. 1990; 395.
17 17 Myrna KE. Neuro‐ophthalmology in the horse. Vet Clin North Am Equine Pract 2017; 33(3): 541–549.
18 18 Pont RT and Beltran E. Clinical approach to equine neuro‐ophthalmology. In Practice 2019; 41(8): 383–393.
10 Miosis, mydriasis, anisocoria, and Horner syndrome
Degrees of miosis (constricted pupil), mydriasis (dilated pupil), and anisocoria (asymmetric pupil size) occur in many ocular diseases, often accompanied by degrees of visual impairment. Large animal patients are not very frequently presented because of these problems alone; however, identifying them on a neurologic examination greatly helps in localizing the lesion. Texts discussing the evaluation and treatment of eye problems in large animals should be consulted for ophthalmic diseases.1–6
The pupillary constriction (CN III) and dilation (ocular sympathetic) pathways should be reviewed (Figure 2.7 and 2.8). Normal resting pupil size will depend on the emotional state of the patient and the amount of ambient light reaching the retinas. Usually, a nonfrightened large animal patient has a brisk initial pupillary light reflex (PLR). However, a common problem uncounted during examination is the patient blinking when a light is directed into one eye—the dazzle response—thus hiding the initial fast constrictive phase of the PLR. This can be averted by allowing the patient to accustom to the light, starting at say 30–40 cm from the eyes, swinging it from focusing into each eye in turn while moving closer, and observing for tapetal reflexes that highlight pupillary diameters. After determining pupil size and symmetry, the PLR can be assessed using a one second bright light flash directed to the area centralis in the midlateral (temporal) field where photoreceptor density is greatest. Interpretation should consider the phenomena of pupil escape following light‐on, and the postillumination pupil response occurring after light‐off (Figure 10.1).
Figure 10.1 Diagram of pupillary response to light‐on and to light‐off. Note that latency to start of constriction from light‐on is ~200ms.
Source: Modified from Hall and Chilcott,9 figure 1 (CC BY 4.0).
Of interest here is the newly recognized, intrinsically photosensitive, retinal ganglion cells (ipRGCs), which rely on a unique photopigment, melanopsin, and they are now known to have a major role in nonvisual light pathways including the PLR. Use of red and blue light PLR testing has now allowed the testing of retinal cell subpopulations.7–9 In general terms, low intensity, dark‐adapted (scotopic), blue light PLR tests rod function, high intensity, dark adapted, blue light tests ipRGC function, and high intensity, photopic, red light PLR tests cone function. Better understanding of the details of such testing and use of handheld pupilometers10 will allow for a more accurate assessment of visual and light pathways in our large animals.11
Results