Page 1224 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

Eyes 1199

VetBooks.ir clinical signs in a consistent situation and are ame- affected that they cannot be ridden at their intended
level in a discipline, or even in some cases ridden or
nable to the procedure. If signs resolve under the
effect of local anaesthesia then this confirms that
at rest, affected horses may be retired. However, where
the signs are due to facial pain. It does not determine handled safely at all. Where clinical signs do not occur
the origin of that facial pain. There is evidence that signs occur even at rest, in cases which are refractory
the procedure is unreliable, so failure to respond to to treatment, euthanasia on humane grounds should
diagnostic local anaesthesia does not rule out clinical be considered.
signs being due to facial pain. The procedure is inva-
sive and not without risk, so should be considered EQUINE MOTOR NEURON DISEASE
carefully before it is performed.
The remainder of investigations are required to Definition/overview
eliminate other causes of headshaking and should ide- EMND is an oxidative neurodegenerative disor-
ally include clinical examination, oral examination, der of the somatic lower motor neurons in horses
ophthalmic examination, upper respiratory tract and deprived of adequate dietary vitamin E for an
guttural pouch endoscopy and CT of the head. extended period of time. While the neurological
disease is the primary complaint in most cases,
Management ophthalmological disease can occur concurrently.
A true and purely photic headshaker should be Non-ophthalmic aspects are covered elsewhere.
manageable by eliminating exposure of the eyes to
sunlight by maintaining the horse in a darkened Aetiology/pathophysiology
environment, or the use of an eye mask, tinted Vitamin E is a fat-soluble antioxidant that counter-
contact lenses or even blindfolding. However, this acts the harmful free radicals normally produced
may not be practical or sufficient, and there are no during metabolism in animals. A deficiency in these
robust data on the treatment of photic headshakers. protective antioxidants is believed to predispose ani-
Treatments used for TMH should be considered. mals to neurotoxic and/or oxidative injury. The pho-
Unfortunately, little is known about the causes and toreceptor outer segments in the neurosensory retina
mechanisms of TMH, and advances in treatment have a high proportion of polyunsaturated fatty
will remain limited until we understand the aetio- acids in their lipids, which are extremely susceptible
pathogenesis of the condition. It is certainly pos- to oxidative stress. In cases of EMND, accumulation
sible that there is more than one cause with the same of ceroid-lipofuscin in the retinal pigmented epithe-
clinical manifestation, leading to different response lial cells over the tapetal and non-tapetal fundus is
rates to treatment. Regularly used treatments for thought to be the result of light-generated oxidative
TMH are: nose-nets; pharmaceuticals such as gaba- injury to the retina. This accumulation leads to the
pentin or carbemazepine alone or in combination increased retinal pigmentation visible on fundoscopy
with cyproheptadine; EquiPENS™ neuromodula- in affected animals. The remaining clinical find-
tion; and caudal ablation of the infraorbital nerve ings of EMND are the result of dysfunction and/or
via coil compression. All of these treatments have death of somatic efferent motor neurons, which leads
different success and complication rates, and careful to axonal degeneration in the ventral roots and the
consideration of these is required prior to deciding peripheral and cranial nerves.
on the actual treatment plan for each horse.
Clinical presentation
Prognosis Retinal lesions are very common (50%) and may
The prognosis for TMH is guarded because no treat- be seen on fundoscopic examination as yellow–
ment has proven consistently effective. The progno- brown to black pigmentation found in an irregular
sis for photic headshaking is unknown. Some 5% of mosaic (reticulated) pattern and/or horizontal band
horses with TMH can be expected to recover spon- at the tapetal–non-tapetal junction or generalised
taneously. However, horses can become so severely throughout the fundus (Fig. 11.109). The effect on