![]() Anticholinergics such as atropine, homatropine, tropicamide, scopolamine, and cyclopentolate lead to mydriasis and cycloplegia by inhibiting parasympathetic M3 receptors of the pupillary sphincter and ciliary muscles. Pharmacologic anisocoria can present as mydriasis or miosis following administration of agents that act on the pupillary dilator or sphincter muscles. Causes include physical injury from ocular trauma or surgery, inflammatory conditions such as uveitis, angle closure glaucoma leading to iris occlusion of the trabecular meshwork, or intraocular tumors causing physical distortion of the iris. Mechanical anisocoria results from damage to the iris or its supporting structures. Examples include aniridia, coloboma, and ectopic pupil. Physiologic anisocoria may be intermittent, persistent, or even self-resolving.Ĭongenital anomalies in the structure of the iris may contribute to abnormal pupillary sizes and shapes that present in childhood. Light and near responses are intact, and the degree of anisocoria is typically equal in light and dark. The exact cause is unknown, but it is thought to be due to transient asymmetric supranuclear inhibition of the Edinger-Westphal nucleus that controls the pupillary sphincter. It is a benign condition with a difference in pupil size of less than or equal to 1 mm. Physiologic (also known as simple or essential) anisocoria is the most common cause of unequal pupil sizes, affecting up to 20% of the population. An injury or lesion in either pathway may result in changes in pupil size. Generally, anisocoria is caused by impaired dilation (a sympathetic response) or impaired constriction (a parasympathetic response) of pupils. Thus, thorough clinical evaluation is important for appropriate diagnosis and management of the underlying cause. It is relatively common, and causes vary from benign physiologic anisocoria to potentially life-threatening emergencies. © 2019 Neuro-ophthalmology Virtual Education Library: NOVEL Īnisocoria indicates unequal pupil sizes. Pathology should be performed if the underlying cause of the glaucoma is suspected to be neoplasia.Anisocoria. The optic nerve has little give in a cat, and it is essential that NO pressure be applied on the globe when it is removed, to prevent damage to the optic nerve at the chiasm. Removal of an enlarged cat’s eye can result in the patient waking up blind due to damage to the optic nerve on the fellow eye. ![]() ![]() IT IS RECOMMENDED THAT ENUCLEATION OF AN ENLARGED CAT’S EYE BE PERFORMED BY AN EYE SPECIALIST. If the eye is enlarged and the IOP is not responding to therapy, eye removal is recommended. Medical management can be attempted if the IOP is less than 35mmHg and may be successful and avoid the need for eye removal. Once a cat’s eye develops buphthalmos (is enlarged) it is blind. Osmotic Agents – Rarely used and can have significant systemic side effects. Prostaglandin antagonists like latanoprost (Xalatan®) are not effective in reducing intraocular pressure but can cause marked constriction of the pupil. These are used twice to three times daily depending on IOP readings. These are the mainstay of glaucoma treatmenet in cats. ![]() Topical carbonic anhydrase inhibitors: Dorzolamide (Trusopt®). Treating the uveitis is very important as it is usually the underlying cause. Systemic anti-inflammatory therapy: oral cortisone or NSAID depending on the health of the cat and the individual case. Topical NSAID drops: Diclofenac 0.1% (Voltaren®) is also every effective. Regularly recheck the intraocular pressure and avoid if ulceration in present. Topical cortisone drops: Prednisolone acetate (Prednefrin Forte®) or Dexamathasone eye drops (Maxidex®) are extremely effective but some studies have shown a percentage of cats developing elevated intraocular pressure with long term use. The uveitis must be managed as well as the glaucoma. Medical management is the principal way of controlling intraocular pressure and maintaining comfort.
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