The oculomotor nerve innervates 4 out of the 6 extraocular muscles (superior rectus, medial rectus, inferior rectus and inferior oblique), the sphincter pupillae muscle, the ciliary muscle and the levator palpebrae muscle. Oculomotor (third) nerve palsy varies in presentation and etiology. Ninety percent of cases occur in women between the ages of 20-40 years, 80% of cases are unilateral, and 70% of cases are associated with decreased deep tendon reflexes (Adie’s syndrome). Aberrant reinnervation and upregulation of post-synaptic receptors lead to the clinical presentation of a tonically dilated pupil with near stimulation that is poorly reactivity to light. Further pharmacologic workup (see diagnostic procedures) is useful in confirming Horner’s and distinguishing the order of the lesion.Īdie’s tonic pupil results from damage to the parasympathetic ciliary ganglion or short ciliary nerves that innervate the sphincter pupillae and ciliary muscle. Postganglionic or third-order neuron lesions include carotid artery dissection, cavernous sinus lesion, otitis media, and head or neck trauma. Preganglionic or second-order neuron lesions may be caused by a Pancoast tumor, mediastinal or thyroid mass, cervical rib, and neck trauma or surgery. Central or first-order lesions are often caused by stroke, lateral medullary syndrome, neck trauma or demyelinating disease. Anisocoria is greater in the dark due to a defect in the pupillary dilator response secondary to lesions along the sympathetic trunk. Horner’s syndrome (oculosympathetic palsy) is classically described by the triad of ptosis, miosis and anhydrosis, although clinical presentation may vary. Sympathomimetics such as adrenaline, and phenylephrine cause mydriasis through their actions at ɑ-1 receptors of the pupillary dilator muscle.
The use of pilocarpine, a non-selective muscarinic receptor agonist in the parasympathetic nervous system, may result in a small and poorly reactive pupil. 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 iritis or uveitis, angle closure glaucoma leading to iris occlusion of the trabecular meshwork, or intraocular tumors causing physical distortion of the iris. Mechanical anisocoria is an acquired defect that results from damage to the iris or its supporting structures. Examples include aniridia, coloboma and ectopic pupil. However, many cases are persistent.Ĭongenital anomalies in the structure of the iris may contribute to abnormal pupillary sizes and shapes that present in childhood. Physiologic anisocoria may be intermittent and even self-resolving. Light and near responses is 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. A deficit of parasympathetic innervationĬorrect Answers: Anisocoria may be do to any of these items.Įxplanation 3 : “Generally, anisocoria is caused by impaired dilation (a sympathetic response) or impaired constriction (a parasympathetic response) of pupils. Question: Which of the following may cause anisocoria?ģ.
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