In bright lighting, the pupils measured 4 mm OD and 3 mm OS. There was 1 mm of left upper lid ptosis and 1 mm of left lower lid inverseptosis. On examination, his vision was central, steady, and maintained in botheyes. He displayedleft upper extremity weakness with almost no motor strength in the left hand.His left pupil was noted to be smaller than his right pupil by his mother. A 4-month-old boy was born by complicated vaginaldelivery with a resultant brachial plexus injury on the left side. A diagnosis of Klumpke paralysis was made by the neurologist.The anisocoria secondary to a left-sided Horner syndrome was confirmed on3 separate office visits.Ĭase 2. Because of the left upper extremity weakness, a magneticresonance image of the cervical and thoracic spine was ordered. Computed tomography results of the abdomen and pelvis werenormal with no masses. The patient's mother reportedthat he was sleepier than usual that afternoon, but by evening his activitylevel had returned to baseline.Ĭomputed tomography findings of the head, cervical spine, and neck werecompletely normal. The left pupil increased from 2 mmto 4 mm, resulting in a reversal of the anisocoria. The patient was evaluated 1 hour later, and in normal roomlighting, the right pupil remained 3 mm. We instilled 1% apraclonidine in each eye prior to any other pharmacologicagent that day. The patient kept his left hand fisted with flexion contracturesof the third, fourth, and fifth fingers. Neurologic evaluation showed full range of motionof his neck and back.

Motility was full, and the patient was orthotropic atnearby light reflex testing. The conjunctiva, cornea, iris, and lens appearedhealthy in both eyes. No inverseptosis (elevation of the lower lid) was present, but there was approximately1 mm of left upper lid ptosis. Inthe dark, the size of the pupils changed to 5 mm OD and 3 mm OS. In normal room lighting, the pupils measured 3 mm OD and 2 mm OS. His parents reported that they did not notice any anisocoria beforethe infant was 4 months of age. His developmentwas age-appropriate, and he reached for objects preferentially with his righthand.

Therewas no evidence of shoulder dystocia, and his health had been good. He was found to have a nuchal cord and mild neck bruising. Forceps were not used during the delivery.There was some fetal bradycardia related to contractions toward the end ofthe labor. He was the product of an uncomplicated pregnancy andwas born full-term by vaginal delivery. To our knowledge, there is no prior reportof the use of apraclonidine as a diagnostic test in a pediatric patient.Ĭase 1 A 6-month-old boy was first seen in our office because of a 2-month history of anisocoria. For comparison, wediscuss 2 children pharmacologically tested with apraclonidine who had anisocoriabut did not have Horner syndrome. We discuss 4 pediatric patients with a diagnosis of Horner syndromewho underwent pharmacologic testing with apraclonidine. Four patientshad postganglionic Horner syndrome (third-order neuron) and 2 had preganglionicHorner syndrome (first-order and second-order neurons). In every case, the mioticpupil on the Horner side dilated to become larger than the healthy side, whereasthe size of the pupil on the unaffected side remained unchanged. In fact, all patientsexperienced a reversal of their baseline anisocoria. A prior study 4 of6 adult patients with Horner syndrome showed that instillation of 1% apraclonidineinto both eyes produced mydriasis in the affected eye only. 3Īpraclonidine hydrochloride is an α-adrenergic receptor agonistthat is approved for the treatment of elevated intraocular pressure followingargon laser trabeculoplasty. The Horner pupil dilates poorly in comparison with thehealthy pupil. The diagnosis of this condition may be confirmed by instilling topicalcocaine in each eye. Other causes include neuroblastoma, trauma, and brainstem processes. Acquired Horner syndrome in children is oftenpostsurgical. 1 Congenital Horner syndrome is most commonly idiopathicor due to a traumatic birth. Horner syndrome refers to a condition where oculosympathetic pathwaydamage or dysfunction can cause ptosis, miosis of the pupil, and anhydrosis.

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Dx code for miotic pupil