Acute comitant esotropia in Chiari 1 malformation.

Abstract

In their report entitled “Treatment of Acute Comitant Esotropia in Chiari 1 Malformation” (Ophthalmology 1999;106:2368–71), Weeks and Hamed review the clinical course of two patients with Chiari 1 malformation and acute comitant esotropia with diplopia. On the basis of the clinical course of their two patients and on their review of previously reported cases, they suggest it might be advisable to treat the underlying Chiari 1 malformation first, reserving strabismus surgery for cases that do not resolve after decompression. We wish to report a patient with Chiari 1 malformation who had acute comitant esotropia and whose clinical course, we believe, supports their conclusion.A 14-year-old girl was referred for neuro-ophthalmic evaluation 16 months after the onset of horizontal double vision. Uncorrected visual acuity was 20/20 in each eye. A comitant esotropia of 40 prism diopters was measured at distance and near. A moderate-frequency, high-amplitude, right-beating nystagmus was present in right gaze. Horizontal pursuit eye movements were poor, especially to the right. Infrared eye movement recordings showed normal abducting saccadic velocities in each eye. A magnetic resonance imaging scan disclosed a Chiari 1 malformation.She underwent a suboccipital decompression with C1 and C2 laminectomy. Four months later, her esotropia was unchanged. She received 3.0 units of botulinum A toxin in the left medial rectus muscle, and her diplopia resolved within a few days. Six months later, she was orthophoric at distance and near. Her nystagmus had resolved and her pursuit eye movements were clinically normal. Her double vision has not recurred in 15 years.We believe our case supports Weeks’ and Hamed’s suggestion that definitive neurosurgical treatment of the Chiari 1 malformation be done initially, with strabismus treatment reserved for those patients whose esotropia does not resolve after suboccipital decompression. We also point out that these patients may be excellent candidates for treatment of their esotropia with botulinum A toxin. In their report entitled “Treatment of Acute Comitant Esotropia in Chiari 1 Malformation” (Ophthalmology 1999;106:2368–71), Weeks and Hamed review the clinical course of two patients with Chiari 1 malformation and acute comitant esotropia with diplopia. On the basis of the clinical course of their two patients and on their review of previously reported cases, they suggest it might be advisable to treat the underlying Chiari 1 malformation first, reserving strabismus surgery for cases that do not resolve after decompression. We wish to report a patient with Chiari 1 malformation who had acute comitant esotropia and whose clinical course, we believe, supports their conclusion. A 14-year-old girl was referred for neuro-ophthalmic evaluation 16 months after the onset of horizontal double vision. Uncorrected visual acuity was 20/20 in each eye. A comitant esotropia of 40 prism diopters was measured at distance and near. A moderate-frequency, high-amplitude, right-beating nystagmus was present in right gaze. Horizontal pursuit eye movements were poor, especially to the right. Infrared eye movement recordings showed normal abducting saccadic velocities in each eye. A magnetic resonance imaging scan disclosed a Chiari 1 malformation. She underwent a suboccipital decompression with C1 and C2 laminectomy. Four months later, her esotropia was unchanged. She received 3.0 units of botulinum A toxin in the left medial rectus muscle, and her diplopia resolved within a few days. Six months later, she was orthophoric at distance and near. Her nystagmus had resolved and her pursuit eye movements were clinically normal. Her double vision has not recurred in 15 years. We believe our case supports Weeks’ and Hamed’s suggestion that definitive neurosurgical treatment of the Chiari 1 malformation be done initially, with strabismus treatment reserved for those patients whose esotropia does not resolve after suboccipital decompression. We also point out that these patients may be excellent candidates for treatment of their esotropia with botulinum A toxin. Author’s replyOphthalmologyVol. 108Issue 5Preview Full-Text PDF