mapping blood flow in the microcirculation. Ultrasound Med Biol 1997;23:997–1015. 5. Bioeffects Committee of the American Institute of Ultra- sound in Medicine. Safety considerations for diagnostic ultrasound. Bethesda, MD: The Institute, 1984. Use of Latanoprost in the Treatment of Glaucoma Associated With Sturge-Weber Syndrome Charles B. Yang, MD, Sharon F. Freedman, MD, Jonathan S. Myers, MD, Edward G. Buckley, MD, Leon W. Herndon, MD, and R. Rand Allingham, MD PURPOSE: To determine if latanoprost reduces in- traocular pressure in eyes with glaucoma associ- ated with Sturge-Weber syndrome. METHODS: We conducted a prospective study in which eyes with uncontrolled intraocular pressure associated with Sturge-Weber syndrome were treated with latanoprost 0.005% once daily. All eyes were already receiving at least two other antiglaucoma medications. Intraocular pressure was measured at baseline and after treatment for at least 1 month. All intraocular pressure measure- ments were taken within 24 hours of drug instil- lation. RESULTS: Six eyes of six patients received latano- prost. Two (28%) of the six eyes demonstrated an intraocular pressure decrease that averaged 8.8 mm Hg. These two responders had juvenile onset glaucoma, whereas the four nonresponders had congenital onset glaucoma. CONCLUSIONS: Latanoprost may significantly re- duce intraocular pressure in selected patients with glaucoma associated with Sturge-Weber syndrome. (Am J Ophthalmol 1998;126:600 – 602. © 1998 by Elsevier Science Inc. All rights reserved.) S TURGE-WEBER SYNDROME IS CHARACTERIZED BY facial cutaneous, ipsilateral meningeal, and ocu- lar hemangiomas. Glaucoma develops in the ipsilat- eral eye of approximately 33% of patients with Sturge-Weber syndrome. The onset of glaucoma can be either congenital, juvenile, or adult. The mechanism of increased intraocular pressure is thought to be related to increased episcleral venous pressure, developmental angle anomalies, or both. 1 Medications and laser trabeculoplasty are often inadequate. 2 Goniotomy or trabeculotomy may con- trol intraocular pressure for a limited duration. 2 Filtration surgery is risky because of an increased incidence of suprachoroidal hemorrhages. 3 Latanoprost is a prostaglandin F 2  analogue that lowers intraocular pressure by increasing aqueous humor outflow through the uveoscleral pathway. 4 This is a poorly understood pathway in which aqueous humor is thought to pass through the ciliary body where it is then absorbed by vessels in the suprachoroidal space or passed through the sclera. We hypothesized that latanoprost might lower in- traocular pressure in patients with glaucoma and Sturge-Weber syndrome by circumventing the ab- normal trabecular outflow channels and elevated episcleral venous pressure. This prospective study identified all patients with glaucoma associated with Sturge-Weber syndrome currently under care at Duke University Eye Center. Those who had undergone filtering or cyclodestruc- tive surgery were excluded. Patients with unsatisfac- tory intraocular pressure control on at least two antiglaucoma medications were offered treatment with latanoprost 0.005%. Intraocular pressure was recorded at baseline and after treatment once nightly for at least 1 month’s duration. All intraoc- ular pressure measurements were taken within 24 hours after instillation of the medication. One eye from each of six patients was treated with latanoprost. The pretreatment characteristics of these six patients are listed in Table 1. Two patients had Klippel-Trenaunay-Weber syndrome, a variant of Sturge-Weber syndrome in which hem- angiomas extend onto the limbs and trunk. The pretreatment and posttreatment intraocular pressure measurements, as well as concurrent antiglaucoma medications, are shown in Table 2. Only two of six eyes showed a clinically signifi- cant intraocular pressure decrease after treatment with latanoprost, but these two responders demon- strated an average intraocular pressure reduction of Accepted for publication April 1, 1998. From the Eye Physician Associates, S.C., Milwaukee, Wisconsin, (C.Y.), Wills Eye Hospital, Philadelphia, Pennsylvania (J.S.M.), and Duke University Eye Center, Durham, North Carolina (S.F.F., E.G.B., L.W.H., R.R.A.). Inquiries to R. Rand Allingham, MD, Duke University Eye Center, Box 3802, Duke University Medical Center, Durham, NC 27710-3802. AMERICAN JOURNAL OF OPHTHALMOLOGY 600 OCTOBER 1998