Clinical Research Visual Function is Stable in Patients Who Continue Long-Term Vigabatrin Therapy: Implications for Clinical Decision Making *Scott R. Paul, *Gregory L. Krauss, * , ²Neil R. Miller, ²Marianne T. Medura, *Tracy A. Miller, and ‡Mary A. Johnson Departments of *Neurology and ²Ophthalmology of the Johns Hopkins Medical Institutions, and the ‡Department of Ophthalmology of the University of Maryland Medical Center, Baltimore, Maryland, U.S.A. Summary: Purpose: Vigabatrin (VGB) has been shown to cause visual field constriction and other forms of mild visual dysfunction. We determined the safety of continuing VGB therapy in patients who had received prolonged treatment (>2 years) with the drug by serially monitoring changes in visual function over a 1-year period of continued therapy. We also followed up patients who discontinued VGB to see whether alternative therapies are effective. Methods: Fifteen of 17 patients who continued VGB therapy had visual-function testing (visual acuity, color vision, kinetic and static perimetry) every 3 months for 1 year. Eighteen pa- tients who discontinued VGB were given alternative antiepi- leptic drugs (AEDs); their seizure responses were measured after 3 months of treatment. Results: Patients continuing VGB showed no worsening of visual acuity, color vision, or visual-field constriction beyond that measured in the initial test. Many patients who discontin- ued VGB had good seizure control with either newer or previ- ously unsuccessful AEDs. Conclusions: For patients who have an excellent response to VGB and only mild visual changes, continued therapy may be safe with close visual monitoring. Patients who do not have a significant reduction in seizures or who experience consider- able visual dysfunction with VGB may respond well to alter- native therapies. Key Words: Vigabatrin—Visual fields— Vision—Opthalmology—Epilepsy—Visual field constriction. Vigabatrin (-vinyl aminobutyric acid; VGB) is an effective antiepilepsy drug (AED) used to treat partial- onset seizures and infantile spasms (1–3); however, it causes visual-field constriction in 40–45% of patients receiving long-term therapy as well as reductions in elec- troretinogram (ERG) potentials in ∼70% of patients (4– 8). Other visual disturbances, including minor reductions in visual acuity and color vision, also have been demon- strated in some patients after long-term use of VGB (6, 7,9). Because VGB is particularly effective in patients re- fractory to standard treatment (3,10), and because uncon- trolled seizures can lead to significant disability or even death (11), the risk of visual sensory dysfunction, par- ticularly visual-field constriction, must be weighed against the benefits associated with VGB treatment (12). We previously showed that most of the visual distur- bances are mild and asymptomatic (7). In this study, we attempted to determine if the visual defects associated with VGB are progressive or stable with continued therapy. This has potential significance for determining whether it is safe for patients to continue treatment with VGB. We assessed the status of visual function over a 1-year period of continued VGB therapy in 15 patients who had been given prolonged treatment. In addition to evaluating risks associated with continued VGB therapy, we also determined seizure responses for patients who discontin- ued VGB to see if alternative therapies are available for this patient population. These patients were subsequently treated with AEDs that they had previously taken or with new AEDs that were not available when the patients started VGB. METHODS The study group was a subset of 39 adult patients with previously uncontrolled complex-partial and secondarily- generalized tonic–clonic seizures treated for 2–7 years with VGB by one of us (G.L.K.) at Johns Hopkins Hos- Accepted August 9, 2000. Address correspondence and reprint requests to Dr. G. L. Krauss at Department of Neurology, 600 N. Wolfe St./Meyer 2-147, Baltimore, MD 21287-7247, U.S.A. E-mail srp@jhu.edu Epilepsia, 42(4):525–530, 2001 Blackwell Science, Inc. © International League Against Epilepsy 525