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Vigabatrin-associated retinal damage: potential biochemical mechanisms.

Authors
Type
Published Article
Journal
Acta Neurologica Scandinavica
1600-0404
Publisher
Wiley Blackwell (Blackwell Publishing)
Publication Date
Volume
126
Issue
4
Pages
219–228
Identifiers
DOI: 10.1111/j.1600-0404.2012.01684.x
PMID: 22632110
Source
Medline
License
Unknown

Abstract

Vigabatrin (VGB), an irreversible inhibitor of gamma-aminobutyric acid (GABA) transaminase, is approved as adjunct treatment of refractory partial seizures as well as infantile spasms. Although VGB has been proven to be effective, its use is limited by the risk of retinopathy and associated peripheral visual field defects. This review describes and analyzes current literature related to potential pathophysiologic mechanisms underlying VGB-mediated cellular toxicity. Animal data suggest that GABA mediates neural excitotoxicity. The amino acid taurine is concentrated in retinal cells, and deficiency of this amino acid may be involved in VGB-mediated retinal degeneration and possible phototoxicity.

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