Vigabatrin-attributed visual field defect: molecular mechanisms & dependencies

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What it does

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What acts on it

Out of 88 patients exposed to vigabatrin in infancy, 28 were able to perform formal visual field testing, mild vigabatrin-attributed visual field defect was found in four patients and severe defect in one, median vigabatrin treatment duration for those with normal visual field was 11 months compared to 19 months for those with the defect, optical coherence tomography showed concomitant attenuated retinal nerve fiber layer in three children, and the overall prevalence after exposure in infancy is lower than the 52% which has been reported after exposure in adulthood while the risk increases with longer treatment duration.
Vigabatrin → Vigabatrin-attributed visual field defect source_derived_draftungraded
Experimental context and source evidence
evidence_span
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experimental_model
Retrospective population-based perimetry and optical coherence tomography at school age in children exposed in infancy
exposure
Vigabatrin given for infantile spasms, with visual fields and retinal nerve fibre layer measured years later
limitations
Only 28 of 88 exposed patients could perform formal visual field testing, which limits the prevalence estimate in both directions.
nutrient_topic
GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. · Gamma-aminobutyric acid
organism
Human
plain_language
The drug that raises brain GABA costs some patients their peripheral vision, and the longer they take it the likelier that is.
primary_references
[gb-p34716587] Visual field defects after vigabatrin treatment during infancy: retrospective population-based study. (2022). https://pubmed.ncbi.nlm.nih.gov/34716587/ DOI: 10.1111/dmcn.15099
tissue_or_cell_type
Retina
GABA: a ligand with no sign of its own, the cofactor that limits its synthesis, the barrier that keeps it out of the brain, and the immune settings where the same molecule protects and harms (2026-09-22) · lines 170–181
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Retrospective population-based perimetry and optical coherence tomography at school age in children exposed in infancy · source_derived_draft · unverified_draft
### gb-duration-drives-the-field-loss Out of 88 patients exposed to vigabatrin in infancy, 28 were able to perform formal visual field testing, mild vigabatrin-attributed visual field defect was found in four patients and severe defect in one, median vigabatrin treatment duration for those with normal visual field was 11 months compared to 19 months for those with the defect, optical coherence tomography showed concomitant attenuated retinal nerve fiber layer in three children, and the overall prevalence after exposure in infancy is lower than the 52% which has been reported after exposure in adulthood while the risk increases with longer treatment duration. Condition category: normal nutrient_topic: GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. plain_language: The drug that raises brain GABA costs some patients their peripheral vision, and the longer they take it the likelier that is. organism: Human tissue_or_cell_type: Retina experimental_model: Retrospective population-based perimetry and optical coherence tomography at school age in children exposed in infancy limitations: Only 28 of 88 exposed patients could perform formal visual field testing, which limits the prevalence estimate in both directions. exposure: Vigabatrin given for infantile spasms, with visual fields and retinal nerve fibre layer measured years later evidence_span: {"source_cache": "artifacts/gaba-research/34716587.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "30459a805ac23ba0a6f0cb4c9484da96a968609466a4bb1fc7c41636542ba887", "start_char": 0, "end_char": 1403, "text_sha256": "30459a805ac23ba0a6f0cb4c9484da96a968609466a4bb1fc7c41636542ba887"} [gb-p34716587] Visual field defects after vigabatrin treatment during infancy: retrospective population-based study. (2022). https://pubmed.ncbi.nlm.nih.gov/34716587/ DOI: 10.1111/dmcn.15099
Complete structured claim and evidence

Where it participates (unsigned role)

A close relationship between vigabatrin-induced retinal toxicity and light exposure was observed, vigabatrin-treated mice reared in darkness preserved better visual function and retinal architectures as verified by optokinetic tests, optical coherence tomography and electroretinography, the retinal taurine level of vigabatrin-treated mice exposed to light was significantly lower than that of vigabatrin mice reared in darkness, and the vigabatrin-induced morphological and functional impairments could be partially alleviated by taurine treatment.
Retinal taurine concentration → Retinal function measured by electroretinography and optokinetic testing source_derived_draftungraded
Experimental context and source evidence
evidence_span
{"source_cache": "artifacts/gaba-research/27941319.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "92835398ef34fe87d3c084d1933722427a474b40c88c30ada21a6ede8f4d875a", "start_char": 0, "end_char": 1596, "text_sha256": "92835398ef34fe87d3c084d1933722427a474b40c88c30ada21a6ede8f4d875a"}
experimental_model
Electroretinography, optical coherence tomography and optokinetic testing in mice reared in light or darkness
exposure
Vigabatrin with and without light exposure, and with taurine supplementation
limitations
A mouse study. It identifies two contributing factors and shows partial rescue, not that taurine prevents the human visual field defect.
nutrient_topic
GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. · Gamma-aminobutyric acid
organism
Mouse
plain_language
The retinal damage needed light to happen, went with a fall in retinal taurine, and was partly undone by giving taurine back.
primary_references
[gb-p27941319] The Vigabatrin Induced Retinal Toxicity is Associated with Photopic Exposure and Taurine Deficiency: An In Vivo Study. (2016). https://pubmed.ncbi.nlm.nih.gov/27941319/ DOI: 10.1159/000453143
tissue_or_cell_type
Retina
GABA: a ligand with no sign of its own, the cofactor that limits its synthesis, the barrier that keeps it out of the brain, and the immune settings where the same molecule protects and harms (2026-09-22) · lines 183–194
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Electroretinography, optical coherence tomography and optokinetic testing in mice reared in light or darkness · source_derived_draft · unverified_draft
### gb-light-and-taurine-both-matter A close relationship between vigabatrin-induced retinal toxicity and light exposure was observed, vigabatrin-treated mice reared in darkness preserved better visual function and retinal architectures as verified by optokinetic tests, optical coherence tomography and electroretinography, the retinal taurine level of vigabatrin-treated mice exposed to light was significantly lower than that of vigabatrin mice reared in darkness, and the vigabatrin-induced morphological and functional impairments could be partially alleviated by taurine treatment. Condition category: normal nutrient_topic: GABA research collection; topical membership is not evidence of a direct clinical effect, and the sign of a GABA response depends on the chloride gradient of the cell it was measured in. plain_language: The retinal damage needed light to happen, went with a fall in retinal taurine, and was partly undone by giving taurine back. organism: Mouse tissue_or_cell_type: Retina experimental_model: Electroretinography, optical coherence tomography and optokinetic testing in mice reared in light or darkness limitations: A mouse study. It identifies two contributing factors and shows partial rescue, not that taurine prevents the human visual field defect. exposure: Vigabatrin with and without light exposure, and with taurine supplementation evidence_span: {"source_cache": "artifacts/gaba-research/27941319.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "92835398ef34fe87d3c084d1933722427a474b40c88c30ada21a6ede8f4d875a", "start_char": 0, "end_char": 1596, "text_sha256": "92835398ef34fe87d3c084d1933722427a474b40c88c30ada21a6ede8f4d875a"} [gb-p27941319] The Vigabatrin Induced Retinal Toxicity is Associated with Photopic Exposure and Taurine Deficiency: An In Vivo Study. (2016). https://pubmed.ncbi.nlm.nih.gov/27941319/ DOI: 10.1159/000453143
Complete structured claim and evidence

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Vigabatrin-attributed visual field defect