Epilepsy patients treated with vigabatrin exhibit reduced ocular blood flow

Hosking, SL; Hilton, E J Roff; Embleton, Sally J; Gupta, AK

doi:10.1136/bjo.87.1.96

Cited by 15 publications

(19 citation statements)

References 39 publications

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“…Alternatively, the relative preservation of the central retina could be explained by a reduced redundancy of the photoreceptor population in the temporal retina or by unknown neuroprotective mechanisms that prevent cell death. Pre‐existing ischemia could be linked to the severity of visual field loss, as previous evidence suggests that ocular blood flow is reduced in patients receiving VGB (Roff Hilton et al, 2002; Hosking et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

“…The typical appearance of VGB‐attributed visual field loss is a bilateral concentric peripheral constriction that is most severe nasally (Wild et al, 1999; Roff Hilton et al, 2002; Hosking et al, 2003). Accurately identifying and quantifying the degree of VGB‐induced visual field loss is a vital step toward the successful medical management of these patients.…”

Section: Visual Field Investigation Protocols Used In Studies Of Visumentioning

confidence: 99%

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Visual Field Severity Indices Demonstrate Dose‐Dependent Visual Loss from Vigabatrin Therapy

2007

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SUMMARYPurpose: The aims of this study were to develop an algorithm to accurately quantify Vigabatrin (VGB)-induced central visual field loss and to investigate the relationship between visual field loss and maximum daily dose, cumulative dose and duration of dose. Methods: The sample comprised 31 patients (mean age 37.9 years; SD 14.4 years) diagnosed with epilepsy and exposed to VGB. Each participant underwent standard automated static visual field examination of the central visual field. Central visual field loss was determined using continuous scales quantifying severity in terms of area and depth of defect and additionally by symmetry of defect between the two eyes. A simultaneous multiple regression model was used to explore the relationship between these visual field parameters and the drug predictor variables. Results: The regression model indicated that maximum VGB dose was the only factor to be significantly correlated with individual eye severity (right eye: p = 0.020; left eye: p = 0.012) and symmetry of visual field defect (p = 0.024). Conclusions: Maximum daily dose was the single most reliable indicator of those patients likely to exhibit visual field defects due to VGB. These findings suggest that high maximum dose is more likely to result in visual field defects than high cumulative doses or those of long duration.

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Section: Discussionmentioning

confidence: 99%

Section: Visual Field Investigation Protocols Used In Studies Of Visumentioning

confidence: 99%

Visual Field Severity Indices Demonstrate Dose‐Dependent Visual Loss from Vigabatrin Therapy

2007

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“…Optic disc pallor, retinal pigmentation changes, vascular sheathing, optic atrophy, retinal surface wrinkling and reduced ocular blood flow may also occur. [321][322][323][324] A characteristic retinal and optic disc atrophy pattern has been described in infants. [325] Though some patients demonstrate optic disc changes, electroretinogram (ERG) abnormalities suggest that retinal dysfunction results in visual field deficits.…”

Section: Cnsmentioning

confidence: 98%

The Safety and Tolerability of Newer Antiepileptic Drugs in Children and Adolescents

Sarco

Bourgeois

2010

CNS Drugs

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The newer antiepileptic drugs (AEDs) provide more therapeutic options and overall improved safety and tolerability for patients. To provide the best care, physicians must be familiar with the latest tolerability and safety data. This is particularly true in children, given there are relatively fewer studies examining the effects of AEDs in children compared with adults. Since we now have significant paediatric literature on each of these agents, we provide a comprehensive and current literature review of the newer AEDs, focusing on safety and tolerability data in children and adolescents. Because the safety profiles in children differ from those in adults, familiarity with this literature is important for child neurologists and other paediatric caregivers. We have organized the data by organ system for each AED for easier reference.

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“…We addressed this question by comprehensively assessing two components of the ocular circulation in patients with epilepsy. Two key findings emerged from our investigations: (1) retinal microvascular blood flow and pulsatile ocular blood flow are reduced in epilepsy patients when compared with normal healthy volunteers () (Hosking et al ., 2002; Roff Hilton et al ., 2002b); (2) the reduction in pulsatile ocular blood flow was further exacerbated in vigabatrin‐treated epilepsy patients compared with those treated with conventional AEDs (Hosking et al ., 2002).…”

Section: Vigabatrin Blood Flow and The Eyementioning

confidence: 99%

“… Mean values (±S.E.) for retinal blood volume measured with scanning laser Doppler flowmetry and pulsatile ocular blood flow (POBF) for a normal and epilepsy group (Hosking et al ., 2002; Roff Hilton et al ., 2002b). …”

Section: Vigabatrin Blood Flow and The Eyementioning

confidence: 99%

Neurotoxic effects of GABA‐transaminase inhibitors in the treatment of epilepsy: ocular perfusion and visual performance

Hosking

Hilton

2002

Ophthalmic Physiologic Optic

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Vigabatrin is a GABA (gamma-aminobutyric acid) transaminase inhibitor that elicits an antiepileptic effect by enhancing inhibitory neurotransmission in the brain. Vigabatrin has been previously associated with concentric peripheral visual field loss and visual electrophysiological abnormalities. Recently, visual function deficits of the central retina have been identified in a proportion of patients receiving vigabatrin; these include disturbances in colour perception, contrast sensitivity and short-wavelength automated perimetry. Consequently, it is suggested that vigabatrin-associated retinal toxicity is diffuse inducing subtle central visual dysfunction and more severe peripheral visual defects. Reductions in cerebral blood flow and cerebral metabolic rate for glucose occur in epilepsy patients receiving antiepileptic drug therapy. Despite the known cerebral haemodynamic alterations in epilepsy and the visual consequences of vigabatrin therapy, ocular blood flow has only recently been investigated in this group. We present findings from a series of novel investigations that identify compromised retinal microvascular perfusion and pulsatile ocular blood flow (POBF) in epilepsy patients. The reduction in POBF was exacerbated in epilepsy patients treated with vigabatrin compared to conventionally treated epilepsy patients. A number of theories are presented to explain compromised ocular blood flow in vigabatrin treated epilepsy patients, and the possibility of a GABAergic mechanism of toxicity is discussed.

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Epilepsy patients treated with vigabatrin exhibit reduced ocular blood flow

Cited by 15 publications

References 39 publications

Visual Field Severity Indices Demonstrate Dose‐Dependent Visual Loss from Vigabatrin Therapy

Visual Field Severity Indices Demonstrate Dose‐Dependent Visual Loss from Vigabatrin Therapy

The Safety and Tolerability of Newer Antiepileptic Drugs in Children and Adolescents

Neurotoxic effects of GABA‐transaminase inhibitors in the treatment of epilepsy: ocular perfusion and visual performance

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