Patients with glaucoma exhibit low levels of circulating glutathione, suggesting a general compromise of the antioxidative defense.

Visual disturbances are a common side-effect of many antiepileptic drugs. Non-specific retino- and neurotoxic visual abnormalities, that are often reported with over-dosage and prolonged AED use, include diplopia, blurred vision and nystagmus. Some anticonvulsants are associated with specific visual problems that may be related to the mechanistic properties of the drug, and occur even when the drugs are administered within the recommended daily dose. Vigabatrin, a GABA-transaminase inhibitor, has been associated with bilateral concentric visual field loss, electrophysiological changes, central visual function deficits including reduced contrast sensitivity and abnormal colour perception, and morphological alterations of the fundus and retina. Topiramate, a drug that enhances GABAergic transmission, has been associated with cases of acute closed angle glaucoma, while tiagabine, a GABA uptake inhibitor, has been investigated for a potential GABAergic effect on the visual field. Only mild neurotoxic effects have been identified for patients treated with gabapentin, a drug designed as a cyclic analogue of GABA but exhibiting an unknown mechanism while carbamazepine, an inhibitor of voltage-dependent sodium channels, has been linked with abnormal colour perception and reduced contrast sensitivity. The following review outlines the visual disturbances associated with some of the most commonly prescribed anticonvulsants. For each drug, the ocular site of potential damage and the likely mechanism responsible for the adverse visual effects is described.

Aim: To determine the ocular haemodynamic response to gas perturbations in glaucoma. Methods: Intraocular pressure (IOP), systemic systolic and diastolic blood pressure (SBP and DBP), and retrobulbar blood flow velocities, measured by colour Doppler imaging (CDI), were recorded at two visits. CDI was used to measure peak systolic and end diastolic velocities (PSV and EDV) and resistance index (RI) in the ophthalmic artery (OA), central retinal artery (CRA), and short posterior ciliary arteries (SPCAs). At the first visit, measurements were taken at baseline (B1: breathing room air) and during isoxic hypercapnia (end tidal PCO 2 increased 15% above baseline) in 16 normal subjects and 12 patients with glaucoma. On another day, measurements were repeated at a second baseline (B2) and during hyperoxia (100% oxygen breathing) for 15 normal subjects and 13 glaucoma patients. Baseline systemic data were compared using paired t tests; REANOVA was performed to compare group differences at baseline and to determine the vessel response to each condition. Fisher's LSD was used for post hoc comparison. Results: Baseline OA PSV was lower for the glaucoma than for the normal group (p = 0.047); the groups were otherwise similar at baseline. IOP demonstrated no response to hypercapnia, but reduced during hyperoxia for both the normal subjects (p,0.0001) and glaucoma patients (p = 0.04). During hypercapnia, SBP increased in normal subjects (p = 0.03) and glaucoma patients (p = 0.01); DBP increased in normal subjects (p = 0.021). There was a corresponding increase in ocular perfusion pressure (OPP) for normal subjects (p = 0.01) and glaucoma subjects (p = 0.028), and as a result OPP was included as a covariate in the REANCOVA model. Hypercapnia resulted in increased PSV in the CRA of normal subjects (p = 0.035) and increased PSV and EDV in the SPCAs of glaucoma patients (p = 0.041 and p = 0.030 respectively). Hyperoxia resulted in reduced PSV and EDV in the ophthalmic arteries of normal subjects only (p = 0.001 and 0.031 respectively). Conclusions: These findings suggest the presence of relative vasoconstriction in glaucoma patients, which is at least partially reversed by hypercapnia.

Summary:Purpose: To investigate visual function in the central 10 degrees in patients who have undergone vigabatrin (VGB) antiepileptic drug (AED) therapy with the aim of identifying a clinical regimen for assessing central visual function.Methods: The sample comprised 12 epilepsy patients (mean age, 38.6 ± 11.7 years) who had been treated with VGB (either as monotherapy or polytherapy). A number of central visualfunction tests were carried out for each eye, including highcontrast LogMAR visual acuity, short-wavelength automated perimetry (SWAP 10-2), spatial contrast sensitivity (CSV-1000), and Farnsworth-Munsell (FM) 100-hue colour discrimination.Results: The group mean cumulative VGB dose was 5,086 ± 3,245 g. The average SWAP 10-2 mean deviation (MD) for the group was -3.24 ± 3.23 dB; 14 eyes of eight patients showed defects (range, -1.62 to -9.46 dB). The square root of the group mean total error score for FM 100-hue was 7.42 ± 3.84; nine eyes of five patients were classified as abnormal with an unsolved colour axis suggestive of complex drug interactions. For contrast sensitivity, 15 eyes of eight patients yielded abnormal results in one or more spatial frequencies. Defects were more prominent at higher spatial frequencies. Overall, four patients had defects in all three visual-function tests, six patients had mixed defects, and two patients were normal.Conclusions: Visual-function deficits in epilepsy patients treated with VGB are present in the central 10 degrees of the retina. We recommend a battery of investigations, including SWAP 10-2 and spatial contrast sensitivity testing, to assess central visual function.

Purpose To investigate intraocular pressure (IOP) and ocular haemodynamics following small incision cataract surgery. Methods Systemic and ocular haemodynamics, and IOP, were measured pre-operatively and 1 month post-operatively, in 25 eyes of 25 patients (mean age 72.677.9 years) scheduled for small incision cataract surgery and intraocular lens implantation; these values were compared to an untreated age-matched healthy group (n ¼ 25, mean age 72.375

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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.

Capillary blood flow in the retina, neuroretinal rim and lamina cribrosa decreases with advancing age. This may be of consequence in the progression of chronic ocular diseases such as glaucoma, and should be considered in the longitudinal determination of change in disease monitoring.