© 2003 BMJ Publishing Group
CLINICAL SCIENCE
Epilepsy patients treated with vigabatrin exhibit reduced ocular blood flow
1 Neurosciences Research Institute, Aston University, Aston Triangle, Birmingham B4 7ET, UK
2 City Hospital NHS Trust, Dudley Road, Birmingham B18 7QH, UK
Correspondence to:
Correspondence to:
Sarah L Hosking, PhD, Neurosciences Research Institute, School of Life and Health Sciences, Aston University, Aston Triangle, Birmingham B4 7ET, UK;
s.l.hosking{at}aston.ac.uk
Background/aim: Reduced cerebral blood flow and decreased glucose metabolism have been identified in epilepsy patients receiving vigabatrin. It is likely that such a change may extend to the eye and may be linked to previously reported irreversible visual field defects. The aim of this study was to determine whether patients who have undergone anti-epileptic drug (AED) therapy with vigabatrin have altered ocular haemodynamics.
Methods: The study cohort comprised 11 normal subjects (mean age 42.6 (SD 12.7) years and 17 epilepsy patients, of which 10 were either currently or previously treated with vigabatrin (38.6 (11.7) years) and seven were treated with AEDs excluding vigabatrin (46.0 (9.8) years). The three groups were matched at baseline for pulse rate, diastolic and systolic blood pressure, and intraocular pressure (IOP). At a single visit, the ocular blood flow analyser (OBFA; Paradigm Medical Instruments Inc, UT, USA) was used to measure pulsatile ocular blood flow (POBF) and pulse amplitude (PA) in each eye of all subjects. One way ANCOVA (with age as a covariate) was used to identify differences in POBF and PA between the groups. For the vigabatrin group only, Pearson's product moment correlation coefficient was used to explore potential interactions between ocular blood flow parameters and cumulative vigabatrin dose, duration, and maximum dose.
Results: Both the vigabatrin treated epilepsy group and conventionally treated epilepsy group exhibited significantly reduced POBF (p=<0.001, p=0.040) and PA (p=<0.001, p=0.005) compared to normal subjects. Patients treated with vigabatrin exhibited a further reduction in POBF (p=0.046) and PA (p=0.034) compared to conventionally treated epilepsy patients. No significant correlations were found between drug dosage and POBF and PA for the vigabatrin treated epilepsy group.
Conclusions: A significant reduction in POBF and PA is apparent in epilepsy patients treated with AEDs when compared to normal subjects. A further reduction in POBF and PA is apparent between vigabatrin treated and conventionally treated patients. The reduction in ocular perfusion, which is more pronounced in patients previously treated with vigabatrin, may have implications in the impairment of visual function associated with the drug.
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