vigabatrin ( vgb ) is an antiepileptic drug that irreversibly inhibits brain -aminobutyric acid ( gaba ) transaminase ( 1 ) . vgb is used as first - line treatment for infantile spasms , especially those secondary to tuberous sclerosis , and as an adjunct therapy for medically resistant localization - related childhood epilepsies ( 2 ) . following an initial report of 3 patients who experienced concentric visual field losses following vgb treatment ( 3 ) , several additional studies showed visual field constriction during vgb therapy . cross - sectional studies have estimated the prevalence of vgb - associated visual field defects ( vfds ) as 20 - 50% in patients receiving vgb mono- or adjunct therapies . various groups have found that longer treatment ( 4,5 ) and higher total doses ( 6 - 8 ) are associated with greater visual field losses in adults , while other studies dispute these correlations ( 9,10 ) . a characteristic pattern of ocular dysfunction has been observed in vgb - treated patients , including peripheral visual field constriction primarily in the nasal area , which is rarely seen in other conditions ( 11 - 13 ) . although these studies have shown evidence of vgb - associated vfd , vgb is highly effective and has a low occurrence of side effects or metabolic interactions . thus , it is still commonly used in the clinic , especially for treatment of infantile spasms and tuberous sclerosis with intractable epilepsy . most studies on vgb - associated vfd to date have been performed in adult patients , in part because it is difficult to estimate the frequency of this condition in pediatric patients , who are generally unable to cooperate in visual field testing . we therefore sought to estimate the prevalence , type , severity , and risk factors of vgb - attributed vfds in pediatric patients . we retrospectively investigated the medical records of 67 pediatric epileptic patients who were treated with vgb at the department of pediatrics of the asan medical center and had undergone ophthalmological examinations . for inclusion , each patient was required to have a diagnosis of epilepsy , no evidence of ophthalmologic disease upon initial examination , and a history of treatment with antiepileptic drugs , including vgb , during the observation period . patients were excluded if they had poor compliance or non - concentric vfds , which corresponded to brain organic lesions ( e.g. intracranial hemorrhage ) . the enrolled patients had been given full ophthalmologic examinations , including visual acuity , ophthalmoscopy , measurement of intraocular pressure , and visual field examination using program 30 - 2 of the humphrey field analyzer . the severities of the vgb - attributed vfds were scored as grade i ( minimal , 25 - 30 ) , grade ii ( moderate , 20 - 30 ) , grade iii ( moderate to severe , < 20 ) , or grade iv ( severe , ring scotoma)(fig . data were analyzed by fisher 's exact test and student 's t - test using spss , version 10.01 . the patient population consisted of 67 vgb - treated patients , 41 males ( 61.2% ) and 26 females ( 38.8% ) , with a mean age of 13 yr ( range ; 6 6/12 yr to 21 yr old ) . of the 67 patients , 15 ( 22% ) had vfds , which we attributed to vgb , and 52 ( 78% ) did not . of the patients with vgb - attributed vfds , 13 had nasal arcuate type , 1 had nasal and temporal constricted type , and 1 had nasal constricted type ( table 1 ) . seven patients had grade i vgb - attributed vfds , 5 had grade ii , 2 had grade iii , and 1 had grade iv ( table 2 ) . to identify potential risk factors for vgb - attributed vfds , we compared the vfd and non - vfd patient groups with respect to medications and other clinical parameters . there were no significant differences between the vfd and non - vfd patients in terms of mean age at the beginning of treatment , total treatment duration , cumulative vgb dose , maximum vgb dose , sex distribution , structural abnormalities in the brain , or whether vgb was given alone or in conjunction with another drug ( p>0.05 each ) ( table 3 ) . however , there were no cases of vgb - attributed vfds in patients with total treatment durations < 2 yr ( table 4 and cumulative doses < 10 g / kg ( table 5 ) . our results indicate that the prevalence of vfds in vgb - treated children is 22% . this is consistent with recent reports of vfd prevalences ranging from 15 to 20% in western children ( 7,13 - 17 ) , but is lower than the about 30% previously observed in vgb - treated children . this may be due to our patient population , which was limited to older patients capable of cooperating with ophthalmologic and visual field examinations . the exclusion of younger patients may have decreased the estimated prevalence of vgb - associated vfds , because these younger patients , especially those with infantile spasms , require high dose , sustained treatment with vgb and might be more prone to vfds . in addition , we used automated static perimetry to detect vgb - attributed vfds , which may have influenced our results . the utilized 30 - 2 humphrey field analyzer has the advantages of being generally available , investigator independent , easy to use , simple to standardize , and highly effective at detecting nasal field defects . however , because of its limited spatial context , the humphrey field analyzermay miss mild to moderate visual field defects in the temporal fields . these are more reliably demonstrated by other techniques , such as kinetic ( goldmann ) perimetry ( 10,18 ) . however , vgb - associated vfds typically present as concentric peripheral losses that are most severe nasally , with relatively milder temporal losses ; these characteristics indicate that although some mild - to - moderate defects may be underestimated using this technique , the static humphrey field analyzer should reliably detect vgb - attributed vfds . a final limitation in the present work is our inability to conclusively identify a causal link between vgb therapy and the observed vfds ; for this to be possible , we would have to enroll only patients who had completed vfd testing prior vgb therapy , which is rare . however , this is a limitation in most , if not all , retrospective studies on pediatric vbg - attributed vfds . here , we believe that the noted vfds are vgb - attributed vfds because they have the nasal - dominated pattern that is characteristic of vgb - attributed vfds but is not seen in vfds due to other causes . interestingly , our analysis did not reveal any correlations between the incidence of vgb - associated vfds and the mean age at the beginning of treatment , total treatment duration , cumulative dose or maximum dose . however , we did note that no vgb - attributed vfds were seen in patients with total treatment durations < 2 yr and cumulative doses < 10 g / kg . the latter trends are consistent with previous findings in adults , wherein longer treatment durations ( 5 ) and higher total doses of vgb ( 7 ) were associated with greater losses in visual fields . these possible associations are particularly important in pediatric patients , because high dose , sustained vgb treatment is commonly used to treat infantile spasms , especially those from tuberous sclerosis ( 19 ) . if the treatment duration and cumulative dose of vgb are related to vfd , shorter treatments or lower doses should be investigated by linear regression analysis and prospective trials for their abilities to be therapeutically effective while minimizing the occurrence of vfds . another important finding was that the most common type of vgb - attributed vfd in our study population was the nasal arcuate type , and that severity grades i and ii were most frequent . these findings are consistent with previous reports that vgb - associated vfds involve the nasal field ( 10 ) , and indicate that automated perimetry is likely to be more reliable for identifying vgb - associated vfds . however , automated perimetry tends not to lend itself to assessment of pediatric patients , suggesting the need for more reliable and cooperation - independent testing methods . while vgb - attributed vfd was originally considered irreversible ( 20 ) , more recent studies have shown that this condition can be reversed in adult ( 21 - 23 ) and pediatric ( 13,24,25 ) patients after discontinuation of vgb therapy . these reports suggested that patients can recover their retinal function despite apparently permanent damage to retinal cells . although the mechanism by which vgb causes vfd is still not known , studies have suggested that vgb causes a general defect in the retinal network rather than damaging the outer retinal layer ( 26 ) . theoretically , such a defect could functionally recover , at least to some extent , in younger people whose neuronal systems still possess significant plasticity . in the future , it may be possible to perform follow - up visual field examinations on our study population , in an effort to examine reversibility in pediatric patients . in sum , the results of the present study suggest that vfd occurs in vgb - treated children , but at a lower prevalence than that seen in adults ( 5,9 - 11,14,26 - 29 ) . our results also suggest that there is a relationship between vgb - attributed vfds and the duration and total dose of vgb . therefore , we recommend that the total dose and duration of vgb treatment should be reduced as much as possible , and that patients receiving vgb should be given visual field examinations prior to vgb treatment , and at regular intervals thereafter . overall , the clinical decision to use vgb should be based on a risk - benefit analysis of each individual case .