Vigabatrin-Associated Visual Field Constriction - Optometry in Practice

Optometry in Practice Vol 7 (2006) 1–16 

Vigabatrin-Associated Visual Field 

Constriction: A Review 

Mark Lawden BMBCh MA PhD FRCP 

Department of Neurology, Leicester General Hospital, Leicester, UK 

Accepted for publication 20 December 2005 

Introduction 

Until the mid-1980s the treatment of epilepsy was based 

upon a small number of long-established drugs such as 

phenytoin and carbamazepine. Vigabatrin (γ-vinyl-GABA: 

VGB) was the first of the new antiepileptic drugs to be 

introduced, a group that now has nine members. It was 

first synthesised in 1974 and licensed for clinical practice 

in the UK in 1989. VGB was also the first antiepileptic drug 

whose mode of action was known from the outset; it 

irreversibly inhibits the enzyme GABA-transaminase, 

which breaks down GABA (γ-aminobutyric acid), one of 

the major inhibitory transmitters in the brain and retina. 

This in turn increases availability of GABA within the 

central nervous system and increases inhibitory as 

compared to excitatory tone, reducing the likelihood of 

propagation of paroxysmal epileptic neuronal activation. 

VGB was soon established as a powerful antiepileptic drug 

that could be used, usually adjunctively with other older 

drugs, to treat epileptic seizures of focal onset, with or 

without secondary generalisation. Although its role in 

epilepsy management is now much diminished in view of 

its propensity to cause visual field constriction, it still has 

a role in the treatment of infantile spasms and for patients 

with focal epilepsy unresponsive to other drugs. 

Initially the side-effects of VGB were believed to be 

uncommon and mostly minor. Sedation was never a major 

problem, in contrast to most of the older drugs, and 

although psychiatric disturbances were occasionally 

provoked, these can occur with any antiepileptic drug and 

indeed may sometimes be a paradoxical consequence of 

successful seizure control. Concerns arose when it was 

shown in preclinical toxicity studies that VGB was 

associated with the appearance of microvacuolation 

(intramyelinic oedema) in the white matter of mice, rats 

and dogs (Butler et al. 1987, Graham 1989), but no such 

lesions have ever been found in monkeys or in human 

cases at autopsy (Pedersen et al. 1987). 

© 2006 The College of Optometrists 

1 

Initial Reports of Vigabatrin-Associated Visual 

Field Constriction 

In 1997 Tom Eke, John Talbot and I published the first 

three cases of what has come to be known as VGBassociated 

visual field constriction (VAVFC) (Eke et al. 

1997). In each case the subject reported constricted visual 

fields and one reported a tendency to bump into objects. 

Visual acuities were normal and Goldmann visual fields 

revealed marked concentric field constriction, in one case 

with a nasal predominance. Ophthalmic examination 

revealed slight optic disc pallor in two of three patients. 

Magnetic resonance imaging of their brains revealed no 

relevant abnormality, and electrodiagnostic testing 

revealed an abnormal electro-oculogram (EOG), reduced 

oscillatory potentials in the electroretinograms (ERGs), 

but normal a- and b-wave latencies and amplitudes and 

normal visual evoked potentials. Visual fields failed to 

improve when VGB was stopped. We suggested that the 

field constrictions arose because of a toxic effect of VGB 

upon the retina. 

At the time of this initial publication very few other cases 

had come to light. One probable case of bilateral field 

constriction associated with VGB had been referred to 

briefly in an Italian publication in 1993 (Faedda et al. 

1993). A single German case report (Dieterle et al. 1994) 

of unilateral field constriction probably arose because of an 

optic neuropathy, whether ischaemic or inflammatory; 

another case of unilateral optic neuritis in a patient taking 

VGB was probably coincidental (Crofts et al. 1997). By 

January 1997 just nine cases of visual field defect had been 

reported to the Committee on Safety of Medicines under 

the Yellow Card system and this figure included our three 

cases. The then manufacturer of VGB (Hoechst Marion 

Roussel) had received 28 reports of visual field 

abnormalities worldwide out of an estimated 140 000 

patients treated, and a review of the records of 713 VGBtreated 

patients by Wong et al. (1997) yielded a single 

possible symptomatic case. Other correspondents 

suggested that chronic refractory epilepsy rather than its 

treatment might be the cause of visual field defects (Wilson 

Address for correspondence: Dr M Lawden, Department of Neurology, Leicester General Hospital, Leicester, LE5 5PW, UK.

M Lawden 

& Brodie 1997), or that this might be a class effect of 

antiepileptic drugs (Harding 1997). 

What is the Prevalence of Vigabatrin- 

Associated Visual Field Constriction? 

When visual field defects apparently associated with VGB 

were first reported there was some scepticism that such 

an important adverse effect could have remained 

undetected for so long (9 years from its introduction). 

Based upon self-reporting of visual symptoms by patients, 

figures of ‘less than 0.1%’ were quoted by the 

manufacturer (Backstrom et al. 1997) and 0.14% from a 

review of a long-term observational study (Wong et al. 

1997). A prescription event monitoring study conducted 

between 1991 and 1994 analysed questionnaires returned 

by 10 033 patients taking VGB and identified four patients 

with objective evidence of visual field defect (Wilton et al. 

1999). A long-term follow-up study of 4741 patients still 

taking VGB at the end of the above study identified an 

additional 29 cases of visual field defect thought to be 

probably or possibly associated with VGB, giving a 

prevalence of 0.7%. These figures proved to be 

underestimates to a truly massive degree. 

The first published study to estimate prevalence of visual 

field defects in exposed patients was that by Arndt et al. 

(1999), who found them in 12 of 20 (60%) consecutive 

patients (though one patient had a hemianopsia following 

occipital head injury and has been excluded from the 

figures quoted in Table 1). Further early studies showed 

prevalence figures of 29% (Daneshvar et al. 1999), 41% 

(Kälviäinen et al. 1999), 48% (Lawden et al. 1999) and 

‘nearly 50%’ (Miller et al. 1999). The figures quoted by 

Kälviäinen et al. (1999) were particularly valuable as these 

patients had been treated with VGB as monotherapy 

rather than as an adjunctive treatment with other 

antiepileptic drugs, which might have produced field 

defects of their own. 

Prevalence data from those published studies based either 

upon unselected patients or on consecutive series of 

patients assessed for temporal lobe surgery (Hardus et al. 

2000a, Malmgren et al. 2001) are given in Table 1. The 

study of Miller et al. (1999) does not provide exact 

prevalence figures and was excluded. The study of 

Kälviäinen et al. (1999) was not included (except for 

figures relating to epileptic controls) as these patients were 

included in a larger series published later (Nousiainen et al. 

2001). Where possible, separate figures are quoted for male 

and female subjects, and a distinction is drawn whether the 

method of visual field analysis was based upon static 

2 

perimetry (mostly using the Humphrey Allergan visual 

field analyser) on kinetic (Goldmann) perimetry, or both. 

The range of the estimates of prevalence is indeed large, 

extending from 17% by Hardus et al. (2000a) to 83% by 

Midelfart et al. (2000), but this may well reflect differing 

methods of field assessment, different criteria used in 

classifying fields as normal or abnormal and differences in 

patient groups. 

It is of interest that the two studies giving the lowest 

prevalence figures (Hardus et al. 2000a, Malmgren et al. 

2001) are the two series based upon patients who were 

being assessed for temporal lobe surgery. By their nature 

these patients had medically intractable epilepsy and 

would therefore have tended to spend less time on VGB, 

which must have proved ineffective, than patients in other 

studies, many of whom would be seizure-free on 

continuing maintenance therapy. It follows that the 

patients in the two surgical series would be expected as a 

group to have a lower cumulative exposure to VGB than 

would be found in unselected consecutive patients 

attending a conventional epilepsy clinic. At least 52% of 

Malmgren’s patients had cumulative VGB exposure of less 

than 1kg, while in Lawden’s unselected series only 12% had 

exposures this low. High levels of exposure greater than 3kg 

were found in only 14% of Malmgren’s patients, but in 52% 

of Lawden’s. Prevalences of visual field deficits in the lowexposure 

groups were 4% from Malmgren, 0% for Lawden; 

figures for the high-exposure groups were 71% and 54% 

respectively. 

Combining figures for all methods from all series we obtain 

an overall prevalence of 34% visual field constriction in 

patients exposed to VGB, rising to 39% if we exclude the 

two surgical series, which might have been skewed towards 

lower cumulative doses. Series employing static perimetry 

using the Humphrey Allergan visual field analyser or 

similar devices tend to report a greater prevalence of visual 

field defects (46% overall) than series based on Goldmann 

kinetic perimetry (26%), and males show higher prevalence 

(38%) than females (25%). This difference in sensitivity 

between kinetic and static perimetry is noteworthy, as 

several authors have proposed that the kinetic method of 

field assessment should be more suited to identification of 

a predominantly peripheral field defect than the static 

method as the former tests more eccentric areas of the 

visual field than the latter. In fact the reverse appears to be 

the case, with the static method being more sensitive than 

the kinetic. 

If visual field defects can be detected in at least a third of 

patients exposed to VGB, how can we explain the fact that 

nothing of the sort was detected in pre-licensing trials of 

the drug nor for 9 years thereafter, and why did initial

Table 1 Published estimates of vigabatrin-associated visual field defects 

3 

Vigabatrin-Associated Visual Field Constriction: A Review 

Method of Male Female Both Symptomatic VFDs in 

measurement constriction controls on 

other antiepileptic 

drugs 

Arndt et al. (1999) Static + kinetic 8/9 (89%) 3/10 (30%) 11/19 (58%) 2/19 (11%) – 

Lawden et al. (1999) Static 5/10 (50%) 7/15 (47%) 12/25 (48%) 3/25 (12%) 0/16 (0%) 

Daneshvar et al. (1999) Static – – 12/41 (29%) 4/41 (10%) – 

Wild et al. (1999) Static + kinetic 17/45 (38%) 12/54 (22%) 29/99 (29%) – 0/42 (0%) 

Manuchehri et al. 

(2000) 

Static 8/12 (67%) 3/8 (38%) 11/20 (55%) 0/20 (0%) 1/11 (9%) 

Midelfart et al. (2000) Static 9/9 (100%) 6/9 (67%) 15/18 (83%) – 0/5 (0%) 

Hardus et al. (2000a) a Static + kinetic 15/53 (28%) 5/65 (8%) 20/118 (17%) – 0/39 (0%) 

Mauri-Llerda et al. Static – – 6/10 (60%) 2/10 (20%) – 

(2000) 

Toggweiler & Wieser Kinetic – – 9/15 (60%) – 1/12 (8%) 

(2001) 

Malmgren et al. (2001) a Kinetic – – 19/99 (19%) 0/99 (0%) 5/55 (9%) 

Nousiainen et al. (2001) Kinetic 11/25 (44%) 13/35 (37%) 24/60 (40%) – 0/18 (0%) b 

Schmitz et al. (2002) Static + kinetic – – 13/29 (45%) – 3/31 (10%) 

Jensen et al. (2002) Kinetic 2/5 (40%) 1/5 (20%) 3/10 (30%) 1/10 (10%) 0/10 (0%) 

Van der Torren et al. 

(2002) 

Static + kinetic – – 19/29 (66%) – – 

Newman et al. (2002) Kinetic 6/46 (13%) 14/54 (26%) 20/100 (20%) – 0/10 (0%) 

Nicolson et al. (2002) Static – – 42/98 (43%) 1/98 (1%) – 

Total purely static Static 22/31 (71%) 16/32 (50%) 98/212 (46%) – 1/32 (3%) 

Total purely kinetic Kinetic 19/76 (25%) 28/94 (30%) 75/284 (26%) – 6/105 (6%) 

Total all methods Both 81/214 (38%) 64/255 (25%) 265/790 (34%) 13/322 (4%) 10/249 (4%) 

Total excluding Both 66/161 (41%) 59/190 (31%) 226/573 (39%) 13/223 (6%) 5/155 (3%) 

surgical series 

VFD, visual field defect. 

a Series based upon patients evaluated for epilepsy surgery. 

b Data from Kälviäinen et al. (1999).

M Lawden 

estimates of prevalence underestimate the prevalence by a 

factor of at least 50? The answer is that a large majority of 

VAVFC are asymptomatic and would not be identified 

unless specifically sought by formal visual field assessment. 

Figures for symptomatic constriction (excluding vague 

symptoms such as blurring) are more difficult to compare 

between different series as the results obtained will depend 

greatly on exactly what questions the patient was asked, 

whether this was before or after visual field assessment, 

and what was accepted as evidence of symptomatic 

constriction. However, using the figures in Table 1, an 

overall estimate that about 4% of VGB-exposed patients 

complain of visual field constriction seems reasonable. 

This means that over 90% of the patients who actually have 

visual field defects fail to notice them, explaining much of 

the discrepancy between initial and later estimates of 

prevalence referred to above. 

Visual field measurement is much more difficult in 

children than in adults and estimates of the prevalence of 

VGB-associated visual field defects are accordingly much 

scarcer. The first report of VAVFC in two children aged 10 

and 15 years was published by Vanhatalo & Pääkkönen 

(1999). An early Spanish study (Argumosa et al. 1999) 

found no defects either in 12 children treated with VGB 

monotherapy or in controls treated with carbamazepine or 

valproate. By contrast, Wohlrab et al. (1999) found five 

cases of visual field constriction in 12 VGB-treated 

children (42%), but also in one of 12 matched controls 

treated with other antiepileptic drugs. That they were able 

to test visual fields in only 12 children out of a total cohort 

of 153 shows the difficulty of visual field measurement in 

children. The largest published study is of 91 children by 

Vanhatalo et al. (2002), who found significant visual field 

constriction in 17 (18.7%) of them. Other reported 

prevalence figures in paediatric patients include Luchetti 

et al. (2000) 8/13, Iannetti et al (2000) 4/21, Russell-Eggitt 

et al. (2000) 10/14, Gross-Tsur et al. (2000) 1/17, Prasad et 

al. (2001) 2/12, Harding et al. (2002b) 4/12, and Ascaso et 

al. (2003) 3/15. This gives an overall risk of VAVFC of 

64/219 (29%), slightly lower than the adult figure. 

Do Visual Field Defects also Occur as a Result 

of Epilepsy or with other Antiepileptic Drugs? 

When the first report linking VGB to visual field defects 

was published, it was often suggested that these defects 

could also be caused by other antiepileptic drugs (Harding 

1997) or perhaps by the epileptic disorder itself (Wilson & 

Brodie 1997). Trojan (1967) had reported a case in which 

visual fields appeared reversibly constricted in the 

immediate aftermath of an epileptic seizure. One much- 

4 

quoted study had attempted to assess the prevalence of 

visual field defects in patients treated for epilepsy (Ludwig 

& Marsan 1975) and the prevalence of such defects was 

indeed high (20% of 55 patients). However, this patient 

group was selected by the presence of occipital 

electroencephalogram foci and many had structural lesions 

in the occipital lobes. Figures derived from this highly 

atypical group cannot be applied to the whole epileptic 

population, amongst whom occipital lobe epilepsy is very 

rare. 

Regarding the traditional antiepileptic drugs, there were a 

few case reports of visual field defects, but these were again 

highly atypical. One such report described constricted 

visual fields apparently caused by phenytoin, but this was 

said to be the result of prolonged toxic blood 

concentrations in a patient with a rare defect of drug 

metabolism (Lorenz & Kuck 1988). Another report 

implicated oral diazepam taken in large and surely sedative 

doses as an anxiolytic agent, but the relevance of this to 

epilepsy practice is not clear (Elder 1992). Intravenous 

diazepam has been reported to cause reversible visual field 

constriction, but this effect disappeared when fields were 

measured with the upper eyelid taped and is likely to be 

due to ptosis (Takahashi et al. 1989). Steinhoff et al. 

(1997a, b) had described several rather minor effects of a 

variety of antiepileptic drugs on various aspects of vision 

other than visual field. Arndt et al. (2002) have presented 

data suggesting that VAVFC are more severe in patients 

treated concomitantly with sodium valproate than in those 

treated with carbamazepine. 

Since the first reports of VAVFC several other novel 

antiepileptic drugs have been introduced, some of which 

also affect GABAergic transmission. A single case was 

reported of visual field constriction associated with 

epilepsy treatment with the as-yet unlicensed GABAagonist 

drug progabide and this persisted 6 months after 

the drug was withdrawn (Baulac et al. 1998, Nordmann et 

al. 1999). Tiagabine is perhaps the most closely related to 

VGB as it is believed to exert its antiepileptic effect by 

blocking reuptake of GABA at the synapse, thus prolonging 

its neurotransmitter action, whereas VGB inhibits its 

breakdown. Although one possible case of a visual field 

defect associated with tiagabine has been published 

(Kaufman et al. 2001), the severity of the field defect was 

minor. Nousiainen et al. (2000a) failed to find any such 

defects in 15 consecutive patients treated with tiagabine 

monotherapy using methods that had previously identified 

a high prevalence of visual field defects in VGB-treated 

patients. These findings were replicated by Krauss et al. 

(2003), who found that visual fields of 12 tiagabine-treated 

patients were similar to epilepsy control patients and quite 

different to those of patients treated with VGB. It seems

unlikely that this is a class effect common to GABAergic 

drugs. 

What then of the other possibility, that epilepsy itself 

might be responsible? Eleven of the studies cited above 

attempted to investigate this by measuring visual fields in 

patients taking other antiepileptic drugs who had never 

been exposed to VGB and, where available, the prevalence 

of such defects is included in Table 1. Seven studies 

reported finding no attributable defects at all in their 

control populations while the other four report abnormal 

fields in 8–10%. Combining these figures, an overall figure 

of 4% abnormal fields in control subjects emerges, which is 

clearly much less than the 34% found in the VGB-exposed. 

It is possible that the occasional identification of visual 

field defects in patients with epilepsy who have never 

taken VGB represents no more than the inherent difficulty 

of visual field measurement itself and it has yet to be 

convincingly demonstrated that either epilepsy or other 

antiepileptic drugs cause visual field defects. 

What are the Characteristics of Vigabatrin- 

Associated Visual Field Defects? 

Our initial report of VAVFC (Eke et al. 1997) showed 

concentric constriction of the visual field in both eyes to a 

variety of isopters in Goldmann kinetic fields. In one case 

the nasal fields appeared more affected than the temporal 

fields, but in the other two cases there was no such nasal 

predominance. Our subsequent case series (Lawden et al. 

1999) employed static perimetry. Typical results for both 

kinetic and static perimetry in a moderately affected case 

are shown in Figure 1. While severely affected cases 

showed concentric constriction, milder cases had a 

distinctive pattern in which the field loss was 

proportionately more extensive in the nasal field, resulting 

in a characteristic pattern of binasal field loss extending in 

an annulus across the horizontal midline, with a tendency 

for sparing of the temporal field. 

These findings were confirmed and extended by Wild et al. 

(1999), who reported on a total of 42 abnormal visual 

fields attributed to VGB exposure. The patients came from 

a variety of sources and visual fields were measured by 

either static or kinetic methods. Static perimetry was 

available for 39 of these patients and 34 (87%) showed the 

distinctive pattern of predominantly binasal field loss, 

while 3 (8%) more severely affected cases were classified as 

concentric and 2 (5%) had other patterns of deficit. These 

field deficits had another distinctive and unusual feature in 

that they had steep borders with a sudden dramatic fall-off 

in sensitivity. Both eyes were equally affected in most 

cases. In those 21 cases where both Humphrey static and 

5 


Goldmann kinetic perimetry was available, the VAVFC was 

identifiable by both methods. 

Whether the pattern of field defect found in VAVFC is 

uniquely characteristic is controversial. Several authors 

have contested this point and asserted that the field 

restriction is concentric and affects the temporal field to 

the same proportionate degree as the nasal field. What is 

clear is that those studies employing static perimetry have, 

without exception, commented upon a nasal 

predominance of the field defect giving a characteristic 

binasal pattern when the fields of both eyes are viewed 

together (Ascaso et al. 2003, Daneshvar et al. 1999, Gross- 

Tsur et al. 2000, Lawden et al. 1999, Manuchehri et al. 

2000, Mauri-Llerda et al. 2000, Midelfart et al. 2000, 

Prasad et al. 2001, Wild et al. 1999). By contrast, those 

studies relying on kinetic perimetry have mostly found 

nasal and temporal fields to contract in proportion, 

without any uniquely distinctive pattern (Fledelius 2003, 

Kälviäinen et al. 1999, Hardus et al. 2000a, 2001a, 

Malmgren et al. 2001, Miller et al. 1999, Vanhatalo et al. 

2002). Of course, patients start with a temporal field that 

is greater in extent (almost 90º) than the nasal field (about 

60º). If VGB caused both nasal and temporal fields to 

shrink proportionately, this field defect would impinge first 

upon the nasal field during static perimetry, as the area of 

field tested is centred symmetrically upon the fixation 

point. A good example of the different field appearances 

generated in the same patient by static and kinetic 

perimetry was given by Reuther et al. (1998); the 

characteristic binasal pattern was obvious with static 

perimetry, and subtle with kinetic perimetry. 

All the above field measurements were made with the 

subject in a fully light-adapted state against a diffusely 

illuminated background. They were therefore derived 

exclusively from the cone system, whereas of course the 

predominant photoreceptor type in affected peripheral 

regions of retina is rods. Banin et al. (2003) assessed 

peripheral rod-derived dark-adapted visual fields and 

found them also to be constricted in patients having 

VAVFC on light-adapted fields. This important finding 

showed that VGB retinal toxicity was not confined to the 

cone system. 

What then is the method of field analysis most suited to 

the identification and monitoring of VAVFCs? In my 

opinion the optimal strategy is to use Humphrey static 

perimetry using the Central 30-2 full-threshold program. 

The prevalence figures given in Table 1 suggest that static 

perimetry is more likely to identify VAVFCs than kinetic 

perimetry. As the field defect is undoubtedly peripheral, 

the Central 30-2 program (extending to 30º eccentricity) is 

clearly more likely to encounter it than the more

M Lawden 

Figure 1 Goldmann kinetic visual field (top) and Humphrey full-threshold Central 30-2 static perimetry (bottom) for 

a patient with a typical vigabatrin-associated visual field constriction. 

6

estricted Central 24-2 program (extending to 21º 

eccentricity), which samples less of the peripheral field. It 

is quite possible that even more cases could be picked up 

by using the Peripheral 30/60 program, which takes the 

field analysis out to 60º, but there are no established agerelated 

confidence limits available beyond 30º eccentricity 

and the risk of false-positive results must be significant. It 

is unlikely that any VAVFC of visual significance to the 

patient would be missed by a Central 30-2 threshold test 

whilst being detectable on the Peripheral 30/60 test. While 

screening programs such as the Full Field 120-point 

screening test can certainly be used to identify patients 

with possible VAVFC expeditiously, these provide 

insufficient quantitative information for sequential 

monitoring of patients who choose to continue treatment 

and in my opinion have few, if any, advantages. In skilled 

hands there is no doubt that Goldmann kinetic perimetry 

will identify those VAVFCs that are of visual significance, 

but the pick-up rate is likely to be lower than with static 

perimetry and the extra expenditure of operator time 

seems unjustified. It is possible that some patients who 

prove unable to produce reliable data with the automated 

Humphrey field analyser might manage the more 

interactive Goldmann perimetry better. One definite 

advantage of automated static perimetry is that the binasal 

shape of VAVFC that it produces is quite characteristic, 

easily recognised and quite unlike any other field defect 

routinely encountered in the clinic. It is theoretically 

possibly for such a defect to be caused by compression of 

the chiasm from both sides simultaneously, but this is 

exceedingly rare. This advantage does not apply to 

Goldmann kinetic fields in which VAVFCs for the most part 

simply appear concentrically constricted without uniquely 

distinctive features. Frisén (2004) has recently presented 

evidence that a more sophisticated method of perimetry 

called rarebit (or microdot) perimetry could be more 

informative and sensitive than kinetic perimetry in 

patients with VAVFC, though this technique has yet to be 

compared with static perimetry using the Humphrey field 

analyser, which is now the international standard. 

Does Vigabatrin Affect Aspects of Vision 

other than Visual Field? 

Most reports of VAVFC have emphasised that visual acuity 

and sensitivity of the macular visual field remained normal, 

even in the presence of extensive field deficit. Nousiainen 

et al. (2000b) found abnormally high error scores using the 

Farnsworth-Munsell 100 hue test in 32% of patients treated 

with VGB and there was an approximate correlation 

between visual field constriction and total error score. 

Abnormal colour vision was also found in 28% of patients 

7 


treated with carbamazepine, so this may not be specific to 

VGB. Mecarelli et al. (2001) found that a single dose of 

VGB in healthy volunteers produced a detectable 

impairment of blue colour perimetry, but the effect was 

minor and less marked than with carbamazepine. 

Nousiainen et al. (2000c) found that VGB impaired 

contrast sensitivity slightly in those with VAVFC. 

Ophthalmoscopic Findings 

Although ophthalmoscopic abnormalities have been 

described in association with VAVFC, these were mostly 

minor and insufficiently distinctive to be useful in 

diagnosis. In two of the original three cases, Eke et al. 

(1997) described the optic disc as appearing ‘slightly pale’ 

and in one case the peripheral retina ‘seemed slightly 

atrophic’. In the next four cases to be described, Krauss et 

al. (1998) described narrowed retinal arteries, retinal 

surface wrinkling and abnormal macular reflexes. In the 12 

patients considered by Lawden et al. (1999) to have 

definite VAVFC, four had optic disc pallor, five had slightly 

pale discs and three had normal discs. Miller et al. (1999) 

described non-specific retinal abnormalities in 23/32 VGB 

patients and no such abnormalities in any of their 10 

epilepsy controls. Apparently acquired non-specific 

pigmentary retinal changes or disc pallor were observed in 

4/21 VGB-treated children by Koul et al. (2001). Jensen et 

al. (2002) reported attenuated retinal vessels in 3/10 VGBtreated 

patients, though only one had VAVFC. Viestenz et 

al. (2003) reported a single case of VAVFC in a 70-year-old 

man associated with optic disc pallor and pathological 

reduction of retinal nerve fibre layer thickness. Optic disc 

pallor was reported by Daneshvar et al. (1999) in 4/12 

patients with field abnormalities, and also by Russell-Eggitt 

et al. (2000) (3/14), Mauri-Llerda et al. (2000) (2/6) and by 

Ponjavic & Andréasson (2001) (1/12). No significant 

ophthalmoscopic findings were reported in the studies of 

Arndt et al. (1999), Ascaso et al. (2003), Banin et al. 

(2003), Besch et al. (2002), Gross-Tsur et al. (2000), 

Hardus et al. (2000a, b), Iannetti et al. (2000), Kälviäinen 

et al. (1999), Manuchehri et al. (2000), Midelfart et al. 

(2000), Newman et al. (2002), Prasad et al. (2001), 

Schmitz et al. (2002), van der Torren et al. (2002), 

Vanhatalo et al. (2002) and Wohlrab et al. (1999). 

The only studies of VAVFC specifically aimed at evaluation 

of funduscopic appearances were those of Frisén & 

Malmgren (2003) and Buncic et al. (2004). Frisén & 

Malmgren (2003) performed retrospective analysis of 

digitally enhanced ocular fundus photographs from 25 

patients with VAVFC and found evidence of atrophy of the 

nerve fibre layer and optic disc in 21 (84%). In mildly 

affected eyes only the nasal quadrant was affected, whereas

M Lawden 

in severely affected eyes all quadrants were affected except 

the temporal one, which contains the papillomacular 

bundle serving central vision. They suggested that this 

pattern of vulnerability of ganglion cell axons could arise if 

fibres with longer intraocular unmyelinated courses were 

affected first. There was a rough correlation between the 

severity of atrophy and cumulative VGB dose and with 

degree of visual field constriction. 

Buncic et al. (2004) reported on three children with 

VAVFC, all of whom had a distinctive pattern of disc 

change that the authors term ‘inverse optic atrophy’. This 

affects all areas of the nerve fibre layer and optic disc, 

conspicuously sparing fibres originating from the macula 

and hence also sparing the temporal part of the optic disc. 

This is the opposite of the pattern shown in most forms of 

optic neuropathy such as that following optic neuritis, in 

which there is temporal pallor. There appeared to be a 

fairly sharp line of demarcation separating normal from 

atrophic areas of the nerve fibre layer corresponding 

roughly to the temporal vascular arcades. Changes in the 

macula area were limited to minor wrinkling. An identical 

pattern of atrophy in the retinal nerve fibre layer was 

shown in an adult patient with VAVFC by Choi & Kim 

(2004). 

90 

80 

70 

60 

50 

%VFC 

40 

30 

20 

10 

0 

0 5 

Cumulative VGB dose (kg) 

Malmgren et al. (2001) 

All others 

All combined 

Figure 2 Frequency of visual field constriction (VFC) and 

cumulative vigabatrin (VGB) dose. 

8 

Do Vigabatrin-Associated Visual Field Defects 

Change? 

It is now clear that visual field defects occur in a high 

proportion of patients taking VGB, but that a large majority 

of these are asymptomatic. Is the probability of developing 

VAVFC related quantitatively to duration of VGB exposure 

or to cumulative dose? Lawden et al. (1999) found that the 

mean cumulative VGB dose was larger (4.4kg) in those 

patients with VAVFC than in those with normal fields 

(1.7kg), though patient numbers, particularly of those with 

normal fields, were small. Kälviäinen et al. (1999) could 

demonstrate no correlation between visual field extent and 

the duration, maximum dose and cumulative dose of VGB, 

and these findings were later confirmed (Nousiainen et al. 

2001). However, these two papers provided no details of 

individual patient dosages and visual fields. By contrast 

Manuchehri et al. (2000) found a strong correlation 

between the amount of visual field loss and cumulative 

dose; hardly any patients had VAVFC with cumulative 

doses below 1.5kg. Hardus et al. (2000a) found that loss of 

visual field was significantly more extensive in patients 

who had used VGB for 2–4 years than in those exposed for 

< 2 years and Toggweiler & Wieser (2001) showed a 

correlation between treatment duration and extent of field 

constriction. In a careful study of 92 patients whose drug 

history was precisely known, Hardus et al. (2001a) 

employed a novel method to calculate percentage surface 

loss of the visual field as measured kinetically using the 

Goldmann V/4 stimulus. Although data were widely 

scattered, there was a clear correlation between 

cumulative VGB dose and percentage field loss, with 

significant field loss almost unknown with cumulative 

doses below 1kg. 

Malmgren et al. (2001) also found a clear correlation 

between cumulative dose and frequency of VAVFC. Field 

defects were found in only 2/51 patients (4%) with 

cumulative doses less than 1kg, but in 10/14 patients (71%) 

with cumulative doses greater than 3kg. Malmgren’s series 

differs from most others by including many patients who 

had been exposed to VGB, but had low cumulative doses. 

This probably explains why this paper provides an 

unusually low estimate of VAVFC prevalence, but 

demonstrates an unusually clear correlation between 

VAVFC frequency and cumulative dose. In Figure 2 the 

observed frequency of VAVFC has been plotted for a range 

of cumulative VGB doses. This figure compares data from 

Malmgren et al. (2001) with data derived from all those 

adult case series where enough data was given to allow 

approximate cumulative VGB doses to be calculated for 

patients whose fields could be classified as normal or 

abnormal (Arndt et al. 1999, Besch et al. 2002, Daneshvar 

et al. 1999, Hardus et al. 2001a, Jensen et al. 2002, Lawden

et al. 1999, Manuchehri et al. 2000, Midelfart et al. 2000, 

van der Torren et al. 2002). The data for zero cumulative 

dose came from the combined figure of 4% found in Table 

1. Although there was quite wide variation, particularly at 

lower cumulative doses, there was rough agreement that 

the frequency of visual field constriction increased with 

increasing cumulative VGB dose, that field defects were 

rare, though not unprecedented, at cumulative doses below 

1kg, and that cumulative doses above 5kg did not appear to 

impart any further increase in risk. 

With regard to duration of treatment, the position is less 

clear. In the very short term a single dose of 3000mg VGB 

had no detectable effect on either static or kinetic 

perimetry in a double-blind placebo-controlled cross-over 

study in 24 healthy volunteers (Tiel-Wilck et al. 1995). A 

similar study in healthy volunteers with a maximum of 9 

days’ exposure likewise demonstrated no detectable effect 

on visual field (Harding et al. 1999). A case report 

(Karabiyik 2003) of a patient who had taken a large 

overdose of VGB stated that he developed an irreversible 

concentric visual field deficit, though as this patient had 

been taking VGB for 4 years before the overdose, this was 

difficult to evaluate except in comparison with previous 

visual fields, which the author did not provide. The first 

three symptomatic cases reported by Eke et al. (1997) first 

noticed their symptoms after VGB treatment lasting 

between 24 and 38 months. Hardus et al. (2000a) were 

able to show that visual field loss was significantly more 

extensive in patients who had used VGB for 2–4 years than 

in those exposed for < 2 years. Hardus et al. (2001a) later 

used linear regression to look for the most powerful 

combination of parameters to predict visual field loss and 

found that, while cumulative dose contributed 

significantly, neither mean daily dose nor duration of 

treatment added further precision to the prediction. While 

the large majority of patients with VAVFC had taken VGB 

for at least 1 year, some series contain occasional affected 

patients whose exposure duration was much less than this. 

For example, Midelfart et al. (2000) included one patient 

with a field defect described as ‘severe’ who had taken VGB 

for just 6 months and whose cumulative dose was a 

maximum of 0.1kg. A case report by Kiratli & Turkcuoglu 

(2001) gave details of a 60-year-old woman who developed 

symptomatic VAVFC after just 6 months of VGB treatment 

with a maximum cumulative dose of 0.4kg. As most 

patients were asymptomatic, the observation that almost 

all had been taking VGB for at least a year before VAVFCs 

were detected may be a result of the logistics of visual field 

screening in the treated population rather than the time 

course of the drug’s toxic effect. 

If VGB is discontinued, is there any evidence that VAVFC 

recover? The initial report of VAVFC described visual field 

9 


constriction as ‘persistent’ on the basis that none of the 

three patients showed any tendency to improve despite 

withdrawal of VGB for up to 4 years (Eke et al. 1997). In a 

subsequent series Lawden et al. (1999) reported modest 

improvement in three out of 12 patients with VAVFC after 

drug withdrawal, but most subsequent series have 

observed little or no tendency for fields to improve once 

VGB was withdrawn. Yet several cases of apparently 

significant improvement after drug withdrawal have been 

reported. Versino & Veggiotti (1999) reported a case of a 

10-year-old child whose apparently severely constricted 

visual fields reverted to nearly normal 5 months after drug 

discontinuation. Though the patient’s symptoms (bumping 

into objects) also disappeared, the initial abnormal fields 

do show the characteristic cloverleaf pattern observed as 

an artefact in subjects who fail to maintain concentration 

after the initial initialisation procedure performed by the 

Humphrey field analyser. Other such cases of apparent 

reversibility were reported by Giordano et al. (2000), Jain 

et al. (2004) and Krakow et al. (2000), so it is likely that 

occasional cases do improve. 

Several case series have attempted to evaluate progression 

and reversibility explicitly. Hardus et al. (2000b) reported 

no tendency for VAVFC to improve after drug withdrawal, 

but a small tendency for fields to worsen in patients who 

elected to continue VGB. Studies by Graniewski-Wijnands 

& van der Torren (2002), Hardus et al. (2003), Johnson et 

al. (2000), Nousiainen et al (2001) and Schmidt et al. 

(2002) found no evidence of improvement in VAVFC 

following VGB withdrawal for up to 3 years. By contrast, 

Fledelius (2003) reported that 4/8 patients who withdrew 

from VGB showed significant improvement, but that this 

was only found in 1/18 patients who either reduced VGB 

dose or continued therapy unchanged. 

What if patients with detectable field defects elect to 

continue therapy with VGB? Paul et al. (2001) investigated 

this question in 15 patients who were assessed at 3monthly 

intervals while continuing therapy for 1 year. All 

had received VGB for at least 2 years prior to the study. 

Initially nine had normal fields and six had constricted 

fields. Thirteen showed no significant change in field 

extent over the year and one showed some initial 

improvement, probably a practice effect. One patient did 

show apparent progressive worsening of field extent, 

actually moving from the normal to the impaired group 

over that time. The authors discounted this patient’s 

worsening performance on the grounds that his results 

were felt to be unreliable, though it appears odd that he 

became progressively more unreliable as his familiarity 

with the testing procedure increased. Absence of 

identifiable progression in at least the large majority of 

patients followed over 1 year suggests that fields remain

M Lawden 

stable for long periods with continuing VGB treatment, 

whether or not they are initially impaired. It remains 

possible that progression occurs over a period greater than 

a year, perhaps in a minority of patients. Best & Acheson 

(2005) followed 16 patients with definite VAVFC who 

elected to continue VGB for at least 18 months, and found 

evidence of progression in only one of them. 

What Electrophysiological Abnormalities are 

Associated with Vigabatrin-Associated Visual 

Field Defects? 

The initial description of VAVFC (Eke et al. 1997) 

mentioned that two of the three patients had an abnormal 

EOG and reduced oscillatory potentials in the ERG. Since 

then a large number of publications have reported on 

electrophysiological abnormalities associated with VAVFC 

and/or with VGB treatment. Electrophysiology has the 

potential both to teach us more about the pathological 

process underlying VAVFC and to allow diagnosis in 

patients unable to cooperate with visual field testing due to 

age or learning disability. The situation is complex as 

electrophysiological results can be affected by the precise 

recording techniques employed, by the presence and 

severity of VAVFC, by whether the patient was taking VGB 

at the time of recording and by concomitant treatment 

with other drugs known to affect ERG, such as 

carbamazepine. The electrophysiological literature is now 

extensive, but somewhat unilluminating for the nonspecialist 

as both methods of measurement and 

terminology differ between research groups, making it 

difficult to know how to compare studies from different 

units and how to reconcile differences in findings. 

As this topic is of limited interest to optometrists, analysis 

of work in this field will not be attempted here. Harding et 

al. (2000a, b) and Hardus et al. (2001b) attempted to 

distinguish between the effect of VAVFC itself, the effect of 

ongoing VGB therapy and the effect of ongoing therapy 

with other antiepileptic drugs. Broadly, while flash ERG 

abnormalities are not uncommon in patients with VAVFC, 

none correlates closely and consistently with VAVFC 

presence or extent in a diagnostically useful manner. EOG 

abnormalities correlated more with ongoing VGB therapy 

than with VAVFC. Some variables connected with 30Hz 

flicker and with oscillatory potentials correlated with 

severity of VAVFC and appeared unaffected by ongoing 

VGB therapy. In a further analysis Harding et al. (2002a) 

concluded that the best indication of severe VAVFC 

independent of current treatment was provided by 

amplitude of 30Hz flicker, and that this variable was 

unaffected by current as opposed to previous VGB therapy. 

10 

Visual evoked responses (VER) have been reported to be 

normal in most patients with VAVFC (eg Lawden et al. 

1999, Miller et al. 1999, Zgorzalewicz & Galas- 

Zgorzalewicz 2000). Harding et al. (2002b) have employed 

an ingenious modification of the VER technique using 

central and peripheral checker patterns reversing at 

different rates in order to generate separable signals from 

outer and inner regions of the visual field. Their aim was to 

develop a diagnostic tool capable of identifying VAVFC in 

patients as young as 2 years of age unable to cooperate with 

conventional perimetry, and this appears to be successful 

with acceptable levels of sensitivity (75%) and specificity 

(71%) (Spencer & Harding 2003). It remains to be seen 

whether this technique will be adopted clinically, given the 

steep decline in the use of VGB in epilepsy practice. 

What Pathological Changes Occur in the 

Retina? 

From the outset, it appeared likely that the retina was the 

primary site of damage causing VAVFC. This was supported 

by the pattern of the field defect, and eventually by 

identification of electrophysiological abnormalities 

correlated to the field loss. Several pathological and 

pharmacological studies of the effect of VGB on the retina 

in rats have now been published. Butler et al. (1987) 

showed that in albino but not in pigmented rats, VGB had 

a dose-dependent toxic effect on the outer retina 

characterised by disruption of the outer nuclear layer 

containing photoreceptor nuclei. Sills et al. (2001) showed 

that VGB accumulated in the retina of albino rats after a 

single dose in concentrations five times greater than in the 

brain. Concentrations of GABA were likewise elevated 

more in retina than in brain, and later work by Neal et al. 

(1989) suggested accumulation of GABA in retinal glial 

cells. Tiagabine, by contrast, showed no tendency to 

accumulate in the retina and did not alter GABA 

concentrations. Retinal accumulation of VGB was 

confirmed in a later study, which also showed no such 

tendency with two other antiepileptic drugs, gabapentin 

and topiramate (Sills et al. 2003). 

Duboc et al. (2004) treated albino rats with VGB for 45 

days and demonstrated a significant irreversible reduction 

in photopic (but not in scotopic) ERG amplitudes and also 

in 30Hz flicker and oscillatory potential responses. Retinal 

histology revealed severe disruption of the peripheral outer 

retina with histochemical evidence of gliosis affecting the 

entire retina, with evidence of widespread damage to cone 

(but not rod) photoreceptors. Although GABA is 

physiologically an inhibitory transmitter, it can apparently 

become excitatory and potentially excitotoxic in damaged

neurons and when present in excessive concentrations 

(Lukasiuk & Pitkanen 2000, Staley et al. 1995, Van den Pol 

et al. 1996, Xu et al 2000;). All retinal neurons express 

GABA receptors, with the noticeable exception of rod 

photoreceptors. Ponjavic et al. (2004) have reported 

similar findings in rabbits. 

Izumi et al. (2004) examined the effect of light on VGB 

toxicity in albino rat retinas. When retinas were incubated 

with VGB under bright light for 20h, damage to 

photoreceptors could be demonstrated. Incubation with 

VGB in darkness caused no damage; nor did incubation 

with GABA or tiagabine in the presence or absence of light. 

Retinas from rats exposed to bright light for 20h after VGB 

injection showed similar outer retina damage, but this was 

not present in animals treated with VGB that were kept in 

the dark. At least in this situation VGB was only toxic to 

the retina in a short time if combined with light and this 

toxicity did not appear to result from heightened GABA 

levels as GABA itself was not toxic, whatever the lighting. 

The relevance of these acute effects in rats to much more 

chronic effects in humans remains to be established. 

A single case of VAVFC with pathological retinal 

examination has now been reported (Ravindran et al. 

2001). The patient was a 41-year-old man with severe 

symptomatic VAVFC who died of a cardiac arrest shortly 

after VGB withdrawal. Histological assessment of the 

retinas showed severe loss of ganglion cells in the 

peripheral retina with much less marked changes at the 

macula. In addition there was partial loss of nuclei in inner 

(bipolar and amacrine cells) and outer (photoreceptor) 

nuclear layers, atrophy in inner and outer plexiform layers, 

and marked atrophy of the optic discs, nerves, chiasm and 

tracts, always with relative preservation of macular fibres. 

There was no evidence of intramyelinic oedema at any 

location. This case confirmed that the retina was the 

primary site of damage and that there was consecutive 

optic nerve atrophy. The loss of ganglion cells was 

consistent with the irreversibility of VAVFC reported by 

the majority of workers, and the relative sparing of macular 

retina explained preservation of acuity and colour vision, 

and the comparative rarity of detectable disc pallor. 

Several antiepileptic drugs are known to decrease cerebral 

blood flow, including VGB (Spanaki et al. 1999). Hilton et 

al. (2002) used scanning laser Doppler flowmetry to 

measure ocular blood flow in epilepsy patients on a variety 

of antiepileptic drugs and found a significant reduction 

when compared to non-epileptic controls. Hosking et al. 

(2003) went on to show that pulsatile ocular blood flow was 

significantly lower in the eyes of patients exposed to VGB 

than in patients on other antiepileptic drugs. No 

11 


correlation was attempted with visual field measurements, 

nor was it clear how many of the VGB-exposed group were 

still taking VGB at the time of examination, so the 

relevance of these findings to VAVFC remains to be 

established. 

One issue that remains to be resolved is the question why 

most patients who develop VAVFC remain asymptomatic, 

and show no tendency to progress with continued VGB 

treatment (at least over a year or two), while a small 

minority progress until they become symptomatically 

visually disabled due to tunnel vision. It seems likely that 

the latter are genetically more susceptible to VGB-induced 

retinal damage, but the reason for this is unknown. One 

early suggestion was that genetic variation in the 

mitochondrial enzyme ornithine δ-transaminase might be 

to blame (Roubertie et al. 1998), but no such genetic 

variation could be identified (Hisama et al. 2001). 

Conclusion 

According to the National Society for Epilepsy, epilepsy is 

the most common serious neurological condition in the 

UK. One in every 130 adults and children in the UK has 

epilepsy, so there are around 450 000 people with epilepsy 

in the UK. VGB is significant as the first of the new 

antiepileptic drugs to be introduced, but the number of 

patients taking it is small and likely to be declining. 

Although the proportion of patients who will develop 

visually disabling VAVFC is small, the insidious and 

irreversible nature of this side-effect now limits the use of 

VGB to those patients who have already either failed to 

respond or to tolerate all alternative antiepileptic drugs. I 

estimate that there are 18 antiepileptic drugs that could 

reasonably be used in the UK for the outpatient treatment 

of epilepsy, so the likelihood that VGB will be initiated in 

new patients in the future is low. A possible exception to 

this is in infants suffering from the severe epilepsy 

syndrome of infantile spasms. VGB has been shown to be 

highly effective in this condition and has definite 

advantages as regards side-effects compared to the best 

alternative treatment (adrenocorticotrophic hormone 

injections). It is unlikely that such infants will be able to 

cooperate with visual field testing and many have severely 

disabling underlying brain disorders. Most epilepsy clinic 

lists still contain patients who are well controlled on VGB 

therapy that was initiated before VAVFC were first 

reported. Some of these will wish to continue taking a drug 

that has served them well. Such patients will need visual 

field assessment at intervals of 4–6 months for as long as 

they continue VGB therapy.

M Lawden 

Visual field constriction is a common accompaniment of 

VGB therapy, occurring in between a third and a half of 

patients. When measured by static perimetry there is a 

distinctive pattern of binasal field loss that is readily 

recognisable. Using kinetic perimetry the appearances are 

not distinctive and consist of a generalised field 

constriction. The large majority of VGB-associated visual 

field constrictions (about 90%) produce no symptoms, 

though a minority of patients (about 4%) progress to 

develop visually disabling tunnel vision. The risk of 

developing VAVFC seems to go up with increasing 

cumulative dose, though clearly there are large variations 

in individual susceptibility. Men appear to be more at risk 

than women and co-medication with sodium valproate 

may be a risk factor. As the field constriction is insidious, 

patients taking VGB, where possible, should have visual 

fields assessed prior to commencing therapy and at 4–6month 

intervals thereafter. Visual field constriction 

appears to be largely irreversible if therapy is stopped, but 

should not then progress any further. Ophthalmoscopic 

abnormalities are found, but are subtle and not reliable for 

diagnosis. Electrophysiological investigations have 

implicated the retina as the site of damage in the visual 

system, but are not yet able reliably to diagnose VAVFC 

with acceptable sensitivity and specificity. Where patients 

who might benefit from VGB are unable to cooperate with 

visual field assessment, the decision to treat must be based 

upon a calculation of the balance of benefit and risk for the 

individual. Although it will be important in future to screen 

novel antiepileptic drugs for effects on visual field during 

development, the evidence so far suggests that this toxic 

effect is specific for VGB and does not occur with any of the 

other mainstream antiepileptic drugs, even those that work 

by modulation of the GABA transmitter system. 

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Multiple Choice Questions 

1. How is vigabatrin believed to exert its antiepileptic 

effect? 

(a) by reducing GABA reuptake 

(b) by blocking sodium ionic channels 

(c) by inhibiting the breakdown of GABA 

(d) by increasing GABA synthesis 

2. Among patients taking vigabatrin, what proportion 

have detectable visual field constriction? 

(a) fewer than 10% 

(b) 10–30% 

(c) 30–50% 

(d) more than 50% 

3. Which of the following appear to increase the risk of 

developing visual field constriction with vigabatrin 

treatment? 

(a) female sex 

(b) treatment with carbamazepine 

(c) treatment with valproate 

(d) frequent convulsive seizures 

4. The following statements concern the pattern of visual 

field defect associated with vigabatrin. Which is true? 

(a) Kinetic perimetry appears more sensitive to the defect 

than static perimetry 

(b) In static perimetry the field loss usually has a 

distinctive binasal pattern 

(c) The severity of visual field loss is often asymmetrical 

between the two eyes 

(d) Clinically many conditions cause binasal visual field 

loss 

5. What proportion of vigabatrin-treated patients 

complain of noticeable visual field constriction? 

(a) fewer than 1% 

(b) about 5% 

(c) about 10% 

(d) about 30% 

6. The following ophthalmoscopic abnormalities have 

been associated with vigabatrin-associated visual field 

constriction: 

(a) retinal arterial narrowing 

(b) macular holes 

(c) temporal disc pallor 

(d) peripapilliary retinal atrophy 

15 


This paper is reference C-3111. Three credits are available. Please use the inserted answer sheet. Copies can be obtained from Optometry 

in Practice Administration, PO Box 6, Skelmersdale, Lancashire WN8 9FW. There is only one correct answer for each question. 

7. Presence of vigabatrin-associated visual field 

constriction appears to be most closely correlated with 

which of the following? 

(a) peak vigabatrin dose 

(b) cumulative vigabatrin dose 

(c) duration of vigabatrin treatment 

(d) frequency of daily doses 

8. Which of the following statements is true? 

(a) Most studies have demonstrated a tendency for VAVFC 

to improve after vigabatrin withdrawal 

(b) Most studies have demonstrated a tendency for VAVFC 

to progress despite vigabatrin withdrawal 

(c) If vigabatrin treatment is continued in a patient with 

detectable but asymptomatic VAVFC, the field defect 

usually remains stable 

(d) In some patients continuing vigabatrin therapy, 

VAVFC have been shown to regress 

9. The following electrophysiological abnormalities are 

associated with VAVFC: 

(a) increased latency of flash-evoked visual evoked 

potentials 

(b) increased EOG Arden index 

(c) increased oscillatory potentials 

(d) decreased 30Hz flicker response 

10. In human pathological material, vigabatrin treatment 

has been associated with the following: 

(a) intramyelinic oedema in cerebral white matter 

(b) loss of ganglion cells from the peripheral retina 

(c) loss of macular cone photoreceptors 

(d) increased vascularity of the choroidal circulation 

11. According to all combined studies, what cumulative 

dose of vigbatrin led to a >70% frequency of visual field 

constriction? 

(a)

M Lawden 

13. Which of the following was revealed to be abnormal by 

electrodiagnostic testing in patients with VAVFC? 

(a) b-wave amplitude 

(b) a-wave latency 

(c) electro-oculogram 

(d) visual evoked potentials 

14. The overall risk of VAVFC in paediatric patients 

compared with adult patients is: 

(a) exactly the same 

(b) slightly higher 

(c) slightly lower 

(d) impossible to say as visual field measurement is more 

difficult in children 

15. Which method of field analysis is regarded as the 

international standard for identifying and monitoring 

VAVFC? 

(a) Humphrey static perimetry extending to 60º 

eccentricity 

(b) Goldmann kinetic perimetry 

(c) Humphrey static perimetry extending to 30º 

eccentricity 

(d) Rarebit perimetry 

16

Optometry in Practice Vol 7 (2006) 17–22 

Posterior Staphyloma: Can it be Retinal 

Detachment or Tumour? 

Nonavinakere P Manjunatha 1 MD MRCOphth (Lon), Shrivatsa P Desai 1 MS FRCS, 

Aravind Reddy 2 MS FRCS and Siddharth Goel 1 MRCOphth (Lon) FRCS (Edn) FRCS (Gls) 

1 Doncaster and Bassetlaw NHS Foundation Trust, UK 2 Bradford Teaching Hospitals NHS Foundation Trust, UK 

Accepted for publication 23 January 2006 

Posterior staphyloma is often a feature of pathological 

myopia. The complex optics in high refractive error and 

the difficulties in viewing the fundus in myopic eyes can 

lead to a mistaken diagnosis of retinal detachment or 

tumour on routine examination. This can cause anxiety to 

patients. We report two such cases. Curtin (1977) 

suggested a classification for posterior staphyloma and we 

have used it in the description of our cases. 

Case 1 

A 45-year-old female was referred urgently by her 

optometrist with suspicion of bilateral retinal detachments 

to the emergency eye clinic at Doncaster Royal Infirmary. 

She had been for a routine check-up and was 

asymptomatic. There was a history of high myopia and in 

the past she had had right-eye squint surgery. The vision 

had been poor in both eyes since childhood. 

Her best corrected visual acuity was 6/24 in the right eye 

and 6/36 in the left eye. The refraction was 

–31.00DS/–1.50DC axis 10 in the right eye and 

–31.00DS/–2.00DC axis 180 in the left eye. Anterior 

segments of both eyes were unremarkable except for deep 

anterior chambers. Examination showed myopic 

degeneration in both eyes. Posterior staphyloma Curtin 

type VIII was seen in both eyes (Curtin 1977; Figure 1). 

There was an area of ectasia centred around the disc 

extending 4 disc diameters nasal to the optic nerve and 

temporally to within 1 disc diameter of the macula with 

single step along the nasal wall of the staphyloma. Neither 

retinal detachment nor retinal tears could be seen in either 

eye. The axial lengths were: right eye 35.79mm, left eye 

35.55mm. Ultrasound B-scan confirmed the staphyloma 

and retinal detachment was ruled out (Figure 2). The 

patient was reassured and discharged back to the optician. 

© 2006 The College of Optometrists 

17 

Case 2 

A 72-year-old woman was referred urgently to the 

emergency eye clinic at Bradford Royal Infirmary by the 

optometrist who had noticed an elevated area in the right 

fundus and suspected choroidal melanoma. Once again it 

was a ‘routine’ eye check-up and the patient was 

asymptomatic. There was a history of bilateral myopia and 

the right eye was amblyopic. 

On examination the patient’s best corrected visual acuity 

was 6/60 in the right eye and 6/6 in the left eye. The 

refraction was –7.00DS/–2.00DC axis 135 in the right eye 

and –1.75DS in the left eye. Anterior segments of both eyes 

were unremarkable. Examination showed myopic fundal 

degeneration in both eyes but posterior staphyloma only in 

the right eye. It was of Curtin type V with an area of ectasia 

around the disc, extending 1 disc diameter above the disc 

to about 5 disc diameters inferiorly (Curtin 1977). No 

staphyloma was found in the other eye. Ultrasound B-scan 

of the right eye showed only staphyloma but no tumour 

(Figure 3). The axial lengths of the right and left eye were 

29.3mm and 22.48mm respectively. The patient was 

reassured and discharged. 

Discussion 

The word ‘myopia’ is derived from the ancient Greek 

myops, half-closing the eyes, a reference to the stenopaeic 

effect achieved by so doing. It is a refractive condition that 

results when the image of a distant object is focused in 

front of the retina by the relaxed eye. Myopia can be 

classified into simple myopia and pathological myopia. 

Simple myopia is the most common eye disorder 

worldwide. Pathological myopia, also called progressive 

myopia, involves structural alterations to the globe, which 

may threaten sight and ocular health. 

Pathological myopia is due to the development of 

structural defects in the posterior segment of the eye. It 

comprises 2% of all myopias. It is thought to result from a 

Address for correspondence: Mr NP Manjunatha, Ophthalmology Department, Doncaster Royal Infirmary, Armthorpe Road, Doncaster, South 

Yorkshire, DN2 5LT, UK.

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