Documenta Ophthalomologica 78: 177-181, 1991. 9 1991 Kluwer Academic Publishers. Printed in the Netherlands.
On the relation between glare and straylight T.J.T.P. VAN DEN BERG The Netherlands Ophthalmic Research Institute and Laboratory of Medical Physics and Informatics, University of Amsterdam, The Netherlands Accepted 15 August 1991
Key words: Glare, straylight, contrast sensitivity, light scatter, disability glare, discomfort glare Abstract. An overview is given of the basic phenomena that may lead to glare complaints in
patients. Prominent among them is increased intraocular straylight; this can be measured. Other causes may include: increased sensitivity to normal straylight, the length of (increased) light and dark adaptation times, (small angle) neuronal lateral interaction. Distinction must be made between disability glare and discomfort glare. Tests have been proposed to determine glare-induced loss of various visual functions. Often the test results are thought to be directly related to straylight but this may be untrue.
Introduction When reading glare literature one realizes that the very concept of glare is not well defined [1], at least not in a generally accepted way. Of course, the classical literature has concluded that so-called disability glare in normal subjects is the effect of retinal contrast loss due to intraocular straylight [2]. This can safely be assumed to be the cause of glare complaints from oncoming head lights during night driving. But if a patient comes with a glare complaint, is it safe to assume that he suffers from increased intraocular straylight? One may wonder. Let us consider some possibilities. Patients may use the word glare for situations where scattering is not at all the relevant issue. For instance, after leaving a dark cinema (or a tunnel) in the middle of a bright day. Then many people cannot see too well for some period of time. But this is probably related to the sluggishness of the light adaptation, which is located in the retinal cells, and in the limitations of the pupillary reflex. In this case one is blinded by the sudden bright light and it therefore seems natural to use the word glare. In pathological conditions of the retina (or pupillary reflex), this form of blinding may be increased and the corresponding complaint might be misinterpreted as being due to the optic media. A complication is that sometimes both retinal and preretinal factors may
178 be involved, for instance in age-related conditions, in diabetes or in retinitis pigmentosa. Interviewing patients about the typical situations in which glare is experienced may help to decide whether the glare complaints are neuronal or optical in origin. On the other hand, interviewing a patient about glare may not be straightforward. It is not the same as visual acuity. A patient can easily tell you whether he can read the newspaper. Patients may report on glare in a much more confusing way. Glare is a more complicated phenomenon. First, glare is as a rule dynamic. In the situation of (night) driving, for example, glare is dynamic because of the movement of the cars. On the other hand, glare is also dynamic because of the evasive reaction of the patient himself. This subjective response may differ significantly between patients. Some patients may subjectively be much more disturbed by glare than others, resulting in rather different evasive reactions. Because this subjective disturbance is so clearly a separate entity in glare, early researchers gave it a separate name, 'discomfort glare'. It is a serious complaint deserving attention, since the evasive reaction resulting from it may in itself result in decreased visual ability. This adds to the disabilitating effect already present which is called 'disability glare'. We should realize that in glare research the outcome of tests may be influenced by both phenomena. Inter- and intra-individually, disabilitating effects of discomfort may be rather variable. I have noticed that spending time talking with patients about glare phenomena makes them better able to cope with glare, possibly by reducing the feeling of discomfort, which may again reduce the disabilitating effects. In present test designs, discomfort effects are never considered, as far as I know. It is generally assumed that the tests are concerned with disability glare only. Whether this is true or not depends on the design of the test and the instructions given to the patient. Another complicating factor in glare research is that glare disturbance is already present in normal non-pathological conditions. Everybody is disabilitated by glare. Often this is not realized because the effects are experienced from early childhood and are accepted as normal visual experience. It is sometimes difficult to convince normal subjects that their eyes are not normal and that, for instance, the haloes perceived around light sources at night are indications of abnormalities in their own eyes and should not be there. But sometimes patients with a pathological condition of the retina become aware of their normal straylight. The corresponding complaint can easily be misinterpreted as due to early defects in the preretinal media, whereas it may in fact be the result of aggravation, due to the pathological retinal condition of normal glare effects. My impression is that this happens in retinitis pigmentosa patients in the earlier stages [3]. Thus, apart from (increased) straylight, a variety of phenomena may be involved in the complaint of glare. As far as I know, no systematic study has
179 been carried out on the whole spectrum of glare complaints. We shall restrict ourselves to glare caused by bright sources at a distance. Since the 1960s it has been clear that the glare experienced by normal subjects in such a case is caused by the imperfect optical condition of the normal eye. Following Cobb's line of thought [4], the effect of a glaring light source was quantified by means of the so-called 'equivalent luminance' [5, 6]. This is the luminance of a background with equally strong blinding effects as the glare source. An important argument in favor of the straylight hypothesis was that this assumption correctly predicted equivalent luminance to be linearly related to the intensity and size of the glare source. Equivalent luminance has been shown over many decades to be strictly proportional to glare source intensity [7]. Correspondingly, increase in the number of glare sources was also shown to have a linear effect [8]. This linearity test should be used to evaluate glare testing procedures. Such a test has been performed [9] in an evaluation of the procedure of Paulsson and Sj6strand [10]. Although this procedure was very well designed, the outcome was negative. Another indication of the optical origin of the effect of a distant glare source can be derived from patient research. If the glare source is projected on blind retinal areas, it is unlikely that effects are caused by neuronal interaction. We studied retinitis pigmentosa patients [3]. Projection of the glare source on blind areas of their visual field did not disturb the measurement of the foveal effect in terms of equivalent luminance. When there were no media opacities the values found were comparable to those for the normal population. In the case of a patient with some cataract, typical for the later stages of retinitis pigmentosa, elevated values were found. This is of special relevance to the present discussion. Retinitis pigmentosa patients with poor visual fields cannot perceive the glare source, but they are well aware of its presence because of its foveal effects. It further reduces their already reduced foveal function. But the validity of the straylight hypothesis has its limits. The classical studies were performed at large angles (and with specific test and background configurations). It is possible that, at small angles (and with other test and background configurations) neuronal effects may play a role. It would be pertinent to know, for each condition, what angle would be the borderline between neuronally and optically dominated effects. In the case of the classical studies it seems safe to assume that, for the normal eye at 1 degree, the optical effect dominates [2], but under the conditions of the present glare testers we just do not know. In one tester [11], using a glare source at a distance of 13 degrees, neuronal influence proved to be present [12, 13]: for patients with a slight elevation of light scattering, sensitivity declined less than expected, or even improved, upon presentation of the glare source. (This finding does not imply that neuronal influence spreads over 13 degrees. Neuronal influence may be exerted by the direct surround-
180 ings of the test area in this tester. Realize that the surroundings are also illuminated with scattered light). How do we precisely imagine straylight to cause glare? Straylight throws a veil of light over the retina. This veil of light lowers retinal contrast, thus reducing effective contrast sensitivity. The veil reduces all contrasts to the same extent, so that the contrast sensitivity function shifts as a whole [14]. Some contrasts become invisible: this is glare. The high spatial frequency end of the contrast sensitivity curve corresponds to visual acuity. Because at this end the contrast sensitivity function is very steep, the highest spatial frequency visible does not change much and neither does visual acuity. So it would be unwise to use the visual acuity as criterion in a glare test. Yet several glare testers do so. The effects of scattered light may be enhanced under conditions of low light adaptation. The scattered light can cause a dark-adapted retina to light-adapt. Subsequently the subject can still be blinded when the glare source has long been removed. With pathologically increased dark adaptation times the effect can be stronger. There are also glare testers which are intended to assess this effect. The effect of a straylight source on contrast sensitivity must be differentiated from the direct effect of the optics of the eye on contrast sensitivity. Contrast sensitivity has been shown to be decreased, especially for higher spatial frequencies, in cataract patients [15, 16]. The retinal contrast of a grating image itself also reflects light scattering. But only small angle scattering is reflected properly. Larger angle scatter, as is relevant in most glare situations, cannot be judged properly from contrast sensitivity alone. For this, a peripheral light source must be added. In conclusion, how can we assess glare? At present, there is no definite answer to this question. As discussed above, the term 'glare' applies to many different conditions. Glare complaints derive from a variety of (pathological) phenomena and glare depends on the visual environment. Must several test(er)s be designed, one for each type of glare? For the important class of straylight-induced glare, matters could be simpler. As indicated above, however, present tests for the straylight type of glare fail on validation research. Also, in clinical use, the reliability of glare testing seems to be questionable [17-20]. A problem is the absence of a generally accepted reference, a golden standard for glare. If the chosen reference is the one applied in one test, naturally that test performs well, whereas dissimilar tests perform less well [18]. Another approach would be to use the patient's subjective experience as the reference [19]. A more generally applicable approach would be to determine the straylight itself. This would give direct information on optical imperfections as the primary cause of glare. The results would be applicable for all visual environments. The contrast loss, as the direct cause of glare, could be derived. A first attempt was made by Paulsson and Sj6strand [10]. A
181
method free from neuronal interference has been designed by us [14, 21]. Maybe this method, or a similar one, may in the future form a better basis for clinical glare assessment. References 1. Aulhom E. Blendung bei degenerativen Augenerkrankungen. In: Degenerative Erkankungen des Auges (ed. O-E Lund& TN Wanbke), Ferdinand Enke Verlag Stuttgart 1983: 189-96. 2. Wos JJ. Disability glare: A state of the art report. CIE-Journal 1984; 3 (2): 39-53. 3. van den Berg TJTP. Red glasses and visual function in retinitis pigmentosa. Doc Ophthalmol 1990; 73: 255-273. 4. Cobb PW. The influence of illumination of the eye on visual acuity. Am J Physiol 1911; 29: 76-99. 5. Stiles WS. The effect of glare on the brightness difference threshold. Proc Roy Soc 1929; 104B: 322-355. 6. le Grand Y. Recherches sur la diffusion de la lumi6re dans l'oeil humain. Rev Opt 1937; 16: 201-214; 241-266. 7. Vos JJ. On mechanisms of glare. Thesis. Utrecht, 1963. 8. Crawford BH. The integration of the glare effects from a number of glare sources. Proc Roy Soc 1936; 123B: 69. 9. Yager D, Rumei Yuan, Mathews S. What is the utility of the psychophysical 'light scattering factor'? In: Technical Digest on Noninvasive Assessment of the Visual System, Vol 1. Washington DC: O.S.A. 1991: 244-247. 10. Paulsson LE, Sj6strand J. Contrast sensitivity in the presence of glare light. Invest Ophthalmol Vis Sci 1980; 19: 401-406. 11. Ginsburg AP, Osher RP, Blauvelt K, Blosser E. The assessment of contrast and glare sensitivity in patients having cataracts. Suppl Inv Opthalmol Vis Sci 1987; 28: 397. 12. van den Berg TJTP, de Waard PWT, IJspeert JK, de Jong PTVM. Intraocular light scattering assessed quantitatively in age related cataract. Invest Ophthalmol Vis Sci 1989; 30 Suppl.: 499. 13. de Waard PWT, IJspeert JK, van den Berg TJTP, de Jong PTVM. Intraocular light scattering in age-related cataracts. Submitted 1991. 14. van den Berg TJTP. Importance of pathological intraocular scatter for visual disability. Doc Ophthalmol 1986; 61, 327-333. 15. Hess R, Woo G. Vision through cataracts. Invest Ophthalmol Vis Sci 1978; 17: 428-435. 16. Elliott DB, Gilchrist J, Whitaker D. Contrast sensitivity and glare sensitivity changes with three types of cataract morphology: Are these techniques necessary in clinical evaluation of cataract? Ophthal Physiol Opt 1989; 9: 25-30. 17. Prager TC, Urso RG, Lewis JW, Ruiz RS. Methodological considerations in glare testing in patients with cataract. Arch Ophthalmol 1988; 106: 1501. 18. Neumann AC, McCarty GR, Locke J, Cobb B. Glare disability devices for cataractous eyes: A consumer's guide. J Cataract Refract Surg 1988; 14: 212-216. 19. Elliott DB, Hurst MA, Weatherill J. Comparing clinical tests of visual function with the patient's perceived visual disability. Eye 1990; 4: 712-17. 20. Rubin GS et al. Contrast sensitivity and glare testing in the evaluation of anterior segment disease. Ophthalmology 1990; 97, 1233-1237. 21. van den Berg TJTP, IJspeert JK. The straylightmeter. In: Technical Digest on Noninvasive Assessment of the Visual System, Vol 1. Washington DC: O.S.A. 1991: 256-259.
Address for correspondence: T.J.T.P. van den Berg, Laboratory of Medical Physics & Informatics, AMC, Meibergdreef 15, 1105 AZ Amsterdam, The Netherlands. Tel. 020 5664583.
On the relation between glare and straylight T.J.T.P. VAN DEN BERG The Netherlands Ophthalmic Research Institute and Laboratory of Medical Physics and Informatics, University of Amsterdam, The Netherlands Accepted 15 August 1991
Key words: Glare, straylight, contrast sensitivity, light scatter, disability glare, discomfort glare Abstract. An overview is given of the basic phenomena that may lead to glare complaints in
patients. Prominent among them is increased intraocular straylight; this can be measured. Other causes may include: increased sensitivity to normal straylight, the length of (increased) light and dark adaptation times, (small angle) neuronal lateral interaction. Distinction must be made between disability glare and discomfort glare. Tests have been proposed to determine glare-induced loss of various visual functions. Often the test results are thought to be directly related to straylight but this may be untrue.
Introduction When reading glare literature one realizes that the very concept of glare is not well defined [1], at least not in a generally accepted way. Of course, the classical literature has concluded that so-called disability glare in normal subjects is the effect of retinal contrast loss due to intraocular straylight [2]. This can safely be assumed to be the cause of glare complaints from oncoming head lights during night driving. But if a patient comes with a glare complaint, is it safe to assume that he suffers from increased intraocular straylight? One may wonder. Let us consider some possibilities. Patients may use the word glare for situations where scattering is not at all the relevant issue. For instance, after leaving a dark cinema (or a tunnel) in the middle of a bright day. Then many people cannot see too well for some period of time. But this is probably related to the sluggishness of the light adaptation, which is located in the retinal cells, and in the limitations of the pupillary reflex. In this case one is blinded by the sudden bright light and it therefore seems natural to use the word glare. In pathological conditions of the retina (or pupillary reflex), this form of blinding may be increased and the corresponding complaint might be misinterpreted as being due to the optic media. A complication is that sometimes both retinal and preretinal factors may
178 be involved, for instance in age-related conditions, in diabetes or in retinitis pigmentosa. Interviewing patients about the typical situations in which glare is experienced may help to decide whether the glare complaints are neuronal or optical in origin. On the other hand, interviewing a patient about glare may not be straightforward. It is not the same as visual acuity. A patient can easily tell you whether he can read the newspaper. Patients may report on glare in a much more confusing way. Glare is a more complicated phenomenon. First, glare is as a rule dynamic. In the situation of (night) driving, for example, glare is dynamic because of the movement of the cars. On the other hand, glare is also dynamic because of the evasive reaction of the patient himself. This subjective response may differ significantly between patients. Some patients may subjectively be much more disturbed by glare than others, resulting in rather different evasive reactions. Because this subjective disturbance is so clearly a separate entity in glare, early researchers gave it a separate name, 'discomfort glare'. It is a serious complaint deserving attention, since the evasive reaction resulting from it may in itself result in decreased visual ability. This adds to the disabilitating effect already present which is called 'disability glare'. We should realize that in glare research the outcome of tests may be influenced by both phenomena. Inter- and intra-individually, disabilitating effects of discomfort may be rather variable. I have noticed that spending time talking with patients about glare phenomena makes them better able to cope with glare, possibly by reducing the feeling of discomfort, which may again reduce the disabilitating effects. In present test designs, discomfort effects are never considered, as far as I know. It is generally assumed that the tests are concerned with disability glare only. Whether this is true or not depends on the design of the test and the instructions given to the patient. Another complicating factor in glare research is that glare disturbance is already present in normal non-pathological conditions. Everybody is disabilitated by glare. Often this is not realized because the effects are experienced from early childhood and are accepted as normal visual experience. It is sometimes difficult to convince normal subjects that their eyes are not normal and that, for instance, the haloes perceived around light sources at night are indications of abnormalities in their own eyes and should not be there. But sometimes patients with a pathological condition of the retina become aware of their normal straylight. The corresponding complaint can easily be misinterpreted as due to early defects in the preretinal media, whereas it may in fact be the result of aggravation, due to the pathological retinal condition of normal glare effects. My impression is that this happens in retinitis pigmentosa patients in the earlier stages [3]. Thus, apart from (increased) straylight, a variety of phenomena may be involved in the complaint of glare. As far as I know, no systematic study has
179 been carried out on the whole spectrum of glare complaints. We shall restrict ourselves to glare caused by bright sources at a distance. Since the 1960s it has been clear that the glare experienced by normal subjects in such a case is caused by the imperfect optical condition of the normal eye. Following Cobb's line of thought [4], the effect of a glaring light source was quantified by means of the so-called 'equivalent luminance' [5, 6]. This is the luminance of a background with equally strong blinding effects as the glare source. An important argument in favor of the straylight hypothesis was that this assumption correctly predicted equivalent luminance to be linearly related to the intensity and size of the glare source. Equivalent luminance has been shown over many decades to be strictly proportional to glare source intensity [7]. Correspondingly, increase in the number of glare sources was also shown to have a linear effect [8]. This linearity test should be used to evaluate glare testing procedures. Such a test has been performed [9] in an evaluation of the procedure of Paulsson and Sj6strand [10]. Although this procedure was very well designed, the outcome was negative. Another indication of the optical origin of the effect of a distant glare source can be derived from patient research. If the glare source is projected on blind retinal areas, it is unlikely that effects are caused by neuronal interaction. We studied retinitis pigmentosa patients [3]. Projection of the glare source on blind areas of their visual field did not disturb the measurement of the foveal effect in terms of equivalent luminance. When there were no media opacities the values found were comparable to those for the normal population. In the case of a patient with some cataract, typical for the later stages of retinitis pigmentosa, elevated values were found. This is of special relevance to the present discussion. Retinitis pigmentosa patients with poor visual fields cannot perceive the glare source, but they are well aware of its presence because of its foveal effects. It further reduces their already reduced foveal function. But the validity of the straylight hypothesis has its limits. The classical studies were performed at large angles (and with specific test and background configurations). It is possible that, at small angles (and with other test and background configurations) neuronal effects may play a role. It would be pertinent to know, for each condition, what angle would be the borderline between neuronally and optically dominated effects. In the case of the classical studies it seems safe to assume that, for the normal eye at 1 degree, the optical effect dominates [2], but under the conditions of the present glare testers we just do not know. In one tester [11], using a glare source at a distance of 13 degrees, neuronal influence proved to be present [12, 13]: for patients with a slight elevation of light scattering, sensitivity declined less than expected, or even improved, upon presentation of the glare source. (This finding does not imply that neuronal influence spreads over 13 degrees. Neuronal influence may be exerted by the direct surround-
180 ings of the test area in this tester. Realize that the surroundings are also illuminated with scattered light). How do we precisely imagine straylight to cause glare? Straylight throws a veil of light over the retina. This veil of light lowers retinal contrast, thus reducing effective contrast sensitivity. The veil reduces all contrasts to the same extent, so that the contrast sensitivity function shifts as a whole [14]. Some contrasts become invisible: this is glare. The high spatial frequency end of the contrast sensitivity curve corresponds to visual acuity. Because at this end the contrast sensitivity function is very steep, the highest spatial frequency visible does not change much and neither does visual acuity. So it would be unwise to use the visual acuity as criterion in a glare test. Yet several glare testers do so. The effects of scattered light may be enhanced under conditions of low light adaptation. The scattered light can cause a dark-adapted retina to light-adapt. Subsequently the subject can still be blinded when the glare source has long been removed. With pathologically increased dark adaptation times the effect can be stronger. There are also glare testers which are intended to assess this effect. The effect of a straylight source on contrast sensitivity must be differentiated from the direct effect of the optics of the eye on contrast sensitivity. Contrast sensitivity has been shown to be decreased, especially for higher spatial frequencies, in cataract patients [15, 16]. The retinal contrast of a grating image itself also reflects light scattering. But only small angle scattering is reflected properly. Larger angle scatter, as is relevant in most glare situations, cannot be judged properly from contrast sensitivity alone. For this, a peripheral light source must be added. In conclusion, how can we assess glare? At present, there is no definite answer to this question. As discussed above, the term 'glare' applies to many different conditions. Glare complaints derive from a variety of (pathological) phenomena and glare depends on the visual environment. Must several test(er)s be designed, one for each type of glare? For the important class of straylight-induced glare, matters could be simpler. As indicated above, however, present tests for the straylight type of glare fail on validation research. Also, in clinical use, the reliability of glare testing seems to be questionable [17-20]. A problem is the absence of a generally accepted reference, a golden standard for glare. If the chosen reference is the one applied in one test, naturally that test performs well, whereas dissimilar tests perform less well [18]. Another approach would be to use the patient's subjective experience as the reference [19]. A more generally applicable approach would be to determine the straylight itself. This would give direct information on optical imperfections as the primary cause of glare. The results would be applicable for all visual environments. The contrast loss, as the direct cause of glare, could be derived. A first attempt was made by Paulsson and Sj6strand [10]. A
181
method free from neuronal interference has been designed by us [14, 21]. Maybe this method, or a similar one, may in the future form a better basis for clinical glare assessment. References 1. Aulhom E. Blendung bei degenerativen Augenerkrankungen. In: Degenerative Erkankungen des Auges (ed. O-E Lund& TN Wanbke), Ferdinand Enke Verlag Stuttgart 1983: 189-96. 2. Wos JJ. Disability glare: A state of the art report. CIE-Journal 1984; 3 (2): 39-53. 3. van den Berg TJTP. Red glasses and visual function in retinitis pigmentosa. Doc Ophthalmol 1990; 73: 255-273. 4. Cobb PW. The influence of illumination of the eye on visual acuity. Am J Physiol 1911; 29: 76-99. 5. Stiles WS. The effect of glare on the brightness difference threshold. Proc Roy Soc 1929; 104B: 322-355. 6. le Grand Y. Recherches sur la diffusion de la lumi6re dans l'oeil humain. Rev Opt 1937; 16: 201-214; 241-266. 7. Vos JJ. On mechanisms of glare. Thesis. Utrecht, 1963. 8. Crawford BH. The integration of the glare effects from a number of glare sources. Proc Roy Soc 1936; 123B: 69. 9. Yager D, Rumei Yuan, Mathews S. What is the utility of the psychophysical 'light scattering factor'? In: Technical Digest on Noninvasive Assessment of the Visual System, Vol 1. Washington DC: O.S.A. 1991: 244-247. 10. Paulsson LE, Sj6strand J. Contrast sensitivity in the presence of glare light. Invest Ophthalmol Vis Sci 1980; 19: 401-406. 11. Ginsburg AP, Osher RP, Blauvelt K, Blosser E. The assessment of contrast and glare sensitivity in patients having cataracts. Suppl Inv Opthalmol Vis Sci 1987; 28: 397. 12. van den Berg TJTP, de Waard PWT, IJspeert JK, de Jong PTVM. Intraocular light scattering assessed quantitatively in age related cataract. Invest Ophthalmol Vis Sci 1989; 30 Suppl.: 499. 13. de Waard PWT, IJspeert JK, van den Berg TJTP, de Jong PTVM. Intraocular light scattering in age-related cataracts. Submitted 1991. 14. van den Berg TJTP. Importance of pathological intraocular scatter for visual disability. Doc Ophthalmol 1986; 61, 327-333. 15. Hess R, Woo G. Vision through cataracts. Invest Ophthalmol Vis Sci 1978; 17: 428-435. 16. Elliott DB, Gilchrist J, Whitaker D. Contrast sensitivity and glare sensitivity changes with three types of cataract morphology: Are these techniques necessary in clinical evaluation of cataract? Ophthal Physiol Opt 1989; 9: 25-30. 17. Prager TC, Urso RG, Lewis JW, Ruiz RS. Methodological considerations in glare testing in patients with cataract. Arch Ophthalmol 1988; 106: 1501. 18. Neumann AC, McCarty GR, Locke J, Cobb B. Glare disability devices for cataractous eyes: A consumer's guide. J Cataract Refract Surg 1988; 14: 212-216. 19. Elliott DB, Hurst MA, Weatherill J. Comparing clinical tests of visual function with the patient's perceived visual disability. Eye 1990; 4: 712-17. 20. Rubin GS et al. Contrast sensitivity and glare testing in the evaluation of anterior segment disease. Ophthalmology 1990; 97, 1233-1237. 21. van den Berg TJTP, IJspeert JK. The straylightmeter. In: Technical Digest on Noninvasive Assessment of the Visual System, Vol 1. Washington DC: O.S.A. 1991: 256-259.
Address for correspondence: T.J.T.P. van den Berg, Laboratory of Medical Physics & Informatics, AMC, Meibergdreef 15, 1105 AZ Amsterdam, The Netherlands. Tel. 020 5664583.
