Cataract morphology, classification, assessment and referral  
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Correspondence:
Dr. Konrad Pesudovs
Department of Optometry
University of Bradford
Bradford
West Yorkshire
BD7 1DP, UK
E-mail: K.Pesudovs@bradford.ac.uk

Konrad Pesudovs
BScOptom, PhD, MCOptom,
FVCO, FAAO
Bradford University and Flinders University
(Australia)


David B Elliott
PhD, MCOptom
FAAO
Bradford University
 

Abstract

Cataract is the most common condition requiring assessment and referral from optometric practice. This article examines the features of the main morphological types of age-related cataract: nuclear cortical and posterior subcapsular. The steps to take in the assessment and management of cataract patients are discussed including: examination for cataract, visual assessment methods to confirm whether vision loss is present, discussion with the patient to establish if visual disability is present, and establishing criteria for referral.

Keywords

Cataract, disability, morphology, referral vision.

Introduction

Cataract is a frequent condition found in patients attending an optometric practice and, given the demographic changes within the population, their numbers will increase in the coming years. This article discusses the optometric assessment and management of age-related cataract. The scope includes the categorisation of cataract morphology, the assessment of vision, the assessment of visual disability, and how to determine when to refer a patient for surgery.

Cataract morphology

Cataract increases substantially with age. Cataract causing a visual acuity (VA) of worse than 6/9 has a prevalence of approximately 5% in the 55-64 age group and over 40% in the over 75s1. There are three main types of age-related cataract: cortical, nuclear and posterior subcapsular. In the UK, cortical cataract is the most prevalent (63%), followed by nuclear (41%) and posterior subcapsular cataract (24%)2. Around 30% of eyes have mixed cataract, i.e. more than one morphological type.

Cortical cataracts

Cortical cataracts are cuneiform or wedge shaped opacities found in the anterior and/or posterior lens cortex (Figure 1A). The base of the wedge or spoke is in the periphery of the lens, so that the cataract is often hidden behind the iris. Cortical cataracts are most often found in the inferionasal part of the lens, which may implicate ultra-violet radiation involvement in their aetiology3. Cortical opacities are often associated with water clefts, which are optically clear wedges that can be seen with slit-lamp biomicroscopy. This association gives a clue as to the pathology of cortical cataract, which is fundamentally due to water imbibition into the lens leading to disruption of the regular order of lens fibres4. The disrupted, displaced and swollen lens fibres dissolve and precipitation of components leads to an opaque suspension within the lens. These structural changes create light scattering centres with a considerable variation in refractive index. Opacification is due to the scattering of light when it meets irregular interfaces between regions of differing refractive index. The visibility of cortical cataracts at the slit-lamp results from gross backscatter (i.e. towards the observing clinician), however, forward scatter (i.e. towards the retina) also occurs and this is responsible for the degradation of vision. It is important to note that backscatter and forward scatter are not necessarily highly correlated5, thus a cortical spoke which is highly visible at the slit-lamp may not necessarily be causing a decrease in the patient’s vision. In addition, vision is only affected if the cortical spokes enter the pupillary area. Cortical cataracts can cause astigmatic changes and monocular diplopia (Table 1).

Cortical cataract  
Prevalence (UK) ~63% of all cataracts
(including mixed cataract)
Description
Risk factors
 Wedge-shaped opacity in the lens cortex with the base in the lens periphery, see Figure 1a.
Age, ultra-violet light, female gender
Refractive changes
Idiosyncratic symptoms/signs		 Possible astigmatic changes.
Monocular diplopia, sometimes asymptomatic despite obvious cataract on slit-lamp examination.
Tints for disability glare (vision loss with glare) No, patients with these cataracts see worse with a larger pupil
Table 1. Cortical cataract clinical pearls

 

Nuclear cataracts

Nuclear cataract presents as a homogeneous increase in light scatter and absorption in the lens nucleus (Figure 1B), and can be associated with increased yellowing or brunescence of the lens. Vision loss is due to both light scatter and absorption. The pathology of the opacity is fundamentally an increase in molecular size through a cross-linking of proteins within and between cells in the lens nucleus6.

This change results in an increase in optical density (and a decrease in transparency) by large molecules that absorb light and cause some light scatter. The increased yellowing and brunescence of some nuclear cataracts is indicative of wavelength-dependent light absorption by lens proteins. Nuclear cataracts can produce a marked myopic shift2, which is known as index myopia. Indeed a -0.50DS shift over two years in an elderly patient is highly indicative of developing nuclear cataract2. The average shift over 4 years is -1.50DS, giving a rate between -0.25 and -0.50DS per year. Obviously some shifts can be much larger than this. Large myopic shifts can become the basis for referral (Table 2).

Prevalence (UK) ~41% of all cataracts (including mixed cataract)
Description Homogeneous increase in light scatter in lens nucleus. Blue wavelength absorption also leads to increased yellowing, see Figure 1b.
Risk factors Age, smoking, low levels of anti-oxidant vitamins.
Refractive changes Myopic shift
Idiosyncratic symptoms/signs Colour vision changes (blue-yellow confusion)
Tints for blue disability glare
(vision loss with glare)		 These patients already have a built-in blue disability absorbing tint
Table 2. Nuclear cataract clinical pearls

 

Posterior subcapsular cataract

Posterior subcapsular (PSC) cataract presents centrally, at the back of the lens just in front of the posterior capsule (Figure 1C). These opacities are epithelial cells that migrate aberrantly to the posterior pole of the lens7. The migratory cells which cluster around the posterior pole interdigitate with adjacent lens fibres leading to breakdown and liquefaction of the posterior cortex with formation of globules8. The posteriorly migrating epithelium coalesce into larger "bladder cells"9. These cells and globules form large, well spaced, discrete light scattering centres. The size and spacing of the particles causes a great deal of forward scatter with comparatively little backscatter, making the opacities difficult to view at the slit-lamp yet very visually debilitating. PSC cataracts also cause a dramatic reduction in vision because they are generally centrally positioned within the pupillary area. These opacities can also present earlier than the other morphological types, at about age 55 years. PSC cataracts can be associated with other ocular and systemic diseases, such as retinitis pigmentosa and diabetes8 and are found as a side effect of systemic drugs such as oral corticosteroids10. These are the most visually disabling cataracts, and may be missed with a direct ophthalmoscope because they can be hidden behind the Purkinje images (Table 3).

Prevalence (UK) ~24% of all cataracts (including mixed cataract)
Description Circular opacities in the centre of the pupil just in front of the posterior capsule, see figure 1c.
Risk factors Age, smoking, diabetes, steroid use, trauma
Refractive changes None reported
Idiosyncratic symptoms/signs Can be very visually debilitating, especially under glare, near VA worse than distance VA, can be difficult to spot with direct ophthalmoscopy, occur in younger age groups.
Tints for disability glare (vision loss with glare) Yes, patients with small, central PSC see disability better with a larger pupil.
Table 3. Posterior subcapsular cataract clinical pearls

Clinical cataract classification schema

These systems basically involve classifying the cataract morphology and grading features of the cataract seen at the slit-lamp by comparing them with standard diagrams and/or photographs. Valid systems for the classification of cataract are useful for epidemiological studies, anti-cataract drug trials, clinical trials where generation of cataract may be a risk, or in clinical studies where cataract severity is compared to other measures. Most importantly, cataract classification can be used in the clinical setting to provide a quantitative record of cataract severity.

Numerous schemes exist for the classification of cataract11-25. Almost all are for age-related cataract and independently classify the three morphological types: nuclear, cortical and PSC. Most systems are designed for slit-lamp based assessment where grading is by comparison with standard diagrams, with the alternatives of microscopic or photographic grading. The nature and complexity of the scaling varies markedly between systems26,27. Two of the most popular schema are The Oxford Clinical Cataract Classification and Grading System and the Lens Opacities Classification System III (LOCS III).

Sparrow et al developed the Oxford Clinical Cataract Classification and Grading System14. This technique, which has found wide acceptance and has been used in many clinical trials28, is a slit-lamp-based system in which cataract features are classified morphologically. This carefully designed system has the merit of equal interval steps between the grades14.

The LOCS III22 evolved following experiences with 2 earlier versions15,17,22,29. LOCS III grades cataract in four dimensions: nuclear colour (NC) nuclear opalescence (NO) cortical opacity (C) PSC (P) (Figure 2). Nuclear opalescence and colour are rated on a decimal scale from 0 to 7 in steps of 0.1 and cortical and PSC are rated on a decimal scale from 0 to 6. This is a thoroughly validated system which has been used extensively for clinical trials29-32.

Alternatively, cataracts can be classified and approximately graded without these systems. The conventional 0 to 4 grading system can be used, where 0 is a clear lens, + or 1+ represents a mild cataract, ++ or 2+ a moderate cataract, +++ or 3+ a marked cataract and ++++ or 4+ a severe cataract. Alternatively, PSC and cortical cataract can be graded by the percentage of the (dilated or otherwise) pupillary area they occupy or by a brief sketch.

Assessment of vision in the cataract patient

There are many ways in which vision is affected by cataract, including increasing myopia and astigmatism, monocular diplopia, reduced light transmission and changes in colour perception33. However, visual loss in cataract is principally due to increased intraocular light scatter. Light from the object itself is scattered, reducing the contrast of its retinal image. In addition, wide-angle light scatter from peripheral glare sources can produce a veiling luminance on the retina, further reducing the contrast of the retinal image. Not surprisingly, visual decrement is greatest in glare or bright light conditions (notes on prescribing tints and coatings for cataract patients are found in Table 4).

Tints for discomfort glare Tints can be useful to alleviate discomfort.
Tints for disability glare
(vision loss with glare)		 In general tints provide no benefit as the effect of the reduction in glare light is balanced by the reduction of light from the object of regard. In general, broad- brimmed hats are better. Some patients with small, central PSC cataract may benefit from a tint due to its effect on pupil size (see Table 3)
UV-blocking tints These can alleviate some disability glare from fluorescence within the lens and perhaps slow cataract progression, particularly of cortical cataract.
AR lens coatings These may be useful for patients with cataract, especially those who drive at night or use a VDU.
Table 4. Spectacle tints and coatings for use in the cataract patient

 

It is well established that some patients with cataract, who retain good VA, have significant visual problems. In these cases contrast sensitivity and glare testing can be used to evaluate the level of disability.

Contrast Sensitivity

Contrast sensitivity at low to intermediate spatial frequencies can be reduced in patients with cataract when VA is good34,35. In these cases cataract surgery can return contrast sensitivity to age-matched normal values35. Additionally, in cataract patients, contrast sensitivity can be a better indicator of various aspects of real world vision than VA, such as driving, orientation, mobility and face expression recognition35-37. The best available test for use in cataract patients is the Pelli-Robson chart (Figure 3). At the recommended working distance of 1m, the letters are equivalent to 6/273 Snellen, and the chart gives an indication of contrast sensitivity at a spatial frequency of approximately 0.5 to 2 c/deg (just below the peak of the contrast sensitivity curve). In many cataract patients, Pelli-Robson contrast sensitivity will be normal (1.50 log contrast sensitivity or above). Any patient with a log contrast sensitivity of 1.35 or below, is likely to be complaining of poor vision, no matter how good the VA is. Poor contrast sensitivity is more likely with nuclear and PSC cataracts38-42.

Glare testing

Increased forward light scatter causes cataract patients to see poorly in bright light or glare conditions. Consider the effect of a dirty windscreen on your vision when driving. Vision is satisfactory until sunlight or light coming from car headlights hits the screen, when vision can be reduced dramatically. Similarly, with some cataract patients, VA can be adequate in the relatively low illumination conditions of the examination room, but considerably reduced when outdoors or when driving at night (Panel 1).

A healthy 45-year-old prison guard complained of a gradual decrease in vision over the previous year. This decrease only occurred in bright sunlight, such as when guarding prisoners working outside. Before his visit, his loss of vision had been so great as to allow two convicts to escape! His VA was measured to be 6/6 in both eyes in the examination room. However, VA measured in bright light levels was 6/120! Slit-lamp examination with a dilated pupil revealed small PSC cataracts.
Panel 1. Typical PSC and glare case report52.

 

The case history in (see Panel 1) highlights that a patient attending for an examination in the UK in the winter with no symptoms and a VA of 6/9 or better, could have profoundly reduced vision in a sunny environment Any suggestion of small PSC cataracts should immediately indicate glare testing and pupillary dilation with a careful slit-lamp examination.

Glare tests measure the reduction in a patient's vision due to a glare source (glare loss), and indicate the effect on vision of increased light scatter and a smaller pupil. Glare test scores have been shown to correlate with VA measured outdoors and to correlate better with glare symptoms than conventionally measured VA in patients with cataract43,44. Simple methods of measuring disability glare involve measuring VA under glare conditions, such as while directing a bright penlight or ophthalmoscope light into the patient's eye45. Due to the inverse square law and light scatter varying as a function of the square of the glare angle (the angle of the glare source to the visual axis), it is very important to standardise the angle and distance of the penlight to the eye. Typical standards are 10cm and 30 degrees. A more standardised version of such tests is the Brightness Acuity Tester (BAT, Figure 4).

Disability glare scores are usually taken as the level of VA under the glare condition. Alternatively, the impact of glare can be recorded as glare loss i.e. the number of lines on the chart lost when the glare source is introduced. Testing can be done using conventional VA, low contrast VA or contrast sensitivity charts.

Assessment of disability in the cataract patient

The decision of when to refer a patient for cataract surgery should be primarily dependent on whether the patient’s reduced vision interferes with their desired lifestyle. Referral should NOT be based on VA measurements alone. For example, if a patient is a taxi driver and cataract is reducing his vision so that he cannot see well enough to drive at night or on sunny days, he should be referred for surgery. Conversely, if a patient is perfectly happy with their vision and has no restrictions on their lifestyle, despite having 6/18 or even 6/24 VA, there is no need to refer for surgery, although you may discuss the possibility of future referral with them46. Therefore, it is important to determine whether the patient’s desired lifestyle is affected by their reduced vision. When cataract is identified, it is useful to ask some specific questions which relate to cataract-induced visual loss. For example, "Do you have any problem with glare or in bright sunlight?" and if pertinent "Do you have any problems driving at night?, or on sunny days?". In addition, ask about the effect of vision on the patient's job, sports or hobbies. There are formal instruments (questionnaires) for the measurement of visual disability caused by cataract such as the VF-14 and the VDA47,48. While these questionnaires may not be appropriate for routine use in optometric practice, they do contain questions which the optometrist may find helpful to ask.

Deciding on the need for surgery: the nexus between vision, disability and cataract grading

The referral of patients with cataract for surgery must be based on whether the patient’s reduced vision is interfering with their desired lifestyle. Referral is then justified using clinical vision tests such as distance and near visual acuity, contrast sensitivity, disability glare and for monocular pseudophakes, anisometropia and stereopsis. The presence of co-morbid eye disease (including amblyopia) needs careful assessment to determine whether or not the cataract is the major cause of the visual loss. An apportionment of the visual loss and the visual disability to each condition using potential vision tests49-51 and clinical acumen should be made. This last quality is the most difficult to teach, but in simple terms it involves an assessment of whether the level of vision, severity of cataract and degree of symptoms seem in balance. Finally, a discussion of the risk and benefits of cataract surgery as well as the costs and inconvenience is important, and this should follow the line of an informed consent discussion, similar to that which the patient will encounter when they meet the cataract surgeon. (Figure 5).

Acknowledgments

Konrad Pesudovs is supported by an Australian National Health and Medical Research Council (NHMRC) Sir Neil Hamilton Fairley Research Fellowship.
 
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1. Klein BE, Klein R, Linton KL. Prevalence of age-related lens opacities in a population. The Beaver Dam Eye Study. Ophthalmology 1992;99:546-52.

2. Brown NAP, Hill AR. Cataract, the relation between myopia and cataract morphology. Br J Ophthalmol 1987;71:405-414.

3. Coroneo MT. Albedo concentration in the anterior eye: a phenomenon that locates some solar diseases. Ophthalmic Surg 1990;21:60-6.

4. Brown NP, Harris ML, Shun-Shin GA, Vrensen GF, Willekens B, Bron AJ. Is cortical spoke cataract due to lens fibre breaks? The relationship between fibre folds, fibre breaks, water clefts and spoke cataract. Eye 1993;7:672-9.

5. Elliott DB, Hurst MA, Weatherill J. Comparing clinical tests of visual function in cataract patients using a quantification of forward light scatter. Eye 1991;5:601-606.

6. Harding JJ, Crabbe MJC. The Lens: development, proteins, metabolism and cataract. In: Davson H, Ed. The Eye. New York: Academic Press, 1984: vol. 2.

7. Eshagian J, Streeten B. Human posterior subcapsular cataract, an ultrastructural study of posteriorly migrating cells. Arch Ophthalmol 1980;98:134-43.

8. Eshagian J. Human posterior subcapsular cataract. TOSUK 1982;102:364-8.

9. Zagorski Z. Histopathological studies of the human lens. Lens Eye Toxic Res 1991;8:311-8.

10. Edgar DF, Gilmartin B. Ocular adverse reactions to systemic medication. Ophthal Physiol Opt 1997;17 Suppl 2:S2-8.

11. Chylack LTJ. Classification of human cataracts. Arch Ophthalmol 1978;96:888-92.

12. Chylack LTJ, Lee MR, Tung WH, Cheng HM. Classification of human senile cataractous changes by the American Co-operative Cataract Research Group (CCRG) method. I. Instrumentation and technique. Invest Ophthalmol Vis Sci 1983;24:424-31.

13. Chylack LTJ, Ransil BJ, White O. Classification of human senile cataractous change by the American Co-operative Cataract Research Group (CCRG) method: III. The association of nuclear color (sclerosis) with extent of cataract formation, age, and visual acuity. Invest Ophthalmol Vis Sci 1984;25:174-80.

14. Sparrow J, Bron A, Brown N, Ayliffe W, Hill A. The Oxford clinical cataract classification system.Int Ophthalmol 1986;9:207-25.

15. Chylack LTJ, Leske MC, Sperduto R, Khu P, McCarthy D. Lens Opacities Classification System. Arch Ophthalmol 1988;106:330-4.

16. West SK, Rosenthal F, Newland HS, Taylor HR. Use of photographic techniques to grade nuclear cataracts. Invest Ophthalmol Vis Sci 1988;29:73-7.

17. Chylack LT, Jr, Leske MC, McCarthy D, Khu P, Kashiwagi T, Sperduto R. Lens opacities classification system II (LOCS II). Arch Ophthalmol 1989;107:991-997.

18. Laser H, Hannen K, Wienert J, Hockwin O. A new method for an objective classification of lens opacities. Investigations about cataract morphology and cataract progression. Dev Ophthalmol 1989;17:145-51.

19. Sharma YR, Vajpayee RB, Bhatnagar R, Mohan M, Azad RV, Kumar M, Nath R. A simple accurate method of cataract classification. Cataract-I. Ind J Ophthalmol 1989;37:112-7.

20. Klein BE, Klein R, Linton KL, Magli YL, Neider MW. Assessment of cataracts from photographs in the Beaver Dam Eye Study. Ophthalmology 1990;97:1428-33.

21. Sasaki K, Shibata T, Obazawa H, Fujiwara T, Kogure F, Obara Y, Itoi M, et al. Classification system for cataracts. Application by the Japanese Co-operative Cataract Epidemiology Study Group. Ophthalmic Res 1990;22 Suppl 1:46-50.

22. Chylack LT, Jr, Wolfe JK, Singer DM, Leske C, Bullimore MA, Bailey IL, Friend J, et al. The lens opacities classification system III. Arch Ophthalmol 1993;111:831-6.

23. Duncan DD, Shukla OB, West SK, Schein OD. New objective classification system for nuclear opacification. J Opt Soc Am A 1997;14:1197-204.

24. Sasaki K, Sakamoto Y, Fujisawa K, Kojima M, Shibata T. A new grading system for nuclear cataracts--an alternative to the Japanese Co-operative Cataract Epidemiology Study Group's grading system. Dev Ophthalmol 1997;27:42-9.

25. Braccio L, Camparini M, Graziosi P, Baratta G, Ferrigno L, Williams SL, Rosmini F, et al. An independent evaluation of the Age-Related Eye Disease Study (AREDS) cataract grading system. Curr Eye Res 1998;17:53-9.

26. Taylor HR, West SK. The clinical grading of lens opacities. Aust NZ J Ophthalmol 1989;17:81-86.

27. Hall AB, Thompson JR, Deane JS, Rosenthal AR. LOCS III versus the Oxford Clinical Cataract Classification and Grading System for the assessment of nuclear, cortical and posterior subcapsular cataract. Ophthalmic Epidemiol 1997;4:179-94.

28. Deane JS, Hall AB, Thompson JR, Rosenthal AR. Prevalence of lenticular abnormalities in a population-based study: Oxford Clinical Cataract Grading in the Melton Eye Study Ophthalmic Epidemiol 1997;4:195-206.

29. Chylack LTJ, Wolfe JK, Friend J, Khu PM, Singer DM, McCarthy D, Carmen del J, Rosner B. Quantitating cataract and nuclear brunescence, the Harvard and LOCS systems. Optom Vis Sci 1993;70:886-895.

30. Karbassi M, Khu PM, Singer DM, Chylack LTJ. Evaluation of lens opacities classification system III applied at the slitlamp. Optom Vis Sci 1993;70:923-928.

31. Khu PM, Karbassi M, Singer DM, Chylack LTJ. Effect of cataract type and severity on lens grading. Ophthalmic Res 1994;26:61-67.

32. Durant JS, Sparrow JM, Frost NA. The effect of analysing different regions of interest on nuclear densitometry with the case 2000 CCD camera. Invest Ophthalmol Vis Sci 1997;38:S346.

33. Brown NA, Bron AJ, Ayliffe W, Sparrow J, Hill AR. The objective assessment of cataract. Eye 1987;1 ( Pt 2):234-46.

34. Hess RF, Woo G. Vision through cataracts. Invest Ophthalmol Vis Sci 1978;17:428-35.

35. Elliott DB. Evaluating visual function in cataract. Optom Vis Sci 1993;70:896-902.

36. Rubin GS, Bandeen Roche K, Prasada-Rao P, Fried LP. Visual impairment and disability in older adults. Optom Vis Sci 1994;71:750-60.

37. Pesudovs K, Coster DJ. The relationship between subjective visual disability and objective measures of visual function. Optom Vis Sci 1995;72(12s):118.

38. Skalka HW. Arden grating test in evaluating "early" posterior subcapsular cataracts. Southern Med J 1981;74:1368-70.

39. Lempert P, Hopcroft M, Lempert Y. Evaluation of posterior subcapsular cataracts with spatial contrast acuity. Ophthalmology 1987;94:14-18.

40. Drews-Bankiewicz MA, Caruso RC, Datiles MB, Kaiser-Kupfer MI. Contrast sensitivity in patients with nuclear cataracts. Arch Ophthalmol 1992;110:953-959.

41. Pesudovs K, Coster DJ. Visual performance and cataract morphology: the nexus between subjective disability and objective measures of visual function. Asia Pac J Ophthalmol 1994;6:12-18.

42. Elliott DB, Situ P. Visual acuity versus letter contrast sensitivity in early cataract. Vis Res 1998;38:2047-52.

43. Neumann AC, McCarty GR, Steedle TO, Sanders DR, Raanan MG. The relationship between cataract type and glare disability as measured by the Miller-Nadler glare tester. J Cat Refract Surg 1988;14:40-5.

44. Koch DD. Glare and contrast sensitivity testing in cataract patients. J Cataract Refract Surg 1989;15:158-64.

45. Williamson TH, Strong NP, Sparrow J, Aggarwal RK, Harrad R. Contrast sensitivity and glare in cataract using the Pelli-Robson chart. Br J Ophthalmol 1992;76:719-2.

46. Latham K, Misson G. Patterns of cataract referral in the West Midlands. Ophthal Physiol Opt 1997;17:300-6.

47. Steinberg EP, Tielsch JM, Schein OD, Javitt JC, Sharkey P, Cassard SD, Legro MW, et al. The VF-14: An index of functional impairment in patients with cataract. Arch Ophthalmol 1994;112:630-8.

48. Pesudovs K, Coster DJ. Validation of a new tool for the assessment of subjective visual disability. Br J Ophthalmol 1998; 82:617-624

49. Hurst MA, Douthwaite WA. Assessing vision behind cataract - A review of methods. Optom Vis Sci 1993;70:903-13.

50. Barrett BT, Davison PA, Eustace P. Clinical comparison of three techniques for evaluating visual function behind cataract. Eye 1995;9:722-727.

51. McGraw PV, Barrett BT, Whitaker D. Assessment of vision behind cataracts. Ophthal Physiol Opt 1996;16:S26-32.

52. Rubin ML. The little point that isn't there. Surv Ophthalmol 1972;17:52-3..