The ideal sight for the non-athletic person is about —1.50 dioptres of myopia. The occasional use of spectacles or contact lenses will give excellent distance vision. For studying and other detailed close work no spectacles are required, even into advanced old age. Many young people, however, do not consider it this way, and ask for operations to correct this small degree of myopia. If such operations are carried out, the strong likelihood is that, when the patient reaches middle age, he will regret losing his ability to see near to without spectacles, which he would otherwise have retained.

Spectacles for short sight not only reduce the size of object- images; they also tend to make them brighter, unless the spectacle lens has been manufactured or coated with a tint. Many very short-sighted people prefer, and may even be advised by their practitioner, to use tinted glasses. Furthermore, the abnormal length of the eye, from the cornea to the back of the retina, which is usually the cause of myopia, often means that the jelly between the crystal lens and the retina is not as firmly attached as it should be. If the eye then changes its contour or volume, as it tends to from early middle age onwards, its internal structures (retina and vitreous jelly) are put under great pressure to adapt, which they cannot readily do, to the new shape. The only way they can adapt is by the retina being unduly stretched and the jelly becoming less solid.

The contact lens operates slightly differently from the spectacle lens. It is in contact (hence the name) with the cornea either directly or with a variable thickness of tear film in- between. Between the spectacle lens and the eye, on the other hand, there is a volume of air. Because the contact lens only has air in front of it, light must be bent to correct short sight almost entirely by its front surface. The reason for this is that, where the fitting of the contact lens permits, the eye and tear fluids have almost as much negative refractive power as the artificial lens itself. Therefore, after light has passed through the contact lens, it will not be further bent until it reaches the lens inside the eye. The contact lens becomes, in effect, the new front of the eye, the new cornea. But because of its proximity to the natural optic system, and because of the materials used in its manufacture, the contact lens is necessarily much thinner than a spectacle lens. For short-sighted eyes, the contact lens also has an additional advantage: it tends to correct any non-spherical problems of the cornea, since the power of the cornea has now been negated (by the additionally thick layer of fluids). The image formed on the retina will now be of a size either equal to that of a normal eye, or larger, and of course the correction itself curves with the eye. But although from an optical point of view the contact lens is significantly more efficient than the spectacle lens, there are some problems associated with the use of contact lenses.

The opposite of short sight is long sight. This occurs when the optical power of the whole eye is too weak to bring the image on to the retina, but instead projects it some distance beyond. The eye is simply too short for the focal length of its lens system. A small degree of long-sightedness can be corrected by `accommodation‘ of the inner lens to a higher power, but if more than two dioptres of accommodation is required in each eye there occurs a simultaneous stimulus for the eyes to converge. But if accommodation is thus required to correct long sight and obtain a clear image of distant objects, this synchronized convergence is of no value since it becomes no longer possible to direct both eyes in the correct direction. Therefore, when there is more than two dioptres of long sight, only one eye is held straight, whilst the other drifts into a corner. Such behaviour is known as strabismus or squinting of the eye. This condition is most common when long sight of high degree is present from birth.

Long sight is very often inherited (as is short-sightedness). It may be due to eyes that have failed to develop to a correct length as the rest of the body grows, or it may be due to a weakness in the cornea or crystal lens. A combination of both factors is also a possibility. Someone suffering from long sight, whilst able to focus easily on distant objects, may find the extra effort required for near vision just too much and consequently develop symptoms of eye-strain. As with short sight, substantial long sight can and should be corrected by the use of spectacles or contact lenses, only in this case the power of the artificial lens needs to be positive in order to bring the image forward on to the retina. Long-sighted spectacles increase the power of the individual’s optics.

There are other surgical techniques for flattening the curve of the cornea, all involving removal of tissue, but all more serious in their complications than Radial Keratotomy. They are used only in correcting more substantial degrees of myopia, say from six to sixteen dioptres.

However, the cornea may be artificially flattened without recourse to surgery by using small, hard contact lenses. Unlike ordinary contact lenses they are purposely designed to bring sustained pressure on the cornea; but at best they can only correct up to two dioptres of vision, and in many cases the correction is only temporary, so that after a while it again becomes necessary to wear the lenses. There is also the risk of creating irregular curves on the cornea, which will cause visual distortions.

Other mechanical techniques of flattening the cornea have been attempted. Various ways of relaxing the outside eye muscles (which help to make the eyes `bulge’), including acupuncture and electrolysis, have had their advocates, though the results have been far from conclusive. There also exist techniques that combine the mechanical with the psychological. Of these the ‘Bates Method’ is the best known. Certainly it is the one for which the most exaggerated claims have been made.

William H. Bates was a New York ophthalmologist who practised at the beginning of this century. The title of his famous book speaks for itself: Better Eyesight without Glasses. In it he recommends the treatment of short-sightedness by non-medical and non-optical methods. (Glasses, wrote one of his disciples, are to be regarded as ‘eye crutches’.) Aldous Huxley, who was almost blind, is reputed to have gained relief by doing the exercises that Bates advises. The very short-sighted, Bates suggests, should be taught to make the best use of object outlines as a method of recognition. For those with a smaller degree of short-sightedness various eye relaxation and eye-muscle exercises are recommended, along with ‘palming’ (a way of applying pressure to the eyes using the hands), and ’swinging’, a callisthenic exercise that massages the eyeballs by rhythmically alternating the body’s centre of gravity. While, individually, none of these practices is likely to cause harm, and may even help (`palming’ certainly helps, if only because it means the patient is unlikely to read too excessively), in their collective presentation they amount to an attempt to make the patient think his way out of trouble. Other similar programmes involve homoeopathic medicine, stimulation to the neck muscles, even hypnosis. Together they constitute a field of practice where the suggestive personality is most likely to find help. None of the techniques is scientifically proven, but they gain adherents among sufferers who have failed to find succour from orthodox practitioners. However, although a mildly short-sighted person will almost certainly improve his or her sight without recourse to glasses or spectacles by learning how to relax the eyes and avoid all close work, little succour is offered to the busy city executive or eager student.

So much, then, for the cornea. We come briefly to the crystalline lens. It has been stated that if the inner lens could be made to flatten its curves, this too would reduce the total eye power and therefore bring the image back into place on the retina. Very simply, this can be done by looking in the distance and avoiding all close work. Not realizing the mechanics of this, it is surprising how often a patient will tell his doctor that he has been seeing better during a trip to the mountains. Eye-drops containing drugs which act upon the eye’s internal muscles of accommodation (the ciliary muscle), thus releasing tension in the ligaments that keep the crystal lens in position, can be very effective. But such drugs dilate the pupil and cause excessive sensitivity to light, and so are only useful when short sight is sudden in onset and related to a spasm induced by near-sight tasks. It is not possible to move the inner lens forwards or backwards by mechanical (surgical) means. The crystal lens can be removed, and this will correct very high powers of short sight (say —18 dioptres), but such removal is a procedure that is liable to weaken the eye in other ways.

The mechanical methods of correcting short sight are still limited, therefore, and it is still the case that, in nearly every instance, the preferred solution is to use optical aids, i.e. spectacles and contact lenses.

Meanwhile, as we discover how the genetic programming of our body operates, it seems more not less remarkable that the eye grows from a ball 17 mm in diameter to one 24 mm in diameter without being noticed. The cornea and crystalline lenses make the necessary changes without any disruption to `normal services’, so that the image falls consistently on the film at the back of the eye. Is there some method by which eye- growth is controlled from the nervous system in such a way that the nervous system ‘knows’ how the image is formed? In other words, if the image goes out of focus, even fractionally, does the nervous system plot the necessary realignments in all parts of the optical system so that a good picture can be swiftly restored? The alternative would be to say that the pattern of development is pre-set and will operate irrespective of any one part being out of step with the rest, that each part will grow to its required size and optical function of its own accord. While both possibilities are perfectly compatible with the diverse ways in which genetic coding operates, the second theory seems to provide a better explanation of the occurrence of visual defects, in so far as those defects are not caused by environmental factors. But as yet the genetic machinery is not fully understood; when it is, clinicians will be better able to discover ways of diagnosing early malfunctions and therefore be in a better position to suggest ways of correcting, and even preventing, them.

Counselling apart, genetic ophthalmology as a practical science belongs to the future. Abnormal developments must therefore be discussed as they occur, not as they ‘would otherwise’ occur. In general there are three areas in which optical malfunctions may take place, the three related optical components of the eye: the cornea, the crystalline lens, and the retina. Aberrations may affect any or all of these, individually or in combination. If the cornea is too steeply curved, its power will be too great and the image will fall in front of the retina, thus causing shortsightedness. This state of affairs can be theoretically corrected by reducing the length of the eye, or by moving the crystalline lens backwards, or by reducing the power of the crystalline lens in some other way (e.g. replacing it with a weaker lens). In normal circumstances it is possible to lose up to one dioptre of power by stopping reading and all other close work and by applying drugs that relax the eye for distant vision. Alternatively, if the cornea is flattened, then its power can also be reduced. This can be done in more than one way. Since the cornea is maintained in its curvature by pressure and the elasticity of its own tissues, deep cuts in its surface, allowing the tissue to expand, will cause a flatter curve to be formed. Such an operation is called Radial Keratotomy. It is relatively simple to carry out, but as it only corrects up to between three and four dioptres of myopia it is of little help to patients whose problems are more acute. However, since in most patients the scale of myopia is only between one and eight dioptres, Radial Keratotomy is of great interest.

It is not uncommon for a patient to ask his practitioner whether he would recommend surgery, almost as though such surgery was an obvious solution which the practitioner had momentarily overlooked. What are the risks? The answer is that, in the long term, we don’t know yet. The operation produces several scars on the cornea in areas away from its centre. While clear vision is not affected, in theory at least it should slightly decrease the cornea’s ability to collect light rays from its periphery.

In tribal societies a child’s education involves learning just as much as it does in post-industrial societies. What differs is the technique of knowledge acquisition. While there are no exact figures as to the number of separate bits of knowledge a member of a tribe must learn, it must nevertheless be considerable and compare with what a ‘civilized’ child must learn. But this is done by word of mouth and by example, not through books. It is also most usually, in terms of a teacher—student ratio, a one-to- one process. Children learn from their parents or tribal elders all they need to know about survival, and they are told, either directly or through ritual, about their culture. The ‘civilized’ child must complete a very different course. Oral and performative instruction still occurs, and perhaps to a much greater degree than some modern pedagogues are ready to admit, but the emphasis is on book-learning, both as regards developing survival skills, and as regards culturization. The cultural background studies require proof of acquisition of knowledge by memorizing reading matter. Thus from an early age children of our times will probably find themselves reading print, and progressively smaller print, for several hours a day. This accommodation to close vision, together with sustained convergence of the eyes, will, in some instances, not relax sufficiently when the reading period is over. The power of the eyes remains set for close vision, and if this continues as an habituation the child will develop near sight. This is slightly simplified, but essentially it is what may happen. Also to be taken into account is the effect near-focusing has on the internal system of eye pressures, and the effect those pressures in turn have on the length of the eye. Children who read too much, or read in circumstances where they have constantly to ’strain’ the eyes, are likely to increase the physical length of the eye artificially, and, this is the main cause of short sight. But it does not happen to alt children who thus use, or overuse their eyes, and so such ‘acquired’ short sight needs to be seen as the result of an interaction between genetic composition (tendency) and environment.

Cause and effect are simple in theory. But explanations become more complicated as we increase the number of factors that are taken into consideration. Primitive society is less well equipped to detect small degrees of short-sightedness, and this in itself may be one reason why there are more people with short sight in post-industrial communities. There may even be a problem of language involved. It is possible, for example, that in some bygone societies the difference between being a ‘good hunter’ and being an average or even bad one may have been a difference, inter alia, in visual performance without actually being referred to as such. Again, it may be that certain children have an innate desire for the acquisition of knowledge, or at least looking at small objects, while other children may be naturally more extrovert. The questions arise: are personality traits inherited? and, are there more important considerations than short-sightedness? Some people will only become short-sighted if the pattern of close work is present, while others (a small minority) will become short sighted whatever the circumstances. (Acquired short-sightedness cannot of course be passed on, but a hereditary tendency to become short-sighted is eminently likely.) Yet the acquisition of knowledge from books is related to intelligence. No two children, given the same set of materials to read, are likely to ‘learn’ identically. (But there again, by the time a child is able to read, he or she has already been sufficiently socially conditioned to make it very hard indeed to judge how much intelligence is innate, and how much has been developed through environmental influence.) Furthermore, among social groups more given to reading than others (teachers for instance) interbreeding is likely, again making it difficult to distinguish between genetic factors and environmental influence.

A development period of just over twenty years must be considered short by comparison with other technical advances such as the television and aeroplane. As with all technology, the advances depend almost entirely upon knowing the objectives and then having the resources to overcome the problems. What these objectives are vis-a-vis the contact lens we will come to. At first glance the contact lens appears to be a simple, one- component device and therefore not technically difficult to produce, but in fact the demands made upon size, thickness, replicability of material and lens forms, quite apart from consistency of optic definition, provide a formidable task, while the funds that have been available to individual researchers have been only a fraction of the moneys available for more obviously commercial ventures (and infinitesimal compared to world- destruct weapons systems).

Because the contact lens lies on the eye, its back surface must be perfectly compatible with the complex and sensitive tissue of the eye. Indeed, compatibility is the main prerequisite, and not a perfect, glove-like fit. In fact, for the normal eye, a perfect fit is the opposite of what is required, because the cornea can only remain clear if gases are permitted to flow backwards and forwards over its tear film. This is a form of respiration. Just as the lungs permit our red blood cells to get rid of their unwanted carbon dioxide and replenish themselves with oxygen, so too cells in the cornea take up 02 and disgorge CO,, and it does this from the gases on its surface. The cornea’s ability to do this depends upon a very complex network of metabolic cycles, which, like all complex entities, is very readily disturbed. The placing of a layer of plastic over the cornea must not be allowed to interfere with the cornea’s respiratory system. Where interference does take place, the result can be oedema, or corneal swelling. When a small lens is used (such as an ordinary hard contact lens) the swelling is localized centrally and associated with an unwanted steepening of the corneal curve, which therefore increases short sight. This is usually transitory, but in some patients can be long-lasting. When a contact lens practitioner tells you to ‘come back and see me in six months’ he is not thinking about his consultancy fee but about your health, and you’d be foolish to ignore the instruction.

There are other complications arising from the use of contact lenses. There is, for example, some likelihood of gradual distortion, common among wearers of hard contact lenses who wear their lenses day-in day-out over a period of years, especially if the lenses themselves are too thick. This creates a dependence on the contact lens for, unlike spectacles, if the lenses are abandoned for a few weeks there is very little tendency for the eye to improve of its own accord. Like a bad analyst, the hard contact lens may create problems which only it can correct. Other problems are more serious, but the majority reverse themselves once the patient stops using contact lenses. All lenses produce some surface changes to the cornea as they rub against its surface, but the degree of tolerance is a very individual matter. There are some people who simply cannot wear contact lenses, while others experience no difficulty. The damage done can only be seen by magnification and oblique illumination. By using a dye called fluorescein the injured cells on the superficial layer of the cornea can be highlighted. The cornea that has been so dyed has a green mottled appearance, the density of the dye being greater wherever the injury is most severe.

If, however, you have overworn your contact lenses, or if a significant foreign body has inserted itself between the lens and the cornea, then the corneal surface may be more seriously affected.

The syndrome of overwear is a very individual problem. Some patients are chronic overwearers. They are often wearing unsuitable lenses in bad environments, and as soon as a painful red-eye episode begins they decrease their wearing time or stop for a few days, and then continue. This chronic situation may be the result of a hyper-sensitivity to the lenses or to preparations used with the lenses. On the other hand some patients do not know they have overworn their lenses. The damage done by overwear usually takes place under the lens, and whilst the lens is worn there is no pain. Shortly after removing the lens the pain commences and in some instances becomes sufficiently severe for the patient to seek advice at a hospital (usually in the middle of the night). While the lesion to the eye is unlikely to be severe, the pain is, and leads to spasms of the lids and an inability to open or move the eye.

A less severe syndrome occurs with soft lenses. After a long period of overwear the cornea becomes cloudy, the eyes red. The lenses may hitherto have been perfectly satisfactory, but suddenly a change has occurred, either in the properties of the plastic or in the environment.

With some very rare exceptions, the problems associated with overwear are not pathologically serious, and provided you learn to recognize the symptoms at an early stage no great damage will be done. While overwear typically affects people whose jobs or social life demands that they are ‘on show’ for long stretches of time, the prolonged wear of suitable lenses, night and day, may not cause any greater problems than ordinary daily wear except for a periodic blurring of vision and a more frequent change of lenses; and if you don’t develop any of the symptoms characteristic of overwear, either while you are wearing the lenses or after you have taken them out, it is most unlikely that the eye is suffering any damage, trivial or otherwise.

The compatibility between patient and lens varies from individual to individual. Without exception it is the quality of the tears, of the eye’s lubrication system, that determines whether good contact lens wear can be achieved and maintained. But before we turn to tears, let us look at the whole media of the eye and some of the problems associated with it.

When a spectacle wearer changes over to contact lenses there are usually alterations in his or her behaviour and personality. A short-sighted person in contact lenses is often a more extroverted individual. It is small wonder that contact lenses are held in such high repute. People will talk about them, openly and without encouragement, in a way they never did about glasses.

Some ophthalmologists and optometrists have put forward theories and some proof that contact lens wearers with short sight have less need to accommodate because of the larger image size, or because the internal ocular pressure becomes slightly decreased when contact lenses are being worn. In clinical practice it does appear that there is slower progression of short sight in contact lens wearers in the age group 8-16. Also, the need to change contact lenses, or at any rate their prescription, becomes less since the optical tolerances of the device are cruder than is the case with spectacles. Thus though the short-sighted eye may have changed by half a dioptre, the patient still sees the small letters on the distance chart, whereas with glasses there is no such tolerance of change.

The contact lens in its small form is a modern invention, dating from the 1950s. Contact lenses did exist before that time, but they were much larger, covering the whole of the front of the eye. And it was not until the late 1960s that softer materials were used (`soft’ contact lenses), and only in very recent years have soft coloured and very thin optical forms been available.

At present there are three ways of classifying a contact lens:

Classification according to size

Scleral (haptic): 13-26 mm in diameter Corneal: 7.5 to 13 mm

(most contact lenses are of the second, smaller size)

Classification according to material

Hard or rigid

Soft hydrophilic (water content over 60 per cent) Soft silicone rubber

Classification according to gas permeability

High gas (or oxygen) Low gas (or oxygen) No gas

By and large, hard contact lenses cover only part of the cornea over the centre of the iris and can be gas-permeable, while soft contact lenses cover the whole iris, or cornea, and are gas- permeable in varying degrees. Both sorts of contact lens are worn daily, but taken out at night, though a recent development has produced a semi-permanent soft contact lens that stays in contact with the cornea for periods up to six months. More recently still, in Japan, a semi-permanent gas-permeable hard lens has been manufactured. These latter varieties, though they have obvious user advantages, carry with them certain risks, mainly that they can cause damage to the cornea and lids. Some practitioners will not prescribe them, or will only prescribe them if the patient provides a written undertaking that the practitioner will not be held responsible for any injury incurred. They do, however, have a real application for certain kinds of eye disease, and for individuals unable to handle lenses on a daily basis; and they are the logical goal for perfection in contact-lens performance. The ordinary soft contact lens is also reputedly more comfortable to wear, though it requires a good deal more attention in its care (at night they have to be specially cleaned, sometimes heated, and allowed to soak in a prepared solution), whereas the hard contact lens, which takes more getting used to, needs only to be cleaned. The hard contact lens has a much longer life, indeed it may last indefinitely, and so is less expensive than the soft contact lens, which generally must be renewed every one to two years. In advising you which sort of contact lens to adopt, hard or soft, the practitioner may well make an undisclosed assessment of your character, whether or not you are the sort of person who takes good care of things, and to a lesser degree he may assess your financial well-being.

But what causes these changes? What causes glaucoma? Is it genetic? Is the decay built into our genes or is it due to outside factors? Can glaucoma be brought on by the wrong diet, by drugs, or by other environmental factors? Perhaps the answer lies, once more, in a combination of both genes and environment. Some people may be genetically programmed to be vulnerable to certain sorts of environment. This at least would explain why some diets seem to have an adverse effect on some individuals and not on others. Certainly some types of glaucoma recur in the same family (though of course members of one family will tend to react the same way to an environmental etiology).

Equipment has been designed to measure accurately the pressure in the eye and to test the field of vision. There are also tests to measure the flow of aqueous fluid from the eye when stress is put upon the eye-pressure system. But even if an early diagnosis is made, treatment is not necessarily effective, and the final outcome can be almost complete loss of the fields of vision except at the centre of sight. Affected individuals can still see clearly in the distance, and can read clearly, but they are unable to move about with any confidence, because they cannot see anything that is not directly in front of them. They have lost their peripheral vision, and in acute cases they may even have difficulty in following a line of print. Such a condition is called `tunnel vision‘, and is accounted a form of blindness, a fact little _understood or appreciated by the general public.

The onset of this kind of glaucoma is very slow and many patients do not know that they are affected. Sometimes the first noticeable indication is a loss of colour hue discrimination. It occurs most frequently in post-industrial ‘civilized’ communities, but this may simply be because in such communities the average life-span is longer, or because, in technological societies, people are more likely to damage their eyes by too much close-work. Even so, senile or elderly glaucoma has a relatively low incidence. About two per cent of the population over fifty will have eye-pressure above the normal, but only in perhaps 0.2 per cent (one in every five hundred) of the age group will specific treatment be sought or required.

Because it tends mostly to affect people over fifty there are possible connections with senile peripheral blood vessel degeneration, which affects other sensitive tissues in the body. There are, however, other causes and types of the glaucomous condition, of raised intra-ocular pressure. Some of these are too rare to be worth describing here, but others are not.

Infantile glaucoma occurs when the baby is born with an abnormal outflow of fluid from the eye. This often means that the angle of the eye has developed without adequate outflow channels. At birth the tissues of the eye are soft, and as the eye-pressure increases the eye becomes bigger. This can be a painful condition, and the baby may be distressed and unhappy. The cornea of the infant suffering glaucoma appears especially large and is sometimes cloudy. The eyes, also unnaturally big, will look red. There will be quiet periods, without pain, but diagnosis is essential. The condition can be treated either with drugs (eye-drops) or with surgery, opening up new channels for drainage of the fluid from the eye. If treatment is not provided, however, the eye may become very severely affected, and treatment at a later stage will be pointless.

There is also a condition of juvenile glaucoma, equally rare, but, like the infantile form, capable of leading to a loss of vision. It is generally considered a late development of the infantile condition.

Some doctors consider minor forms of glaucoma to be present in children who subsequently become myopic. Early high eye- fluid pressure, in this view, causes the eye to elongate and thus cause short-sightedness. Increased pressure owing to excessive close-work is often cited as the classic explanation of myopia, but in fact this has never been substantiated clinically.

At the Oxford Ophthalmological Congress the eye surgeon Harold Ridley reported the results of eight operations that he had performed to insert a Perspex lens. He thus founded a completely new branch of ophthalmic surgery. Ridley had treated many ocular injuries suffered by members of the Royal Air Force during World War II. Aircraft windshields (made of Perspex) had shattered after explosions or the impact of bullets, and Perspex fragments had penetrated the eyes of plane crews. Ridley had noticed how inert Perspex was in the eye and how little inflammation it caused.

None the less, lens implantation was not immediately adopted by the world’s surgeons. Complications were common in the early days, mainly because of unsophisticated surgical equipment and imperfect lens design. Only a few surgeons, mostly in Holland, Italy, and Britain, retained their interest.

The first intraocular lens was an almost exact replica of the human model. The cataract was removed by the extra- capsular method and a small lenticulus (artificial lens), of the same size and power, was inserted into the space previously occupied by the cataract. The lenticulus was made from polymethylmethacrylate (Perspex), a material much heavier than the biological lens that it replaced. Positioned as it was in the very fragile capsule just in front of the vitreous face, its weight meant that it was ill-supported. There was a strong tendency for it to dislocate because it put too great a strain on the zonular fibres.

To overcome this problem a new generation of ‘anterior chamber’ implants was designed. These lenses are placed in the fore part of the eye, in front of the iris. They are supported by a number of legs which stand on the iris itself. Although the lens is thereby more stable, it may rub against the back of the cornea. This may happen during insertion, may be caused by the lens being not precisely the right size, or may be due to the iris itself having been pushed forward. In any event, the contact between lens and cornea causes loss of corneal cells, which in turn may lead to loss of transparency.

An alternative to this type of lens is the ‘iris-supported’ lens. In this case the lens may be positioned either in front of or behind the pupil. It is held in place by a number of loops which hook the lenticulus to the iris. Although this method reduces the likelihood of the lens rubbing on the cornea, it interferes with the normal functioning of the pupil.

Another solution is to implant a posterior chamber `capsular fixated’ lens. This type of lens is the one which most closely mimics a human lens. Resembling the original Ridley lens it is, however, equipped with flexible loops attached to the lens edge. Following an extra-capsular extraction, this new lens is inserted into the capsular bag. The loops are then allowed to expand in order to hold the lens firmly in place without either distorting the pupil or endangering the cornea. The lens is held rigidly in the correct position.

The image presented to the retina by any intraocular lens is almost the size of that in the normal eye. For this reason intraocular lenses are particularly appropriate for patients who retain good vision in one eye. It is most useful for those who have had one of their eyes damaged by injury — for instance, in a road-traffic accident. Indeed, this is sometimes the only acceptable method of optical correction.

Since implanted lenses mimic normal human lenses, it might seem proper to give every patient a plastic lens. However, the long-term effects of placing plastic in the eye are unknown. It is possible that the human body’s defence mechanism will attack the implanted lens, whose plastic will then deteriorate. Moreover, if the corneal cell loss (and consequent impairment of transparency) is extensive, sight will deteriorate. If there has been previous corneal damage from another eye disease (for example, glaucoma, or a long-term inflammatory condition), the danger of further cell loss is unacceptable.

Any degeneration at the back of the eye, which might lead to a detached retina in, for instance, very shortsighted people or diabetic patients who are at risk of developing retinal complications, is considered by many surgeons to contra-indicate an implant — particularly of the iris-supported type of lens. It is necessary to dilate the pupil widely in order to examine the back of the eye satisfactorily. If an intraocular lens is present, this procedure becomes difficult, and the lens itself may be dislodged during the inspection.

Despite these complications, there is undoubtedly an important place for the intraocular lens implant. The design and manufacture of the lenses are being continuously researched. Better lens materials have been developed. Ways of making the operation itself simpler and safer are being investigated. Methods of avoiding and treating subsequent problems are being explored. In the early 1970s the popularity of the operation increased rapidly. This was due largely to the introduction of the operating microscope, the development of finer surgical instruments and suture materials, and an increasing appreciation by ophthalmic physiologists of the eye’s response to the introduction of foreign materials. Today more implant operations are being undertaken, although the practice is by no means universal.

The reasons why the two eyes do not work together, either temporarily or permanently, can be several. Normally the two eyes move together, maintaining fixation on the same object or objects in the distance. As the object comes closer, the eyes converge somewhat to maintain fixation. However, when an object is placed very close to the eyes such dual fixation is no longer possible, and it is normal for one eye to wander. What is abnormal is for one eye to wander when the object is still in the middle or far distance. This state of affairs can occur to anyone in special circumstances, when they are very tired, or ill, or under the influence of drugs and/or alcohol. But a permanent deviation by one eye, either inwards, outwards, upwards or downwards, is an abnormality which, if allowed to go uncorrected, can destroy stereoscopic vision and lead to monocular blindness. In children the deviation is most commonly inwards; in adults, when a squint develops afresh, it tends to be outwards.

When such a deviation occurs, there are two broad categories of cause. Either it may be sensory, some malfunction in the image-making processes of the optic system, or it may be motor-related. The abnormality may involve the eye itself, or it may involve any part of the nerves, muscles and brain concerned with visual functions. Thus almost anything that affects the stimulus of sight may be held responsible for the fact that one eye squints. For example, one eye may from birth only be able to form a blurred image so that even when this is optically corrected later on, the brain is unable to fuse its picture with that of the other normal eye. Or the two eyes may be normal in every way, but the brain itself is unable to fuse their pictures.

The commonest explanation of squint among children is excessive long sight. Such children attempt to correct their vision by accommodation, causing the muscles that converge the eyes to contract reflexly. To maintain fusion, to avoid seeing double, the brain subconsciously chooses one eye to fixate whilst the other strays into a corner. Sometimes the eyes alternate in this way, so that first one and then the other is used. Whilst most squints of this type are treatable and preventable by the early use of optical correction, the young age of the child often hinders diagnosis. If an eye stays in a corner and is not used then, in the first place, its visual stimulation is inhibited or suppressed, and, eventually, it may become deprived of sight. If the condition remains untreated for several years during the child’s development then critical good vision may never be regained. When this happens the result is called amblyopia.

Diagnosis at a very early age is difficult, but, with the help of electro-diagnostic methods, it is sometimes possible to find out which part of the visual system is at fault and hence to decide whether treatment will be of any value. Treatment itself may take many forms, but essentially involves stimulation of the weak eye while the good eye is occluded. After a child has reached the age of seven or eight the likelihood of a successful treatment diminishes.

Among adults the development of a squint is most commonly associated with the loss of vision in one eye. Provided that the patient’s binocular vision was normal beforehand it may become possible again once sight is restored to the affected eye. The most usual cause of this type of squint is injury to the eye with resultant cataract formation. Once the cataract is removed and vision is restored, using either a contact lens or intra-ocular implant, binocular vision becomes possible once more. However, the same thing happening to a young child, with a traumatic cataract in one eye while the other stays normal, will rarely result in good vision, even where the cataract is expertly removed and a contact lens worn. The reason for this is the much greater plasticity of the young person’s brain. Even when amblyopia is the result of only a few weeks’ lost vision in one eye, the effect, in a young child, can be decisive. The brain refuses to confuse the good image with the bad one, and so, even during treatment, the strong eye remains dominant, and the weaker one is suppressed.

Apart from injury to the eye, however, squint may be caused by abnormalities in the brain itself, in the nerves, or even in the muscles of the eye. As with sensory malfunction, motor malfunction may be subject to any one of a number of explanations. For example, that part of the brain which co-ordinated eye- movement may be deficient from birth. On the other hand, an injury at birth may prevent a particular eye-muscle from functioning. Again, injury and accident can put a nerve out of action, temporarily or permanently. Providing the sensory part of the eye and of the brain remain unaffected, the result of such a malfunction will be seeing double (diplopia), either part of the time and in particular areas of the visual field, or in the whole field and at all times. Whereas the child easily suppresses one of the images, the adult cannot do this as the neural pathways between the eyes and the visual cortex are too firmly established. The only remedy for double vision of this sort is to keep one eye covered up.

The modern, effective treatment of cataract is to remove it from the lens capsule, or, if necessary, remove the whole lens itself. From about the age of fifty onwards the ligaments which hold the crystal lens in place become weaker. The lens can therefore be quite easily removed from the eye by rupturing the ligaments, especially if they have been ‘prepared’ by appropriate weakener-enzymes. Special forceps or a ‘freezing probe’ then lift the lens out of the eye. Usually the surgeon will supply counter-pressure to facilitate this operation. Another technique makes an opening in the eye and tears out the lens capsule. The hard nucleus of the lens may be ‘broken up’ whilst it is still in the eye, and the debris then washed out.

Once the nucleus has been removed the cortex, which is softer, naturally disintegrates so that it too may be washed out.

Once the inner lens has been removed the surgeon will decide whether to replace it with an artificial lens, or not to replace it at all.