Are you suffering from optical delusions?

Life being what it is – a temporary experience –insightful readers will be familiar with the question that arises when visiting a doctor. ‘Is this it?’

And anyone who has sat in the waiting room for a first visit to the ophthalmologist will know the inner voice which asks, ‘How am I going to face the possibility of going blind?’

Both anxieties, while reasonable, tend to exaggerate the likelihood of catastrophe. When it comes to eyes, the exaggeration is greater. As far as we know, everybody, in the end, gets an interview with St Peter, but very, very few people become blind, at least in the sense that the word is generally understood.

The distinction between properly blind (unable to see) and technically blind is worth making. The difference between them is great, and the scope for unnecessary worry and distress equally great.

Blind means blind. It means you cannot see – the lights have gone out. But the threshold for eligibility for registration as a person with severe sight impairment is lower –and looser - than you might imagine.

The great majority of people registered as blind can see. Their sight may be blunt and their field of vision restricted, but they can see. The lights are still on.

Having satisfied ourselves that we are unlikely to become totally blind, let’s consider what eye trouble we are actually likely to develop. What are the principal disorders? Why do we get them? How shall we experience them? What is to be done?

Cataracts

The cataract is as good a place to start as any.

If you haven’t already been told you’ve got one – or even two – it is only a matter of time before you will.

In the meantime, plenty of your friends and relations will already be on a waiting list, or have had their cataract ‘done’. If you define a good operation as a favourable benefit:risk ratio, cataract surgery is the best operation in the history of medicine.

Cataract is the name given to the lens in your eye when it has become less than perfectly clear. ‘Cataract’ because of the River Nile, where, over time, the water loses its youthful clarity, foaming white over six waterfalls or cataracts.

And the thing in your eye was originally called a cataract because it looked white – as densely opaque as Nile cataracts. Modern microsurgical techniques have changed all that, and now any lens that is less than absolutely clear can be operated upon – but it is still called a cataract.

The processes by which the lens may lose its youthful transparency and optical perfection are intriguing and varied. They share the common feature of accumulating disorganisation of cells and proteins.

Why does the lens lose its transparency? More interestingly, how does it? The lens is a highly organised body of accumulating cells, permitting light rays to be cleanly transmitted, to focus a clear image at the back of the eye.

Associated conditions, including diabetes and steroid treatment, inflammation, and trauma, may contribute to the process.

But the end result is the same: a lens which can no longer focus a clear image for the light receptors in the retina, at the back of the eye, to convert into nerve signals to send to the visual brain.

The effect of cataract on your vision is a gradual reduction in clarity. It is often associated with glare or dazzle in the face of oncoming car headlights.

There is also an unnoticed progressive reduction in transmission of short-wavelength (green and blue) light, due to filtering of these rays by the developing cataract. The instant restoration, and intensity, of these colours, when the cataract has been removed, is commonly a subject of happy celebration.

Cataract surgery takes 20 minutes, give or take. You are wide awake, the eye is magically numbed, and the lens with the cataract is replaced with a plastic one (intraocular lens or IOL) of appropriate focussing power.

The eye’s optical geometry is measured to calculate the right power of IOL to implant. It also provides a useful opportunity to correct pre-existing long or shortsightedness by adding the power of previously worn glasses.

Some surgeons offer to cure presbyopia (the need for glasses to see close up) and astigmatism (aspheric focal error) while dealing with your cataract, by implanting a non-standard multifocal, accommodating, or toric IOL. These options are generally available only in the private sector at an often high, additional cost.

No surgery comes with a guarantee, and there are risks that a cataract operation may not go according to plan. If things go badly wrong, the operated eye may lose sight completely.

There can be serious surgical complications. The eye can develop an infection. In less severe cases, you may still see, though less well than you had hoped. While low, the risk of a suboptimal outcome is not negligible.

The benefit side of the risk:benefit equation depends on the magnitude of your existing visual problem. You don’t have to have your cataract removed. Opt for surgery when you estimate the visual trouble you are currently experiencing is great enough that the risks of surgery are outweighed by the potential benefit.

Age-related macular degeneration

Just as the performance and organisation of the lens fibres deteriorate over time, giving rise to cataract, the performance of cells in the retina may deteriorate after many years of faithful service.

These cells – rod and cone receptors, and their close relations the bipolar and ganglion cells –receive light rays and process the optical image into a pattern of nerve impulses. These are conveyed to the occipital cortex of the brain, where the visual experience is produced.

Structural and functional deterioration occurs particularly in the macula, the central zone of the retina, where the cells are most hard-working. AMD causes progressive loss of central visual definition, and with it the frequent, though unwarranted fear of impending blindness.

AMD does cause difficulty with tasks that require sharp central vision (‘acuity’), such as reading print and car numberplates, and recognising faces. But it always spares peripheral vision – that element of the visual experience we use to orientate and navigate our way through life.

People developing AMD are sometimes told they are blind, or will become blind. Their dismay is understandable but misplaced. In reality, they will never become blind, but will always retain the peripheral vision required for getting around, and for independent living.

AMD is classified as “dry” and “wet” (neovascular). Dry AMD is the commoner one. It describes a general wearing-out of the macular cells and their metabolic support. It is not catastrophic, but causes a gradually progressive blurring of central vision over a period of years.

No treatment usefully reverses the process. Various dietary vitamin and mineral supplements are often suggested though none is of any convincing value.

Wet AMD describes the less common condition, in which capillaries beneath the retina leak and bleed. The consequence can be a deeper, more rapid impairment of central vision. But injections of ingenious antibody-based agents can stabilise, and sometimes reverse, the process. The treatment may need a number of repeat injections and imaging to assess the response.

Glaucoma

Glaucoma isn’t a single disease. It is the name given to a number of otherwise unrelated conditions.

They each have three common features: raised intraocular pressure

(IOP), loss of retinal nerve fibres serving the visual periphery, and a corresponding reduction in the field of vision (without compromising central vision: the converse of AMD).

The glaucoma most people get, or are told they have, is chronic (which means it is not here-and-gone) open-angle glaucoma. It doesn’t hurt, and generally people seem not to have noticed its effect by the time they are diagnosed.

It is believed that high pressure in the eye damages retinal nerve fibres, and that treatment to reduce the pressure helps to preserve the peripheral field. That is the theory but, as there are a number of assumptions and many unknowns, the truth may be more complicated.

Treatments for chronic open angle glaucoma include drops, surgery and laser treatment. Like all treatments, each has its benefits and risks. Treatment with drops for glaucoma generally reduces intraocular pressure moderately well, but not always sufficiently.

The drops often cause inflammation as a side effect. Because they need to be used in the long term, this can be a serious ongoing problem.

Around 70% of operations for glaucoma are successful, producing a once-and-for-all solution by permanently reducing IOP. Some surgeons augment this surgery by adding agents intended to inhibit scarring. This may increase the success rate, but adds an additional risk of complications.

Finally, laser treatment (argon or selective laser trabeculoplasty –ALT or SLT) is sometimes used either instead of, or to supplement, treatment with drops

If your vision becomes problematic, you first have to discover whether you need a change of glasses or have a disorder that needs treatment. Visit a reputable high street optometrist (aka optician) who is trained to recognise eye disease – free for the over 60s.

If there’s a condition, you’ll be referred to an ophthalmologist (aka eye doctor). This specialist surgeon will diagnose and treat the condition, either medically or surgically, on the NHS or privately.

For further information, go to www.nhs.uk and search eye care