Types of squintBinocular single vision (BSV) is the simultaneous use of the two eyes to give a single mental impression under normal conditions of seeing. Anyone who has a squint or cast of the eye, such that the two eyes are not pointing towards the object of regard, is seriously disadvantaged, both socially and physiologically. Squinting eyes are most commonly convergent, but divergent squint and vertical squint — with one eye looking higher or lower than the fixing eye — occur as well. Where the squint is constant, the vision in the deviating eye is ignored or suppressed, resulting in reduced acuity. When this defective visual acuity persists after correction of any refractive error it is called amblyopia (literally ‘blunt vision’).
Consequences of squintingSquints may be constant, intermittent, or latent. An intermittent, divergent squint on distant viewing may disappear on looking at near targets, with recovery of BSV. There can be latent squint when a tendency to squint is controlled by the individual's quality of BSV. Depending upon the angle of a constant squint, the patient may have some low quality or degraded BSV, or even none at all. Here the lack of depth perception can reduce the ability to do detailed close work or to pour liquids accurately, and can make driving even more hazardous than it is already. These problems assume a lesser degree of importance when the faculty of BSV has never developed than in the case of a normal-sighted adult who suddenly loses the ability to fuse the images from the two eyes and is afflicted with double vision (diplopia).
Application of animal studiesThe infant visual system, comprising eyes, optic pathways, relay stations, and visual cortex, is partly pre-programmed, and the remaining development is governed by the visual environment. Important experimental work with kittens and cats, by Hubel and Wiesel at Harvard in the early 1960s, and later by Blakemore (Professor of Physiology at Oxford), established how columns of nerve cells in the visual cortex could be tuned to respond to the length, orientation, and direction of movement of lines in their field of vision. Amblyopia was produced by unilateral lid suturing, by unilateral squint (induced by surgery or prisms), by defocusing the image optically, or by using atropine. Amblyopia caused a decrease in the number of cortical cells receiving input from the deprived eye, with corresponding cell shrinkage in the layers of the relay station. The number of binocularly-driven visual cortical cells fell from 80% to less than 20%, with a shift in cortical dominance to the side of the non-deprived eye. Some of the changes could be rectified by reverse lid suturing — that is, opening the sutured lids of the visually-deprived eye and suturing the lids of the fellow eye. Similar processes were demonstrated in immature monkey visual systems by von Noorden, at Baylor, Texas. Animal experiments showed that there was a sensitive period of limited duration when cortical cell responses could be reversed and, by analogy with results from occluding the preferred eye in amblyopic children, there is a sensitive period in humans, although its extent cannot be determined so precisely. Certainly this work has led to modifications in the management of childhood amblyopia — for example, part-time occlusion instead of total occlusion or atropinization of the preferred eye. Surgical straightening of congenital convergent squint has only rarely been done as early as 4 months of age, but many surgeons will operate by 9–12 months of age. However, there are many different types of squint, in some of which treatment at four to five years of age can be successful.
Refractive correctionDonders, Professor of Ophthalmology in Utrecht, as long ago as 1864, laid the foundations of the importance of correcting refractive errors in squinting children. In particular, if a child has to exert marked accommodation to overcome hypermetropia (long-sightedness) for clear sight, the normal close link is broken between focusing the eyes and attaining just the right amount of convergence. The excessive focusing power produces over-convergence, which drives one eye too far inwards. If corrective spectacles are not worn this convergent squint may become permanent.
In some children, the focusing of the two eyes is widely different, usually with one being much more hypermetropic than the other. The more hypermetropic eye never receives a clear image, so visual cortical cells fail to be properly stimulated. Full spectacle correction may not be tolerated because of the large difference in image size on each retina. Instead, contact lenses can be used, as they cause a much smaller difference in image size between the two eyes, thus allowing central fusion.
Early detectionBecause of the importance of early correction of obstacles to binocular vision, enthusiastic programmes to visually screen all children by 3–4 years of age have been undertaken, but this is a doctrine of perfection. Their cost-effectiveness — in terms of eventual outcome versus the time and effort expended by orthoptists — has been challenged.
Both parents and family doctors must be educated about the importance of early detection of squints. Any child in a family where either parent or a sibling is hypermetropic or has a history of squint should be screened by an orthoptist. If the results are clearly positive, or equivocal, the child must be referred on to the consultant ophthalmologist, for detailed examination of the eyes, their refractive errors, and their movements. Appropriate therapy, if indicated, can then be started and supervision continued by the orthoptist. Once best visual acuities have been achieved, with glasses if needed, any residual squint is treated by surgical realignment of the eyes under general anaesthesia. This involves moving ocular muscle attachments to new positions in the eyeball and shortening their antagonist muscles. Ideally, fusion of the images of the two eyes can be (re)established, but a more usual result is significant improvement in appearance, with good acuity bilaterally but no or only low-grade fusion.
Double vision in adult squintsIn the adult, or visually-mature child of 8 years or older, ‘paralytic’ squint may develop suddenly as the result of injury or illness. Road traffic accidents are a continual cause of head injury, despite seat belts, as are other means of personal transport — such as cycling, roller blades, and skiing — and also body contact sports. Damage to the cranial nerves which control the eye muscles, or direct orbital injury to the muscles and their connective tissues, causes uncoordinated eye movements with diplopia. This is a dramatic symptom, demanding medical help urgently. Illnesses capable of such devastating visual results include diabetes, high blood pressure, multiple sclerosis, cerebral aneurysms, and tumours.
In the early stages of paralytic squint, very thin, plastic Fresnel prisms can be pressed onto spectacle lenses to restore fusion. Fresnel, a French physicist, used racks of glass prisms to direct the beam from a lighthouse. Plastic spectacle prisms, based on the same principle, are invaluable orthoptic aids to therapy. Later, in adult patients, surgical repositioning of ocular muscles using adjustable sutures under local anaesthesia gives the best results. Botulinum toxin (Botox) (in minute doses, as this is one of the most powerful poisons known) may be injected directly into the antagonist of a weakened ocular muscle to let the eye move into a more central position. For example, in damage to the sixth cranial nerve, which paralyses outward movement, causing horizontal diplopia, this treatment may allow useful binocular vision with a compensatory head posture, and it may even hasten recovery. Botox can be used to create cosmetically straighter eyes in patients embarrassed by noticeable squint. The improvement may only last a matter of months, but a significant number of such patients prefer repeated top-up injections of Botox to a series of squint operations.
Donders, F. C. (1864). On the anomalies of accommodation and refraction of the eye. The New Sydenham Society, London.
Mein, J. and and Harcourt, B. (1986). Diagnosis and management of ocular motility disorders. Blackwell Scientific Publications, Oxford.
See also eye movements; gaze; orthoptics.
squint / skwint/ • v. 1. [intr.] look at someone or something with one or both eyes partly closed in an attempt to see more clearly or as a reaction to strong light: the bright sun made them squint. ∎ [tr.] partly close (one's eyes) for such reasons. 2. [intr.] have eyes that look in different directions: Melanie did not squint. ∎ (of a person's eye) have a deviation in the direction of its gaze: her left eye squinted slightly. • n. 1. a permanent deviation in the direction of the gaze of one eye: I had a bad squint. 2. inf. a quick or casual look: let me have a squint. 3. an oblique opening through a wall in a church permitting a view of the altar from an aisle or side chapel. DERIVATIVES: squint·er n. squint·y adj. [often in comb.] squinty-eyed.
Hence squint sb. strabismus XVII; hagioscope XIX. Aphetic of ASQUINT.