Squint, or strabismus, refers to the misalignment of the visual axes of the eyes and is thought of as a disorder of eye movement. Normal eye movement is dependent on correct functioning at three levels:
Normal range of movement and various terms used to describe them are as follows (click on table1/figure1 to enlarge):
Coordinated eye movement and alignment allow for both eyes to be directed towards the same object. An image of said object is created on corresponding parts of each retina, and fed back to processing centres in the brain. The two retinal images are then fused and interpreted by the higher cortical centres as a single image. Because each eye has a slightly different angle and field of vision, the images formed on each retina are slightly different to each other. The brain processes these disparities to construct a 3D image of the object being viewed. This gives rise to two important concepts:
Pathological changes in squint
Abnormalities of eye movement and misalignment of the eye, as in squint, inteferes with these two functions. Because both eyes are focused on different fields of view, the retinal images are too disparate to fuse together into a single 3D image. This can manifest in two common ways:
Squint, or strabismus, is a misalignment of the visual axes of the eyes. A squint can be described in a number of ways - the common terminology used is discussed in table 2.
Another important system of classifying squints, based on aetiology and pathogenesis is as follows:
These two terms are illustrated in figure 2:
Non-paralytic squints may be idiopathic, developing in a child with otherwise normal eyes, or may arise secondary to another eye problem. Idiopathic cases are postulated to be related to disordered central control of eye movement), while secondary squints are related to disorders that distort retinal images produced by each eye, asymmetrically. The brain, unable to process two different images, attempts to compensate by altering eye movement and positioning. Common causes of secondary squint include:
Other risk factors for developing squint include family history, prematurity, neonatal jaundice, neurological illness (meningitis, encephalitis, cerebral palsy) and craniofacial abnormalities (including syndromes associated with dysmorphism such as Down's).
Good history taking is important, particularly in young babies, where it is essential to differentiate pathological squint from the self-remitting squint of new borns. Key features of the latter include:
Examination is aimed at
(1) Ruling out pseudostrabismus. This refers to certain facial features that cause a person with normally aligned eyes to look like they have a squint. On examination look for features known to be associated with pseudostrabismus:
(2) Confirming Squint: the following tests help identify presence of a squint
(3) Identifying the underlying problem. This includes testing eye movements, stereopsis, refraction and examination of the cornea, lens and retina
Management of a non-paralytic squint involves:
Squint surgery is required when there is no identifiable/treatable cause, or in large squints, that have not responded to correction. When indicated, it is recommended that surgery be done as early as possible, to reduce the risk of amblyopia. The surgery is variable in its results as under- or over-correction may occur. These patients may require further procedures to get satisfactory realignment. Occasionally adjustable sutures may be used, allowing for minor correction in alignment to be made in the awake patient, without having to return to theatre. A few patients go on to develop a second squint, despite initially good results after surgery.
Early intervention with glasses, patching and/or surgical realignment can greatly improve vision in the squinting eye and prevent amblyopia. Surgical realignment, where successful, also reduces the psychoscoial ramifications of squint. However, while these children will develop good binocular single vision, they very rarely develop good stereopsis.
Paralytic squint is caused by decreased function of one or more EOMs, due to:
Diplopia in paralytic squint is binocular - i.e. double vision is corrected when one eye is occluded. It should be differentiated from monocular diplopia (i.e. patient still sees double when one eye is occluded), which is usually due to refractive error or cataract.
Notably, paralytic squint is not typically associated with amblyopia as the affected patient is usually older and has surpassed the critical period of visual development. Even in cases of congenital paralytic squint, amblyopia does not develop as there is usualy binocular vision in most directions of gaze, including primary position - squint is only manifest in one or two cardinal positions.
Cranial nerve palsies
The presentation of cranial nerve palsies along with common causes are discussed in the table below. Diplopia associated with cranial nerve palsies is usually constant:
A few of the important EOM pathology associated with double vision and squint are described in the table below:
Management of non-paralytic squint:
Although the mains aims of managing squint are the reduction of double vision and the prevention of amblyopia, it is important to be respectful and considerate about the holistic impact that squint can have on the individual. Patients may feel extremely self-conscious or develop negative body image. They may feel the stigma of having a squint in other aspects of their life as well, including peer-interaction, job opportunities and relationships. Studies have shown that both children and adults find squints disturbing to look at, irrespective of their degree of personal experience with them.
Additionally, new onset diplopia has ramifications for driving. Patients are required to inform the DVLA and cease driving, until their diplopia has been adequately corrected by glasses/wearing a patch while driving.
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