Eye chamber and lens

Structures and function are discussed from anterior to posterior (Figure 28-1). The first structure that light hits after it is reflected from an image is the cornea. (Technically, light first hits the tear layer, which has its own structure and rests on the corneal surface.) Corneal tissue is completely transparent. Light is refracted, or bent, to the greatest degree by the cornea because the light rays must pass through different media, which change in density, as in going from air to water.² The refraction of light can be observed by noting how a stick placed into water appears bent where it enters the water (Figure 28-2).

Damage to the cornea from abrasions, burns, or congenital or disease-related processes can alter the spherical shape of the cornea and disturb the quality of the image that falls on the retina. Radial keratotomy, a surgical procedure done in the 1980s to reduce nearsightedness by placing spokelike cuts in the cornea, sometimes had the side effect of scarring the cornea and causing distorted vision. This surgery is no longer done. The newer surgeries such as laser-assisted in situ keratomileusis (LASIK) are far superior and more predictable in their reduction of refractive error (nearsightedness, farsightedness, or astigmatism) and induce virtually no scarring or distortion. In keratoconus the cornea slowly becomes steeper and more cone shaped, distorting the image and causing reduced vision.³

Iris

Behind the cornea is the iris, or colored portion, which consists of fibers that control the opening of the pupil, the dark circular opening in the center of the eye. The constriction and dilation of the pupil control the amount of light entering the eye in a similar fashion to the way the f-stop on a camera changes the size of the aperture to control the amount of light and the depth of field.⁴ Under bright light conditions the opening constricts, and under dim light conditions it dilates, allowing light in to stimulate the photoreceptor cells of the retina. This constriction and dilation are under autonomic nervous system (ANS) control, with both sympathetic and parasympathetic components.⁵ Under conditions of sympathetic stimulation (fight or flight) the pupils dilate, perhaps giving rise to the expression “eyes wide with fear.” Under parasympathetic stimulation the pupils constrict. The effect of drugs that stimulate the ANS can be observed.⁶ For example, someone who has taken heroin will have pinpoint pupils.

Lens

Behind the iris is the lens. The lens is involved in focusing, or accommodation. It is a biconvex, circular, semirigid, crystalline structure that fine-tunes the image on the retina. In a camera the lens is represented by the external optical lens system. The ability to change the focus on the camera is achieved by turning the lens to change the distance of the lens from the film, which effectively increases or decreases the power of the lens, allowing near or distance objects to be seen more clearly. The same effect, a change in the power of the lens, is achieved in the eye by the action of tiny ciliary muscles, which act on suspensory ligaments, thereby changing the thickness and curvature of the lens. A thicker lens with a greater curvature produces higher power and the ability to see clearly at near distances. A thinner lens and flatter curvature produces less optical power, which is what is needed to allow distant objects to be clear (Figure 28-3). The process of lens thickening and thinning is accommodation.^4,5

Ideally the lens will bring an image into perfect focus so that it lands right on the fovea, the area of central vision. If the focused image falls in front of the retina, however, then a blurred circle will fall on the fovea (Figure 28-4). In this case the lens is too thick, having too high an optical power. One simple remedy is to place a negative (concave) lens externally in front of the eye in glasses (or contact lenses) to reduce the power of the internal lens and allow the image to fall directly on the fovea. In presbyopia (old eyes), the flexibility of the lens fibers decreases and the lens becomes more rigid.⁷ Accommodation gets weaker until the image can no longer be focused on the retina. Normal-sighted individuals first begin to notice these changes in their early forties. When this occurs, a plus (positive) lens (or bifocals, progressive lenses, bifocal or monovision contact lenses) may be worn to aid in reading.⁴

Other solutions to the problems of aging can be implemented during the time of cataract surgery, where a bifocal implant may be inserted, or monovision implant correction performed in each eye.

The lens can be affected by the age-related process of cataract development, in which the general clarity of vision is impaired from a loss of transparency of the crystalline lens. Incoming light tends to scatter inside the eye, causing glare problems. When vision is impaired to such a degree that it affects function, the lens may be removed surgically and replaced with a silicone implant placed just posterior to the iris.

Vitreous chamber

The space behind the lens, which is filled with a gel-like substance, is called the vitreous chamber. As we age, the gel tends to liquefy, and some of the remnants of embryological development that were trapped are released to float freely. This can cause the very common perception of “floaters,” the shadows cast by these particles onto the macular region. They can be disturbing but generally float out of view over time.⁵

Retina

The retina at the back of the eye is the photosensitive layer, like the film in a camera, receiving the pattern of light reflected from objects. The topography of the retina (Figure 28-5) includes the optic disc, which is where the optic nerve exits and arteries and veins emerge and exit. This is also the blind spot because there are no photoreceptor cells on the disc. The macula is temporal to the optic disc and contains the fovea, providing central vision. The surrounding retina provides peripheral vision and defines a 180-degree half-sphere.⁵

Visual pathway

The visual pathway begins with the photoreceptor cells, which begin a three-neuron chain exiting through the optic nerve. This chain consists of the rods and cones, which synapse with bipolar cells that synapse with ganglion cells (Figure 28-6).^5,8

There are two types of photoreceptor cells: rods and cones. The cone or rod shape is the dendrite of the cell. Variation in shape and slight variation in pigment give each one different sensitivities. The rod cell has greater sensitivity to dim light but less sensitivity to color, whereas the cone cell has greater sensitivity to color and high-intensity light and less to reduced light conditions. The highest concentration of cone cells is in the fovea and macula, with decreasing concentration of cone cells and increasing concentration of rod cells moving concentrically away from the macula. The high degree of low-light sensitivity can be most appreciated in survival mode conditions such as being lost in the woods on a moonless night. By swinging the eyes side to side one can maximize the image and keep the macula from interfering.

The phenomenon responsible for the high degree of neural representation of the foveal region and that accounts for the tremendous conscious awareness of the central view is called convergence.⁵ At the periphery of the retina the degree of convergence is great; many photoreceptor cells synapse on one ganglion cell, which accounts for poor acuity but high light sensitivity. The closer to the macula, the less the degree of convergence, until, finally, at the fovea there is no convergence. This means that one photoreceptor cell synapses with one bipolar cell and one ganglion cell.

The awareness of what is seen is directly related to the amount of convergence, which reflects the extent of neural representation. The 1:1 correspondence between photoreceptor and ganglion cell at the fovea means that there is a high degree of neural representation of the foveal image in the brain. It is even greater than the neural representation of the lips, tongue, or hands.⁹ This accounts for the primary awareness of what is in the foveal field and secondary awareness of the peripheral field. Conscious awareness of the environment is whatever is in the foveal field at the moment. But continuous information about the environment is flowing over the peripheral retina, usually subconsciously. Attention quickly shifts from foveal to nonfoveal stimulation when changes in light intensity or rapid movement are registered. This type of stimulus arouses attention immediately because it could have specific survival value. For example, a person is driving down the street and senses rapid motion off to the right. The foveas swing around immediately to identify a small red ball bouncing into the street. This information goes to the association areas, in which “small ball” is associated with “small child soon to follow.” Frontal cortical centers are aroused and a decision is made to initiate motor areas to take the foot off the accelerator and put it onto the brake, while simultaneously moving the wheel away from the ball and scanning for the object of concern, that is, the child.

Exercise 28-3: peripheral central awareness

We have a unique ability to change our awareness by consciously shifting attention from our foveal or central awareness to our peripheral awareness. For example, as you read these words, become aware of the background surrounding the paper; note colors, forms, and shapes; continue to expand your awareness to include your clothes, the floor, walls, and ceiling if possible. You are consciously stimulating your primitive, phylogenetically older visual system. The ability to do this has considerable therapeutic value because a typical pattern of visual stress is associated with foveal concentration to the exclusion of peripheral information. The ability to expand the peripheral awareness at will is a skill that can help you to relax while you drive, can improve reading skills, and can be used in visual training techniques.

The moment light hits the retina, the photographic film model must be abandoned for the image processing or computerized image enhancement model. The primary visual pathway at the retinal level is a three-neuron chain. From back to front the first neuron is the photoreceptor cell, rods or cones. They synapse with a bipolar cell, which in turn synapses with a ganglion cell. The axon of the ganglion cell exits by means of the optic nerve. Image enhancement occurs at the two junctions of the three–nerve-cell pathway. Lateral cells at the neural junctions have an inhibitory action on the primary three-neuron pathway, and through the inhibition of an impulse the image is modulated. For example, at the first junction between photoreceptor cell and bipolar cell, there are horizontal cells. These cells enhance the contrast between light and dark by inhibiting the firing of bipolar cells at the edge of an image. This makes the edge of the image appear darker than the central area, which increases the contrast and thereby increases attention-getting value. After all, it is by perceiving edges that we are able to maneuver around objects. In a similar manner, amacrine cells act at the second neural junction between bipolar and ganglion cells to enhance movement detection.¹⁰

This image enhancement process continues throughout the visual pathway. The process has been likened to the way in which a computer enhances a distorted picture of outer space received from a satellite. The image goes through a series of processing stations in the inner workings of the computer. The computer-generated, enhanced image shown on the screen is like the end product in the brain: the perceived image.

The visual pathway continues through the brain (Figure 28-7). The ganglion cell axons exit the eyeball by means of the optic nerve, carrying the complete retinal picture in coded electrochemical patterns. From there the patterns project to different sites within the central nervous system (Figure 28-8). Projections to the pretectum are important in pupillary reflexes; projections to the pretectal nuclei, the accessory optic nuclei, and the superior colliculus are all involved in eye movement functions.⁵ The largest bundle, called the optic tract, projects to the lateral geniculate body in the hypothalamus, where additional image enhancement and processing occurs. The next group of axons continues to the primary visual cortex and from there to visual association areas.

At what point does the retinal image become a perception, and with what part of the brain does one see? Current theory regarding visual perception is the result of Nobel prize–winning research by Hubel and Wiesel in the 1960s called the receptive field theory.¹¹ This theory states that different neurons are feature detectors, defining objects in terms of movement, direction, orientation, color, depth, and acuity. Research in 1990 by Hubel and Livingstone¹² was able to locate a segregation of function at the level of the lateral geniculate body. They identified two types of cells, one type being larger and faster magno cells, which are apparently phylogenetically older and color blind but which have a high contrast sensitivity and are able to detect differences in contrast of 1% to 2%. They also have low spatial resolution (low acuity). They seem to operate globally and are responsible for perception of movement, depth perception from motion, perspective, parallax, stereopsis, shading, contour, and interocular rivalry. Through linking properties (objects having common movement or depth) emerges figure-ground perception. Much of this perception occurs in the middle temporal lobe.

The other type of cell, called the parvo cell, is smaller, slower, and color sensitive and has a smaller receptive field. These cells are less global and are primarily responsible for high-resolution form perception. Higher-level visual association occurs in the temporal-occipital region, where learning to identify objects by their appearance occurs. It appears that these two types of cells are functionally and structurally related to the two visual systems represented in retinal topography—the foveal (central) and peripheral visual systems.

Eye movement system

The eye movement system consists of six pairs of eye muscles: the medial recti, lateral recti, superior and inferior recti, and superior and inferior obliques (see Figure 28-8). Together they are controlled by cranial nerves III (oculomotor), IV (trochlear), and VI (abducens). The eye movement system has both reflex and voluntary components. Reflexive movements are coordinated through vestibular interconnections at a midbrain level. The vestibuloocular reflex (VOR) functions primarily to keep the image stabilized on the retina. Through connections between pairs of eye muscles and the semicircular canals, movement is analyzed as being either external movement of an object or movement of the head or body. From this information the VOR is able to direct the appropriate head or eye movement.⁵

Two types of eye movements are the result. Smooth, coordinated eye movements are called pursuits, and rapid localizations are called saccades. Voluntary control of both these motions indicates cortical control. Pursuits are used for continuously following moving targets, and they are stimulated by a foveal image. Saccades are stimulated by images from the peripheral system, where a detection of motion or change in light intensity results in a rapid saccadic eye movement to bring the object into the foveal field. Either difficulties in the eye movement system or altered functioning of the vestibular system can affect the coordinated, efficient functioning of eye movement skills.

A third type of eye movement is specifically related to eye aiming ability. This is the coordinated movement of both eyes inward toward the nose, as in crossing the eyes, or outward along the midline, as when looking away in the distance. The inward movement is called convergence, and the outward movement is called divergence. The most important result of efficient vergence abilities is depth perception, or stereopsis. Small errors in aiming can dramatically affect stereopsis. Problems such as double vision, wandering eyes, and strabismus are discussed in greater depth in a later section.

Accommodation

Accommodation is the ability to bring near objects into clear focus automatically and without strain. Relaxation of accommodation allows distant objects to come into focus. The primary action is that of the ciliary muscles acting on the lens, and the primary system of control is the ANS, with sympathetic and parasympathetic components.⁵

Both accommodation and pupil size changes are reflexes that work in concert: as accommodation relaxes the pupil dilates and as accommodation increases the pupil constricts.⁴ As a person focuses on a near object, the lenses thicken, allowing the near object to come into focus. At the same time the pupils constrict to increase depth of focus (just as in a camera). As a person looks into the distance, the lens gets flatter, relaxing accommodation, and the pupil dilates, decreasing the depth of field.

Accommodative ability is age dependent. A young child can focus on small objects just a few inches in front of the eyes. At about the age of 9 years, the accommodative ability slowly begins to decrease. By the mid 40s the reserve focusing power diminishes to the point that near objects begin to blur. At this stage, reading material is pushed farther away until the arms are not long enough, and then reading glasses are needed. This is called presbyopia (old eyes).

Problems in accommodation may contribute to myopia, hyperopia, and presbyopia. Symptoms include blurriness at either near or far distance, depending on the age and the problem.

Accommodation is important mainly for up-close activities: reading, hygiene, dressing (specifically, closing fasteners), use of tools, typing, tabletop activities, and games.

Vergence

Vergence includes convergence and divergence. It is the ability to smoothly and automatically bring the eyes together along the midline to singly observe objects that are near (convergence) or conversely to move the eyes outward for single vision of distant objects (divergence). Specific brain centers control convergence and divergence.

With regard to reflexes, vergence is associated with accommodation: convergence with accommodation, and divergence with relaxation of accommodation. The function of this reflex is to allow objects to be both single and clear, at either near or far positions. Vergence has both automatic and voluntary components. Most of the time it is not necessary to think about moving the eyes inward while looking at a close object; yet if asked to cross the eyes, most people can do this at will.

Problems can occur in vergence ability when the eye movement system is out of sync with accommodation or from damage to cranial nerves III, IV, or VI. Problems can be slight, in which there is merely a tendency for the eyes to converge in or out too far, or the eyes can be grossly out of convergence. Tendencies to underconverge or overconverge are called phorias and are not visible except by special testing in which they are elicited. An individual may be asymptomatic, but symptoms may occur under conditions of increased stress or fatigue such as excessive reading or working at a computer terminal or from drug side effects (prescription and recreational).

Some phorias may worsen to the extent that binocularity breaks down, at which point the individual becomes strabismic. There are two main types of strabismus: esotropia and exotropia. An esotropia is an inward turning of the eye, and an exotropia is an outward turning. A third, less common type of strabismus is hypertropia, in which one eye aims upward relative to the other eye. Strabismus and dysfunctional phorias are discussed in greater detail in the next section.

Vergence ability is needed for singular binocular vision; thus it is basic to all activities. At near positions the patient may have difficulty finding objects; eye-hand coordination may be decreased, affecting self-care and hygiene tasks; and reading may be difficult. Distance tasks that may be affected include driving, sports, movies, communication, and, frequently, ambulation. Individuals with impaired vergence ability may also have difficulty focusing and may have decreased or no depth perception. Interpreting space can be quite difficult and confusing. If decreased vergence is a result of traumatic head injury or stroke, it may contribute to the patient’s confusion, and he or she may not be able to identify or communicate the problem.

Pursuits and saccades

Eye movement skills consist of pursuits and saccades. Pursuits are the smooth, coordinated movements of all eye muscles together, allowing accurate tracking of objects through space. Perception is continuous during pursuit movements. Saccades are rapid shifts of the eyes from object to object, allowing quick localization of movements observed in the periphery. The systems involved in eye movement skills are the oculomotor system with the VOR, in conjunction with coordination of the central and peripheral visual systems. The peripheral visual system is finely tuned for detecting changes in light levels and small movements.

Problems in pursuits or saccades can be the result of a dysfunction of any individual muscles, the VOR, or areas of the brain controlling pursuits or saccades.13–15 Because the VOR helps to stabilize the image on the retina and to differentiate image movement from eye movement, simple tracking can be more difficult. In addition, visual field loss, either central or peripheral, can dramatically affect localization ability. People with blind half- or quarter-fields can be observed to do searching eye movements rather than directly jumping to the object.

Activities affected include searching for objects; visually directed movement for fine motor tasks, gross movement, and ambulation tasks; eye-hand coordination; self-care; driving; and reading.

Memory also may be affected by an eye movement dysfunction. Research by Adler-Grinberg and Stark¹⁶ and Noton and Stark¹⁷ examined patterns of eye movements as subjects looked at a picture. Distinct eye movement patterns, called scan paths, became apparent. When the subject was asked to recall the picture, the same eye movement pattern was elicited as when the subject originally saw the picture. It would appear that a type of oculomotor praxis is involved in recall. Applying this idea to the clinical setting, if a patient has inaccurate eye movement with poor pursuits or excessive saccades, then perhaps the stored memory is less efficiently stored and consequently more difficult to reconstruct from memory. Additionally, if a patient has a type of brain damage with generalized dyspraxia, the eye movement system could quite likely be affected and might be involved in the patient’s perceptual dysfunction.

Another more recent example of the relationship between eye movements and memory is the use of eye movement desensitization and reprocessing (EMDR) therapy to help individuals with posttraumatic stress disorder reintegrate traumatic experiences.¹⁸ Although the exact mechanism is at this time unknown, the prevailing hypothesis is that the lateral eye movements elicit an orienting response, scanning the environment for further danger, and that this is an investigatory reflex associated with a relaxed physical state.¹⁹

Near point blur

Blurred vision up close is not a symptom that by itself is indicative of a problem in any one area. It could indicate farsightedness (hyperopia), astigmatism, or reduced accommodative ability (insufficiency). The client may move objects or the head farther or closer, may complain of eye strain or headaches, may squint, or may even avoid near activities as much as possible. The therapist might observe excessive blinking, and the patient may complain of glasses not working well.

Distance blur

Distance blur could also have a number of different causes, including nearsightedness (myopia), a pathological problem (such as beginning cataracts or macular degeneration), or accommodative spasm. Most people have some experience with accommodative spasm. After spending long periods of time either studying or reading a novel and then glancing up at the wall across the room, it may be blurry and then clear up slowly. For some individuals, this spasm eventually develops into nearsightedness if the reading habits continue for a long time.

Clients with distance blur may make forward head movements and frequently squint in an attempt to see. They may not respond or orient quickly to auditory or visual stimuli beyond a certain radius. The therapist may also note excessive blinking and a withdrawn attitude because the patient cannot see well enough to interact with the environment.

Visual hygiene can be recommended to assist in the development of good visual habits. This should include attention to good lighting and posture, taking frequent breaks, and monitoring the state of clarity of an environmental cue such as a clock across the room.

Phoria and strabismus

The next area of eye alignment problems can be divided into two types of problems: phoria and strabismus. A phoria can be defined as a natural positioning of the eyes in which there is a tendency to aim in front of or behind the point of focus. It may or may not be associated with symptoms. Fusion is intact, and depth perception may also be intact to some degree.

Everyone has a phoria, just as everyone has a posture. It may be within normal range, or, just as someone may have scoliosis, a high phoria may cause problems. The following phorias may cause problems:

Phoria is measured in units of prism diopters, which indicate the size of the prism needed to measure the eye position in or out from the straight-ahead position.⁴

Phorias tend to produce subtle symptoms. These include having difficulty concentrating, frontal or temporal headaches, sleepiness after reading, and stinging of the eyes after reading.

A strabismus, or tropia, is a visible turn of one eye, which may be constant, intermittent, or alternating between one eye and the other. The person may have double vision, or if the strabismus is long term, the person may suppress or “turn off” the vision in the wandering eye. Suppression is a neurological function that is an adaptation to the confusing situation of double images. In the developing brain the individual must choose (unconsciously) which eye is dominant, and the image is confirmed by motor and tactile inputs as being the “real” image. The other fovea’s image is then neurologically suppressed. The peripheral vision in the suppressing eye is still normal, and the eye still contributes to other aspects of vision such as orientation and locomotion.

The essential concept in understanding the difference between phoria and strabismus is that in strabismus fusion and depth perception are not present. Definitions of different types of strabismus are presented in Box 28-2. It is not a conclusive list; many other types and permutations are beyond the scope of this discussion. The intent here is to expose the therapist to different terms that may be used by the physician in diagnosing the type of strabismus.

In strabismus, one eye appears to go in, out, up, or down, and there is frequently an obvious inability to judge distances, especially if the strabismus is of recent onset (acquired). The client may underreach or overreach for objects, cover or close one eye, complain of double vision, or exhibit a head tilt or turn during specific activities. He or she may appear to favor one eye, have difficulty reading, appear spaced out, or avoid near activities. In addition, especially if the patient sees double but is unable or unwilling to talk about it, she or he may be confused or disoriented.

Certain postures may facilitate fusion for some clients. The eye doctor will be able to determine which head position may be best. Frequently, many clients will automatically move around to the best position. At other times, however, head position will be used to avoid using one eye. Head and body position, therefore, are important aspects to consider.

Many convergence problems are amenable to vision therapy,20–22 but some are not.²³ Whether a particular problem can be helped by vision therapy can be determined by an eye doctor, who can prescribe specific exercises.

Oculomotor dysfunction

Oculomotor dysfunction is a very common sequela of neurological deficits, with an incidence as high as 90% according to Ciufredda and colleagues.^24,25 Commonly the smooth pursuit system will be affected, such that the smooth movement is interrupted by a series of fixation stops and the movements appear jerky. Damage anywhere along the visual motor pathway may cause a variety of eye movement disorders. This includes injury to the pontine and mesencephalic reticular formation, oculomotor nucleus in the brain stem, caudate nucleus and substantia nigra, cerebellum, and vestibular nuclei.²⁴

Patients with oculomotor disorders frequently also experience dizziness, nausea, and balance difficulties. Many times an eye movement will elicit dizziness and disorientation. It is thought that these symptoms are in part caused by a loss of integration of information coming from the two aspects of the visual system that process central vision (parvocellular pathway) and peripheral vision (magnocellular pathway).

As mentioned previously, detection of peripheral targets serves to direct an eye movement with a specific velocity and direction to bring the foveas in line for purposes of identification. Therapy for rehabilitation of eye movement disorders should be directed at using peripheral awareness with slow controlled eye movement toward the target. Once these movements are tolerated, head movement can be added, then slowly body movement.^26,27

While doing any sort of tracking activity, the client is encouraged to maintain peripheral awareness. This technique will help the client keep her or his place. The oculomotor system is guided by the peripheral location of an object.

Visual field defects—hemianopsia and quadrantanopsia

Visual field loss may indicate damage that is prechiasmic, at the optic chiasm, postchiasmic, in the visual radiations of the thalamus, or in the visual cortex. The resultant visual field loss is characteristic (even diagnostic) in each case. The visual field loss pattern will generally reflect the location of the lesion. It could be bitemporal (outer half of each field), half-field loss (hemianopsia) with or without macular involvement, or quarter-field loss (see Figure 28-7). Some symptoms of field loss are an inability to read or starting to read in the middle of the page, ignoring food on one half of the plate, and difficulty orienting to stimuli in a specific area of space.

Hemianopsia is a loss of half of the visual field in each eye, and quadrantanopsia is loss of a quarter of the visual field in each eye. Homonymous hemianopsia refers to the inner or nasal half and the outer or temporal half of each eye being affected. The retina itself is intact, but a neurological lesion has interrupted the ability of the visual cortex to receive recognition of the image. Vision processing may be occurring at lower centers, such as the lateral geniculate body, but if signals are not being received by the cortex, then they are not recognized as “seen.” In 1979, Zihl and von Cramon²⁸ published their findings that damaged visual fields could be trained by use of a light stimulus presented repeatedly at the border of the visual field defect. Balliet and co-workers²⁹ (when attempting to repeat the experiment, adding controls for oculomotor fixations) proposed that subjects were actually learning to make small compensatory eye movements rather than experiencing true improvements in the visual fields. In the 1980s and 1990s a group of German researchers developed a computer-based field training system for researching the question of visual field training. They found in their research that visual fields did expand on average by 5 degrees, with functional improvements noted by more than 80% of their patients (Figure 28-9).^30–34 A company called NovaVision introduced the computer-based visual field restitution training program in the United States with good results (see Appendix 28-A). This author has also noted documentable and functional improvements in visual fields even when trained with less sophisticated methods.

Compensation training may also be required to allow the client to resume activities such as reading. Compensation techniques include use of margin markers and reading with a card with a slit in it (typoscope) to isolate one line or a couple of lines at a time. Holding reading material vertically also can help.

The incidence of retinopathy of prematurity is increasing because of the improved survival of premature infants as a result of improved ventilation.³⁵ Immature retinal vessels are sensitive to high oxygen tension. The effect on the vessels is vasoconstriction, eventually leading to obliteration of the vessels. This creates a state of ischemia, which stimulates the growth of new blood vessels. These small, fragile vessels bleed easily, leading to fibrosis and traction on the retina. As a result of the traction, the macula gets stretched, interfering with the function of central vision.

The temporal vessels are most affected because they develop last. The degree of damage may be mild or severe, depending on the amount of prematurity.⁷

Age–related conditions

Cataracts.

The most common malady affecting vision in elderly persons is cataracts. General clarity of vision is impaired from a loss of transparency of the crystalline lens of the eye.

In the senile cataract the lens slowly loses its ability to prevent oxidation from occurring, and liquefaction of the outer layers begins. The normally soluble proteins adhere together, causing light scatter.³ Vision slowly declines as opacification and light scatter increase, until the lens must be removed.

Age-related macular degeneration.

Age-related macular degeneration (AMD) is the leading cause of blindness in the Western world and is the most important retinal disease of the aged (affecting 28% of the 75- to 85-year-old age group).⁷

Loss of central vision results from fluid that leaks up from the deeper layers of the retina, pushing the retina up and detaching it from the nourishing layer. New vessel growth and hemorrhage and atrophy further destroy central vision. There is much research going on regarding treatments for AMD. The most promising at this time is the use of bevacizumab (Avastin) or ranibizumab (Lucentis), which is injected into the eye; then the eye is treated with a laser. The drug targets the neovascular network of blood vessels, and the laser treatment obliterates the vessel network, sparing the photoreceptors.³⁷

This condition has significant implications for independent functioning. Mobility tends to be less impaired because the peripheral visual system is still intact. All activities involving fine detail such as reading, computer use, sewing, and cooking are affected. Safety also can be affected.

Arteriosclerosis.

In arteriosclerosis, vision may or may not be affected. There is a hardening of the retinal arteries, which may eventually lead to ischemia, with the areas of retina deprived of sufficient oxygen eventually dying.

Hypertension.

Hypertension is usually accompanied by arteriosclerosis. There may be retinal bleeding and edema, which can affect central vision if the macula is involved.

Diabetes.

Diabetes can affect the lens. In the diabetic “sugar cataract,” sorbitol collects within the lens, causing an osmotic gradient of fluid into the lens, which leads to disruption of the lens matrix and loss of transparency. As the fluid increases and decreases within the lens, the patient’s vision also can fluctuate, depending directly on the sugar level. This makes prescribing glasses during this time quite difficult. The cataract will need to be removed if vision is worse than 20/40.

The retinal effects include microvascular damage and the development of microaneurysms. Central vision may be reduced as a result of retinal ischemia. The ischemia leads to new blood vessel growth (neovascularization). These new vessels are weak, frequently leaking and causing hemorrhage. The hemorrhage leads to fibrosis, which puts traction on the retina, pulling it off and leading to retinal detachment and blindness. Laser treatment of the bleeding retinal vessels will stop the bleeding but also burns photoreceptors, creating blind spots. This result is far preferable to total retinal detachment and blindness.

Glaucoma.

Glaucoma occurs in 7.2% of the 75- to 85-year-old age group.⁷ It is generally caused by an increase in the intraocular pressure. This pressure interferes with the inflow and outflow of blood and nutrients at the optic disc. As it progresses, glaucoma can cause tunnel vision and, in some, complete blindness. Because of the type of vision loss affecting the periphery, mobility and safety are significantly impaired. Try walking around holding a paper towel tube to your eye while closing the other eye, and see what happens to your ability to maneuver around obstacles or find your destination.

A less common type of glaucoma is low-tension glaucoma, in which the internal eye pressures are essentially normal. The mechanism is not understood, and the disease is treated with eye drops to lower internal pressure, just like the other types of glaucoma.

In one type of glaucoma, called open-angle glaucoma, the outflow of aqueous humor is reduced, leading to increased intraocular pressure. There are no overt symptoms. In another type, closed-angle glaucoma, the outflow is blocked by the iris. Symptoms are a painful, red eye, which may be confused with conjunctivitis.

Corticosteroids used to treat many conditions in the elderly for long periods of time may have side effects in some people, such as glaucoma and cataracts.

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