Ординатура / Офтальмология / Английские материалы / Ocular Periphery and Disorders_Dartt, Bex, Amore_2011

abnormalities in V1. Moreover, although human electroretinogram (ERG) studies are equivocal, after optimizing optical focus, fixation alignment, and fixation stability, Robert Hess and colleagues found no pattern ERG deficit in deep amblyopes, in a spatial frequency range where there were obvious psychophysical deficits for the same stimuli. Although it is possible that retrograde degeneration may affect the lateral geniculate nucleus (where there is some shrinkage of the cells in the parvocellular layers) and retina, it seems unlikely that these effects contribute significantly to the behavioral losses. In contrast, amblyopia results in profound alterations in V1 both in cats and monkeys. In monkeys, visual deprivation (via lid suture) leads to a massive loss of neurons in V1 that can be driven by the deprived eye. Experimentally induced blur during development leads to a selective loss of V1 neurons tuned to high spatial frequencies and the spatial tuning of neurons may be markedly different when tested through the two eyes. Experimentally induced strabismus disrupts the binocular connections of cortical neurons. It is difficult to draw distinctions based on the type of rearing from the physiology, because the effects of abnormal visual experience are complicated by the onset, duration, and depth of deprivation; however, there is evidence that the physiological deficits in amblyopia do not fully explain the behavioral losses (in the same monkeys), suggesting that there may be deficits downstream from V1.

The most dramatic changes in V1 involve alterations in binocularity. Specifically, neurons that appeared to be monocular often demonstrate clear binocular interactions during dichoptic stimulation. In strabismic (prism-reared) monkeys, there is marked binocular suppression during dichoptic stimulation suggesting that inhibitory connections are less susceptible to the effects of strabismus than excitatory connections. Interestingly, even very brief periods (just 3 days) of prism-induced strabismus at the height of the critical period (4 weeks in monkeys, which translates to about 4 months in humans) increased the prevalence of V1 neurons that exhibited binocular suppression without altering their sensitivity to interocular spatial phase disparity. This result suggests that the earliest change in V1 is increased binocular suppression and, importantly, that the suppression originates at a site downstream from where information from the two eyes is first combined.

Very much less is known about the physiological effects of amblyopia on visual areas downstream from V1. Brainimaging studies using positron emission tomography and functional magnetic resonance imaging show a clear deficit in V1, and several studies have also found deficits in other areas (e.g., V2). However, it is difficult to discern whether these downstream losses are simply a pass-through effect from V1 or whether the V1 losses are amplified downstream. However, several imaging and psychophysical

studies are consistent with the idea that the abnormalities in V1 are amplified in V2 and possibly beyond. These studies show losses in second-order detection global form and motion integration, symmetry detection, and counting.

Sensitive Periods for the Development of Amblyopia

Clinicians are well aware that amblyopia does not develop after 6–8 years of age, suggesting that there is a sensitive period for the development of amblyopia; however, in humans with naturally occurring amblyopia, the age of onset of the amblyogenic condition(s) is difficult to ascertain, and the effects of intervention combine to make it difficult to obtain a clear picture of the natural history of amblyopia development. Thus, much of our current understanding of the development of amblyopia accrues from animal studies, and from retrospective studies of clinical records. Technological improvements in infant testing have also provided more direct data on the development of naturally occurring amblyopia in humans and monkeys. All of these studies provide strong evidence for amblyopia induced by early deprivation.

While the upper limit for susceptibility of binocular interactions (binocular summation and stereopsis) is not yet certain, it appears to be later than that for acuity or contrast sensitivity in monkeys, and may extend to at least 7 or 8 years (and possibly more) in humans. Psychophysical studies of interocular transfer in humans with a history of strabismus provide an indirect estimate of the period of susceptibility of binocular connections. The results of both studies suggest that binocular connections are highly vulnerable during the first 18 months of life, and remain susceptible to the effects of strabismus until at least age 7 years.

Traditional Treatment of Amblyopia

For centuries, the primary treatment for amblyopia has consisted of patching or penalizing the fellow preferred eye, thus forcing the brain to use the weaker amblyopic eye. Typically, patients with mild to moderate amblyopia are prescribed complete occlusion for 2–6 waking hours per day, over several months to more than a year. Patients with moderate to severe amblyopia are often prescribed 6–10 h or more a day, and some clinicians recommend more aggressive full-time occlusion for severe amblyopia. As reported in a recent large-scale clinical study of children (3–8 years of age), the dose–response rate for occlusion is approximately 0.1 log unit (1 chart line) per 120 h of occlusion, and the treatment efficacy is 3–4 logMAR lines. The dose–response curve appears to plateau only after 100–400 h. The treatment outcome is dependent on

occlusion dose, the depth of amblyopia, binocular status, fixation pattern, the age at presentation, and patient compliance. Recent clinical studies suggest that atropine penalization may be just as effective as patching.

The notion that there is a sensitive period (or periods) for the development of amblyopia has often been taken to indicate that there is also a critical period for the treatment of amblyopia. This concept grew out of the work of Claude Worth in 1903. Worth suggested that the presence of a sensory obstacle (e.g., unilateral strabismus) arrested the development of visual acuity (amblyopia of arrest), so that the patient’s acuity remained at the level achieved at the time of onset of strabismus. In this view, the depth of amblyopia is a direct function of the age of onset of the sensory obstacle. Worth further suggested that, if amblyopia of arrest were allowed to persist, amblyopia of extinction could occur as a result of binocular inhibition. In Worth’s view, only this extra loss of sensory function (i.e., the amblyopia of extinction) could be recovered by treatment. Although this latter notion is open to question in the light of present knowledge, the ideas of Worth have had a powerful influence upon both clinicians and basic scientists. Many of our currently held concepts of amblyopia, such as plasticity, sensitive periods, and abnormal binocular interaction, were already described more than a century ago, and gained currency with the work of Hubel and Wiesel in 1970 and the many anatomical and physiological studies that followed. Consequently, while amblyopia can often be reversed when treated early, treatment is generally not undertaken in older children and adults. Below we consider both experimental and clinical evidence for plasticity in the adult visual system that calls into question the notion of a sensitive period for treatment.

Clinical Studies

It is often stated that humans with amblyopia cannot be treated beyond a certain age; however, a review of the literature suggests otherwise. Recent clinical trials suggest that in children, 2 h of patching per day may be just as effective as 6 h per day. Moreover, treatment may be just as effective in older (13–17 years) patients who have not been previously treated as in younger (7–12 years) children.

Plasticity in adults with amblyopia is also dramatically evident in the report of amblyopic patients whose visual acuity spontaneously improved in the wake of visual loss due to macular degeneration in the fellow eye. There are also reports suggesting that some adult amblyopes recover vision in their amblyopic eye following loss of vision in their fellow (nonamblyopic) eye. These studies are consistent with the notion that the connections from the amblyopic eye may be suppressed rather than destroyed. Loss of the fellow eye would allow these existing connections to be unmasked, as occurs in adult cats with retinal lesions (Figure 1).

Experimental Treatment of Amblyopia Beyond

the Sensitive Period

Adults are capable of improving performance on sensory tasks through repeated practice or perceptual learning (‘yes, you can teach old dogs new tricks!’), and this learning is considered to be a form of neural plasticity that also has consequences in the cortex. Specifically, in adults with normal vision, practice can improve performance on a variety of visual tasks, and this learning can be quite specific (to the trained task, orientation, eye, etc.). Interestingly, similar neural plasticity exists in the visual system of adults with naturally occurring amblyopia due to anisometropia and/or strabismus, suggesting that perceptual learning may be a useful approach for amblyopia treatment. Perceptual learning can improve visual functions in amblyopia on a wide range of tasks, including: Vernier acuity, positional acuity, contrast sensitivity, and letter identification. Practicing each of these tasks results in improved performance on the practiced task.

The specificity of perceptual learning noted above poses some interesting difficulties. If the improvement following practice was solely limited to the trained stimulus, condition and task, then the type of plasticity documented here would have very limited (if any) therapeutic value for amblyopia, since amblyopia is defined primarily on the basis of reduced Snellen acuity. Importantly, perceptual learning of many tasks (e.g., Vernier acuity, position discrimination, contrast sensitivity) appears to transfer, at least in part, to improvements in Snellen acuity, as does practicing contrast detection. In addition to visual acuity improvement, other degraded visual functions such as stereoacuity and visual counting improve as well.

Figure 1 The postnatal development of visual function. Cartoon illustrating visual functions (sehfunktion) developing at somewhat different rates, while the developmental potential (entwicklungspotenz, in the lower panel) dissipates over the years (Jahre). Reproduced from Teller, D. Y. and Movshon, J. A. (1986) Visual Development. Vision Research 26: 1483–1506.

Figure 2 Improvement in positional acuity (solid circles) and Snellen acuity (open circles) of a severe juvenile amblyope (observer AL, 8.8 years old, with unilateral strabismus). The triangle shows the improvement based on occlusion alone. The gray line shows the improvement based on occlusion alone (OT: occlusion therapy) in 2 amblyopes (aged 6–8) with acuities similar to that of AL. Replotted from Li et al., 2007; Stewart et al., 2004, 2005, 2007.

Perceptual Learning as a Clinical Tool for Treating Amblyopia

Occlusion therapy is the gold standard method for treating amblyopia. In all previous perceptual learning studies, the subjects are occluded while performing the visual task, so it is reasonable to ask whether active perceptual learning actually provides an added benefit over occlusion alone. Recent work suggests that occlusion plus perceptual learning may be more effective than occlusion alone (Figure 2). Combining occlusion with perceptual learning may be a useful method for obtaining the optimal treatment outcome in the shortest possible time. Eliminating or reducing the need to wear an eye patch in public would eliminate, or at the very least reduce, the emotional stress that often accompanies occlusion therapy.

Over the centuries, there have been numerous attempts to increase the effectiveness of treatment. These attempts have a long and chequered history, ranging from the sublime to the ridiculous, and include: subcutaneous injection of strychnine, electrical stimulation of the retina and optic nerve, flashing lights, red filters and rotating gratings, administration of Levodopa/Carbidopa and shocks to the brain via transcranial magnetic stimulation. Few were subjected to rigorous scrutiny, and those that were often failed to stand up to it. Thus, any promising new method should be examined critically and there is a clear need for careful controlled studies.

Acknowledgment

See also: Astigmatism.

Further Reading

Ciuffreda, K. J., Levi, D. M., and Selenow, A. (1991).

Amblyopia: Basic and Clinical Aspects. Stoneham, MA: Butterworth-Heinemann.

Fahle, M. (2004). Perceptual learning: A case for early selection.

Journal of Vision 4: 879–890.

Harwerth, R. S., Smith, E. L., III, Duncan, G. C., Crawford, M. L. J., and von Noorden, G. K. (1987). Multiple sensitive periods in the development of the primate visual system. Science 232:

235–238.

Hubel, D. H. and Wiesel, T. N. (1970). The period of susceptibility to the physiological effects of unilateral eye closure in kittens. Journal of Physiology (London) 206: 419–436.

Kiorpes, L. (2006). Visual processing in amblyopia: Animal Studies.

Strabismus 14: 3–10.

Levi, D. M. (2006). Visual processing in amblyopia: Human studies.

Strabismus 14: 11–19.

Levi, D. M. and Carkeet, A. (1993). Amblyopia: A consequence of abnormal visual development. In: Simons, K. (ed.) Early Visual Development, Normal and Abnormal, pp. 391–408. Oxford: Oxford University Press.

Levi, D. M. and Polat, U. (1996). Neural plasticity in adults with amblyopia. Proceedings of the National Academy of Sciences of the United States of America 93: 6830–6834.

Li, R. W., Provost, A., and Levi, D. M. (2007). Extended perceptual learning results in substantial recovery of positional acuity and visual acuity in juvenile amblyopia. Investigative Ophthalmology and Vision Science 48: 5046–5051.

Mckee, S. P., Levi, D. M., and Movshon, J. A. (2003). The pattern of visual deficits in amblyopia. Journal of Vision 3: 380–405.

Polat, U., Ma-Naim, T., Belkin, M., and Sagi, D. (2004). Improving vision in adult amblyopia by perceptual learning. Proceedings of the National Academy of Sciences of the United States of America 101: 6692–6697.

Revell, M. J. (1971). Strabismus: A History Orthoptic Techniques. London: Barrie and Jenkins.

Stewart, C. E., Fielder, A. R., Stephens, D. A., and Moseley, M. J. (2005). Treatment of unilateral amblyopia: factors influencing visual outcome. Investigative Ophthalmology and Vision Science 46: 3152–3160.

Stewart, C. E., Moseley, M. J., Stephens, D. A., and Fielder, A. R. (2004). Treatment dose-response in amblyopia therapy: The Monitored Occlusion Treatment of Amblyopia Study (MOTAS).

Investigative Ophthalmology and Vision Science 45: 3048–3054. Stewart, C. E., Stephens, D. A., Fielder, A. R., and Moseley, M. J.

(2007). Modeling dose-response in amblyopia: toward a child-specific treatment plan. Investigative Ophthalmology and Vision Science 48: 2589–2594.

Teller, D. Y. and Movshon, J. A. (1986). Visual Development. Vision Research 26: 1483–1506.

Vereecken, E. P. and Brabant, P. (1984). Prognosis for vision in amblyopia after the loss of the good eye. Archives of Ophthalmology 102: 220–224.

Wiesel, T. N. (1982). Postnatal development of the visual cortex and the influence of environment. Nature 299: 583–591.

Worth, C. A. (1903). Squint: Its Causes, Pathology and Treatment. Philadelphia: The Blakiston.

Wu, C. and Hunter, D. G. (2006). Amblyopia: Diagnostic and therapeutic options. American Journal of Ophthalmology 141: 175–184.

Glossary

Accommodation – Increase in optical power by the eye in order to maintain a clear image (focus) as objects are moved closer. It occurs through a process of ciliary muscle contraction and zonular relaxation that causes the elastic-like lens to round up and increase its optical power. Natural loss of accommodation with increasing age is called presbyopia.

Amblyopia – Decreased vision in one or both eyes due to an amblyogenic factor (e.g., refraction, strabismus, and cataract) without detectable anatomic damage in the eye or visual pathways. Asthenopia – Vague eye discomfort arising from use of the eyes; it may consist of eyestrain, headache, and/or brow ache. It may be related to uncorrected refractive error or poor fusional amplitudes. Astigmatism – Optical defect in which refractive power is not uniform in all directions (meridians). Light rays entering the eye are bent unequally by different meridians that prevent formation of a sharp image focus on the retina.

Convergence – Inward movement of both eyes toward each other, usually in an effort to maintain single binocular vision as an object approaches. Cycloplegic – An agent (typically eye drops) that paralyzes the accommodation system of the crystalline lens to eliminate variability in retinoscopy or refraction measures.

Emmetropization – An active growth process in which the eye grows toward a refractive error of plano.

Esotropia – Eye misalignment in which an eye deviates inward (toward nose) while the other fixates normally.

Strabismus – Eye misalignment caused by extraocular muscle imbalance: one fovea is not directed at the same object as the other.

Definition and Classifications of

Hyperopia

Hyperopia, also termed hypermetropia or farsightedness, is a common refractive error in children and adults.

In a hyperopic eye, parallel rays of light entering the eye reach a focal point behind the plane of the retina, while accommodation is in a relaxed state. Hyperopia can produce variable symptoms, depending on the magnitude of hyperopia, the age of the individual, the status of the accommodative and convergence systems, and the demands placed on the visual system (distance vs. near). Individuals with uncorrected hyperopia may experience symptoms such as blurred vision, asthenopia, accommodative/binocular dysfunction, amblyopia, and/ or strabismus.

The vast majority of cases of hyperopia are of a physiological nature. In terms of physiological optics, hyperopia occurs when the axial length of the eye is shorter than the refracting components the eye requires for light to focus precisely on the photoreceptor layer of the retina. Hyperopia may result in combination with or isolation from a relatively flat corneal curvature, insufficient crystalline lens power, increased lens thickness, short axial length, or variance of the normal separation of the optical components of the eye relative to each other. Astigmatism, the most common refractive error, is often present in conjunction with hyperopia. High hyperopia is associated with high levels of astigmatism, suggesting a breakdown in the process of emmetropization that results in a component-type refractive error. Hereditary factors are probably responsible for most cases of refractive error, including physiologic hyperopia, with environment playing some role in influencing the development and degree of the error.

The American Optometric Association Clinical Practice Guideline has outlined the classifications for hyperopia in the following ways:

1.Hyperopia can be classified on the basis of structure and function. These three classifications are based solely on the structure of the eye:

. simple hyperopia, due to normal biological variation, can be of axial or refractive etiology;

. pathological hyperopia is caused by abnormal ocular anatomy due to mal-development, ocular disease, or trauma; and

. functional hyperopia results from paralysis of accommodation.

2.Clinically, hyperopia may also be categorized based on degree of the refractive error. The magnitude of hyperopia can be classified in the following three ways:

. low hyperopia consists of an error of þ2.00 diopters

(D)or less;

. moderate hyperopia includes a range of error from þ2.25 to þ5.00 D;

. high hyperopia consists of an error over þ5.00 D.

3.An additional classification may be based upon the outcome of noncycloplegic and cycloplegic (1.0% cycloplentolate) refractions and takes the patient’s accommodative system in consideration:

. manifest hyperopia, the amount of refractive error that is detected by noncycloplegic refraction;

. latent hyperopia, the amount of refractive error that is detected only by cycloplegia, can be overcome by accommodation under noncycloplegic conditions.

The sum of latent and manifest hyperopia is equal to the magnitude of hyperopia.

Active accommodation mitigates some or all of hyperopia’s adverse effects on vision. The impact of accommodation is highly dependent on age, the amount of hyperopia and astigmatism, the status of the accommodative and vergence systems, and the demands placed upon the visual system. Latent hyperopia is typically overcome in the young patient by the action of accommodation, but may not be sustainable for long periods of time under conditions of visual stress. Signs and symptoms such as blurred vision, asthenopia, accommodative and binocular dysfunction, and strabismus may develop. These signs and symptoms occur more readily and to a greater degree in manifest hyperopia. In general, younger individuals with lower degrees of hyperopia and moderate visual demands are less adversely affected than older individuals, who have higher degrees of hyperopia and more demanding visual needs.

Pathological hyperopia is a rarer type of hyperopia, is typically greater in magnitude, and may be due to several etiologies: mal-development of the eye during the prenatal or early postnatal period, a variety of corneal or lenticular changes, aphakia, chorioretinal or orbital inflammation or neoplasms, neurologicalor pharmacologicalbased etiologies, microor nan-ophthalmia, anterior segment malformations, and acquired disorders. A number of congenital and/or genetic developmental disabilities and syndromes are also associated with high hyperopia.

Prevalence

Although it is difficult to discuss the prevalence of hyperopia due to variations in its definition by researchers (e.g., with or without cycloplegia, spherical equivalent, and least hyperopic meridian), the prevalence of hyperopia is age related. Most full-term infants are mildly hyperopic (approximately þ2.00 D), while premature infants and those of low birth weight tend to be either less hyperopic or myopic (approximately þ0.24 D). The prevalence of

Figure 1 Comparison of refractive error distributions between newborns and children illustrates a shift away from hyperopia during the emmetropization process. Reprinted from Cotter,

S. A. (2007). Management of childhood hyperopia: A pediatric optometrist’s perspective. Optometry and Vision Science 84(2): 103–109.

refractive error among full-term infants has a normal bell-shaped distribution (see Figure 1). Up to 9% of 6–9-months-old infants have hyperopia greater than þ3.25 D, but this prevalence decreases to 3.6% in the 1-year-old population. Over the next 10–15 years of life, there is a further decrease in the prevalence of hyperopia and an increase in the frequency of myopia. With the development of presbyopia, latent hyperopia becomes manifest, contributing to an apparent increase in the prevalence of hyperopia.

Normal Time Course of Hyperopia

Emmetropization results in a gradual decrease in the level of hyperopia in most patients (see Figure 2), but in patients who have high degrees of hyperopia the change occurs more rapidly. However, infants with high hyperopia are more likely to remain significantly hyperopic throughout childhood. These infants may also have an increased incidence of against-the-rule astigmatism, which appears to further decrease the reduction in hyperopia during emmetropization compared to hyperopic infants without significant astigmatism.

During the school years, there is a slow but continued decreasing trend in the incidence and the magnitude of hyperopia, except in patients with high hyperopia, whose refractive error is more likely to remain relatively unchanged. During the years of presbyopia development, latent hyperopia may become manifest requiring the implementation of both distance and near correction, yet in older individuals (>75 years of age) a myopic refractive shift may ensue likely due to crystalline lens changes.

Age, y

Figure 2 Mean spherical equivalent refractive errors, as reported by several studies, plotted by age. A smooth curve (single exponential function) was plotted to illustrate the change in refractive error with age. Reprinted from Mayer, L., Hansen, R., Moore, B., Kim, S., and Fulton, A. (2001) Cycloplegic refractions in healthy children aged 1 to 48 months. Archives of Ophthalmology 119: 1625–1628.

Clinical Presentations of Hyperopia

Young persons with hyperopia generally have sufficient levels of accommodation to maintain clear vision without producing asthenopia symptoms. However, when the level of hyperopia is too great or the accommodative reserves are insufficient due to age or fatigue, blurred vision and asthenopia may develop. Presbyopia brings an increase in absolute hyperopia, causing blur, especially at near. The influence of accommodation on the vergence system also plays a role in the presence or absence of symptoms in patients with hyperopia. Individuals with esophoria and inadequate negative fusional vergence ability are frequently symptomatic and may become esotropic as a result of the uncorrected hyperopia.

Among the signs and symptoms of hyperopia are red or tearing eyes, squinting and facial contortions while reading, ocular fatigue or asthenopia, frequent blinking, constant or intermittent blurred vision, focusing problems, decreased binocularity and eye–hand coordination, and difficulty with or aversion to reading. The presence and severity of these symptoms varies widely. Some young patients with hyperopia, including those with moderate and high hyperopia, may be relatively free of signs and symptoms.

Early detection of hyperopia may help prevent the complications of strabismus and amblyopia in young children. In older children, uncorrected hyperopia may affect learning abilities and in individuals of any age, it can contribute to ocular discomfort and visual inefficiency.

Risks of Uncorrected Hyperopia

The major complications of moderate and high physiologic hyperopia in children are amblyopia and strabismus.

Infants with moderate to high hyperopia (>+3.50 D) are up to 13 times more likely to develop strabismus by 4 years of age if left uncorrected, and they are 6 times more likely to have reduced visual acuity than infants with low hyperopia or emmetropia. Children who had significant hyperopia during infancy are much more likely to develop amblyopia and strabismus by 4 years of age. The presence of anisometropic hyperopia further increases the risk of strabismus and amblyopia, especially if found beyond 3 years of age. The American Optometric Association has published guidelines stating that levels greater than 1.00 D of hyperopic anisometropia and 5.00 D of isometropic hyperopia are amblyogenic.

Early detection and treatment of hyperopia may reduce the incidence and severity of consequential amblyopia and strabismus and is a major justification for universal vision evaluation of young children.

Importance of Early Detection of

Significant Hyperopia

Atkinson and colleagues showed that uncorrected hyperopia (>3.5 D in one meridian) might contribute to poor motor and cognitive development in younger children (9 months to 5.5 years) and/or learning problems in some older children. The precise mechanism of this relationship is unclear, but optical blur, accommodative and binocular dysfunction, and fatigue all appear to play roles. In fact, uncorrected infant hyperopia has been associated with mild delays in visuo-cognitive and visuo-motor development, but has appeared to reach the level of their emmetropic counterparts after 6 weeks of full time hyperopic spectacle wear in 3–5-year-olds. The substantial number of school-age children and young adults who have uncorrected significant hyperopia is evidence of the potential impact of this learning-related vision problem and the need for early detection screening programs.

Examination Techniques of Hyperopia

Optical correction should be based on both static (normal accommodation) and cycloplegic (e.g., 1% cyclopentolate) retinoscopy, accommodative and binocular assessment, and AC/A (accommodative convergence/ accommodation) ratio. The correction should then be modified as needed to facilitate binocularity and compliance. Plus-power spherical or sphero-cylindrical lenses are prescribed to shift the focus of light from behind the eye to a point on the retina. Accommodation plays an important role in determining the prescription. Some older patients with hyperopia do not initially tolerate the full correction indicated by the manifest refraction, and many patients with latent hyperopia do not tolerate the full correction of hyperopia indicated under cycloplegia.

However, young children with accommodative esotropia and hyperopia generally require only a short period of adaptation to tolerate full optical correction. Patients with latent hyperopia who prove intolerant to the use of full or partial hyperopic correction may benefit from initially wearing the correction only for near viewing; or alternatively, trial use of a short-acting cycloplegic agent may enhance acceptance of the optical correction. Patients with absolute hyperopia are more likely to accept nearly the full correction, because they typically experience immediate improvement in visual acuity.

Management of Hyperopia

The specific elements of treatment (e.g., final spectacle prescription) should be tailored to individual patient needs. Among the factors to consider when planning treatment and management strategies are: the magnitude of the hyperopia (under dry and cycloplegic conditions), the presence of astigmatism and/or anisometropia, the patient’s age, the presence of an associated esotropia and/or amblyopia, the status of the accommodative and convergence systems, the demands placed on the visual system, and any symptoms.

Among several available treatments for hyperopiarelated symptoms, optical correction of the refractive error with spectacles and contact lenses is the most commonly used modality. Newer high-index lens materials and aspheric lens designs have reduced the thickness and weight of high plus-power lenses, increasing wear ability and patient acceptance. Spectacles, especially those with lenses of polycarbonate material, provide protection against trauma to the eye and orbital area and are imperative in children.

Soft or rigid contact lenses are an excellent alternative for some patients. Contact lenses not only provide better cosmesis and compliance, but they reduce aniseikonia in persons with anisometropia, improving binocularity. Multifocal or monovision contact lenses may be considered for patients who require additional near correction, but resist the use of multifocal spectacles because of their appearance. Patients who wear contact lenses are at increased risk for ocular complications due to corneal hypoxia, mechanical irritation, or infection; but nevertheless, improved vision makes contact lens wear a valuable treatment option for compliant patients.

Vision therapy and modification of the patient’s habits and environment can be important in achieving definitive long-term remediation of symptoms. Such modifications include, but are not limited to, improved lighting, longer near working distances, using better-quality-printed material, taking frequent breaks when reading or working on a computer for sustained periods of time. These modifications all work to reduce the accommodative

demand placed on the patient and can allow, irrespective of spectacle wear, the patient to perform their daily near activities with less symptoms.

Several refractive surgery techniques to correct hyperopia are under development. The major procedures currently being studied as possible therapies for hyperopia are – Holmium: YAG laser thermal keratoplasty, automated lamellar keratoplasty, spiral hexagonal keratotomy, excimer laser, and clear lens extraction with intraocular lens implantation. The American Academy of Ophthalmology has recently reviewed 36 research articles studying the efficacy and safety of refractive surgery for hyperopia and found that the surgery provides an effective and safe correction for lower ranges of hyperopia (<3.00 D). Although still considered to be investigative on a long-term treatment basis, laser-assisted in situ keratomileusis (LASIK) is Food and Drug Administration (FDA) approved for hyperopia up to þ6.00 D.

There is no universal approach to the treatment of hyperopia. The goals of treatment are to reduce accommodative demand and to provide clear, comfortable vision and normal binocularity at all distances. It is not simply determination of the lens power required to focus light onto the retina, but a complex approach encompassing the patient’s visual needs, magnitude of accommodation, coexisting amblyopia and/or strabismus, and sensitivity. The following are specific management strategies appropriate for different age groups and conditions as outlined by the American Optometric Association’s Clinical Guidelines for Hyperopia.

Young children (birth–10 years of age) with low to moderate hyperopia, but without strabismus, amblyopia, or other significant vision problems, usually require no treatment. However, even occasional evidence of decreased visual acuity, binocular anomalies, or functional vision problems may signal the need for treatment. Whereas the effects of uncorrected hyperopia may manifest as visual perceptual dysfunction, reading difficulties, or failure in school, any child with hyperopia who is experiencing learning or other school difficulties needs careful assessment and may require treatment.

In most young hyperopic children, the process of emmetropization leads to a gradual reduction in the degree of hyperopia by 5–10 years of age. Some children do not go through this process, however. They remain significantly hyperopic and at increased risk for developing strabismus and amblyopia. Patients under age 5 who have hyperopia over 3.25 D appear to benefit from early optical correction to reduce the risk for strabismus and amblyopia. Clinical pediatric studies suggest that partial hyperopic prescriptions do not impede infants’ emmetropization by 36 months.

Optical correction of hyperopia should generally be prescribed for young children who have moderate to high hyperopia. However, there are many differences in

prescribing patterns within and between pediatric optometrists and ophthalmologists. Lyons and colleagues surveyed pediatric optometrists and ophthalmologists prescribing thresholds for hyperopia in 2-year-olds and found that 65% of pediatric optometrists used þ3.0 D of bilateral asymptomatic hyperopia as their threshold for prescribing and 25% used þ5.0 D, while pediatric ophthalmologists had less conservative thresholds with 66% using þ5.0 D and 25% using þ3.0 D. It should also be prescribed, along with other interventions (e.g., occlusion or active vision therapy), for all young patients with actual or suspected amblyopia or strabismus. Optical correction may be deferred for some patients with moderate hyperopia, but such patients should be considered at risk and re-examined periodically.

Careful follow-up is essential, and frequent lens changes may be needed. It is not unusual for a significant increase in hyperopia to occur after optical correction has been worn for even a short time, due to the manifestation of latent hyperopia. It is also important to continually monitor for the presence of an esotropia during all follow-up visits. When compliance proves difficult, the clinician may encourage acceptance of the prescribed treatment by using cycloplegic agents to blur uncorrected vision. Contact lenses may be a good alternative for patients who do not comply with prescriptions for spectacle wear, especially those with anisometropia, high hyperopia with or without nystagmus, and hyperopia with accommodative esotropia.

Special consideration should be given to several specific categories of problems in young children who have significant hyperopia. Prior to the onset of accommodative esotropia, which usually becomes evident at about 2–3 years of age, few children exhibit obvious signs of ocular problems, with the exception of intermittent esotropia in children who are ill or very tired. Early screening for refractive error usually detects hyperopia, but due to the relative infrequency of refractive screening, many children with underlying moderate to high hyperopia go undetected until the appearance of frank strabismus. Appropriate treatment includes the use of either single vision or multifocal spectacles depending on the patient’s binocular and accommodative status. Concurrent amblyopia, when present, may be treated by patching and active vision therapy.

Less commonly, young children with bilateral high hyperopia develop isoametropic amblyopia due to the resulting constant state of severely blurred vision. Such patients may have an associated esotropia, or conversely, may not manifest esotropia because they make no attempt to accommodate. Optical correction of this condition is indicated in order to prevent or treat the associated amblyopia and/or strabismus; however, careful monitoring is warranted a previously nonexistent esotropia may present itself following correction. Partial correction may

inadvertently stimulate accommodative esotropia, because the patient now has good reason to attempt to overcome the remaining uncorrected hyperopia. Treatment to improve vision in the child with amblyopia may take a few years, but improvement is usually possible with full time spectacle wear and/or patching or pharmacological penalization.

Many persons between the ages of 10 and 40 years who have low hyperopia require no correction because they have no symptoms. Ample accommodative reserves shelter them from visual problems related to their hyperopia. Under increased visual stress, such persons may develop symptoms that require correction. Wearing prescribed lenses with low amounts of plus power usually alleviates the problem. Patients with moderate degrees of hyperopia are more likely to require at least part-time correction, especially those who have significant near demands or have accommodative or binocular anomalies. Accommodative or binocular dysfunction associated with uncorrected low to moderate hyperopia may be treated by optical correction or vision therapy. Vision therapy may be instituted initially or after optical correction in patients who have significant binocular vision problems. The effects of visual habits and environment play an increasing role in determining the need for and characteristics of treatment.

By the age of 30–35 years, most previously asymptomatic, uncorrected hyperopic patients begin to experience blur at near and visual discomfort under strenuous visual demand. Facultative hyperopia can no longer be sustained comfortably due to decreasing accommodative amplitudes. Latent hyperopia should be suspected when symptoms occur in conjunction with lower amplitude of accommodation than expected for the patient’s age. Cycloplegic retinoscopy can help identify this latent component. By the mid-1930s, accommodation takes noticeably longer while facility decreases, causing associated visual problems in many hyperopic persons previously free of symptoms. A prescription for the distance manifest (noncycloplegic) refraction for the patient to wear as needed (i.e., part time at near) often suffices. The patient may require additional correction with increasing age and visual demands at near. Before prescribing a permanent pair of spectacles, the optometrist may lend the patient a pair of spectacles (i.e., over-the-counter reading glasses) to demonstrate the potential benefits of optical correction of latent hyperopia.

With the onset of presbyopia (loss of accommodation), maintaining focus at near becomes progressively more difficult, especially in poor illumination. Prescribing an optical correction for most or all of the distance manifest refraction, along with a near addition, can greatly improve vision and comfort. Hyperopia equal to or greater than þ1.00 D to þ1.50 D generally requires full-time distance correction, with a near addition for patients over about

age 45. As facultative hyperopia becomes absolute, more plus power at distance is required. Progressive multifocal lenses enable clear focusing at a range of finite distances. A monovision, bifocal, or multifocal contact lens prescription is an option in some patients.

Physiological hyperopia is not progressive. Therefore, the prognosis, which can be given at diagnosis, is generally excellent, except for those patients with both hyperopia and amblyopia or strabismus, for whom it is less certain. Appropriate optical correction almost always leads to clear and comfortable single binocular vision. Younger children who have significant hyperopia associated with amblyopia, strabismus, or anisometropia require intensive follow-up and treatment for their more complex problems, starting as early as 3–6 months of age. The timing of periodic preventive optometric care for uncomplicated hyperopia depends on the patient’s age and circumstances. For children with hyperopia, follow-up may be required as often as every 3–6 months depending on the concern for strabismus and/ or amblyopia, while for asymptomatic adults, every 1 or 2 years is generally sufficient.

The underlying cause, rather than hyperopia itself, is the chief concern in patients with pathologic hyperopia. Because the causes of pathologic hyperopia are both uncommon and diverse, general statements concerning treatment must be limited to the need to correct the hyperopia in the best manner possible, depending on the underlying etiology. Conditions of a developmental or anatomic nature are rarely progressive. When useful vision is thought to be obtainable, the treatment of hyperopia resulting from nonprogressive conditions is similar to that for physiologic hyperopia. Patients with pathological hyperopia require treatment of their underlying conditions and, when indicated, referral to another eye care provider for special services. All patients treated for hyperopia with persistent symptoms require additional follow-up care to remediate their problem.

Conclusion

Hyperopia is a common refractive disorder that has a close association with other consequential disorders, namely amblyopia and strabismus, especially in children. This makes hyperopia a greater risk factor for more permanent vision loss than myopia. In addition, it appears that uncorrected hyperopia has a detrimental effect on a child’s learning and development. Therefore, the early diagnosis

and treatment of significant hyperopia and its consequences can prevent a significant amount of visual disability in the general population. Because hyperopia is usually not readily apparent, preventive examination of all young children is essential. Although there is no clear consensus on the prescribing practices for hyperopia, clinicians must examine the visual needs and binocular system of each patient to best determine their final treatment plan. Periodic eye examinations are needed thereafter to help ensure the provision of treatment appropriate to the changing visual needs of the hyperopic patient.

See also: Abnormal Eye Movements due to Disease of the Extraocular Muscles and Their Innervation; Amblyopia.

Further Reading

AOA Consensus Panel on Care of the Patient with Hyperopia (1997). American Optometric Association Clinical Practice Guidelines: Hyperopia. http://www.aoa.org/documents/CPG-16.pdf (accessed Jun. 2009).

Atkinson, J., Anker, S., Nardini, M., et al. (2002). Infant vision screening predicts failures on motor and cognitive tests up to school age. Strabismus 10(3): 187–198.

Atkinson, J., Braddick, O., Nardini, M., and Anker, S. (2007). Infant hyperopia: Detection, distribution, changes and correlates – outcomes from the Cambridge infant screening programs. Optometry and Vision Science 84(2): 84–96.

Atkinson, J., Nardini, M., Anker, S., Braddick, O., Hughes, C., and Rae, S. (2005). Refractive errors in infancy predict reduced performance on the movement assessment battery for children at 3½ and 5½ years. Developmental Medicine and Child Neurology

47: 243–251.

Cotter, S. A. (2007). Management of childhood hyperopia: A pediatric optometrist’s perspective. Optometry and Vision Science 84(2): 103–109.

Donahue, S. P. (2007). Prescribing spectacles in children: A pediatric ophthalmologist’s approach. Optometry and Vision Science 84(2): 110–114.

Guzowski, M., Wang, J. J., Rochtchina, E., Rose, K. A., and Mitchell, P. (2003). Five-year refractive changes in an older population: The blue mountains eye study. Ophthalmology 110(7): 1364–1370.

Lee, K. E., Klein, B. E. K., Klein, R., and Wong, T. Y. (2002). Changes in refraction over 10 years in an adult population: The beaver dam eye study. Investigative Ophthalmology and Visual Science 43(8):

2566–2571.

Lyons, S. A., Jones, L. A., Walline, J. J., et al. (2004). A survey of clinical prescribing philosophies for hyperopia. Optometry and Vision Science 81(4): 233–237.

Mayer, L., Hansen, R., Moore, B., Kim, S., and Fulton, A. (2001). Cycloplegic refractions in healthy children aged 1 to 48 months.

Archives of Ophthalmology 119: 1625–1628.

Varley, G. A., Huang, D., Rapuano, C. J., et al. (2004). LASIK for hyperopia, hyperopic astigmatism, and mixed astigmatism: A report by the American Academy of Ophthalmology. Ophthalmology 111(8): 1604–1617.

A

AAV see Adeno-associated virus Abducens nerve (CNVI) 17

abnormal eye movements from disorders of 42 LR innervated by 18–19, 19f

Aberrations 193 Ablation profile 193

Abnormal eye movements see also Eye movements EOM and 39, 40f, 41f

brainstem disorders and horizontal movements 40f, 42 brainstem disorders and vertical movements 41f, 43 CNVI, CNIII, CNIV disorders effecting 42 congenital misalignment 43

disorders effecting 39 NMJ disorders and 40, 40f

visual system disorders effecting 44 AC see Adenylyl cyclase; Artificial cornea

ACAID see Anterior chamber-associated immune deviation

Acanthamoeba keratitis 413

adaptive immune system’s resistance to 415 evading 416, 417t

barriers to 414

innate immune system’s resistance to 414, 415, 415t macrophages and 414

mucosal immune system and 416, 416t neutrophils and 414

trophozoites for 417 Accommodation 487, 517, 529

hyperopia and 530 Acinar cells 83

in lacrimal gland 68, 69f, 83, 84f

electrolyte/water secretion mechanisms by 72, 73f in meibomian glands 62–63

Acinus 60, 68 Actinic lesion 91

Active innate immune system see Innate immune system, active Acuity see Visual acuity

ACV see Acyclovir

Acyclovir (ACV) 306–308, 308t Adaptive immune system 347, 367

Acanthamoeba keratitis and 415 evading 416, 417t

antigen trafficking, processing and T cell presentation in 348, 349f innate immune system’s link to 359

PRRS in 347–348

ADDE see Aqueous deficient dry eye Adenine nucleotide translocator 27

transporter 1 (Ant1) 30 transporter 2 (Ant2) 30

Adeno-associated virus (AAV) 330, 331f Adenosine diphosphate (ADP) 27 Adenosine triphosphate (ATP) 27, 284, 288

EOM and buffering system of 28–29 EOM mitochondria generating 31–32 synthase 30–31, 31f

Adenylate cyclase soluble 288

VIP signal transduction and 87, 87f Adenylate kinase (AK) 28–29 Adenylyl cyclase (AC) 87

Adherens junctions (AJs) 219, 286–287

corneal epithelial wound healing and 167, 167t Adhesion complex 143

cell-matrix junctions and 167 hemidesmosomes of 145, 145f

Adhesion molecules 359

corneal epithelium infection response of 455 ADP see Adenosine diphosphate

Adrenergic agonists, signal transduction and 88 Ca2+ and PKC 88, 88f

MAPK 88f, 89 NO 88f, 89

Afferent immune response 390

in autoimmune-based inflammation 386, 386f

corneal graft rejection, mechanisms/components of 392 direct/indirect allorecognition 392 histocompatibility antigens 392

T-lymphocyte activation 393 immunoregulation and 385

AFM see Atomic force microscopy Against-the-rule 506, 507

Age-related macular degeneration (AMD) 378 AJs see Adherens junctions

AK see Adenylate kinase

AKC see Atopic keratoconjunctivitis Akt1 406

Aldehyde dehydrogenase (ALDH) 223 ALDH see Aldehyde dehydrogenase Alignment testing 46

Alkali burn 333

ALL see Anterior limiting lamella Allergen 419

Allergic conjunctivitis 419 Allergic eye disease 114

APCs and 378

Allergies see Ocular allergies Alloantigen 327, 361, 390 Allogeneic 185

Allograft 470

see also Keratolimbal allograft rejection 481

Alloimmunity 478

Alloreactive 390 Alpha-melanocyte-stimulating hormone 369 Alternative splicing 116

AM see Amniotic membrane transplantation Amblyopia 39, 91, 419, 525, 529

as public health problem 525

sensitive periods for development of 526 sites of 525

treatment for 47

clinical studies on 527, 527f

perceptual learning as tool for 527, 528f traditional 526

types of 525

AMD see Age-related macular degeneration Amidases 303

Amniotic membrane transplantation (AM) 139 for CESC culture 187

clinical outcome of 189 indications for 188, 188f

postoperative management for 187t, 189 procedure for 188

surgical procedure for 189 for fibrotic scarring 269 history/concepts of 187

ocular surface reconstruction and 188 AMPs see Antimicrobial peptides Amyloid 226

Androgens 75

Angioblast 465 Angiogenesis 465, 470

corneal avascularity as study platform for 482 process of 470

Angiogenic molecules bFGF 467

in CNV 466

in corneal angiogenic privilege 473, 473t lipid mediators 475

MMPs 475

VEGF 473

Angiogenic privilege see Corneal angiogenic privilege Angiostatin 475, 480

Anion transporters 285, 285f Aniridia 478

Aniridic keratopathy 185