Chapter 46
The Eye and Reading Disorders
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Reading is the foundation of education. Books, papers, articles, and lecture notes all rely on reading to convey the ideas and thoughts used in the educational process. Reading difficulties can lead to lifelong problems that can affect self-esteem, education, vocation, socialization, or daily living activities. Therefore, reading disorders have been the subject of considerable thought and study as their cause and treatment have been explored. Parents, teachers, and physicians all feel the frustration when dealing with this important and complex issue. Unfortunately, quick fix remedies often add to this frustration. This chapter discusses how we read, the current theories on what causes some people to have difficulty reading, and the treatment of reading disorders. Evaluation of treatment methods based on the erroneous belief that reading difficulties are caused by a dysfunction of vision also are evaluated. Finally, the role of the ophthalmologist when faced with these issues is discussed.
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In 1896, Hinshelwood gave a detailed description of a 45-year-old man with dyslexia.1 He credited the term dyslexia to Berlin.2 Samuel Orton, a neurophychiatrist, provided the first insight into the etiology and treatment of dyslexia in 1925. He theorized that dyslexia was caused by a dysfunction in visual perception and vision memory, which was caused by a maturational lag. Treatment, he believed, should be educationally based through the use of tutorials.3 Unfortunately, a full century after its initial description, the etiology and treatment of dyslexia still is an issue of controversy.
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The terms reading disability and dyslexia often are used interchangeably. Dyslexia refers to the ina-bility to develop the capability to read, at an expected level, despite an otherwise normal intellect. Most dyslexics also display poor writing ability. Dyslexia is a primary reading disorder and should be separated from other secondary forms of reading difficulties. Secondary reading disorders include the following: mental retardation; environmental deprivation; educational deprivation; and physical, or organic, diseases. Because there is no one standard test for dyslexia, the diagnosis usually is made by comparing reading ability with intelligence and standard reading expectations.
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Because a universal definition of dyslexia is lacking, it is difficult to arrive at a consensus of the incidence of the disorder from the literature. Most studies suggest an incidence of 5% to 10% of the school-aged population in the United States. It had been thought that boys outnumbered girls by a ratio of 2:1 to 5:1.4,5 However, this prevalence may be a reflection of school referral bias. In a study of students from the Connecticut Longitudinal Study, Shaywitz and associates found a research-identified incidence of reading disability of 8.7% of boys and 6.9% of girls.6 However, a teacher-identified incidence of the same population identified 13.6% of boys and only 3.2% of girls. The authors suggest that greater reports of behavioral difficulties among boys in the classroom may have lead to this bias. Other studies also document a discrepancy in the diagnosis of learning-disabled children between school officials and research teams.7 Until a universally agreed on definition is found, the exact incidence of dyslexia will be difficult to determine.
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In 1879, the French ophthalmologist Javal provided the first description of the eye movements during reading. He noted that the eyes moved in small steps, saccades, from left to right with moments of steady fixation between these saccades. A small percentage of saccades also were made from right to left. Legein and Bouma recently detailed the complex phenomena of ordinary reading.8

Visual information is perceived during periods of fixation. This accounts for 90% of our time reading. Approximately 85% of fixations take place after forward saccades and 15% after backward saccades.9,10 Backward saccades are thought to play a role in comprehension of previously read text. Short words are read with one fixation and longer words are read with two, one at the beginning and the end of the word.10,11 The duration of a fixation varies with the difficulty of the test being read. Fixations may last from 45 to 450 msec, with the mean being approximately 180 msec.9 Because it takes about 90 msec to generate a saccade after a neural impulse derived from the retina, some fixations are so short that the text is not perceived before a new saccade is initiated. It is therefore thought that some saccades generated during reading are controlled by a reflex not associated with fixation.

Saccades during reading bring a new area of text onto the fovea. Unlike the fixation period, it is believed that visual perception is suppressed during saccades. The average distance of a saccade is 2 degrees, or about eight letters of average-sized text.9 The length of saccades varies between readers and affects the speed of reading.12 Saccade length is dependent on the individual's ability to recognize letters and combinations of letters outside of the central visual field, the difficulty of the text being read, and the length of the word before the saccade. A longer word to the right of the new area of regard gives rise to a shorter saccade.11–13

The average backward saccade, or regression, is one half the length of a forward saccade and covers about four letters. These regressions are thought to aid in text comprehension by validating previously read words. Regressions account for approximately 15% of all saccades but increase with the difficulty of the text.9,13,14

Because eye movements of dyslexic readers are similar to those of beginning readers, it is helpful to understand the eye movements seen in early readers. A beginning reader reads slower than an experienced reader. This increased time results from longer fixations, increased number of fixations, shorter saccade length, and more regressions. The early reader averages almost twice the number of fixations and regressions, fixates twice as long, and travels only half as far with each saccade as a better reader.15–17 As the child's reading improves with age, the child decreases fixation number and time and lengthens saccade distance. A child approaches almost two thirds of an adult reading speed by 10 years of age. Further improvement is obtained by decreasing the number of regressions.17

Dyslexics show many of the same type of eye moments as the beginning reader. Furthermore, good readers show the same type of movements when asked to read text in which the letters have been reversed or otherwise changed in position.12 Because dyslexics show normal sequential saccade tracking in other areas of oculomotor functioning, it is believed that the abnormalities seen in dyslexics during reading are a result, and not the cause, of their reading disability.


Vellutino presented a library model to understand the role of memory in reading.18 In this model, the processing of information occurs in three stages. The first stage takes place in a sensory storage system where a replica of the given stimulus is briefly held. The second stage takes place in a short-term working memory. This short-term memory has a limited capacity. Here, a transformed, encoded version of the stimulus is held for up to 30 seconds. This transformation produces an abstract representation of the stimulus to be placed into long-term memory. The third and final stage allows the stimulus to be categorized and stored in long-term memory or discarded.

Printed words are able to be identified through either “whole-word” or “part-whole” processing. Whole-word processing is based on the visual features of a word, its meaning, and its context. Part-whole processing is performed by breaking words down into letter sounds and is based on alphabetic mapping.

The beginning reader uses both the whole-word and part-whole form of processing to identify words. If the child relies too heavily on either strategy, reading difficulties arise. If the whole-word strategy is used excessively, visual memory is overused and letter reversals may occur. However, if alphabetic mapping is overused, the reader misses the salient features of words and has difficulty reading fluently and comprehending the text being read.

Spoken and written words are broken into individual phonemes and stored with a phonologic code in memory. This code is analogous to a file card in Vellutino's library model. Proper coding of these cards is necessary for later retrieval. Poor phoneme segmentation would not allow enough “clues” to be stored on the file card to enable the correct recall of a word that has been read or heard.

Using experiments based on his model, Vellutino was able to explain many of the behavior patterns seen in dyslexic readers. The common etiology of these behaviors were linguistic deficiencies and not visual or perceptual disorders. In one experiment, dyslexic children were able to name the letters of most words in the correct order, although they often named them incorrectly. Furthermore, when they were asked to reproduce words from an unfamiliar writing system, Hebrew, dyslexics did as well as normal readers. Both groups manifested identical tendencies to process the Hebrew letters from left to right. Therefore, when wordlike symbols lacked linguistic associates, visual recall was no different between these two groups. The conclusion was that memory for visual symbols representing words is mediated by the linguistic properties of those words and that difficulties in maintaining proper directionality is a symptom, not a cause, of a reading disorder.

Mirror writing, or reversal errors, is common in dyslexia and may reflect an imbalance between whole-part and part-whole word processing. Children who were taught to identify meaningless words, pseudowords, by a whole-part method made many more reversal errors than children taught to use alphabetic mapping. However, there was no difference in the number of reversal errors between normal and poor readers. The claim that spatial confusion causes these types of errors is not supported by this evidence.

Auditory processing of spoken words also is abnormal in children with reading difficulties. Poor readers demonstrated more trouble recalling lists of recently heard words than normal readers. However, they showed no difference in auditory sensory memory. Like their visual traces, the auditory traces dissipated no faster from a dyslexic's sensory memory than that of a normal reader. This combined difficulty in both visual and aural recall, coupled with normal sensory memory, indicates that it is the linguistic, not visual, processing of written text that is the cause of reading difficulties.

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Neuroanatomic changes that have been observed in the brains of dyslexic patients are located in language-related areas. Galaburda describes two forms of anomalies during postmortem analysis of dyslexic subjects.19 The first abnormality is the absence of the normal asymmetry in the language regions of the brain. Normally, the left planum temporale is larger than the right. The subjects studied showed no difference in the volume between the right and left planum. This lack of asymmetry also has been observed in living dyslexics through the use of magnetic resonance imaging.20 This abnormal symmetry appears to be associated with the linguistic difficul-ties typical of some dyslexics.21

The second brain abnormality observed in dyslexics also is found in language-related areas. Goldman-Rakic and Rakic demonstrated distortion of neuronal microarchitectural arrangement in these areas. This distortion appears to originate from misdirected migration of these neurons during embryonic brain development.22

Neurophysiologic studies have shown differences between dyslexics and normal subjects in the language areas of the parietal and temporal lobes. They also have found differences in the region of the frontal lobes that are important in the planning and sequential transformation of information processed during reading.23 These abnormalities of cortical organization include a smaller size and atypical locations of language areas. This has been demonstrated in abnormal readers undergoing studies of language functions during neurosurgical operations performed under local anesthesia.24 Abnormal brain electrical activity mapping of dyslexics during tests of language and nonlanguage functions may reflect these differences in language localization, which are caused by the small ectopic developmental anomalies in the brains of dyslexics. Defects in the magnocellular subdivision of the visual pathway may be present in dyslexic individuals. This portion of the visual pathway is responsible for conveying fast, low-contrast visual information.25 A defect in this area theoretically could explain why some dyslexics do poorly in tests requiring rapid visual processing. However, other studies have not been able to duplicate these findings or support its hypothesis.26,27 The current neurobiologic data are consistent with an increasingly sophisticated account of dyslexia that does not single out visual deficits. To think of dyslexia as an isolated vision disorder may appear to be logical but is not supported by scientific data.

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Because dyslexia is a language-based disorder, treatment should be directed at this etiology. A thorough evaluation with a trained expert in reading disorders is needed to properly classify the nature of the dysfunction and develop an appropriate treatment plan based on this classification. Early treatment of reading difficulties should involve intensive individualized tutoring targeted at the documented deficiencies observed in the specific individual. A balanced reading program that includes both the holistic/meaning and the analytic/phonetic approaches to reading should be combined with other activities to improve language development.18 Because the supposed association between visual dysfunction and poor reading is so intuitively logical and because it is easy to accept a visual deficit as the cause for reading difficulties, parents and teachers are easily led to believe that therapies aimed at treating visuoperceptual dysfunction offer an effective intervention. The proliferation of so-called evidence of the efficacy of these treatments further escalates the temptation to believe in these scientifically unproven modalities.

Vision therapy has been proposed as a therapeutic intervention for the alleged visual abnormalities responsible for reading disorders. Research supporting vision therapy shows several major flaws in their investigational and interpretative designs. Such research fails to differentiate between normal variation, association, and cause and effect. Most studies involving vision therapy lack matched comparison groups and fail to provide a sham or placebo treatment given to a control group in a masked manner. The foundation of many studies is based on an initial preconception that an isolated visual factor is responsible for reading disabilities. These preconceptions rely too heavily on anecdotal or superficially logical evidence. The efficacy of vision therapy in these reports fails to control for nonspecific gains that may be derived by the product of simply increasing the time and attention given to poor readers during the course of these investigations.28–31 Finally, the claims that show the benefits of vision therapy by and large are reported by groups that have a vested interest, usually financial, in proving the validity of these benefits. Because current available evidence has failed to implicate visual disorders as a cause of reading problems and there remains no scientific evidence that validates vision therapy as a way of treating these problems, the Academy of Pediatrics, the American Academy of Ophthalmology, and the American Association for Pediatric Ophthalmology and Strabismus do not recognize vision therapy as a treatment option for reading disorders.32

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Many authors in the optometric literature proclaim the usefulness of vision therapy for reading and learning disabilities.33–37 The basic tenant of their hypothesis is that children with reading disorders have an increased incidence of vision abnormali-ties.38 Proponents of vision therapy claim that treatment of these abnormalities will therefore help to correct reading deficiencies. However, there is no evidence that there is an increased incidence of visual abnormalities in this population. Helveston and colleagues could not find a statistical relationship between visual function and academic performance in a masked study of a large group of first, second, and third grade students.39 Also, many of the abnormalities that are said to cause problems with reading involve subtle dysfunctions that typically are undefined and unspecified. This makes evaluation of the claims of successful treatment difficult to analyze. Furthermore, most patients are treated with some type of optical aid and with a few standard forms of vision exercises. The almost universal use of these treatment modalities in a disorder so complex and in a population with a low incidence of optical or refractive errors seems to oversimplify the problem and overestimate the role of vision within it.

The ophthalmologist often is consulted after specific recommendations for vision therapy have been made. To properly counsel patients with reading disorders, it is useful for the ophthalmologist to understand the role of vision in reading and also have a working knowledge of the common types of vision therapy prescribed, the theory behind their usefulness, and the flaws in the methodology showing their benefits


Various forms of ocular motility disturbances have been associated with reading disabilities. These disorders include exophoria, esophoria, excessive fixation disparity, amblyopia, and “minimum binocular dysfunction.” Most of these studies claim that patients with these binocular dysfunctions experience visual symptoms that lead to degradation in reading performance.40–44 The link between binocular dysfunction and reading symptoms is assumed, and the small degree of heterophoria in the normal population is not taken into account. In a retrospective study, Grisham and coworkers report an increased incidence of various symptoms in slower readers. They could not show a significant difference in reading ability between readers with normal and abnormal binocular function. Also, there was no proof of cause and effect between decreased binocular function and symptoms or between symptoms and poor reading.45 Other studies also have been unable to find an increase in the incidence binocular disorders in children with reading difficulties or an asso-ciation between motility disorders and reading ability.39,46,47


Several accommodative disorders are said to give rise to reading disorders. Accommodative spasm, accommodative insufficiency, ill-sustained accommodation, and accommodative inertia all have been implicated.36,42,43,48 Accommodative inertia describes the sluggishness that has been reported to occur in some individuals when changing from one level of accommodation to another. Problems said to be caused by these disorders include the following: print blurring, day dreaming, decreased attention span, increased heart and respiratory rate, and poor posture.49–51 Supposedly, the symptoms caused by these problems lead to poor reading. It is argued that treatment of accommodative dysfunctions with low plus lenses will therefore eliminate these secondary problems and their associated symptoms, thereby improving reading efficacy. However, there is no proof that there is a difference in accommodation between normal and abnormal readers or that there is a correlation between reading performance and any specific type of refractive error, including hyperopia.52–54


In 1983, Irlen reported using tinted lenses to successfully treat a group of adults with a long history of reading disorders.55 The author described a new disorder called “scotopic sensitivity syndrome” and claimed that it affected half of all dyslexic readers. People with this syndrome are thought to experience perceptual dysfunctions caused by sensitivities to particular frequencies and wavelengths of light. When subjected to these wavelengths, fatigue and trauma to the visual system occurs, leading to poor coordination, decreased depth perception, sore eyes, and fatigue. Reduction of the offending wavelengths through the use of tinted overlays or lenses corrects these secondary dysfunctions and improves reading ability.56 How scotopic sensitivity relates to reading has not been explained. Retinal rods function under scotopic conditions and are not present in the fovea, where printed text is processed during reading. In a double-blind study of dyslexic children, tinted lens therapy was not shown to improve reading ability subjectively or objectively.57 Studies claiming the efficacy of these lenses have not held up to scientific review.58


An extensive amount of literature supports the use of perceptual-motor training in the treatment of reading disabilities.33,35,36,59–61 Visual perception is the integrative process by which information received from the visual input system (eye) is organized for presentation within the central nervous system so that it may be processed intellectually (cognition) and stored in memory banks for appropriate and timely retrieval. Collectively, perception, cognition, and memory are association functions, their locations within the brain imprecisely determined. Specifically, the anatomic and physiologic sites for visual perception are undetermined. Visual physiologists point out the complexity of visual information processing, which occurs at many levels, including the retina, retinogeniculate tracts, lateral geniculate body, geniculocalcarine tracts, association areas, and centers of higher processing. Unfortunately, the use of terms such as visual-perceptual, visual-perceptual-motor or eye-hand incoordination problems implies a direct relationship between the eye and perceptual difficulties. Such associations have not been established. Perceptual-motor training has not been demonstrated to be useful for reading disorders in other studies, and reviews of the scientific merit of studies supporting their efficacy have shown them to be unfounded.62,63

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Although ophthalmologists do not treat reading disorders, they often are asked to comment on their etiology and proper treatment. Commonly, these questions arise after various forms of treatment have been suggested and the parent has become increasingly frustrated. The ophthalmologist plays an important role in dealing with this frustration. The known facts about reading disorders, including their cause and treatment, should be given to the parent. Equally important, the myths surrounding these disorders should be addressed and dispelled. Any underlying visual disorder should be identified and treated even though it rarely is the cause for the initial consultation. The ophthalmologist needs to be supportive. A parent should not be told that there is nothing wrong if the ophthalmologic evaluation is normal. When a child is performing poorly in school, there is a problem, and this needs to be addressed even if the ophthalmologist is not directly involved in the treatment. Likewise, the ophthalmologist should not decline to be of any assistance to the parent. Providing a list of sources available where a parent or patient can obtain proper help is an invaluable service. Many of these families already have seen countless individuals looking for this information. Every ophthalmologist who sees patients with reading problems should develop a working relationship with a professional with expertise in this area. A referral to such a person often is an overlooked opportunity to provide assistance. It allows the family to seek appropriate professional guidance and makes it less likely that their time and effort will be spent on less-effective therapies provided by people promising an “easy” solution. Treatment requires a multidisciplinary approach involving educators, psychologists, and physicians. Parents need to be warned that this is a complex disorder and there are no quick cures. By dealing with these problems in a logical and straightforward manner, frustration can be minimized and effective intervention can be implemented.
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1. Hinshelwood J: A case of dyslexia: A peculiar form of word-blindness. Lancet 2:1451, 1896

2. Berlin VP: Eine besondere Art der Wortblindheit. Stuttgart: Wiesbaden, 1887

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