Article

Optometric Management of Garth N. Christenson, OD, MSEd John R. Griffin, OD, MSEd : Resolving the Controversy Revisited

Abstract Our intention in this article is to elucidate a validated, good review of the current literature regarding dyslexia. time-tested, method of differentially diagnosing We also recognize the author for acknowledging the fact dyslexia. We refer to this approach as the that most models or classifications for dyslexia stem phonetic-eidetic coding (PEC) model. If dyslexia is from the concepts of Boder.10,11 He stated that defined as a single-word coding problem with exclusion categorization of dyslexia as dysphonesia, dyseidesia or of other adverse factors, we believe this model can be the mixed type (dysphoneidesia) seems to make sense. used to define and diagnose, or rule-out dyslexia, so that However, we disagree with the assertion of Evans that controversy regarding management of dyslexia can be dyslexia is so varied that it defies classification. This resolved. When dyslexia is diagnosed as one of three example of confusion in the literature, as well as our basic subtypes the ability to conceptualize each personal communication with many health-care condition becomes logical. practitioners and educators, leads us to revisit our original attempt to resolve the controversy. Key Words Professionals have tended to view the patient dyslexia, , magnocellular pathway, narrowly through biases of their philosophical bent parvocellular pathway, , visual correlates, relative to their own professional training. Some general reading dysfunction, specific reading pediatricians have equated dyslexia with ADD and tout dysfunction, dyseidesia, dysphonesia, dysphoneidesia the benefits of stimulant medication.12 Some Introduction chiropractors have proposed an “ocular lock” as the basis An article in 1990 discussed the controversy for dyslexia and used cranial skull manipulation as pertaining to optometric involvement in the management treatment.13 Irlen14,15 espoused the “Scotopic Sensitivity of and espoused a classification Syndrome” and offered tinted lenses for a cure. Frank scheme for differentiating three main types of dyslexia.1 and Levinson16 advocated anti-motion sickness Afterwards, related publications regarding optometric medication as a cure for dyslexia. Stein and Fowler17 management of reading disability and dyslexia were argued that there is a lack of ocular dominance and forthcoming.2-7 Even though an optometric statement8 advocated patching of an eye to treat the underlying attempted to clarify matters, the controversy remains. “problem.” Delacato18 hypothesized that creeping and For example, Evans9 mentioned the previously cited crawling would be the answer to reading problems. The classification scheme for dyslexia. His book presents a point is that optometry has a chance to step outside a narrow professional perspective by using the knowledge Correspondence regarding this article can be e-mailed to about treatment of problems that were [email protected] or sent to Garth N. Christenson, OD, 2215 Vine Street, Ste. C, Hudson, WI 54016. All statements are the authors’ pioneered together with the phonetic-eidetic coding personal opinion and may not reflect the opinions of any particular (PEC) model, thus, to clarify the nature of dyslexia as institution or organization. well as the overall treatment of the broader area of reading dysfunction. Christenson G, Griffin J. Optometric Management of Dyslexia: 9 Resolving the Controversy Revisited. Optom Vis Dev We use some of the questions raised by Evans as grist 2005;36(1):23-33. for the mill in clarifying the PEC model of dyslexia.

Volume 36/Number 1/2005 23 Evans is to be commended for his comprehensive review of the literature from the later quarter of the 20th century regarding dyslexia. He also covers the areas of inquiry pertinent to the field, albeit with distorted views in our opinion, regarding ADD, behavioral optometry, and tinted lenses. Additionally, his attempt to bring an evidence-based approach to this field is laudable. However, he arrives at some alarming assertions that we would like to address. We believe these assertions stem from a misguided perception of the true nature of dyslexia. These troubling assertions include: 1) the apparent Figure 1. The Oral Decoding Process underlying premise is to avoid making assumptions as to an exclusive cause Table 1. of dyslexia; 2) associating the Major Causes of Non-Specific Reading Dysfunction behavioral optometric approach with · Low intelligence (e.g., full-scale IQ, 80 or lower on the Wechsler unfounded treatments such as Intelligence Scale for Children – Revised) · patterning and cranial skull Educational deprivation (e.g., child who does not attend school regularly) · manipulation; 3) the assertion that Sociocultural deprivation or differences (e.g., English is child’s second ADD is somehow a plausible ) · explanation for, or significant primary Primary emotional or mental health problems (e.g., schizophrenia) · component of, dyslexia; 4) the Vision problems (e.g., high uncorrected hyperopic astigmatism among many other anomalies of vision) emphasis on the role of tinted lenses in · Auditory problems (e.g., poor auditory perception and processing) the treatment of dyslexia; 5) the · Sensory-integration problems (e.g., poor auditory-visual integrative skills) “unifying theory” of attention and · Attentional problems (e.g., attention-deficit hyperactivity disorder) parallel processing as an explanation · Other problems as well as many possible unknown causes (e.g., allergies for the visual correlates of dyslexia. affecting an individual’s ability to stay on task, poor motivation, poor Arriving at Consensus for a nutrition, speech problems, undetected physical and mental health Model of Dyslexia problems). Evans9 stated that classifications like the PEC model “…seem to make detail.7 Some of the causes of NSRD are listed in Table 1. sense, but are probably an over simplification. Indeed NSRD includes all the general causes of reading some studies have concluded that dyslexia is so varied dysfunction that are not causes of dyslexia. SRD would that it defies classification.” Evans seems to be in favor of include the three main types of dyslexia described by keeping the definition of dyslexia vague and leaving it Boder10,20 and amplified by Griffin and Walton.19 open to varied interpretation. This is the view of many A short elaboration of the PEC model is provided professionals in the field of learning disabilities. On the here. A proposed model of the neuroanatomical loci other hand, we believe dyslexia is a specific reading involved in the decoding of words is shown in Figure 1. disability (SRD) with distinct subtypes that have A written word is presented to the individual. The visual identifiable behavioral characteristics. These image is received by the eyes and neurological impulses characteristics are directly diagnosable using validated are sent to the visual area (VA) in the occipital lobe via 19-22 tests. This concept is based on the contention that the visual pathway. The impulses then travel to the left reading dysfunction (RD) can be divided into posterior hemisphere, probably the angular gyrus (AG). nonspecific reading dysfunction (NSRD) and specific If the word presented is one with which the person is reading dysfunction (SRD), the latter being synonymous familiar (being in his/her sight-word lexicon), then a with dyslexia. The (SRD) rubric has been described in sight-sound match is made quickly. If the word is one for

24 Optometry and Vision Development which the subject has not developed sight recognition, then the impulses travel to a location in the Wernicke’s area where the word more slowly can be syllabicated, sounded out, and blended (i.e., phonetically decoded). This additional interaction between the angular gyrus and Wernicke’s area, apart from being relatively slow, may not always be effective in decoding phonetically irregular words, e.g., “foreign” and “should.” If, however, the person is able to decode the word phonetically, impulses are sent via the arcuate fasiculus to Broca’s area (BA) where, among other functions such as grammar sequencing and motor programming, speech formation is initiated. The signal is then sent to the motor cortex (MC) and relayed to the muscles around the mouth and throat, which are involved in articulation, so the word can be spoken. This over-simplification serves as a model Figure 2. Example of Dyseidetic Encoding for the process of decoding and allows one to understand the reading and problems associated with the three generally recognized types of dyslexia. These types are dyseidesia (“visual”), dysphonesia (“auditory”), and the combined form, dysphoneidesia (“auditory-visual”). Although this neurological- behavioral model is reliable for clinical understanding, further research is recommended as regards exact neuroanaotmical loci and associated language coding functions. We believe the whole-word coding problems (sight-word recognition and orthographic spelling) of the individual with dyseidesia are primarily due to a deficit involving the angular gyrus, although areas in the occipital lobe are also likely to be involved. Common spelling errors include phonetic equivalents for irregularly spelled words, e.g., foren for “foreign” or shud for “should”. (See Figure 2.) Reading is laborious and comprehension is usually reduced Figure 3. Example of Dysphonetic Encoding due to phonetic decoding, which is

Volume 36/Number 1/2005 25 slower than eidetic sight-word recognition, as well as the with dyslexia, they are fundamental prerequisite skills inability to decode many irregularly spelled words. necessary for the patient to be able to benefit from MLT. The dysphonetic type of dyslexia (dysphonesia) In our opinion, Evans9 suggests keeping the causes an individual to have characteristic spelling errors definition of dyslexia open and including all the (e.g., forng for “foreign” and sohld for “should.” (See nonspecific variables as potential causes to justify his Figure 3.) The attempted spelling is not a good phonetic theory of management. We want to point out that we equivalent of the word. Another error often made in believe Evans makes a well intentioned effort to deal these cases is semantic substitution. Since the individual with the ambiguity caused by past, poor defining of has problems in attacking unknown words phonetically, dyslexia. The problem is that ambiguity need not exist if he/she may read, for example, “home” instead of house. we begin with a valid, well-supported model of dyslexia. Reading may be fairly good until the dysphonetic Others have also given explanations for dyslexia which individual comes to an unfamiliar word. Such allow for their method of treatment to be justified. individuals have great difficulty applying the rules of Witness the plethora of treatments that have purported to in decoding, although they may learn to store cure dyslexia: 1. tinted lenses;14,15 2. cranial skull words well for sight recognition. Reading maniupulation;13 3. patching an eye for ocular comprehension is necessarily affected when a significant dominance stability;17 4. creeping and crawling;18 5. number of words are “missing” (undecoded). stimulant medical therapy for ADD/dyslexia.12 6. The individual with dysphoneidesia (combined type anti-motion sickness medication;16 and others. All these of dyslexia) is even more limited in his/her ability to come with their own model of dyslexia. In these cases, recognize and spell words. Decoding and encoding we believe, the model is born out of a desire to justify the errors are characteristic of both dyseidesia and cure. This is similar to how Evans arrives at his final dysphonesia. conclusions in which he presents a “unifying theory” An analogy may be useful in expressing why we feel which attempts to join concepts from ADD, M-pathway it is so important that a definitive classification of deficit theory, tinted lenses, and the Dunlap test (as used dyslexia be universally agreed upon by professionals by Stein and Fowler17) to explain the visual components helping individuals with reading dysfunction. The of “dyslexia.” In all these cases the notion of dyslexia is analogy is as follows. In the field of vision care we manipulated to fit the theory of treatment. The model of endeavor to diagnose and treat problems. A patient dyslexia must be based on a valid construct which presents with the complaint of not seeing well in one eye. underlies and defines a specific written language What is the treatment? We must first differentially problem. It should be based on repeatable behavioral diagnose the problem. Is it a cataract, astigmatism, characteristics owing to underlying language-based myopia, macular degeneration, hyperopia, a corneal scar, neurological functions and validated by genetic or amblyopia (among many other possibilities)? If we do principles as well as prevalence issues, such as in the not make the differential diagnosis, then we are merely PEC model. Commingling all nonspecific variables guessing at the treatment via trial and error. What if it listed in Table 1 with the definition of dyslexia has led to were said that vision problems are so varied that they confusion in the field for over 100 years. A coherent defy classification? Fortunately, there is general definition and uniform classification system for dyslexia consensus as to diagnosis and treatment of most ocular is a desirable goal. There are several reasons why the problems. original Boder model10,11 and others have not been To complete the analogy we assert that dyslexia, embraced in the learning disabilities field. One is that SRD, is not cured with medication therapy for ADD, many tests for single-word decoding skills were untimed tinted lenses, cranial manipulation, occupational and not separated into phonetically regular and irregular therapy, patching an eye for ocular dominance categories. Subtyping as regards dyseidetic and stabilization, or sensory motor integration therapy. This dysphonetic word recognition and attack was not is also true for vision therapy in most cases of dyslexia. If reliable. Likewise, eidetic versus phonetic encoding it is diagnosed and distinguished from the other testing was unreliable. Another reason is economic in nonspecific causes of reading dysfunction, then the most that dyslexia is a disability and educators prefer to have appropriate intervention is multisensory- this as a “medical problem” and not one to be addressed written-language therapy (MLT).7 However, as by educators, much less making differential diagnoses of previously mentioned, if nonspecific causes are subtypes. It is time to apply the valid tools we have for associated the other therapies are often necessary and differential diagnosis and management of reading helpful. Later, we will make special mention of vision problems, including dyslexia. therapy for visual processing problems; when associated

26 Optometry and Vision Development Support for the Phonetic- Table 2. Eidetic Coding (PEC) Model Some Early Proponents of PEC Classification of Dyslexia There is support for the neurological-behavioral PEC Proponents Types model.23-36 A sample list of Camp and Dolcourt (1977) Eidetic and phonetic researchers who are proponents of the Boder (1982) Eidetic and phonetic PEC classification, even though they Hynd and Hynd (1984) Surface and phonologic (deep) may have used different terminology, Roeltgen and Heilman (1984) Lexical and phonologic is shown in Table 2. Temple (1984) Surface and phonologic Shaywitz and associates34 Griffin and Walton (1981) Eidetic and phonetic postulated a variation of our Flynn and Deering (1989) Eidetic and phonetic neurophysiologic model of reading disability based on recent neuroimaging studies such as Position Table 3. Emission Tomography (PET) and Overview of Other Theories of Dyslexia functional Magnetic Resonance Date Name Theory Imaging (FMRI). The model they 1925 Orton Incomplete cerebral dominance have espoused is very similar to the 1925-1959 Monroe Developmental lag one we have briefly described and Fernald Developmental lag schematically presented in Figure 1. Bender Developmental lag The main distinction is the implication 1960-1969 Barsch Incomplete perceptual development that the angular gyrus and Wernicke’s Delacato Incomplete perceptual development area are combined to constitute what Frostig Incomplete perceptual development they call the dorsal (temporal-parietal) Getman Incomplete perceptual development component. They add a ventral Cruickshank Incomplete perceptual development (occipital-temporal) component Kirk Psycholinguistic problems which, by their theory, subserves the Wepman Auditory discrimination problems “late developing word identification De Hirsch Language problems system that underlies fluent word Myklebust Language problems recognition in skilled readers.” Bateman Language problems Conversely the aforementioned dorsal 1970-present Keogh Attention problems system is the early developing Margolis Attention problems phonological system. The only Bannatyne Poor memory question of this model versus the PEC Vellutino Language disorders model is in regard to neurological loci. Satz Maturational lag In either theory, the functional concept Torgesen Mismatch in abilities and education of word recognition is fairly Ingersoll Deflected style consistent, which lends credence to Evans Combination ADD/Binocular the behavioral PEC model of decoding Instability and encoding. Borsting and Ridder33 consistent with the behavioral characteristics in cases of have investigated parallel processing and their work is a 34 step forward in relating neurology to behavioral aspects dyseidesia. Shaywitz and associates and others have of dyslexia. Further electrodiagnostic neurological not presented data relating specific subtypes of should also include subjects with diagnoses of to specific modes of genetic transmission. Validity of the PEC model is also indicated by the dyseidesia and dysphonesia to verify respective loci. 2 It is generally accepted that dyslexia “runs in prevalence factor. Based on prevalence data, there is not families.” Unfortunately, genetic research with much room left over for significant numbers of other subtyping is lacking. The discovery that dyseidesia is “dyslexics.” It clarifies the genetic question in dyslexia inherited via an autosomal dominant mode of and its diagnostic prevalence. The model arises from transmission provides further validity to the PEC model valid constructs. Other diagnostic models are often of dyslexia.36 The notion that an autosomal dominant based on purported cures. We present some of these defect causes a structural problem (not an enzyme deficit competing models of dyslexia in Table 3. as with autosomal recessive) in the angular gyrus is

Volume 36/Number 1/2005 27 Addressing the Unifying Theory back on the age-old dogma that vision therapy does not Evans9 proposed a unifying theory of “dyslexia.” We cure dyslexia. This contention has been agreed to by use quotes to denote the vague definition that includes optometric scholars in that vision therapy does not cure nonspecific factors in reading dysfunction. Evans, to his dyslexia, likewise, the plethora of cures mentioned credit, makes the point that he is attempting to link above. Vision therapy, however, has been shown to interactions between the visual correlates of dyslexia, remediate many problems of vision.53 although admitting that a significant portion of those Evans9 states that the accepted treatment for dyslexia with serious reading problems have language-based, is more intensive schooling. We would amend this to phonological problems which are separate from and not convey that specialized, highly structured, sequential, influenced by his unifying theory for the visual multisensory language therapy MLT, e.g., correlates. In simplified terms, Evans links the Orton-Gillingham type programs, are the most effective M-pathway deficit37-40 to binocular instability, with therapy for the PEC model types of dyslexia.54 An possible mild associations to impaired attention and effective MLT technique is the Vowel Mat of Halapin.55 saccadic dysfunction. This leads to pattern glare as (See Appendix for details.) Introducing this technique to embodied in the Meares-Irlen syndrome.41 Evans does a child with immature visual processing skills, however, indicate that these associations are speculative and is futile. This is abundantly clear to a therapist. Visual endorses more conventional treatments of vision processing skills are necessary and have been shown56 to problems before turning to the Meares-Irlen tinted lens be correlated with reading readiness in grades K to 2. treatment. Nevertheless, we feel the advocacy of tinted In summarizing the discussion on the Evans book we lens therapy is misguided. This whole area has been would like to recognize the author for his attempt to bring reviewed In the past and found to be of questionable clarity to the varied issues that have been confusing to merit.4-7,42,43 The one controlled study we know of which those working in the field. While we agree with many of has used the PEC model of dyslexia and looked at the the points in the book and recommend it as a resource, we question of tinted lenses showed no statistical difference do not concur with the central assertion as to the rejection between those dyslexics wearing blue tinted lenses and of the PEC model of dyslexia, and we do not endorse his those without them.6 This study also discusses the issue unitary theory for the linkage of visual correlates for of past tinted lens studies which have inconsistently reading dysfunction and their treatment via tinted lenses. defined their samples of poor readers so that it is The Deflected Style Theory questionable whether they investigated verified dyslexic This section of the paper will address the deflected subjects. style theory of Ingersoll57 and issues regarding A difficulty that needs to be addressed is Evans’ magnocellular deficits in reading dysfunction. statement that vision therapy for visual processing Proponents of the deflected style theory (DST) assert that problems is lacking in random controlled trials (RCT) the primary cause for reading/spelling problems in and probably does not alleviate reading problems. He “dyslexia” is related to the fact that the individual is indicates a bias toward explaining away visual “stuck” in an inefficient phonetic (auditory) mode of processing problems by concluding that kids with ADD processing (coding) written language. Accordingly, this do not perform well on visual processing tests because of inefficient phonetic style represents a deflection from the poor attention. Additionally, he describes the “normal” pattern of development where words would be relationship of visual processing dysfunctions and processed via the higher order more efficient eidetic, or dyslexia citing the analogy that red wine can cause visual memory, route. Proponents of the DST further headaches, but not all headaches are caused by red wine. postulate that often this occurs as a result of attempting to Therefore, he asserts visual deficits do not seem to be a teach children to read before they are developmentally major cause of dyslexia, but can contribute to a reading ready. In other words, if a child does not yet posses the problem. Unfortunately he does not appear to consider appropriate visual memory and eidetic language the possibility that the attention problems of some, if not processing skills, teaching the child to read may result in many kids, may be due to immature visual processing deflecting toward a style of cumbersome phonetic skills. Furthermore he fails to subject the ADD category (auditory) processing and preventing fluent reading via to the same scrutiny that he uses for visual processing eidetic recall of words. These two models, PEC and therapy (VPT). DST, are a bit like the question of the chicken and the egg. The approach taken by Evans is similar to past However, the rectitude of the two models may be criticisms of vision therapy in the management of elucidated in the ensuing presentation which is indicative reading dysfunctions.44-52 The authors of these reviews questioning the validity of vision therapy continue to fall

28 Optometry and Vision Development of discussions we have had with proponents of the DST reader, and his “reading-disabled-phonetic- spelling” over the years. brother, who excels in all other aspects of intellectual As a prologue to the discussion, a key point regarding life, e.g., playing chess. eidetic recall (visual memory) should be stated. We find Counterpoint 1. this to be a point of some contention and The DST advocate’s first two points involve the misunderstanding among our colleagues. Eidetic genetic issue. The brother who is gifted in spatial memory for matching visual gestalts of whole words abilities but reads slowly and spells phonetically is with sounds of whole words is a separate cognitive skill contrasted by his sibling who is an avid reader. The from eidetic memory for non-linguistic symbols. We question is how this could be possible. The answer believe it is fairly well accepted that eidetic recall for begins with an understanding of the familial nature of words (storage of the sight-word lexicon) occurs in an dyseidesia (DE) in conjunction with it being an area in the left parietal lobe, for most right-handed autosomal dominant (AD) disorder. It would be quite people. Conversely eidetic recall for spatial, non-written possible, even typical, for a monogenic AD trait to be language symbols can occur in the right parietal and expressed in one sibling and not another. In fact the occipital lobes. Many who have not made this distinction theoretical risk of a sibling inheriting such a trait where have mistakenly asserted that tachistoscopic drill of digit one parent is affected is 50%. In most patients we see spans has a salutary effect on spelling of phonetically who have DE, generally half the siblings are affected and irregular words. This correlate would also hold for the half are phenotypically normal. With this type of difference in assessment of eidetic written language inheritance (AD) we should also be aware that the trait recall (as in formal dyslexia testing19) versus clinical can vary in terms of severity and penetrance.36 assessment of visual-spatial memory, e.g, tachistoscopic As to the question of the length of exposure to written digit spans. It should also be pointed out that visual language for mankind, we agree that it has not been a memory testing of digits and geometrical figures does very long time that the masses have been required to be not correlate with testing results of sight-word literate. The printing press was developed in the 1600s. recognition in dyslexic individuals. Realistically, one could argue that, in our culture until the The discussion below summarizes a dialogue we have last generation or two, reading and spelling were not a had with colleagues whom we respect as professionals; necessity to making a living. One author’s (GNC) however, we disagree with them regarding the grandfather, son of Norwegian emigrants, quit school theoretical basis of dyslexia. We present the dialogue in a after the 8th grade to go into the farm implement business. point and counter-point format to allow the reader to In his generation this was not uncommon as many of his make distinctions between these disparate theories. In peers worked on the farm or the railroad or later “drove the opening section of this dialogue we give the active truck” and got by in the presence of dyslexia. We are not voice to those proponents of the DST and offer up the saying that GNC’s grandfather had dyslexia, but are types of criticisms we have heard them present regarding agreeing that was much more optional not so the PEC model. Then in the second section we answer long ago. It seems to us, the less time the species had to those criticisms. We hope this provides a balanced use the specialized cognitive functions the more likely discussion using an interesting format for understanding that there would be wider biological variation in this these competing theories of dyslexia. ability and less time for elimination of this “weak” trait. Point 1. Point 2. The DST proponent criticizes the PEC model as “an The next bone of contention involves the example of a theory of poorly defined brain damage or dysfunctional neurology of reading. The DST proponent structural irregularity as the cause of the various types of explains the depressed neurological activity of the unsuccessful reading behaviors.” There often is strong angular gyrus and excessive activity in the temporal lobe opposition to the notion of genetically determined of poor readers as follows. He/she asserts that this is reading difficulties. For this presentation let’s say the caused by a poor reader’s excessive unsuccessful opponent questions a genetic cause for reading failure, attempts to decode words phonetically, because the because it doesn’t make sense when one considers that decoding style has been deflected rather than as a result the vast majority of the human population has only been of a genetically-based eidetic deficiency. Therefore, the exposed to written text for a few generations? Further DST proponent poses some questions: does it make sense questions include how differences in genetically that dyslexics have a dysfunctional angular gyrus when it endowed brain structure could give rise to the vast only shows up functionally where words are concerned? disparity in reading ability between himself, a good

Volume 36/Number 1/2005 29 Why don’t dyseidetic dyslexics show similar Point 3. dysfunctions where non-linguistic symbols (rather than DST proponents question the PEC model on the basis phonetically based words) are concerned? If the reading that it seems to intimate that those individuals with problem is organically based shouldn’t these dyseidetic dyslexia have “broken or incomplete” brains. individuals show similar types of dysfunction for math Counterpoint 3. facts as for spelling? Furthermore, why are there no We believe that an individual with dyslexia does not Chinese dyslexics? Lastly how could it be possible for a have a “broken or incomplete” brain. Rather, we believe person to be reading disabled in only 3 of the 5 it is correct to say that we all have differential brain that he knew if the etiology is structural? function. Some of us are gifted linguistically, some Counterpoint 2. musically, some artistically. On the other hand, some of We begin with the question: “Does it make sense that us are “tone deaf”, have poor artistic ability, or have dyslexics have a dysfunctional angular gyrus when it dyslexia. The person with dyslexia is no more brain only seems to show up functionally where words are damaged than a person who can’t sing very well. Many concerned?” Other issues raised in this section include individuals with dyslexia are gifted in other skills such as why can dyslexics retain mathematical information if a spatial/mechanical abilities. gyrus is defective and the issue of having dyslexia in one Point 4. language but not another. We bluntly begin by stating Moving away from the DST issue we now address the that we see no incompatibility with the PEC model of assertion that vision plays an important role in reading dyslexia and the issues raised here. Specifically, and vision therapy can be used to treat the reading dyseidesia is a written language-based disorder. The problems caused by dyslexia. Furthermore, some might gyrus (presumably the angular gyrus although there is suggest that visual magnocellular defects cause dyslexia controversy as to this locus) subserves a very specific and they must be treated with vision therapy. kind of eidetic recall for linguistic symbols (where there is a symbol-sound relationship of whole words). This Counterpoint 4. cortical site is where the reader “stores up” his/her Optometric vision therapy can have many salutary sight-word lexicon. As the reader becomes proficient, effects for people with dyslexia. Improved eye teaming, there is little need to process written language tracking, focusing and developmental visual information phonetically. When it comes to eidetic recall of spatial processing are of benefit to individuals with general relations or non-linguistic symbols, the angular gyrus of (nonspecific) reading dysfunction and also for those with the dominant hemisphere for language is probably not specific reading dysfunction (dyslexia). The rationale is involved to a large extent. This underlies the whole working around the dyseidetic dyslexic problem, for concept of hemispheric lateralization of function in example, and is accomplished with phonics training humans to provide for advanced linguistic ability. With using special educational therapy such as the this understanding we can discuss the argument about Orton-Gillingham approach. With this method the “no Chinese dyslexics.” We agree that for an individual reading and spelling abilities of the individual can be with dyseidesia, it may be easier to be taught Chinese or improved but the dyseidetic pattern remains. We have, the Japanese Kanji which are both logographic however, found that dysphonesia is more malleable as a languages where there is relatively little phonetically result of special educational training, especially when based, symbol-sound matching compared with training the strengths of eidetic skills. Dysnemkinesia, languages using the Roman alphabet, as in English. which is a motoric form of dyslexia with reversals of Spatial symbols depict objects and actions, and it is numbers and letters, can be treated with optometric sensible that dyslexics may do better with logographic vision therapy. These latter two types of dyslexia are not languages. Along these lines, a dyslexic individual may as genetically “hard-wired” as dyseidesia, which may have an easier time with a more phonetically regular explain the less favorable prognosis for modifying an language, such as Italian or Spanish. English, French, autosomal dominant trait, which dyseidesia is thought to and Danish, as examples, with their many phonetic be. irregularities are much more debilitating. (Although As regards visual magnocellular defects involving most educational authorities agree that decoding of the “where” pathway, as opposed to the parvocellular words is affected by which language is to be read, there is “what” pathway, a strong association with dyslexia was lack of data, because the question has not been addressed found by Ridder et al.58 who used the subtypes of the from the perspective of the PEC model.) Dyslexia Determination Test (DDT)19 for subject selection in their research. Although there is correlation,

30 Optometry and Vision Development it does not mean that magnocellular defects are the cause cause, vision therapy is the answer; however, this may of dyslexia. Nevertheless, treatment for improved not be so for exclusively dyslexic patients. functioning of the “where” pathway is a goal, The PEC model has remained unrefuted in the particularly in cases of dyslexia. A promising therapy for scientific literature. We assert that the optometric this is that of Lawton.59-62 She conducted a profession should embrace it and treat patients federally-funded controlled study for second-grade consistently with its principles unless someone can students on motion detection discrimination thresholds refute it and offer a valid alternative that can stand the test and corresponding therapy. Her contrast sensitivity and of time. We believe that one of the reasons for some of motion direction discrimination study was similar to that our colleagues to be tentative about accepting the PEC of Ridder et al.58 in that the DDT was used for subject model relates to the fact that for many years some tried to selection; however, low-contrast sine waves of varying “prove” a visual cause for dyslexia. A recent example in contrast and spatial frequency, moving relative to the literature involves a theoretical connection between different frequency backgrounds, were used in her magnocellular function and intermittent central program to stimulate the dorsal “where” pathway suppression.70 Similar to the “visual correlates” theory optimally. Those who were found to have dyslexic of Evans, the author attempts to extrapolate from visual coding patterns (dysphonesia, dyseidesia, deficiencies (which can cause reading problems) to the dysphoneidesia) were grouped as “inefficient readers” specific reading disability which is dyslexia. This leap is and nondyslexics as “efficient readers.” The not compatible with the PEC model and in our opinion nondyslexic group was a grade level higher than the would likely apply to only a small percentage of the those dyslexic group in all reading skills that were evaluated. with dyslexia. Lawton’s computerized vision therapy program We are very proud to be members, of a profession that (patented as Moving-To-Read) was given to each subject has been a leader in clarifying the management of for 5 to 10 minute sessions, biweekly, for 15 weeks. The dyslexia. Additionally, we believe the allied professions results are highly significant, as most inefficient readers of the multidisciplinary team are at a crossroads of doubled their reading speed (p<0.000001 using improving the therapy for our patients with dyslexia. We one-factor ANOVA) and improved over a grade level on hope to see optometry continue to lead the allied team of comprehension, spelling, and word identification; professionals toward a clarified management approach whereas, inefficient readers in the control groups barely for those individuals suffering from dyslexia. improved. It would appear that there may be merit to this References intervention. At the same time we would not advocate 1. Christenson GN, Griffin JR, Wesson MD. Optometry’s role in reading eliminating proven treatments such as multisensory disabilities: resolving the controversy. J Am Optom Assoc language therapy. Further research should address the 1990;61:363-72. 2. Griffin JR. Prevalence of dyslexia. J Optom Vis Dev 1992;23:17-22. appropriate “mixture” of these separate approaches. 3. Cardinal D, Griffin JR, Christenson GN. A neurological-behavioral model of dyslexia. J Behav Optom 1992;3(2):35-39. Summary 4. Cardinal DN, Griffin JR, Christenson GN. Do tinted lenses really help We would like to emphasize why we have endeavored students with reading disabilities. Intervention in School and Clinic 1993;28:275-79. to elucidate the (PEC) model of dyslexia. Optometry is 5. Christenson GN, Griffin JR. Aspects in management of dyslexia by in a unique position, given its rich heritage in helping behavioral optometrists. J Behav Optom 1996;7:123-5. patients with visual processing problems. Visual 6. Christenson GN, Griffin JR, Taylor M. Failure of blue tinted lenses to change reading scores of dyslexic individuals. Optom 2001;72:627-33. processing skills have been shown to be highly correlated 7. Griffin JR, Christenson GN, Wesson M, Erickson G. Optometric with reading ability in the early grades.56 One might management of reading dysfunction. Boston: Butterworth-Heinemann, argue that history shows optometry to be pioneers in 1997. 8. Special Commentary: Vision, learning and dyslexia. J Am Optom dyslexia management by virtue of the fact that Assoc 1997;68:284-86. optometrists have developed diagnostic tests for 9. Evans B. Dyslexia and vision. London and Philadelphia; Wurr 19,21,63-69 Publishers Ltd, 2001. dyslexia. Unfortunately, the reality is that there 10. Boder E. Developmental dyslexia: a new diagnostic approach based on is far from uniform understanding of the PEC model, the identification of three subtypes. J Sch Health 1970;40:289-90. even within our own profession. 11. Boder E. Developmental dyslexia: a diagnostic approach based on three atypical reading patterns. Dev Medic Child Neurol The other part of our motivation comes from our 1973;15:663-78. clinical experience. In our profession of optometry we 12. Richards I. ADHD, ADD and dyslexia. Therapeutic Care and have done much to help patients with general reading Education 3, 145-58, 1994. 13. Ferreri CA, Wainwright RD. Breakthrough for dyslexia and learning problems. In the case of those patients when dyslexia can disabilities, Pompano Beach: Exposition Press of Florida, 1984. be completely ruled out and vision problems are the 14. Irlen H. Successful treatment of learning disabilities. Paper presented to the 91st Annual Convention of the American Psychological Assn. Anaheim, CA, 1983.

Volume 36/Number 1/2005 31 15. Irlen H. Reading by the Colours: Overcoming dyslexia and other Ophthalmology and Otolaryngology, and American Association of reading disabilities by the Irlen method. New York: Avery, 1991. Ophthalmology. Pediatr News 1872;6(2):63-6. 16. Frank J, Levinson HN. Seasickness mechanisms and medications in 45. American Academy of Ophthalmology. Policy statement: learning dysmetric dyslexia and dyspraxia. Acad Thera 1976;12:133-53. disabilities, dyslexia, and vision. J Learn Disabil 1987;20:412-3. 17. Stein J, Fowler S. Effect of Monocular occlusion on visuomotor 46. Goldberg HK. Dyslexia and learning disabilities. Pediatr Clin North perception and reading in dyslexic children. Lancet 1985; Jul Am 1983;30:1195-200. 13;2(8446) 69-73. 47. Kavale K, Mattson PD. “One jumped off the balance beam” meta 18. Delacato CH. The diagnosis and treatment of speech and reading analysis of perceptual-motor training. J Learn Disabil 1983;16:165-73. problems. Springfield, IL: C.C. Thomas, 1963. 48. Helveston EM, Weber JC, Miller K, et al. Vision function and 19. Griffin JR, Walton HN. The Dyslexia Determination Test (DDT). Los academic performance. Am J Ophthalmol 1985;99:346-55. Angeles: Instructional Materials and Equipment Distributors, 1981, 49. Helveston EM. Vol III module 1: Management of dyslexia and related 1987, 2003. learning disabilities. J Learn Disabil 1987;20:415-21. 20. Boder E, Jarrico S. The Boder Test of Reading and Spelling Patterns. 50. Silver LB. The “magic cure”: a review of the current controversial New York: Grune and Stratton, 1982. approaches for treating learning disabilities. J Learn Disabil 21. Griffin JR, Walton HN, Christenson GN. The Dyslexia Screener (TDS). 1987;20:498-504,512. Culver City, CA: Reading and Perception Therapy Center, 1988. 51. Vellutino FR. Dyslexia. Sci Am 1987;256(3):34-41. 22. Guerin DW, Griffin JR, Gottfried AW, Christenson GN. Concurrent 52. Casbergue RM. Greene JF. Persistent misconceptions about sensory validity and screening efficiency of the dyslexia screener. perception and reading disability. J Reading 1988 Dec;198-203. Psychological Assessment 1993;5:369-73. 53. The 1986/87 Future of Visual Development/Performance Task Force. 23. Geschwind N. Specializations of the human brain. Sci Am Special report: The efficacy of optometric vision therapy. J Am Optom 1979;241:180-99. Assoc 1988;59:95-105. 24. Galaburda AM, Kemper TL. Cytoarchitectonic abnormalities in 54. Griffin JR, Walton HN. Therapy in Dyslexia and Reading Problems: developmental dyslexia: a case study. Ann Neurol 1979;6:94-100. Including Vision, Perception, Motor Skills, 2nd edition. Culver City, 25. Duffy FH, Denckla MD, Bartels PH, Sandini G, Kiessling LS. CA: Reading and Perception Therapy Center, 1999. Dyslexia: automated diagnosis by computerized classification of brain 55. Halapin R. Halapin Learning Systems, Inc. Trumbul, CT 06611, 1995. electrical activity. Ann Neurol 1980;7:421-28. 56. Solan HA, Mozlin R, Rumpf DA. Selected perceptual norms and their 26. Fried I. Tanguay PE, Boder E, et al. Development of dyslexia: relationship to reading in kindergarten and the primary grades. J Am electrophysiological evidence of clinical subgroups. Brain Lang Optom Assoc 1985;56:458-67. 1981;12:14-22. 57. Ingersoll, SJ. Syntonics and reading instruction: integrated visual 27. Rosenthal JH. EEG Event-Related Potentials in Dyslexia and its learning. J Optom Vis Dev 2002;33:142-52. Subtypes. In: DAB Lindberg, MF Collen, EE Van Brunt, eds. AMIA 58. Ridder WH, Borsting E, Banton T. All developmental dyslexic Congress on Medical Informatics (1st: 1982: San Francisco). New subtypes display an elevated motion coherence threshold. Opt Vis Sci York: Masson Pub, 1982. 2001;78:510-17. 28. Roeltgen DP, Sevush S, Heilman KM. Phonological agraphia: writing 59. Lawton TL. Training directionally-selective motion pathways can by the lexical semantic route. Neurol (Cleveland) 1983;33:755-65. significantly improve reading efficiency. Human Vision and Electronic 29. Hynd GW, Hynd CR. Dyslexia: neuroanatomical/neurolinguistic Imaging IX, ed. BE Rogowitz and TN Pappas, roc. Of SPIE-IS&T perspectives. Reading Res Q 1984;19:482-98. Electronic Imaging, SPIE. Vol. 5282, 34-45, 2004. 30. Roeltgen DP, Heilan KM. Lexical agraphia. Brain 1984;107:811-827. 60. Lawton T (1997). Reading mediated by inhibitory networks in 31. Flynn JM, Deering WM. Subtypes of dyslexia: investigation of magnocellular streams. Soc Neurosci Abstract. New Orleans, LA, Boder’s classification system using quantitative neurophysiology. Dev 1997. Med Child Neurol 1989;31:215-23. 61. Lawton T (2002). Figure/Ground and left-right movement 32. Hynd GW, Semrud-Clikeman M. Dyslexia and neurodevelopmental discrimination developing when child is learning to read (abstract). pathology: relationships to cognition, intelligence, and reading skill Journal of Vision. 2(7), 32a, , doi:10.1167/2.7.32. acquisition. J Learn Disab 1989;22:204-16. 62. Lawton T. Reading fluency improved significantly by strengthening 33. Ridder WH III, Borsting E, Cooper M, et al. Not all dyslexics are directionally-selective motion pathways, annual meeting of Society for created equal. Optom Vis Sci 1997;74:99-104. Neuroscience, slide presentation, Visual Cortex: Motion. Nov 10, 1 34. Shaywitz SE, Shaywitz BA, Pugh KR, et al. Functional disruption in PM, New Orleans, LA. 2003. the organization of the brain for reading in dyslexia. Proc Natl Acad 63. Wesson MD, Griffin JR, Christenson GN. Pre-dyslexia Letter Coding Sci USA 1998;95:2636-641. Test (PLCT). Culver City, CA: Reading and Perception Therapy 35. Ridder WH III, Borsting E, Banon T. Dyseidetic and dysphonetic Center, 1991. dyslexics display an elevated motion coherence threshold. Inves Ophth 64. Griffin JR, Walton HN. Dyslexia Screener for First-Graders (DFS). Vis Sci (Suppl) 1998;39:401. Culver City, CA: Reading and Perception Therapy Center, 1990. 36. Griffin JR. Genetics of dyseidetic dyslexia. Optom Vis Sci 65. Griffin JR, Christenson GN, Walton HN. The Adult Dyslexia Test 1992;69:148-51. (ADT). Culver City, CA: Reading and Perception Therapy Center, 37. Lovegrove W, Brown C. Development of information processing in 1990. normal and disabled readers. Percept Mot Skills 1978;46:1047-54. 66. Griffin JR, Walton HN, Gonzalez-Lind Y. Spanish Screening Version 38. Badcock D, Lovegrove W. The effects of contrast, stimulus duration, of the Dyslexia Determination Test (DDT). Los Angeles: Instructional and spatial frequency on visual persistence in normal and specifically Materials & Equipment Distributors, 1989. disabled readers. J Exp Psychol Hum Percept 1981;7:495-505. 67. Griffin JR, Walton HN, Christenson GN, Ward L. Test De Dépistage 39. Eskenazi B, Diamond SP. Visual exploration of nonverbal material by De La Dyslexie. Culver City, CA: Reading and Perception Therapy dyslexic children. Cortex 1983;19:353-70. Center, 1996. 40. Williams MC, Brannan JR, Lartigue EK. Visual search in good and 68. Griffin J, Walton H, Ward L. Test De Dyslexie (TDD). Culver City, poor readers. Clin Vis Sci 1987;1:367-71. CA: Reading and Perception Therapy, 1998. 41. Meares O. Figure/ground, brightness contrast and reading disabilities. 69. Griffin JR, Walton HN, Christenson GN. Decoding-Encoding Screener Visible Lang 1980;14:13-29. for Dyslexia (DESD). Los Angeles: Western Psychological Services, 42. Rosner J, Rosner J. The Irlen treatment: a review of the literature. 2005. In press. Optician 1987;194:26-33. 70. Hussey ES. Speculations on the nature of visual motion with 43. Blaskey P, Scheiman M, Parisi M, et al. The effectiveness of Irlen optometric implications. J Behav Optom 2003;14:115-19. filters for improving reading performance: a pilot study. J Learn Disabil 1990;23:604-12. 44. Joint organization statement on the eye and learning disabilities, American Academy of Pediatrics, American Academy of

32 Optometry and Vision Development Appendix. Explanation of Halapin Vowel Mat and Necessary Visual Processing Skills Areview of the vowel mat (multisensory written language therapy technique of Halapin55) demonstrates that the procedure is designed to teach reading dysfunctional persons: 1) the long and short vowel sounds, 2) the ability to blend consonants with vowels in a left to right spatial direction (where the sounds represented by the symbols on the left come earlier in time than the sounds represented by the symbols on the right–as in reading) and 3) the concept of open syllables (where the vowel makes the long sound, e.g., ba) and the concept of closed syllables (where the vowel makes the short sound, eg., ab). This review of the goals of the vowel mat therapy allows for analysis of the requisite visual processing skills which the patient must have mastered in order to be able to engage in the task. A closer look at the procedure itself is useful to illustrate the complexity and level of integrated visual function necessary for the youngster to benefit therapeutically from the task. In one of the higher levels of the therapy with the vowel mat the patient is required to walk through the mat (see Figure 4), stepping alternately on the letter and then the picture, using a cross pattern movement in rhythm with a metronome (usually 60 beats per minute), while calling of ba, ab, bi, ib, bo, ob, bu, ub, be, eb (alternating the long and short sounding of the vowels as described earlier). Analysis of the task, as briefly described, shows that the some of the specific visual processing skills required to accomplish the task include: 1) laterality and directionality, 2) visual form perception, 3) visual figure-ground, 4) visual-motor integration, and 5) auditory-visual integration. This provides part of the rationale for treatment of deficient visual processing skills with vision therapy in cases where dyslexia co-exists with visual processing Figure 4. Halapin Vowel Mat deficiencies.

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