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Several behavioral studies have shown that developmental dyslexics do poorly in tests requiring rapid visual processing. In primates fast, low-contrast visual information is carried by the magnocellular subdivision of the visual pathway, and slow, high-contrast information is carried by the parvocellular division. In this study, we found that dyslexic subjects showed diminished visually evoked potentials to rapid, low-contrast stimuli but normal responses to slow or high-contrast stimuli. The abnormalities in the dyslexic subjects' evoked potentials were consistent with a defect in the magnocellular pathway at the level of visual area 1 or earlier. We then compared the lateral geniculate nuclei from five dyslexic brains to five control brains and found abnormalities in the magnocellular, but not the parvocellular, layers. Studies using auditory and somatosensory tests have shown that dyslexics do poorly in these modalities only when the tests require rapid discriminations. We therefore hypothesize that many cortical systems are similarly divided into a fast and a slow subdivision and that dyslexia specifically affects the fast subdivisions.

Does a third subtype of dyslexia analoguos to the “third alexia” that accompanies Broca's aphasia exist? Statistical analysis of data obtained from 17 young dyslexic adults and 15 reading-disabled children revealed that not only a variety of dyslexia symptomatically similar to the third alexia exists, but also sub-types of dyslexias resembling other forms of alexias exist.

An experimental investigation of a single patient, CAV, with an acquired dyslexia in which there was a significant impairment in his ability to read concrete words compared with abstract words is reported. CAV's ability to identify single letters and non-words was very impaired. His comprehension of words he could not read was poor and semantic primary effects were demonstrated. His concrete word dyslexia was characterized by a lack of consistency and by a high incidence of visual errors. Both quantitative and qualitative aspects of this hitherto undescribed syndrome are in some respects similar to those described in patients with the complementary syndrome of relative impairment of abstract word reading. It is argued that this concrete word reading deficit provides a further example of category specificity in the organization of the semantic systems subserving reading.

It is argued here that the most general information processing deficit in developmental dyslexia lies in phonological processing and that studies of individual differences in reading development where intelligence is controlled generate patterns of associations which are essentially similar to those which arise from studies of developmental dyslexia. Developmental dyslexics are shown to resemble acquired surface dyslexics but they are even more similar to younger children of equivalent reading ability. Also, it is argued that a complete understanding of the development of reading can come only from longitudinal investigations of development itself. Such studies demonstrate typical sequences of interactive growth of related skills. They show how reading changes in nature as it is learned and that a crucial early stage in its development is the adoption of an alphabetic reading strategy. The precursors of the phonological knowledge that forms the foundations of grapheme-phoneme reading are traced back throu...

Two cases of acquired spelling dyslexia and one case of developmental spelling dyslexia are described along with accounts of their performance on various psycholinguistic tasks. It is argued that there is some evidence that spelling dyslexia may exist in developmental form but that parallels are difficult to draw because of the very different histories of child and adult cases. It is also suggested that features of surface dyslexia exist in at least a proportion of spelling dyslexic cases and that this may be influenced by level of premorbid reading skill.

Jorm (1979a) summarized data demonstrating short-term memory(STM) impairment in reading-disabled children, and argued for STM deficit as the cause of developmental dyslexia. In this review it is suggested that evidence for impoverished conceptualization of surface features of language (weak “linguistic access”) among poor readers needs to be accounted for in any overall theory for dyslexia. The possibility that STM deficit is responsible for poor performance in measures of linguistic access is considered and found not to account for all of the data, for example, the finding that training in manipulation of phonemic structure can speed reading acquisition. It is argued that failure on the part of some children to recruit linguistic processes for purposes outside their adaptive specialization may account for both STM impairment and reading difficulties. The need for theory and experiment-based advances in clarifying the concept of linguistic access is noted.

Within the past decade significant advances have been made in articulating the unique neuropsychological and cognitive processes in dyslexic children. The brain mapping procedures and post-mortum studies are especially important in this regard. However, two important issues remain largely unaddressed. First, to date, no recognized nosology for dyslexia or subtypes of dyslexia exist. Second, the functional neurolinguistic system involved in reading and severe reading failure is, as of yet, still not completely understood in regard to subtypes of dyslexia. This article discusses these two areas of priority and proposes a framework for addressing these areas of concern.

It was recognized at a relatively early stage of medical history that injury or disease of the brain in adult patients could cause a loss of a specific cognitive skill such as the ability to name objects or the ability to read. Indeed observations of this type were often employed as an argument in favor of localization of function in the brain. Thus specific anomia or "loss of memory for words" was clearly described in the 16th century and the syndrome of alexia without agraphia was identified in the 17th century. But neither physicians nor educators were as quick to recognize that children might also suffer from specific cognitive disabilities as a consequence of congenital or early acquired disease. It was only in 1853 that the Dublin otologist, William Wilde, published his observations on children who were "dumb, but not deaf," i.e., suffering from specific language disability. As we know, developmental dyslexia went unrecognized until the end of the 19th century when Morgan published his famous case report. As so often happens, once the attention of physicians was called to the condition, they immediately observed it in their practice and a steady stream of papers on dyslexia appeared in the English and German medical literature between 1900 and 1910. Somewhat later, clinical psychologists recognized dyslexia as a distinctive condition and attempted to relate its occurrence to more basic defects in visualization, auditory perception and associational processes. On the other hand, educators were less ready to accept the real existence of "congenital wordblindness" as a clinical entity.

Deep dyslexia is an acquired reading disorder in which the substitution of semantically, but not visually, similar words in single word reading sometimes occurs. For example, city may be read as town or large as big. It has been reported in individuals who have sustained left hemisphere injuries as adults. The purpose of this paper is to provide evidence for a parallel between deep dyslexia and certain kinds of developmental dyslexia. In this chapter, a case of deep dyslexia in an adult female who sustained a left hemisphere cerebrovascular accident is described. In addition, the reading and language behavior of six children with severe reading disorders who show certain characteristics which are similar to the adult deep dyslexic are also described. Deep dyslexia implies the severe impairment of phonological processing in reading because of the nature of the reading errors and the inability to read nonwords. While this impairment of phonological processing influences certain aspects of reading, the performance of deep dyslexics implies that the use of a phonological code is not necessary for word recognition. The nature of the errors in deep dyslexia demonstrates the importance of semantic processing in reading and suggests that semantic networks may be relatively intact, although phonological processing is negligible or nonexistent. In the case of the young children, however, it can be said that semantic processing of the written word may have been developed earlier than phonological processing. It follows that the presence of deep dyslexic symptoms in both adults and children suggests the primacy of semantic processing in the earlier or more primitive stages of reading.

Intensive testing of two dyslexic college students revealed that their symptom complexes have a striking resemblance to those exhibited by some alexic patients who have lost their ability to read as a result of brain damage. Such a similarity provides support to the views that developmental dyslexia manifests in forms of clearly circumscribed syndromes and that its etiology is primarily neurological.

The discovery of biological substrates underlying medical conditions is an important step for their better understanding and for the design of appropriate medical therapies. In the case of developmental dyslexia pedagogic treatment may fail, thus creating a group of individuals in whom medical approaches may be entertained. The biological substrate(s) of developmental dyslexia has yet to be specified, although a few clues are beginning to emerge. In this review I consider the issue of cerebral dominance and brain asymmetry, the development of the cerebral cortex and examples of aberrancy, and diseases of the immune system, all of which relate to recent anatomical and epidemiological findings in developmental dyslexia. These discoveries have been able to lead to the creation of testable hypotheses which, after appropriate experimental work, are apt to enhance our current understanding of this and other developmental learning disorders.

The study of learning disabilities has entered an era in which neural models play a primary role (Chall and Mirsky, 1978; Cruickshank, 1980; Gaddes, 1980; Kinsbourne and Caplan, 1979; Knights and Bakker, 1976). Factors such as family dynamics, emotional adjustment, and motivation, which attracted considerable attention from learning-disability specialists in the past, have been de-emphasized in favor of neurological factors such as perceptual and attentional disorders, neurodevelopmental lag, and cerebral dominance. In this respect, Samuel Orton's (1937) general position with respect to the neural basis of learning disability--a minority viewpoint in the 1920's and 1930's---has become established in the mainstream of contemporary thinking about dyslexia and associated disorders. Prominent among the neural models of dyslexia are those that attribute reading disorders to a defect in cerebral dominance. Thus, not

Despite recent developments in research and theory, investigators and practitioners continue to rely on rather traditional definitions of dyslexia. This paper discusses some of the problems with traditional definitions and reviews a rapidly growing body of research that suggests a more comprehensive definition. According to this definition, dyslexia is a developmental language disorder that involves a deficit(s) in phonological processing. This disorder manifests itself in various phonological difficulties as well as a specific reading disability.

Adult developmental dyslexics showed deficits in the identification of the vowels of English when the sole acoustic cues were steady-state formant frequency patterns. Deficits in the identification of place of articulation of the English stop-consonants [b], [d] and [g] in syllable-initial position were also observed. The average vowel error rate was 29%. The average consonantal error rate was 22%. These error rates are significantly different from those of nondyslexic control groups (p < .01). No single deficit characterized the entire group of dyslexic subjects. The pattern of errors with respect to place of articulation also varied for different groups of subjects. Three dyslexics have high vowel error rates and low consonantal error rates. The data are consistent with the premise that dyslexic subjects may have different perceptual deficits rather than a general auditory deficit involving the rate at which they can process perceptual information. The clinical histories of the present subjects suggest genetic transmission of these speech perception deficits. The presence of genetic variation in the biological substrate relevant to the perception of human speech should be further explored.

This paper investigates the reading performance of two patients with acquired dyslexia. The first patient read aloud all classes of word (85–95 per cent correct), including affixed words, but failed to read aloud non-words. In addition, semantic judgements about written words were shown to be significantly impaired, relative to the ability to read the words aloud. These dissociations support the view that two independent lexical routes are available for reading aloud familiar words, a semantic route and a lexical phonological route. While unable to read aloud non-words, this patient retained the ability to segment orthographic and phonological stimuli. The reading of non-lexical material, therefore, does not appear to be mediated by lexical analogy procedures. Instead, it is suggested that a non-lexical phonological route exists that is clearly independent of lexical phonological procedures. This patient could process isolated written suffixes orthographically, but could only access complete phonological word forms. Suffixed words (but not isolated suffixes) appear to be represented in the phonological word store. The second patient read aloud non-words, but could not give phonetic sounds appropriate to single letters. This dissociation suggests that the reading aloud of non-words is not reliant upon grapheme-phoneme rules.

Theories of dyslexia are characterized by the special emphasis they place on either linguistic or nonlinguistic factors as causes of reading disability. 1 This paper will discuss emerging evidence in favor of the linguistic interpretation of dyslexia. The works of linguistic philosophers, such as Ludwig Wittgenstein, who argue that our personal language reflects our experiences and percep tions of reality, lend support to a linguistic theory of dyslexia. Linguistic philosophers view language as the window through which we perceive meaning in our world (Engle 1970; Wittgenstein 1953, 1958, 1961a, 1961b). When symbols represent real events or thought, language is critical for interpretation. The underlying hypothesis for a linguistic theory of dyslexia is that, regardless of the nature of a child's learning handicap (e.g., perceptual, motor, or memory deficits), the specific problem will eventually manifest itself in language functioning and, as such a child approaches the task of reading, these cumulative verbal deficits will hamper his success in decoding and comprehension (Clinkert 1977). To understand the verbal deficit hypothesis, one must allow an extension of the ordinary definition of language to include the concept of semiotics. Semiotics expands the notion of conventional language to include signs and symbols,2 so that mathematics, for example, is a language with a specialized syntax and vocabulary.

This paper relates the early work of Samuel Orton on cerebral dominance to the current neuropsychological concept of laterality as reciprocal functions of the two cerebral hemispheres. The genetic-cultural perspectives of laterality and functional asymmetry in relation to learning disorders are discussed. A balanced and integrative view of the cognitive contribution of the two hemispheres is needed.

An overview of the literature on developmental dyslexia is offered, moving historically from attempts to identify a single underlying deficit to more recent efforts to define different subtypes of this developmental disorder. Two approaches to the subtyping problem are illustrated and briefly discussed. It is suggested that many of the remaining questions in dyslexia research could be more profitably addressed within the context of a coherent model of reading behaviour. In the latter half of this review, the potential implications of some aspects of the interactive reading theories for the study of reading dysfunction are explored.

Observations and tentative hypotheses regarding recognition, treatment, and management of the symptoms of dyslexia are discussed from within a model of dyslexia as a neurological dysfunction of gen...

Evidence of different syndromes of developmental dyslexia raises the question of the interaction between dyslexic types and patterns of cerebral dominance. Some of the proposed classifications of dyslexia, and most notably the one proposed by Boder (1971), strongly suggest that dyslexic subtypes, that can be identified clinically by reading-spelling patterns, may possess different or opposite cerebral dominance patterns. Thus, research of cerebral dominance in dyslexia (i.e., Orton’s hypothesis) should involve careful selection and classification of subjects. When this is done it can be shown that electrophysiological measures can identify cerebral-dominance abnormalities in at least one subtype of developmental dyslexia.

Two years ago, at the annual meeting of this Society, I was approached by someone who told me that she was distressed to discover that The Orton Society "had now adopted the medical model and had abandoned what should have been its major interest," i.e., the re-education of the dyslexic child. I replied with two statements. The first was that I had seen no evidence at all that the Society had given up its interest in developing training programs for the dyslexic, and, indeed, it is clear both from the program of that meeting and the program of this one that most of the presentations are devoted to this very topic. My second answer was that, after all, this was The Orton Dyslexia Society, and that if one were aware of just what Samuel Torrey Orton had said and done, it would become immediately obvi ous why The Orton Dyslexia Society had decided to devote a portion of its energy to the study of the brain. It is fascinating to reconstruct the history of the awakening of Dr.

The well-constructed study by Seidenberg, Bruck, Fornarolo, and Backman (Applied Psycholinguistics, 6(2)) is an example of the difficulties that occur when good hypotheses and elegant designs are at variance with the realities of developmental reading disorders. My goal in this essay is to use the Seidenberg et al. study as a kind of informal assessment – both of progress in our approaches to dyslexia and of the significant issues that remain, particularly the impact of varied assumptions about homogeneity in severely impaired readers.

The nature of the underlying causes of paralexias produced by a patient exhibiting the syndrome of deep dyslexia was explored by pairing an oral reading task with a picture matching task using the same words. The results suggested two causes of semantic paralexias: word retrieval difficulties and impaired concept arousal. Parallel deficits in language tasks not involving written words were found. It is suggested that the major component of the deep dyslexia syndrome may reflect a deficit which is not specific to the written modality.

This review examines issues and research relating to the involvement of the central nervous system in reading disorders. Questions regarding subtypes, pre- and perinatal influences, genetics, sex differences, and early identification are briefly surveyed along with a summary of major research findings in neuropsychology and neurology. Particular attention is devoted to the assessment of the brain-deficit model vis-à-vis the maturational-lag model of developmental dyslexia. Neither theory can adequately account for the entire population of dyslexics. For progress to be made in this area, attention must be focused on theory articulation and reformulation in addition to methodological and taxonomic advances.

Handwriting is a spatial-temporal activity. It represents a fixed expression of space and motion. Like hypnotism, graphology is being removed from the parlor and included in the professional's kit as a psychodiagnostic tool. Little research in this area has been done in the United States although it has received a great deal of attention in Europe. This paper explores the possibility that certain deviations from norm may indicate the presence of dyslexia.

There is growing interest in differentiating developmental dyslexia,1 as a specific psychoneurological learning disorder, from nonspecific reading retardation. Such differentiation has immediate practical bearing since spe cific dyslexia calls for remedial reading techniques that are not required in the management of nonspecific reading disorders. Moreover, early diag nosis of developmental dyslexia is essential for successful remediation and to prevent school failure with concomitant loss of self-esteem. The need for practical direct diagnostic criteria that would facilitate the early identification of developmental dyslexia has come into the fore front. This need is felt especially by physicians and psychologists, who are often the first to be consulted about the child's inability to read. It is also recognized that the diagnosis cannot be relevant to the educator unless it has immediate implications for remediation. The objectives of this paper are: (1) to present a critical review of pre vailing diagnostic concepts of developmental dyslexia and (2) to briefly describe three atypical patterns of reading and spelling, revealed through

Developmental dyslexia is a condition which means inability to read adequately even with proper teaching. The main purpose of this study was to determine the status of binocular vision skills in relation to developmental dyslexia. The results of the survey indicate that though visual acuity is a non-essential factor, nevertheless binocular eye coordination is evidently a major visual dilemma in dyslexic students.

This paper sets out to providc a theoretical approach to cognitive functions and their acquisition, and includes discussion of brain damage, heredity, and family environment as factors in the genesis of dyslexia. The presence of “noise,” not only in the brain itself, but also in the input data which it has to process, implies that inference must play an important part in many psychological processes; language acquisition in particular appears to be one type of pattern-detection process involving inference. Whenever inferential procedures are used, standards of inference must be adopted. A method of estimating the standard (D) adopted by an individual on a given occasion, in a recognition-learning situation, is described and explained. If a child habitually adopted excessively lax or stringent standards in all matters or in specific areas of cognitive growth such as language or reading acquisition, this overconfident or overcautious attitude would have deleterious effects. It is shown that in 33 families attending a dyslexia clinic, a much higher proportion of the children than of their fathers or mothers had abnormally high or low D values by comparison with normal young adult students.

(1) Twelve cases of reading disability in school children are presented. An assessment of perceptual capacities and skills is reported and the findings are interpreted with reference to the developmental history and familial factors. (2) Reading disability did not occur in isolation in the group. Directional difficulties and difficulties in drawing and copying were characteristic of the group as a whole, but in no case was there an impairment of non-verbal form perception. (3) Confusion among letters was found in 50 per cent of the cases. Letters were confused on the basis of visual resemblance and not acoustic resemblance. This finding, together with the nature of the associated disabilities led to the interpretation that dyslexia in these cases is a disorder of visual perception, often occuring independent of any defect in oral-auditory language development. (4) Evidence of minimal brain damage was found in 58 per cent of the cases. (5) The association of dyslexia with sinistrality and behaviour disorder is discussed.

In this paper I shall attempt to describe what has been and is meant by the terms "dyslexia," "specific dyslexia" and "developmental dyslexia"; common terms, which have become confusing because authors have used them in so many different ways. I shall discuss a number of clinical syndromes involving serious difficulties in learning to read and write in apparently healthy children of average intelligence which have been described in the literature. Some relevant work concerned with difficulties in learning to read and write carried out in the Department of Child Life and Health in the University of Edinburgh will be described.

being done to help the SLD child or adult. With this in mind, I attempted early in 1973 to contact several European colleagues who were involved in the diagnosis and remediation of specific language disabilities, especially dyslexia. Many people made my experience stimulating and informative. Only limitations of space prevent my sharing with readers a wealth of detail con cerning the innovative and valuable procedures these people employ. Any one visit could easily be the subject of an entire paper. It is good to know that so much is going on among our European friends and colleagues in the interest of the children who, whatever their mother tongues, seem so much like our own.

Informative, stimulating, warm and friendly, esthetically delightful and laced with creature comforts might describe any trip to Europe—or to most other places, for that matter. My recent visit was all that, but was focused on dyslexia and most of my time was spent with people who are as deeply interested and as effectively involved in the problem as any of us who are here. Like us, they are eager to learn what their opposite numbers across the water and on their own continent are doing. In the New British Dyslexia Association, now forming as a union of several local groups, a communication network is developing; and there are Polish-Czech interchanges, and within-country connections. However, I found quite frequently some sense of isolation from "dyslexia-international," even where within a country there were contacts and conferences. This was paral leled by interested, enthusiastic reception of your emissary-ecumenical from the Orton Society. For today's talk I thought of apologizing for not bringing you a full grown statistical analysis, but I think you will be glad to be spared that. I have neither the time nor the necessary hard data and, besides, in seven weeks I could only skim off some delicious cream. If you know of a well-funded graduate student or two, well-informed in the language field (for our friends over there are thus sophisticated), I'll be glad to help work out a dissertation plan, for which my trip can serve as a pilot study. I have my eye on one such person, but there's room for more, perhaps on a collaborative project. My next thought was to give you a running account, even though I haven't had time yet to review my 15 tapes and edit properly the 400 or so slides, but I'm not allowed to keep you here long enough for such an account. Besides, The Ancient Mariner was never an acceptable model. These statistics, though, I do have. Not counting a couple of lecture groups, and the children in a score or more of classrooms, I saw individually on professional matters at least 112 of our colleagues (and often also their relatives and non-dyslexia-related friends). Most particularly, I bring you

Developmental dyslexia is a common learning disability characterized by normal intelligence but difficulty in skills associated with reading, writing and spelling. One of the most prominent, albeit controversial, theories of dyslexia is the magnocellular theory, which suggests that malfunction of the magnocellular system in the brain is responsible for the behavioral deficits. We sought to test the basis of this theory by directly measuring the lateral geniculate nucleus (LGN), the only location in the brain where the magnocellular and parvocellular streams are spatially disjoint. Using high-resolution proton-density weighted MRI scans, we precisely measured the anatomical boundaries of the LGN in 13 subjects with dyslexia (five female) and 13 controls (three female), all 22–26 years old. The left LGN was significantly smaller in volume in subjects with dyslexia and also differed in shape; no differences were observed in the right LGN. The functional significance of this asymmetry is unknown, but these results are consistent with the magnocellular theory and support theories of dyslexia that involve differences in the early visual system., Graphical abstract, Highlights • The first direct test of the magnocellular hypothesis of dyslexia in vivo • The first measurements of the LGN in living subjects with dyslexia • The LGN are smaller in subjects with dyslexia and differ morphologically

Spanish-speaking children learn to read words written in a relatively transparent orthography. Variations in orthographic transparency may shape the manifestation of reading difficulties. This study was intended to help clarify the nature of developmental dyslexia in Spanish. Developmentally Dyslexic children (DD) were compared to a chronological age-matched control group (CA). Measures included rapid automated naming, verbal working memory, phonological short-term memory, and phonemic awareness. Results demonstrated that developmental dyslexics show reading-related cognitive deficits in areas such as naming speed, verbal working memory, phonological short-term memory, and phonemic awareness. Our results are consistent with studies conducted in the Spanish language and in other transparent orthographies.

Katz, Healy and Shankweiler investigated poor and good readers' performance on two order recall tasks which were differentiated by the extent to which phonetic memory strategies were employed. Contrary to their predictions, they found that poor readers were significantly impaired on both tasks. They attributed this unexpected finding to the rate at which stimuli were presented. However, results of studies that have experimentally manipulated rate of stimulus presentation in order recall tasks have demonstrated the opposite results to those predicted by these authors. The results of the present study support the hypothesis that poor readers are impaired in recalling the order of rapidly presented successive events.

Publisher Summary This chapter discusses the psycholinguistic nature of dyslexic errors and the additional dysphasic symptoms that appear to accompany the component features of an error taxonomy. A distinction has traditionally been made between pure word-blindness—attributed to a disconnection between visual cortex and language areas—and dyslexia accompanied by dysgraphia, usually in the setting of a more generalized disturbance of language functions. It has been suggested that patients with pure or agnosic alexia tend to be better at letter-naming than word-reading, whereas the converse pattern is associated with aphasic dyslexia. It appears that the acquired disorders of reading can be placed on a continuum according to the extent and severity of the associated symptoms of dysphasia. Furthermore, a number of variables have to be taken into account when describing the restitution or improvement of language skills. These include the etiology and natural history of the disease, the underlying anatomophysiological basis, and the changing pattern of linguistic error. Remedial programs and prognosis are dependent on these and other critical factors.