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Developmental Dyslexia
Developmental Dyslexia MACDONALD CRITCHLEY, M.D., F.R.C.P. (London) 0
The world is like that, a perilous world for those who cannot learn to read. It must be so. We cannot fence every peril so that the unlettered may take no harm from it. There is free and compulsory education: at least everybody has his chance of learning his lessons in school. The world's business is ordered on the understanding that everybody can at least spell out words. vVe walk in obedience to the written word. All about us are boards and placards, telling us to do this thing or to keep from doing that other thing. Keep to the Right, we are bidden, or else we are to Keep to the Left. By this stairway we are to descend to enter the train that goes Westward: by that we go to the Eastward train. Way Out and Way In; Private; Trespassers will be prosecuted; Pit Entrance; the street's name and the name of the railway station-all of these things are cried out to us by that wonderful device of letters, a babble of voices which make no sound. It is hard for us to understand the case of those to whom these many signs and warnings say nothing. They must move as though bewildered, as though they were blind and deaf. No warning touches them, not even that of the board which, like the board of the Southend tramway, cries Danger and Beware. Yet they go about their business in that darkness, in that silence. In some fashion they move, keeping shyly beside us lettered folk. Last month one of them sat near to me in a carriage of the underground railway. He asked me how many stations lay between us and the Monument station. I told him that we were not yet near the Monument, but that he was in the right train. But this was not enough: he must needs tell me that he could not read so much as a station's name. THE
'
CASE OF THE UNLETTERED. LONDON EvENING NEws, AuGUST
9, 1926
From out of the gallimaufry within the population of poor readers, late readers, retarded readers, slow readers, near-illiterates, hopeless spellers and mirror-writers, there emerges a comparatively clear-cut type of problem known as developmental dyslexia. First described in England in 1896 by two physicians, quite independently, the condition was, to begin with, spoken of as "congenital word-blindness." Many other cases were soon recognised and reported, mainly by ophthalmologists, who were often the first specialists to be consulted. Within a few years this condition became identified in other parts of the world, and the first American cases were published 10 years later by Schapringer. " Institute of Neurology, London, England Pediatric Clinics of North America-Val. 15, No. 3, August, 1968
669
670
MACDONALD CRITCHLEY
Congenital word-blindness soon became accepted within the corpus of neurologic teaching, though regarded as something of a rarity. It was looked upon as on a par with other inherent retardations within the domain of language, such as congenital auditory imperception, delayed acquisition of articulate speech and perhaps also constitutional dyscalculia. Neurologists accepted the notion, but were perhaps at fault in neglecting to delve more deeply into some of the obscurities, such as surrounded the questions of aetiology, distribution and prevalence, genetic considerations, association with other neurologic abnormalities, prognosis and rational therapy. An important landmark in the dyslexic scene was the work of Samuel T. Orton of Iowa, who in 1925 drew attention to the errors of writing and spelling shown by children with congenital word-blindness, in particular a tendency towards confusing letters like d and b; a frequent rotation of individual letters so that they were oriented towards the left rather than the right; and reversals of groups of letters or syllables. Sometimes a veritable mirror-writing was encountered. Many normal children go through a brief phase of perpetrating reversals in their earliest efforts to read and write, but Orton pointed out that word-blind children continue to make this type of error for an undue period of time. Orton also found a tie-up with left-handedness. Orton referred to this syndrome as "strephosymbolia," but this term never passed into neurologic currency. After a period of relative neglect, congenital word-blindness once more attracted attention. Perhaps it was the work of various Scandinavian physicians which was responsible for this revival of interest. Hallgren in 1950 became involved in the genetic aspect of the problemthough earlier writers such as C. J. Thomas, J. H. Fisher, S. Stephenson, Hinshelwood, McCready, Plate, Warburg, Illing, Norrie, Skydsgaard and others had already referred to a familial incidence of congenital wordblindness. Hallgren's material, based upon 276 cases, led to the conclusion that a monohybrid autosomal dominant mode of inheritance was operative. Then followed a number of studies of this disability among twins (Hallgren, Norrie, Branden, Ley and Tordeur, Jenkins, Brown and Elmendorf, Schiller). That males were apparently more often affiicted than females also came to light at about this time. From the Scandinavian countries too came some attempt to estimate the frequency of occurrence, and Hallgren considered that 10 per cent of the school population in Sweden were affiicted in this way. About this time the term word-blindness was dropped in favour of the Greek equivalent "dyslexia," often preceded by the adjectives "specific" or "developmental" or both together. The Scandinavians and particularly the Danes were also the pioneers in the rational treatment of dyslexia, and also in this connection the names of Norrie and of Hermann are con-
671
DEVELOPMENTAL DYSLEXIA
spicuous. In Copenhagen there took place the first official attempt upon a governmental scale to identify these cases from out of the population of semi-illiterates, and to provide systematic instruction in a Word-Blind Institute. Nowadays the interest in this subject is considerable, and the centres of principal attention have reverted to Great Britain and to the United States. A special Research Group of the World Federation of Neurology has been set up in order to achieve an international perspective of the problem. Though of topical interest, developmental dyslexia is still surrounded by a number of obscurities regarding its precise nature-its prevalence, world distribution, aetiology, prognosis and appropriate management. It is now realised that the problem of dyslexia is one aspect of the question of general illiteracy, and that peculiar sociologic problems are involved. For example, an important tie-up has been found between untreated dyslexia and juvenile delinquency.
DEFINITION
No adequate definition exists which is both terse and universally acceptable. However, we can tentatively suggest a rather cumbersome attempt at formulation. Developmental dyslexia entails a specific difficulty in learning to read, often genetically determined, which exists despite a level of general intelligence which is at least average; without any primary emotional disturbance or gross brain pathology; without significant impairment in hearing or in vision; and without any deficiency in conventional instruction. In ordinary circumstances, the difficulty in reading persists in some degree into adulthood and is associated with a peculiar difficulty with spelling. Sometimes it is the latter which brings the patient to medical or scholastic attention, and a previous mild dyslexic state may be overshadowed by a veritable "specific spelling disability." The question of the essential aetiologic nature of developmental dyslexia is still a matter of discussion, if not indeed of controversy.
PSYCHOLOGICAL ASPECTS
Though developmental dyslexia has long been accepted within the corpus of accepted neurologic teaching, a different attitude became adopted at one time by many nonmedical and educational psychologists. Stemming in all probability from an opinion put forward two or three decades ago by an authoritarian psychologist of particular eminence, it was accepted without question. Thus it became fashionable at one time
672
MACDONALD CRITCHLEY
to ignore or even deny the existence of developmental dyslexia. In its place was raised the conception of a continuum or a kind of spectrum of reading retardation, ranging from the stupid or inattentive at one end of the scale, to the intelligent but neurotic at the other extremity. In the latter event, environmental or exogenous factors were blamed rather than those which were constitutional or endogenous; circumstances such as broken homes, pupil-teacher hostility, inter-sib jealousy, drunken fathers and wanton mothers were often advanced as causative. Some educationalists proclaimed dyslexia to be a diagnostic myth. Others conceded that it might exist, but that they had never encountered it, or that they were familiar enough with the problem, but that it was a psychologically determined condition, or a manifestation of a mental defect, or perhaps the result of starting a child's reading lessons too early, or too late, or of faulty techniques in teaching. It was even alleged that reading difficulties were the price we pay for the illogical spelling of the English language. So the blame fell upon one scapegoat after another-the teacher, the parents and the child. This way of thinking would not have mattered very much had it not become responsible for about 25 years of neglect of the child who could neither read well nor spell properly. Too often the unfortunate dyslexic became the victim of indignity, even sheer cruelty. If any "treatment" at all were undertaken, it consisted merely in the child being relegated to a guidance clinic and there handled as a problem in paediatric psychology. Individual remedial teaching was but rarely attempted. Within recent years the attitude has changed, and an increasing number of teachers and educational psychologists now admit the existence of a specific developmental type of dyslexia. Pains are taken to differentiate this condition from out of the larger population of poor readers; and furthermore, helpful methods of training are being sought.
OPHTHALMOLOGIC PROBLEMS
Many dyslexics-perhaps most of them-are referred sometime or other to an eye specialist to ensure that the failure to read has not been due to an impairment in visual acuity. It is usually a simple matter to exclude latent refractive errors, retinal disorders and lesions of the optic nerve and of the ocular media. There remain, however, one or two defects which are not as easy to dismiss as nonsignificant. For example, there is the question of faulty eye movements during the act of reading. By employing appropriate techniques it is possible to record the movements of the eyes, and important differences may be found between the performance in good readers and in bad. In the latter, there may be an increased number of fixation pauses, a greater tendency for regressive or backward movements, an unduly short span of words encompassed by each sweep, a liability for the eye to deviate from the middle of one
DEVELOPMENTAL DYSLEXIA
673
line to the line below, and also a difficulty in switching the gaze accurately from the end of one line to the start of the next ( '1inear dyslexia"). Sometimes the defect in ocular mobility is so considerable as to raise the suspicion of an underlying oculomotor apraxia. Defective eye movements during reading may account for the clinical phenomenon which is occasionally found in mild dyslexics, whereby they read large print better than small, for in the latter case the gaze is more apt to wander. Sometimes, however, it is the other way round. Oculomotor imbalance has at one time and in some limited areas been deemed responsible for dyslexia, and orthoptic correction has been practised in an effort to teach children to read. However, this form of training is rarely if ever carried out nowadays. It is usually considered that the faulty eye movements are the result and not the cause of poor reading ability. Yet another ophthalmic hypothesis has been suggested in an effort to explain the dyslexic's difficulty in reading. In the great majority of persons, whatever their handedness, the preferred direction of automatic lateral gaze proceeds from left to right. A contrary state of affairs is alleged to underlie the dyslexic's problem, especially in those who are left-eyed. As most languages are written in a dextrad fashion, notable exceptions being Hebrew and Arabic, the dyslexic would automatically tend to sweep his gaze against the stream, and confusion is the result. Unfortunately there is no evidence whatever to support this hypothesis, and in every dyslexic whom I have tested, the automatic gaze has been from left to right, irrespective of the type of cerebral dominance. There is still another alleged correlation between dyslexia and a visuopsychic defect. It has been asserted that these children who are poor readers also fare badly in Bender's visual-motor Gestalt test, in the detection of buried shapes as in Gottschaldt's embedded figure test, and also in Benton's examination of visual memory and recall. These observations lead one to intrude into the territory of psychopathology, and may uncover processes which are secondary or operative, rather than primary or causal.
"MINIMAL" BRAIN DAMAGE
It is a common experience to find reading and writing difficulties in children diagnosed as "spastics." Some paediatricians, in revolt against the notion of reading retardation as a psychiatric disorder, have suggested that developmental dyslexia might be due to minor brain lesions, either perinatal or originating at a very early age. Clinical testing which goes deeper than the routine practice may, it is said, uncover various "soft" neurologic signs-so subtle as to elude a more cursory examination. Secondly, it has heen argued that a retrospective obstetric study of
674
MACDONALD CRITCHLEY
dyslexic children may bring to light a significant proportion of cases with cerebral trauma. A third argument has been adduced to the effect that electroencephalographic study of a dyslexic may reveal certain minor dysrhythmias. Furthermore, as the child perseveres with the difficult task of reading aloud, the cortical rhythm becomes so disturbed as to amount to a minor degree of subclinical "reading epilepsy." But against the acceptance of the hypothesis of minimal brain damage as being responsible for a primary type of developmental dyslexia are a number of arguments. No history of perinatal trouble or postnatal trauma or disease may be forthcoming. A positive family history of similar troubles with reading and spelling points to an endogenous constitutional disorder, and not one which is acquired. "Soft" neurologic. signs are often not demonstrable, especially in dyslexics in the second and third decades of life. Electroencephalographic abnormalities are inconstant, mild and probably not significant; the evocation of epileptiform discharges during the act of reading must be very rare, and has never occurred in any patient I have tested. The idea that a minor pathologic lesion could give rise to a persistent dyslexia is improbable from what we know of the resilience or plasticity of the juvenile cerebrum.
DYSLEXIA AS A COMMUNICATIVE DISORDER
It has also been suggested that the difficulty in reading is merely one facet of a general failure to achieve communication-a fragment of a congenital "aphasia." The alleged speech defects have been quite diverse and have included anomalies not only in the realm of language, but also in the peripheral articulatory mechanism. There are many objections to this communicative theory, and to describe the dyslexic's imperfect attempts to write as a "congenital dysgraphia" would be a misnomer. True, some developmental dyslexics have been comparatively late in acquiring speech, but this statement does not apply to all cases, or even the majority. The same objection invalidates the assertion that dyslexics talk imperfectly. Most dyslexics use spoken speech in an acceptable fashion from an early age. These "negative" cases -where speech attainment has been normal-argue strongly against any theory of developmental dyslexia as a general communicative disorder.
DYSLEXIA AS AN INSTANCE OF SPECIFIC MATURATIONAL LAG
Today, the most acceptable hypothesis is that of cerebral immaturity. A developmental dyslexic is often spoken of as a "late bloomer".,-to use
DEVELOPMENTAL DYSLEXIA
675
that faintly ridiculous term-but only in respect of the flowering of certain specific faculties. The minor or "soft" neurologic signs which are sometimes detected on close examination are best regarded not as evidence of minimal damage, but of cerebral immaturity. They occur far more often in dyslexics of young age-7 years or less-and they tend to disappear, examination of the older dyslexic being usually negative. Another argument in favor of dyslexia as an instance of cerebral immaturity is the commonly found lack of firm cerebral dominance. The incidence of left-handedness, ambidexterity and crossed laterality is comparatively high. Whether the inadequate unilateral dominance changes with the passage of time is an interesting question which we still cannot answer with confidence. The so-called ambidextrous cases probably show a progressive trend towards a right manual preference. Any study of cerebral dominance, whether in dyslexics or nondyslexics, uncovers a far more complicated state of affairs than is usually imagined. None of these various speculative ideas regarding aetiology touches upon the question of the pathopsychology. This is a quite distinct problem, and indeed it is open to argument whether the modus operandi of the reading difficulty is uniform in cases of developmental dyslexia, or wheijler subtypes exist, each with its own dynamic or physiologic defect. Many aspects of the dyslexia problem are still obscure, and form suitable topics for clinical research. For example, it may be asked whether dyslexia is an "ali-or-none" phenomenon, or whether it is possible to speak of severe cases and mild. And if so, does the difference imply an inherent property of the defect, or is it merely the resultant of associated variables? In the same vein, it is a matter for discussion whether developmental dyslexia is a uniform deficit or whether the underlying psychological mechanism varies quantitatively. The apparent diversity is perhaps due not to contrasting severity of the reading disability, but rather to the interaction of a stable basic deficit with differing influencessuch as, for example, intellectual status, degree of "ego strength," parental attitudes, the age at which the diagnosis is first arrived at, and the amount of remedial teaching the. dyslexic child has received. The foregoing represent some of the unsolved questions surrounding the problem of dyslexia. There are others as well, among which we may refer to the following: 1. The incidence of developmental dyslexia within the general population is not yet known precisely. We have already mentioned that it has been estimated by Scandinavian investigators that 10 per cent of all school-age children are dyslexic. One suspects that this estimate is too high for the United Kingdom and North America. It would be more plausible if it were qualified that the aforementioned 10 per cent referred to poor readers rather than specific dyslexics. The true incidence is a matter for educationalists to determine, and the accuracy of the findings will obviously turn upon the twin factors of definition and differential diagnosis.
676
MACDONALD CRITCHLEY
2. The geographical distribution of dyslexia is still not known. Most of the literature has come from English, American and Scandinavian sources, though dyslexia is also recognised in France, Germany, Italy, Spain, Rumania and Peru. It would be interesting to study the incidence of dyslexia in those races which employ a sinistrad type of script. We have already had experience of dyslexia in Arab and Hebrew-speaking children who have lived for a time in England. Still more intriguing would be a study of dyslexia among people who write from top to bottom (Chinese, Japanese); already the literature holds an isolated case report from Japan ( 1961). 3. We are still in doubt as to the optimum technique for instructing dyslexics. If it should prove correct that subtypes of developmental dyslexia exist, then it is possible that varying techniques should be tailored according to the dyslexic subject. Otherwise it might well prove that as with Kipling's tribal laws, everyone is right. 4. Is there such a state as reading readiness? And arising therefrom, is the question of the early preschool prediction of a dyslexic. Is this a possibility? And if so, can any rational steps be taken? It is clear from the foregoing remarks that the question of a specific type of reading disability constitutes a topical and highly important problem in present-day sociology, paedagogics and psychology.
REFERENCES A full bibliography up to 1964 is to be found in Critchley, M.: Developmental Dyslexia. London, William Heinemann Medical Books, 1964. Subsequent papers which may be consulted include: Critchley, M.: Is developmental dyslexia the expression of minor cerebral damage? The Slow Learning Child, 13:9-19, 1966. Critchley, M.: Some observations upon developmental dyslexia. ln Williams, D., ed.: Modem Trends in Neurology. London, Butterworths, 1967. Lesevre, N.: Les mouvements Oculaires d'exploration. These de Paris, 1964 (full bibliography). Thompson, J. L.: Reading Disability. Springfield, Ill., Charles C Thomas, 1966 (full bibliography). Institute of Neurology Queen Square London W.C. 1, England
The world is like that, a perilous world for those who cannot learn to read. It must be so. We cannot fence every peril so that the unlettered may take no harm from it. There is free and compulsory education: at least everybody has his chance of learning his lessons in school. The world's business is ordered on the understanding that everybody can at least spell out words. vVe walk in obedience to the written word. All about us are boards and placards, telling us to do this thing or to keep from doing that other thing. Keep to the Right, we are bidden, or else we are to Keep to the Left. By this stairway we are to descend to enter the train that goes Westward: by that we go to the Eastward train. Way Out and Way In; Private; Trespassers will be prosecuted; Pit Entrance; the street's name and the name of the railway station-all of these things are cried out to us by that wonderful device of letters, a babble of voices which make no sound. It is hard for us to understand the case of those to whom these many signs and warnings say nothing. They must move as though bewildered, as though they were blind and deaf. No warning touches them, not even that of the board which, like the board of the Southend tramway, cries Danger and Beware. Yet they go about their business in that darkness, in that silence. In some fashion they move, keeping shyly beside us lettered folk. Last month one of them sat near to me in a carriage of the underground railway. He asked me how many stations lay between us and the Monument station. I told him that we were not yet near the Monument, but that he was in the right train. But this was not enough: he must needs tell me that he could not read so much as a station's name. THE
'
CASE OF THE UNLETTERED. LONDON EvENING NEws, AuGUST
9, 1926
From out of the gallimaufry within the population of poor readers, late readers, retarded readers, slow readers, near-illiterates, hopeless spellers and mirror-writers, there emerges a comparatively clear-cut type of problem known as developmental dyslexia. First described in England in 1896 by two physicians, quite independently, the condition was, to begin with, spoken of as "congenital word-blindness." Many other cases were soon recognised and reported, mainly by ophthalmologists, who were often the first specialists to be consulted. Within a few years this condition became identified in other parts of the world, and the first American cases were published 10 years later by Schapringer. " Institute of Neurology, London, England Pediatric Clinics of North America-Val. 15, No. 3, August, 1968
669
670
MACDONALD CRITCHLEY
Congenital word-blindness soon became accepted within the corpus of neurologic teaching, though regarded as something of a rarity. It was looked upon as on a par with other inherent retardations within the domain of language, such as congenital auditory imperception, delayed acquisition of articulate speech and perhaps also constitutional dyscalculia. Neurologists accepted the notion, but were perhaps at fault in neglecting to delve more deeply into some of the obscurities, such as surrounded the questions of aetiology, distribution and prevalence, genetic considerations, association with other neurologic abnormalities, prognosis and rational therapy. An important landmark in the dyslexic scene was the work of Samuel T. Orton of Iowa, who in 1925 drew attention to the errors of writing and spelling shown by children with congenital word-blindness, in particular a tendency towards confusing letters like d and b; a frequent rotation of individual letters so that they were oriented towards the left rather than the right; and reversals of groups of letters or syllables. Sometimes a veritable mirror-writing was encountered. Many normal children go through a brief phase of perpetrating reversals in their earliest efforts to read and write, but Orton pointed out that word-blind children continue to make this type of error for an undue period of time. Orton also found a tie-up with left-handedness. Orton referred to this syndrome as "strephosymbolia," but this term never passed into neurologic currency. After a period of relative neglect, congenital word-blindness once more attracted attention. Perhaps it was the work of various Scandinavian physicians which was responsible for this revival of interest. Hallgren in 1950 became involved in the genetic aspect of the problemthough earlier writers such as C. J. Thomas, J. H. Fisher, S. Stephenson, Hinshelwood, McCready, Plate, Warburg, Illing, Norrie, Skydsgaard and others had already referred to a familial incidence of congenital wordblindness. Hallgren's material, based upon 276 cases, led to the conclusion that a monohybrid autosomal dominant mode of inheritance was operative. Then followed a number of studies of this disability among twins (Hallgren, Norrie, Branden, Ley and Tordeur, Jenkins, Brown and Elmendorf, Schiller). That males were apparently more often affiicted than females also came to light at about this time. From the Scandinavian countries too came some attempt to estimate the frequency of occurrence, and Hallgren considered that 10 per cent of the school population in Sweden were affiicted in this way. About this time the term word-blindness was dropped in favour of the Greek equivalent "dyslexia," often preceded by the adjectives "specific" or "developmental" or both together. The Scandinavians and particularly the Danes were also the pioneers in the rational treatment of dyslexia, and also in this connection the names of Norrie and of Hermann are con-
671
DEVELOPMENTAL DYSLEXIA
spicuous. In Copenhagen there took place the first official attempt upon a governmental scale to identify these cases from out of the population of semi-illiterates, and to provide systematic instruction in a Word-Blind Institute. Nowadays the interest in this subject is considerable, and the centres of principal attention have reverted to Great Britain and to the United States. A special Research Group of the World Federation of Neurology has been set up in order to achieve an international perspective of the problem. Though of topical interest, developmental dyslexia is still surrounded by a number of obscurities regarding its precise nature-its prevalence, world distribution, aetiology, prognosis and appropriate management. It is now realised that the problem of dyslexia is one aspect of the question of general illiteracy, and that peculiar sociologic problems are involved. For example, an important tie-up has been found between untreated dyslexia and juvenile delinquency.
DEFINITION
No adequate definition exists which is both terse and universally acceptable. However, we can tentatively suggest a rather cumbersome attempt at formulation. Developmental dyslexia entails a specific difficulty in learning to read, often genetically determined, which exists despite a level of general intelligence which is at least average; without any primary emotional disturbance or gross brain pathology; without significant impairment in hearing or in vision; and without any deficiency in conventional instruction. In ordinary circumstances, the difficulty in reading persists in some degree into adulthood and is associated with a peculiar difficulty with spelling. Sometimes it is the latter which brings the patient to medical or scholastic attention, and a previous mild dyslexic state may be overshadowed by a veritable "specific spelling disability." The question of the essential aetiologic nature of developmental dyslexia is still a matter of discussion, if not indeed of controversy.
PSYCHOLOGICAL ASPECTS
Though developmental dyslexia has long been accepted within the corpus of accepted neurologic teaching, a different attitude became adopted at one time by many nonmedical and educational psychologists. Stemming in all probability from an opinion put forward two or three decades ago by an authoritarian psychologist of particular eminence, it was accepted without question. Thus it became fashionable at one time
672
MACDONALD CRITCHLEY
to ignore or even deny the existence of developmental dyslexia. In its place was raised the conception of a continuum or a kind of spectrum of reading retardation, ranging from the stupid or inattentive at one end of the scale, to the intelligent but neurotic at the other extremity. In the latter event, environmental or exogenous factors were blamed rather than those which were constitutional or endogenous; circumstances such as broken homes, pupil-teacher hostility, inter-sib jealousy, drunken fathers and wanton mothers were often advanced as causative. Some educationalists proclaimed dyslexia to be a diagnostic myth. Others conceded that it might exist, but that they had never encountered it, or that they were familiar enough with the problem, but that it was a psychologically determined condition, or a manifestation of a mental defect, or perhaps the result of starting a child's reading lessons too early, or too late, or of faulty techniques in teaching. It was even alleged that reading difficulties were the price we pay for the illogical spelling of the English language. So the blame fell upon one scapegoat after another-the teacher, the parents and the child. This way of thinking would not have mattered very much had it not become responsible for about 25 years of neglect of the child who could neither read well nor spell properly. Too often the unfortunate dyslexic became the victim of indignity, even sheer cruelty. If any "treatment" at all were undertaken, it consisted merely in the child being relegated to a guidance clinic and there handled as a problem in paediatric psychology. Individual remedial teaching was but rarely attempted. Within recent years the attitude has changed, and an increasing number of teachers and educational psychologists now admit the existence of a specific developmental type of dyslexia. Pains are taken to differentiate this condition from out of the larger population of poor readers; and furthermore, helpful methods of training are being sought.
OPHTHALMOLOGIC PROBLEMS
Many dyslexics-perhaps most of them-are referred sometime or other to an eye specialist to ensure that the failure to read has not been due to an impairment in visual acuity. It is usually a simple matter to exclude latent refractive errors, retinal disorders and lesions of the optic nerve and of the ocular media. There remain, however, one or two defects which are not as easy to dismiss as nonsignificant. For example, there is the question of faulty eye movements during the act of reading. By employing appropriate techniques it is possible to record the movements of the eyes, and important differences may be found between the performance in good readers and in bad. In the latter, there may be an increased number of fixation pauses, a greater tendency for regressive or backward movements, an unduly short span of words encompassed by each sweep, a liability for the eye to deviate from the middle of one
DEVELOPMENTAL DYSLEXIA
673
line to the line below, and also a difficulty in switching the gaze accurately from the end of one line to the start of the next ( '1inear dyslexia"). Sometimes the defect in ocular mobility is so considerable as to raise the suspicion of an underlying oculomotor apraxia. Defective eye movements during reading may account for the clinical phenomenon which is occasionally found in mild dyslexics, whereby they read large print better than small, for in the latter case the gaze is more apt to wander. Sometimes, however, it is the other way round. Oculomotor imbalance has at one time and in some limited areas been deemed responsible for dyslexia, and orthoptic correction has been practised in an effort to teach children to read. However, this form of training is rarely if ever carried out nowadays. It is usually considered that the faulty eye movements are the result and not the cause of poor reading ability. Yet another ophthalmic hypothesis has been suggested in an effort to explain the dyslexic's difficulty in reading. In the great majority of persons, whatever their handedness, the preferred direction of automatic lateral gaze proceeds from left to right. A contrary state of affairs is alleged to underlie the dyslexic's problem, especially in those who are left-eyed. As most languages are written in a dextrad fashion, notable exceptions being Hebrew and Arabic, the dyslexic would automatically tend to sweep his gaze against the stream, and confusion is the result. Unfortunately there is no evidence whatever to support this hypothesis, and in every dyslexic whom I have tested, the automatic gaze has been from left to right, irrespective of the type of cerebral dominance. There is still another alleged correlation between dyslexia and a visuopsychic defect. It has been asserted that these children who are poor readers also fare badly in Bender's visual-motor Gestalt test, in the detection of buried shapes as in Gottschaldt's embedded figure test, and also in Benton's examination of visual memory and recall. These observations lead one to intrude into the territory of psychopathology, and may uncover processes which are secondary or operative, rather than primary or causal.
"MINIMAL" BRAIN DAMAGE
It is a common experience to find reading and writing difficulties in children diagnosed as "spastics." Some paediatricians, in revolt against the notion of reading retardation as a psychiatric disorder, have suggested that developmental dyslexia might be due to minor brain lesions, either perinatal or originating at a very early age. Clinical testing which goes deeper than the routine practice may, it is said, uncover various "soft" neurologic signs-so subtle as to elude a more cursory examination. Secondly, it has heen argued that a retrospective obstetric study of
674
MACDONALD CRITCHLEY
dyslexic children may bring to light a significant proportion of cases with cerebral trauma. A third argument has been adduced to the effect that electroencephalographic study of a dyslexic may reveal certain minor dysrhythmias. Furthermore, as the child perseveres with the difficult task of reading aloud, the cortical rhythm becomes so disturbed as to amount to a minor degree of subclinical "reading epilepsy." But against the acceptance of the hypothesis of minimal brain damage as being responsible for a primary type of developmental dyslexia are a number of arguments. No history of perinatal trouble or postnatal trauma or disease may be forthcoming. A positive family history of similar troubles with reading and spelling points to an endogenous constitutional disorder, and not one which is acquired. "Soft" neurologic. signs are often not demonstrable, especially in dyslexics in the second and third decades of life. Electroencephalographic abnormalities are inconstant, mild and probably not significant; the evocation of epileptiform discharges during the act of reading must be very rare, and has never occurred in any patient I have tested. The idea that a minor pathologic lesion could give rise to a persistent dyslexia is improbable from what we know of the resilience or plasticity of the juvenile cerebrum.
DYSLEXIA AS A COMMUNICATIVE DISORDER
It has also been suggested that the difficulty in reading is merely one facet of a general failure to achieve communication-a fragment of a congenital "aphasia." The alleged speech defects have been quite diverse and have included anomalies not only in the realm of language, but also in the peripheral articulatory mechanism. There are many objections to this communicative theory, and to describe the dyslexic's imperfect attempts to write as a "congenital dysgraphia" would be a misnomer. True, some developmental dyslexics have been comparatively late in acquiring speech, but this statement does not apply to all cases, or even the majority. The same objection invalidates the assertion that dyslexics talk imperfectly. Most dyslexics use spoken speech in an acceptable fashion from an early age. These "negative" cases -where speech attainment has been normal-argue strongly against any theory of developmental dyslexia as a general communicative disorder.
DYSLEXIA AS AN INSTANCE OF SPECIFIC MATURATIONAL LAG
Today, the most acceptable hypothesis is that of cerebral immaturity. A developmental dyslexic is often spoken of as a "late bloomer".,-to use
DEVELOPMENTAL DYSLEXIA
675
that faintly ridiculous term-but only in respect of the flowering of certain specific faculties. The minor or "soft" neurologic signs which are sometimes detected on close examination are best regarded not as evidence of minimal damage, but of cerebral immaturity. They occur far more often in dyslexics of young age-7 years or less-and they tend to disappear, examination of the older dyslexic being usually negative. Another argument in favor of dyslexia as an instance of cerebral immaturity is the commonly found lack of firm cerebral dominance. The incidence of left-handedness, ambidexterity and crossed laterality is comparatively high. Whether the inadequate unilateral dominance changes with the passage of time is an interesting question which we still cannot answer with confidence. The so-called ambidextrous cases probably show a progressive trend towards a right manual preference. Any study of cerebral dominance, whether in dyslexics or nondyslexics, uncovers a far more complicated state of affairs than is usually imagined. None of these various speculative ideas regarding aetiology touches upon the question of the pathopsychology. This is a quite distinct problem, and indeed it is open to argument whether the modus operandi of the reading difficulty is uniform in cases of developmental dyslexia, or wheijler subtypes exist, each with its own dynamic or physiologic defect. Many aspects of the dyslexia problem are still obscure, and form suitable topics for clinical research. For example, it may be asked whether dyslexia is an "ali-or-none" phenomenon, or whether it is possible to speak of severe cases and mild. And if so, does the difference imply an inherent property of the defect, or is it merely the resultant of associated variables? In the same vein, it is a matter for discussion whether developmental dyslexia is a uniform deficit or whether the underlying psychological mechanism varies quantitatively. The apparent diversity is perhaps due not to contrasting severity of the reading disability, but rather to the interaction of a stable basic deficit with differing influencessuch as, for example, intellectual status, degree of "ego strength," parental attitudes, the age at which the diagnosis is first arrived at, and the amount of remedial teaching the. dyslexic child has received. The foregoing represent some of the unsolved questions surrounding the problem of dyslexia. There are others as well, among which we may refer to the following: 1. The incidence of developmental dyslexia within the general population is not yet known precisely. We have already mentioned that it has been estimated by Scandinavian investigators that 10 per cent of all school-age children are dyslexic. One suspects that this estimate is too high for the United Kingdom and North America. It would be more plausible if it were qualified that the aforementioned 10 per cent referred to poor readers rather than specific dyslexics. The true incidence is a matter for educationalists to determine, and the accuracy of the findings will obviously turn upon the twin factors of definition and differential diagnosis.
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2. The geographical distribution of dyslexia is still not known. Most of the literature has come from English, American and Scandinavian sources, though dyslexia is also recognised in France, Germany, Italy, Spain, Rumania and Peru. It would be interesting to study the incidence of dyslexia in those races which employ a sinistrad type of script. We have already had experience of dyslexia in Arab and Hebrew-speaking children who have lived for a time in England. Still more intriguing would be a study of dyslexia among people who write from top to bottom (Chinese, Japanese); already the literature holds an isolated case report from Japan ( 1961). 3. We are still in doubt as to the optimum technique for instructing dyslexics. If it should prove correct that subtypes of developmental dyslexia exist, then it is possible that varying techniques should be tailored according to the dyslexic subject. Otherwise it might well prove that as with Kipling's tribal laws, everyone is right. 4. Is there such a state as reading readiness? And arising therefrom, is the question of the early preschool prediction of a dyslexic. Is this a possibility? And if so, can any rational steps be taken? It is clear from the foregoing remarks that the question of a specific type of reading disability constitutes a topical and highly important problem in present-day sociology, paedagogics and psychology.
REFERENCES A full bibliography up to 1964 is to be found in Critchley, M.: Developmental Dyslexia. London, William Heinemann Medical Books, 1964. Subsequent papers which may be consulted include: Critchley, M.: Is developmental dyslexia the expression of minor cerebral damage? The Slow Learning Child, 13:9-19, 1966. Critchley, M.: Some observations upon developmental dyslexia. ln Williams, D., ed.: Modem Trends in Neurology. London, Butterworths, 1967. Lesevre, N.: Les mouvements Oculaires d'exploration. These de Paris, 1964 (full bibliography). Thompson, J. L.: Reading Disability. Springfield, Ill., Charles C Thomas, 1966 (full bibliography). Institute of Neurology Queen Square London W.C. 1, England