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Early identification and intervention in children at risk for reading difficultiesRegtvoort, A.G.F.M.

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Citation for published version (APA):Regtvoort, A. G. F. M. (2014). Early identification and intervention in children at risk for reading difficulties

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Summary In most children, learning to read is a process that follows a regular course across several years. While still a pre-reader prior to the onset of formal reading instruction, within half a year a typical child develops into beginning reader, to become an advanced reader in another year. With more experience, reading fluency is acquired enabling the child to process written or printed information (almost) effortlessly. In some children however, learning to read presents a daily struggle and worry, from which they cannot escape: in a literate society every child is expected to become a reader.

Around five per cent in the population has such severe reading problems that they are identified as ‘dyslexic’. People with dyslexia may never obtain a level of reading that is fluent, involuntarily and effortless, and that can be called automatized. For children having one or more close relatives like a (grand) parent or sibling with dyslexic problems the chance of becoming a dyslexic reader is greatly increased with about 20 to 35 per cent. Thus, although having a familial history of dyslexia does not necessarily result in a reading impairment, in pre-readers it should be considered a not-to-ignore risk signalling future reading difficulties.

Among researchers of dyslexia there is broad consensus that developmental dyslexia has a genetic component, that dyslexic brains differ from those of normal readers, both functional and structural, and that a phonological deficit is at the core of the learning disorder. Furthermore, sensory deficits might also be implicated as well a (more general) learning deficit as reflected in problems with the automatization of cognitive skills. Recent cognitive and neurological findings regarding important markers or precursors of later reading skills provide an opportunity to identify children - with and without a familial risk of dyslexia - expected to develop problems with reading acquisition, and act accordingly. Intervention research shows that early intervention is more effective than remediation of reading deficits at a later stage of development. Training in phonological awareness has found to facilitate the process of learning to read, but the effects on reading skill become stronger when incorporating knowledge of grapheme-phoneme correspondences, the most important predictor in a fairly consistent orthography like Dutch. Much less is known about the significance of neural precursors of reading difficulties in pre-readers, in particular with respect to

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early markers outside the literacy domain such as information processing deficits of interest to this thesis.

The aims of the current thesis are to study early identification and intervention in children at risk for later reading difficulties. In the first three studies carried out as part of the DDP, the participants were from the same sample comprising only children from families identified as having a familial history of dyslexia or not. In the fourth study carried out according to the programme ‘Onderwijs Bewijs I’ [Educational Evidence], another sample was recruited in which children were included on the basis of a cognitive risk profile.

The thought that deficits in visual information processing might be implicated in children at familial risk was studied in Chapter 2. The research question whether deficits in the learning mechanisms of dyslexic children may be more general than specific, was investigated using a habituation paradigm. Orienting behaviour to a series of visual standards was recorded with event-related potentials (ERPs) in a sample of pre-reading children with (N = 24) and without (N = 14) a familial risk (FR) of dyslexia. Subsequently, at the end of Grade 2 the acquisition of reading and spelling was assessed in order to relate pre-attentive learning in the pre-reading phase to attentive learning performance as implicated in reading and spelling. After being regrouped into three groups according to literacy level and risk factor, single-trial analyses revealed significant group differences in the N1 and P3 components. No P3 habituation was found in either group, but in the 12 normal-reading noFR controls, the N1 showed the expected decrease in strength of amplitude across 14 trials. In both other groups, strength of N1 to the initial standard was relatively reduced, but interesting differences between these two groups were found to the subsequent standards. The 15 normal FR readers displayed a lack of N1 habituation and prolonged N1 and P3 latencies, indicating possible compensation for their reduced neuronal activity during initial information extraction. In contrast, the group of 9 poor readers showed an increase in N1 strength without prolonged latencies, which might suggest inefficient processing in an early time window and explain automatization difficulties in dyslexic readers.

Chapter 4 relates early identification to early intervention by examining the differential effects of pictorial priming and congruency on word recognition in low (N = 13) and high responders (N = 14) to early literacy intervention recruited as a subsample of the FR kindergartners participating

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in Chapter 3. ERPs were recorded to word-picture pairs in which either the word preceded the picture (unprimed word) or vice versa (primed word). Primed words could be either congruent or incongruent with the picture.

As picture processing may facilitate the activation of phonological information and thereby the integration of phonological and orthographic information, the question was how picture priming would affect phonological encoding and congruency processing in children with low and high phonemic skills under different conditions. Both behavioural responses (accuracy and speed) and neural correlates of priming (topography and extent of brain activation) were analysed. Picture priming appeared to reduce the group difference in accuracy found to unprimed words, and it also modulated the topographic distribution in the time window related to phonological recoding (280-400 ms), such that the group difference to unprimed words was absent to picture-primed words. In a later time window (560-700 ms) only the high responders showed indications of tuning of attentional and integrative processes as a function of congruency. The absent divergence in topographic distribution between congruent and incongruent responding in the lower skilled subgroup suggests that atypical neural responding associated with integrating congruent information signals already at kindergarten age later reading difficulties.

Chapter 3 and Chapter 5 are both dedicated to early intervention in children at-risk for reading difficulties. The main differences between the studies of Chapter 3 versus Chapter 5 are in time of enrolment (kindergarten versus begin Grade 1), inclusion criteria (familial risk versus cognitive risk), tutoring (at home versus at school), and duration (14 weeks versus two years). In both studies the same computer-assisted program was used in which phonological awareness and grapheme-phoneme correspondences were trained in the context of word reading, but whereas in the shorter intervention decoding restricted itself to simple one-syllable words, the longer intervention included training in all relevant word structures. Compared to a FR control group the short intervention appeared to be effective in the short-term, but the improved letter knowledge and phonemic awareness did not transfer to reading ability. In contrast, completing the sustained intervention resulted in better reading skills as compared to the at-risk controls with the proportion of very poor readers (lowest 10% in word reading fluency) in the intervention subgroup approaching norm-referenced standards.

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Chapter 6 discusses the findings and implications of the current studies with regard to the main topics in this thesis. In the first part the central focus is whether and to what extent known behavioural and neurobiological indicators of risk for reading difficulties permit early identification on the individual level. The second part evaluates the benefits of implementing an extended early intervention as opposed to a shorter one. Finally, suggestions for future research and educational practice are given.

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Samenvatting

Leren lezen is een proces dat zich voor de meeste kinderen volgens een vast patroon over verschillende jaren heen voltrekt. Als kleuter ontwikkelen zij geleidelijk het besef dat een woord is op te splitsen in (losse) klanken. Taalspelletjes helpen daarbij. Dat elke klank weergegeven kan worden met een eigen teken, en dat met dezelfde tekens ook andere woorden gevormd kunnen worden, het zogenaamde alfabetisch principe, moet hen expliciet geleerd worden. In Nederland is het gebruikelijk dat de formele leesinstructie begint in groep 3 van het basisonderwijs. Halverwege het schooljaar zijn de meeste klank-tekenkoppelingen geleerd en lezen kinderen eenvoudige woorden en zinnen. Daarna kan het heel snel gaan. Met meer oefenen kost lezen op den duur zo weinig inspanning dat het een geautomatiseerde vaardigheid is geworden: je kunt niet meer níet lezen bij het zien van een tekst.

Foutloos en vloeiend leren lezen is echter niet voor alle kinderen zo vanzelfsprekend. Voor sommigen is leren lezen een dagelijkse strijd die zij geacht worden te winnen: in een geletterde maatschappij moet elk kind kunnen lezen. Ongeveer vijf procent van de bevolking heeft zulke ernstige leesproblemen dat er sprake is van dyslexie. Voor een kind met een dyslectisch familielid in de eerste of tweede lijn is de kans om zelf ernstige lees en/of spellingproblemen te ontwikkelen veel hoger dan 5%, schattingen lopen uiteen van 20 tot 35%. Hoewel het merendeel van de kinderen met een familiair risico op dyslexie geen problemen met leren lezen zal ondervinden, is dyslexie in de familie een niet te negeren signaal.

Onder dyslexieonderzoekers is er brede consensus dat het dyslectische brein functioneel en structureel verschilt van het brein van een goede lezer, en dat een probleem in de verwerking van spraakklanken (fonologisch tekort), de kern van de leerstoornis vormt. Sensorische tekorten worden echter ook niet uitgesloten. Daarnaast zijn er aanwijzingen dat kinderen met dyslexie niet alleen moeite hebben met het automatiseren van lees en spellingvaardigheden maar ook met andere vaardigheden, hetgeen eerder kan duiden op een meer algemene dan specifieke leerstoornis.

Kennis van cognitieve en neurobiologische indicatoren met een voorspellende waarde voor latere leesvaardigheid biedt de mogelijkheid tot identificering en behandeling van kinderen die een verhoogde kans op problemen met het verwerven van leesvaardigheid hebben.

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Interventieonderzoek heeft aangetoond dat vroeg interveniëren effectiever is dan remediëren van leesproblemen. In een transparante orthografie als het Nederlands, waarin veel klank-tekenkoppelingen consistent zijn, blijkt letterkennis een belangrijke voorspeller te zijn van latere leesvaardigheid. Vroege training van het fonemisch bewustzijn (klankbewustzijn) kan de ontwikkeling van de leesvaardigheid faciliteren, maar het effect is groter als de training ook het aanleren van de klank-teken-koppelingen omvat. Over neurobiologische (risico-)indicatoren bij kinderen die nog niet kunnen lezen is veel minder bekend. Dit is met name het geval voor voorlopers van leesvaardigheid die zich niet binnen het domein van lezen manifesteren, maar bijvoorbeeld op een onderliggend niveau van auditieve en visuele informatieverwerking.

In dit proefschrift wordt onderzoek naar de vroege identificatie en behandeling van kinderen met risico op latere leesproblemen beschreven. De eerste drie studies zijn uitgevoerd binnen het Dutch Dyslexia Programme. De deelnemende kinderen kwamen uit twee verschillende steekproeven, bestaande uit kinderen uit een gezin met dyslexie (N = 24, N = 32) of zonder dyslexie (N = 14). De selectie vond plaats halverwege groep 2. De kinderen die gevolgd zijn in de vierde studie, uitgevoerd binnen hetprogramma ‘Onderwijs Bewijs I’, vormden een andere steekproef (N = 137). Screening hiervoor vond plaats begin groep 3 op basis van een cognitief risico profiel. Deze risicokinderen scoorden laag op letterkennis, fonologische vaardigheden en/of beginnende leesvaardigheden vergeleken met klasgenoten. Zij werden random verdeeld over een interventie- en een controle groep.

De veronderstelling dat er bij dyslectici sprake kan zijn van een stoornis in het automatisch verwerken van informatie stond centraal in Hoofdstuk 2. Op een leeftijd dat kinderen met en zonder familiair risico nog niet hadden leren lezen, werd bij hen met elektro-encefalografie (EEG) gemeten of de herhaaldelijke verwerking van nieuwe informatie leidt tot habituatie van de hersenrespons. Op elke nieuwe of onverwachte gebeurtenis in onze omgeving, bijvoorbeeld een geluid, een aanraking, of een plaatje, reageren de hersenen met verhoogde activiteit. Bij herhaling van diezelfde gebeurtenis dooft de opgeroepen hersenrespons langzaam uit. De aanvankelijk nieuwe informatie is voldoende geleerd, de verwerking kost geen aandacht en inspanning meer en de hersenenergie komt beschikbaar voor het uitvoeren van en andere taak. Tijdens het experiment kregen alle kinderen op een monitor veertien keer kort achter elkaar dezelfde,

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onbekende abstracte figuur te zien. De analyse van de EEG data vond plaats nadat de kinderen hadden leren lezen. De twee groepen met en zonder risico werden aan het eind van groep 4 op basis van hun lees- en spellingvaardigheden heringedeeld in drie groepen: een risicogroep zonder leesproblemen (N = 15), een groep met leesproblemen (N = 11) en een controlegroep zonder risico of leesproblemen (N = 12). Met deze werkwijze kon een relatie gelegd worden tussen leren dat geen gerichte aandacht vereist en leren zoals bij lezen en spellen waarvoor wel gerichte aandacht nodig is. De resultaten toonden duidelijke verschillen aan tussen de drie groepen lezers in de herhaaldelijke verwerking van de figuur. Alleen de controlegroep vertoonde een afname in vroege hersenactiviteit over de veertien aanbiedingen van de figuur heen. Vergeleken met deze normaal lezende groep zonder risico reageerde de risicokinderen zonder leesproblemen bij de eerste aanbieding gemiddeld met verminderde en vertraagde vroege hersenactiviteit, die niet afnam. Dit zou kunnen duiden op een compensatiemechanisme voor een minder optimale verwerking van nieuwe informatie. Opvallender was echter dat de groep met leesproblemen op de herhaalde aanbiedingen reageerde met een toename van de vroege hersenactiviteit. Die hersenactiviteit bleek bij de eerste aanbieding van de figuur nóg minder sterk te zijn dan bij de risicogroep zonder leesproblemen, en niet vertraagd ten opzichte van de controlegroep. Inefficiënte verwerking van nieuwe informatie zou de automatiseerproblemen van kinderen met leesproblemen kunnen verklaren. Als nieuwe informatie door een relatief snelle verwerking en lagere hersenactiviteit minder optimaal in het geheugen opgeslagen wordt, kan dit een belemmering zijn voor het snel ophalen uit het geheugen van de juiste informatie.

Hoofdstuk 4 betreft eveneens een EEG studie waarin vroege identificatie gerelateerd werd aan vroege interventie door bij beginnende lezers na te gaan wat de effecten zijn van priming en congruentie op woordherkenning. De onderzoeksgroep bestond uit 27 kinderen met een familiair risico die in groep 2 een kortdurend interventieprogramma ter versterking van (voorbereidende) leesvaardigheden gevolgd hadden (zie hoofdstuk 3). Na afloop van de interventie werden twee groepen gevormd op basis van de mate van beginnende geletterdheid. Tijdens het experiment werd gebruik gemaakt van een computergestuurde reactietaak met gepaarde woorden en plaatjes. De kinderen moesten met een druk op een knop reageren op een woord of plaatje dat congruent was aan het voorafgaande woord of plaatje binnen het paar. Verondersteld werd dat een beginnende

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lezer met zwakke fonologische vaardigheden bij het lezen van een woord (bijvoorbeeld, kip) ondersteund wordt als dat woord voorafgegaan wordt door een plaatje van een kip. Door de vooraanbieding van het plaatje (priming) is de fonologische informatie die plaatje en woord delen reeds geactiveerd, hetgeen mogelijk de integratie met de orthografische informatie van het woord bevordert. Voor de woorden die voor een plaatje kwamen presteerde de risicogroep met hoge beginnende geletterdheid naar verwachting beter dan de andere groep, en werd er eveneens een groepsverschil gevonden in de verdeling van de activiteit over de hersengebieden. Deze groepsverschillen in accuratesse en verdeling van hersenactiviteit waren echter kleiner, respectievelijk afwezig voor woorden die na het corresponderende plaatje kwamen. De faciliterende verwerking van het plaatje op woordherkenning leek dus vooral aanwezig voor de risicogroep met zwakke beginnende geletterdheid. Conform recente bevindingen in neurologisch onderzoek naar de verwerking van gelijktijdig aangeboden congruente of incongruente letterklanken en -tekens, kon voor de risicogroep met hoge beginnende geletterdheid een gedifferentieerde neurale respons voor congruente en incongruente woord-plaatje paren worden waargenomen. Dat dit niet het geval was voor de risicogroep met lage beginnende geletterdheid kan een indicatie zijn dat atypische hersenactiviteit tijdens integratie van congruente informatie een voorloper van leesproblemen is.

Hoofdstukken 3 en 5 zijn beide gewijd aan vroege interventie bij kinderen met een risico op leesproblemen. De belangrijkste verschillen tussen de studies in hoofdstuk 3 versus 5 zijn het tijdstip van selectie (halverwege groep 2 versus begin groep 3), de selectie criteria (familiair risico versus cognitief risico), de tutor (ouders thuis versus schooltutor), en duur van de interventie (14 weken versus twee schooljaren). In beide studies werd gebruik gemaakt van hetzelfde computer-ondersteunende programma gericht op het versterken van het fonemisch bewustzijn en het aanleren van de letter-klank tekenkoppelingen, gecombineerd met leesoefeningen. De korte interventie in groep 2 kan gezien worden als een opstapje naar het leesonderwijs in groep 3: de kinderen oefenden het lezen van korte eenlettergrepige woorden als op en kip met een beperkt aantal letters. Daarentegen werd tijdens de langere interventie, bedoeld als aanvulling voor kinderen die net gestart waren met leren lezen op school, in groep 3 en 4 ook geoefend met andere woordtypen, zoals samengestelde woorden (visnet), woorden met medeklinkercombinaties (melk, klop) en meerlettergrepige

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woorden (kopen, koppen). De kortdurende interventie bleek alleen effectief op de korte termijn. Aan het eind van groep 2 scoorde de interventiegroep (N = 31) hoger op letterkennis en fonemisch bewustzijn dan een vergelijkbare risicogroep (N = 26) die geen interventie gekregen had. De resultaten in groep 3 en 4 toondenechter aan dat, ondanks de betere voorbereidende leesvaardigheden, de interventiegroep niet beter las dan de controle risicogroep. In beide risicogroepen was het percentage kinderen met een leesvaardigheid op het laagste vaardigheidsniveau veel hoger (39%) dan in de landelijke referentiegroep (10%). Afronding van de langdurende interventie (studie in Hoofdstuk 5) resulteerde wel in een betere leesvaardigheid vergeleken met de controle risicogroep (N = 66). De groep die de interventie afgerond had (N = 40) las aan het eind van groep 4 en 5 gemiddeld op het niveau van de landelijk referentiegroep, met een bij benadering vergelijkbaar deel zeer zwakke lezers.

In Hoofdstuk 6 worden de bevindingen van de vier studies samengevat en besproken. Allereerst wordt ingegaan op de betekenis van op groepsniveau vastgestelde cognitieve en neurobiologische voorlopers van dyslexie voor het op individueel niveau signaleren van toekomstige zwakke lezers. Een familiair risico op dyslexie blijkt ook in deze onderzoeksgroepen de belangrijkste indicatie te vormen voor het ontwikkelen van leesproblemen. Het combineren van een familiair en cognitief risicoprofiel voorkomt geen over-identificatie, maar er wordt geen enkel risicokind ‘gemist’. Voor neurobiologische voorlopers van dyslexie kan geconcludeerd worden dat bestaand onderzoek naar de inzet ervan op het niveau van het individuele kind nog onvoldoende uitsluitsel biedt. Vervolgens worden in dit hoofdstuk de kenmerken van een effectieve interventie voor risicokinderen geëvalueerd. Geconcludeerd wordt dat vroege interventie zowel in groep 2 als groep 3 kan starten, maar dat risicokinderen gedurende een langere periode interventie nodig hebben om hun leesvaardigheid optimaal te ontwikkelen. Tot slot volgen enkele suggesties voor verder onderzoek en aanbevelingen voor de schoolpraktijk.

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Dankwoord Geen proefschrift zonder dankwoord. Geen dankwoord zonder namen. Veel namen bevat dit dankwoord niet. Zoveel personen hebben mij gedurende lange of kortere tijd vergezeld tijdens de totstandkoming van dit proefschrift. Vooreerst mijn promotor, mijn co-promotor, (ex-)collega's van POW(L) of elders, familie, vrienden. Zij hebben hun kennis en ervaring gedeeld, mij scherp gehouden, aangehoord, met mij plannen gemaakt en uitgevoerd, van data voorzien, ondersteuning verleend bij de analyse van de resultaten, mijn teksten gelezen en wel/niet naar de digitale prullenbak verwezen, lastige vragen gesteld, geen lastige vragen gesteld. Al die personen weten zelf wat ze voor mij betekend hebben. Mijn dank gaat naar ieder van hen uit.

Niet alleen personen maar ook de tijd vergezelde mij op de lange weg naar afronding. De uitgebreide hoeveelheid longitudinale gegevens in dit proefschrift zijn aan de tijd te danken.

Natuurlijk speciale dank aan alle kinderen, van wie de namen niet genoemd mógen worden, die zich blijmoedig of iets minder blijmoedig ter beschikking stelden voor plakkerige en taaie EEG experimenten, of het wéér moeten lezen van lijsten met (on)mogelijke woorden; aan hun ouders die hun kind(eren) vaak net zo blijmoedig of iets minder blijmoedig vergezelden, en zichzelf onderwierpen aan de voor hen soms confronterende leestests; aan de juffen en meesters die vragenlijsten invulden, en nog meer lijsten en nog meer; aan mijn stagiaires en studentassistenten zonder wie de data niet binnengehaald waren, aan de onmisbare programmeur van de experimentele versies van Bouw!

Een dankwoord kan niet zonder enkele namen. Van Yannick en Niklas, die er waren als inspiratiebron, pre-proefpersoon, assistent, en wat nog meer, en nu met en voor mij blij zijn dat het proefschrift er ligt. Van Wil, die het bestuderen van hersengolfjes als minder boeiend ervoer dan lezen over ‘ervoer of ervaarde’, maar er wel altijd voor me was en zal zijn. Anne Regtvoort Amsterdam, 10 oktober 2014