These presentation notes are not for commercial use. They are strictly for

personal use in conjunction with Professor John Stein’s webinars from

the LDC 2017.

04/03/2017

1

What is Dyslexia; Does it exist?Is it due to sensorimotor Problems

John Stein, MagdalenCollege,

Oxford University, UK

Supported by The Dyslexia Research Trust (www.dyslexic.org.uk), Dyers & Colourists, Esmee Fairbairn, Garfield Weston and Wellcome

Trusts, BBC Children in Need

DRT

The ProblemReading failure is the commonest cause

of childhood misery, depression, even suicide.

Plus illiterates’ frustration and anger with the world, often leads them into aggression and crime. 75% of those in jail are illiterate.

The Programme for International Student Assessment (PISA): <20% of Australians have a reading ability that is worse than 11 year olds’. They are therefore ‘functionally illiterate’; and very ill-equipped for modern life. Illiteracy costs <A$ 50 billion per year.

But most of these people are not dyslexic. They fail for social reasons - bad schooling, lack of family support, truancy

Which children are truly dyslexic?Yet all children struggling to read

deserve all the help they need

Functional illiteracy in Australia

poor readers

Good Readers

Visual blues Visual yellows

Auditory

Social

Good Readers

School Leavers' LiteracyHistory 1

1887- the word ‘dyslexia’ was coined by Rudolf Berlin to describe stroke patients who had lost the ability to read, but retained their sight, hearing and other cognitive skills, ie it was a selective loss, specific to reading– implies discrepancybetween reading and other skills. Now called ‘acquired dyslexia’

1896 – Pringle Morgan first described developmental ‘word blindness’ in ‘Tom’:

a) v. poor reading – he could not even read his own nameb) orally he was the ‘most intelligent boy in the class’ ie discrepancyc) probably ‘congenital’ – hereditary/genetic.

These 3 criteria are still used for the neurological definition of developmental dyslexia

1920s Morgan, Kerr, Hinshelwood, Orton all thought dyslexia was a visual problem: ‘word blindness’, ‘strephosymbolia’

History 2

1930s – The word ‘Dyslexia’ replaced ‘word blindness’ because not all dyslexics do have visual problems1960s – Chomsky’s theory of ‘recursive generative phonology’ ushered in the ‘phonological’ theory, which replaced the visual theory1970s – The phonological theory developed by Isobel Liberman, Utta Frith, Keith Stanovich, Maggie Snowling ?dyslexia became a linguistic/psychological condition and was no longer regarded as medical/neurological1980s – Magnetic imaging renewed interest in the brain basis of dyslexic problems1990s – ‘magnocellular’ theory2000s – genetic studies reinforce brain basisBut now an anti–dyslexia backlash (Keith Stanovich, Linda Siegel, Joe Elliot, DSM5)

Dyslexia, DSM5 & SpLD• In the latest Diagnostic & Statistical Manual of Psychiatric conditions (DSM5)

dyslexia is no longer distinguished from other neurodevelopmental disorders• Dyslexia, dyscalculia, dysphasia, dyspraxia are all now lumped together as

‘Specific Learning Difficulties (SpLD); but you can ‘specify’ an individual’s major problems

• The old IQ-reading discrepancy is now banned!• But problems must be ‘unexpected’– so we must demonstrate discrepancies!• 4 criteria must be met: a) persisted for at least 6ms despite adequate help;

b) measurably below norms for age; c) began at school; d) rule out other causes

• ∴ costly complete IQ testing is not now required for diagnosis, although it may be needed for successful help

• But the original neurological concept of dyslexia is now doubted by some

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(1995)

2015

Anti–dyslexia movement:1. Dyslexia is a middle class

concept – unfair to the poor2. All slow readers have the same

phonological problems3. There are no grounds for

singling out slow readers with higher non reading abilities as ‘dyslexic’. Supported by The Dyslexia Research Trust (www.dyslexic.org.uk), Dyers & Colourists, Esmee

Fairbairn, Garfield Weston and Wellcome Trusts, BBC Children in Need

DRT

This argument probably drives all the others!:1. Middle class children are more likely to get diagnosed as

dyslexic. True2. They often go privately because state Ed. Psychs. avoid a

diagnosis of dyslexia. True3. Therefore middle classes may grab unfair share of help. Perhaps4. All poor readers should get the help they need irrespective of

background. Definitely true!5. But these are not arguments against dyslexia, but for better

teaching for all!

Anti Dyslexia argument

(social)

Supported by The Dyslexia Research Trust (www.dyslexic.org.uk), Dyers & Colourists, EsmeeFairbairn, Garfield Weston and Wellcome Trusts, BBC Children in Need

DRT

1. All poor readers have mainly phonological problems. They do not! Many have mainly visual problems

2. Phonological problems are just the same in dyslexia as in other kinds of reading failure. Of course they are! - because all reading requires translation of letters into phonemes

3. ∴ On the basis of their phonological problems dyslexia cannot be distinguished reliably from other causes of reading difficulty. Of course! But it can be distinguished on the basis of their visual and auditory sequencing problems

4. Dyslexia doesn’t really exist. It does!

Anti Dyslexia argument – phonological basis of

all readingThe Phonological Theory (a tautology? Vision?)

Leading to:• Poor rhyming• Poor segmentation (of

sentences, syllables & phonemes)

• Poor phoneme deletion & substitution

• Poor tongue twisters• Poor spoonerisms• Poor non word reading

• Failure to learn how letters can be translated into sounds (grapheme/ phoneme decoding)

• Failure to learn how to split words into their constituent sounds (phonemes) to match with the letters that represent them

Tests of Phonological ProcessingPossible visual problems ignored!

• Phonological Awareness:Segmenting, deleting or substituting sounds in sentences, words & syllables

• Phonological short term (working) memory:Multisyllable pronunciationNon(pseudo)word repetitionNon word reading

Criticisms of the Phonological Theory

• A useful theory should provide explanations• The phonological theory merely uses different

words to describe poor reading – a tautology• It is set at too high a cognitive level to explain

much• A useful theory would explain why the

phonological weaknesses arise by determining the physiological mechanisms underlying them

• Namely weaknesses in visual and auditory temporal/sequential sensorimotor processing

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Genetic vulnerability

Magnocellular deficit

Visual processing

speed

Auditory processing

speed

Slow temporal

sequencing

Phonology: slow grapheme-phoneme

translation

Poor Reading

Neurobiological Level

Physiological Level

Behavioural Level

Supported by The Dyslexia Research Trust (www.dyslexic.org.uk), Dyers & Colourists, EsmeeFairbairn, Garfield Weston and Wellcome Trusts, BBC Children in Need

DRT

• Reading difficulties in dyslexia are said not to be ‘specific’• Dyslexics’ phonological difficulties are no different to those of any other

poor reader• There need be no ‘discrepancy’ between reading and other cognitive skills • ∴ you can’t distinguish dyslexia on the basis of IQ/reading discrepancy.

You can, if you use tests of rapid visual & auditory sequencing• ∴ dyslexia cannot be distinguished reliably from other causes of reading

difficulty• ∴ Dyslexia doesn’t really exist. It does! It’s a specific sensorimotor problem

Anti Dyslexia argument –

discrepancies?

Discrepancies

• Dyslexia was originally defined as a specificreading disability,

• ie when reading and related skills are unexpectedly & discrepantly low compared with the person’s other cognitive abilities

This discrepancy definition is now criticised because general cognitive ability does not predict dyslexics’ reading ability• Of course not; that’s what makes dyslexia a

specific reading disability! • In practice we do look for discrepancies (spikiness)

in people’s cognitive profiles to identify it, and to distinguish it from social causes of reading failure

Despite recent research advances, currently the definition of dyslexia is in a mess!

• Some people believe dyslexia is no different from social causes of reading problems (home stress, no home support, poor teaching, truancy) because it can’t be distinguished from them on phonological grounds

• NB Education Authorities often have a strong financial incentive NOT to diagnose dyslexia• Criteria for diagnosis of dyslexia, a ‘spiky’ psychometric profile, are unclear, no consensus

and contradictory:• On the one hand officially you’re not allowed to look for discrepancies between general

ability (IQ) and reading, yet discrepancies are what a ‘spiky profile’ imply!• Qualifications required for formal diagnosis are unclear because the Qualifications

Authorities change their requirements repeatedly: specialist teachers, chartered psychologists, educational psychologists?

• No standardisation of which cognitive tests to use; left to practitioners’ personal choice• DSM5 has lumped all learning difficulties together• Screening or diagnosis? Many parents opt for screening, and then have to pay for

diagnosis

WIAT-IIOral Expression Listening Comprehension

ReadingWord ReadingPseudo (non) word decodingReading Comprehension

TOWRE-2Sight Word EfficiencyPhonemic Decoding

Written LanguageSpellingDASH - hand writingWritten Expression

WISC-IV/WAIS-IIIVerbal reasoningNon verbal reasoningVisuospatial skillsWorking Memory Processing Speed

Memory and Learning (WRAML-2)

Verbal MemoryVisual MemoryAttention/Concentration

CTOPP-2Phonological AwarenessPhonological Memory Rapid Naming

OTHERSConnors ADHD Strengths & Difficulties Questionnaires

Ability Tests Attainment Tests

Current Tests for Dyslexia, looking for discrepancies!Typical Spiky Dyslexic

Profile• High oral comprehension*• High non-verbal reasoning*• Normal reading comprehension• Low working (short term) memory• Low processing speed• Low single word reading• V. low spelling*• V. low non word reading*• V. low rapid naming• V. v. low handwriting speed*

(ie she has ‘normal’ reading comprehension, yet clearly dyslexic)2015

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Stick with Pringle Morgan’s 3 crucial features1. Reading & particularly spelling very poor

despite:2. Average or high oral intelligence

ie. It is a specific, selective, reading deficit – discrepancy between oral and written skills. Spiky psychometric pattern

3. Usually a family history –ie hereditary/ genetic; 2-3x more common in males

+ Many other symptoms caused by impaired sensorimotor control

So how should we identify developmental dyslexia as opposed to other causes of

failure to learn to read?

World Federation of Neurology Definition of ‘Dyslexia’ (1968)

"A disorder manifested by difficulty learning to read, despite conventional instruction, adequate intelligence and

sociocultural opportunity. It is dependent upon fundamental cognitive disabilities which are frequently of constitutional

origin."

Implies a discrepancy between reading and other skills (IQ?) & a genetic basis

Genetic vulnerability

Magnocellular deficit

Visual processing

speed

Auditory processing

speed

Slow temporal

sequencing

Phonology: slow grapheme-phoneme

translation

Poor Reading

Neurobiological Level

Physiological Level

Behavioural Level

Magnocellular Systems • Very vulnerable. Impaired m-

cell development has been found in prematurity, foetal alcohol syndrome, developmental dyslexia, dyspraxia, dysphasia, ADHD, ASD, Williams syndrome, schizophrenia, depression

• M- cell high dynamic sensitivity requires high membrane flexibility provided by local environment of omega 3s, found in fish oils

• M- function can be improved using blue or yellow filters, rhythm training, motor mindfulness (embodied cognition), omega 3s

• Large neurones (10%) found throughout the whole brain, specialised for timing: visual, auditory, touch, muscle sensors, cerebral cortex, hippocampus, cerebellum

• Track changes in light, sound, position etc. for direction of visual, auditory & motor attention, hence sequencing

• Large, fast conduction, fast synaptic transmission

• All derive from same lineage; they all express the same surface antigen, CAT 301

Further proof of the M- theory: when we improve dyslexic children’s magnocellular function, this

improves their reading

• Motion training• Eye fixation training• Convergence training• Action video games• Coloured filters – yellow or blue or

many colours?• Auditory: active rhythm training• Motor: embodied cognition• Nutrition – omega 3s

“These results show … a causal relationship between visual

magnocellular (dorsal route) deficits and developmental dyslexia, virtually

closing a 30-year long debate”

Gori, S., Seitz, A. R., Ronconi, L., Franceschini, S., & Facoetti, A. (2015). Multiple causal links between a magnocellular-

dorsal pathway deficit and developmental dyslexia. Cerebral Cortex (New York, N.Y.)

04/03/2017

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No two dyslexics are alike - very great individual differences

Reading is difficult because it requires:

1. Rapid visual identification of letters and their order (orthography); even in experienced good readers this process is rate limiting

2. Rapid auditory translation into the sounds they stand for (grapheme/phoneme translation)

3. Background knowledge of phonology- how words can be split down into separate phonemes

All these processes depend on accurate timing & sequencing carried out by the brain’s

magnocellular nerve cells

Visual processing

2 separate routes for reading: visual whole word and phonological

but note main system used for reading is visual processing • The eyes also have to converge accurately for near vision when reading

• Control of vergence eye movements is dominated by the visual magno system

• The vergence eye movement control system is the most vulnerable to drugs and disease

• Many poor readers have unstable vergence control

Vergence instability

A weak magnocellular system causes unstable vision - oscillopsia

“The letters go all blurry”“The letters move over each other, so I can’t tell which is which”

“The letters seem to float all over the page”“The letters move in and out of the page”“The letters split and go double”“The c moved over the r, so it looked like another c”“The p joined up with the c”“d’s and b’s sort of get the wrong way round”“The page goes all glary and hurts my eyes”“I keep on losing my place”

Visual Symptoms• Letters blur• Go double• Letters ‘fizz’• Move around• Loses his place; uses finger

to keep place• Skips lines when reading• Can't stay on lines• Gets letters in the wrong

order• Says eyes get tired• Reads for only a short time• Closes or covers one eye• Holds things very close• Squints• Rubs eyes frequently

• Reverses letters and words beyond 7 yrs old

• Confuses ‘a’ & ‘o’, b & d, p & q, m & n • Mistakes words with similar spellings:

eg send and spend, pant & pint• Trouble visualizing what is read• Poor visual recall of words• Very poor spelling• Poor copying• Very bad handwriting• Headaches when reading• Moves head excessively• Short visual attention span

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Summary (vision)

• The visual system needs to be able to identify letters and their order in a word

• Letter identification is ok in dyslexics, but letter ordering is not

• M- system stabilises vision and indicates when eyes move

• Thus a rapid and accurate M- system is crucial for sequencing the letters in a word correctly

• The M- system is impaired in dyslexics• Hence their letter ordering is impaired• Therefore their orthographical memory is impaired• Hence their phonological memory is affected too

Auditory Sequencing for Reading

• Need to be able to sequence words in sentences, syllables in words, phonemes in syllables

• Requires hearing accurately the changes in the amplitude and/or frequency of the sounds

• These enable you to sequence the sounds correctly

• Dyslexics are slower and less accurate at this sequencing

• Probably due to impaired development of their auditory magnocellular system

• Improving their detection of AM & FM improves their reading

Auditory Symptoms

• Mispronunciations, lisps & other speech disorders

• Poor pronunciation of multisyllablewords

• Missequencing sounds in words –‘tefelone’ for telephone, ‘hospital’ for hospital

• Spoonerisms – ‘town drain’ for down train, ‘par cark’ for car park

• V. bad at tongue twisters• Poor short term auditory memory-

Cannot remember telephone numbers

Impaired auditory magnocellsin dyslexics?

• Large ‘magnocellular’ neurones in the auditory brainstem signal changes in sound frequency and amplitude

• Dyslexics have smaller magnocellular neurones in the medial geniculate nucleus

• They have lower frequency, AM & FM sensitivity• Frequency sensitivity predicts their non word reading skills• Poor phonological skill may result from impaired

development of auditory magnocells• Musical training, particularly in rhythm, may improve

auditory m- cell responses, hence improve reading

What is the Future for Dyslexia Testing?

• Genetics?• Improved phonological or

orthographic testing?• Neuroimaging?• Improved psychophysical tests?• EEG Biomarkers?

Dyslexia is highly hereditary; 15 chromosomal sites and 9 genes have so far been discovered; these

strongly imply a neurological basis

C6p ? KIAA 0319 gene -cell~cellrecognition and immune control (MHC system); also DCDC2

C18p, omega 3s?

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3 dyslexia genes (KIAA0319, DCDC2, ROBO) control neuronal migration and may cause these ectopias. KIAA0319 is also involved in setting up speech laterality and whether you are right or left handed

Genetic Testing?• The ‘missing heritability problem’ - even if all the effects of the

9 gene variants that have so far been associated with dyslexia are summed together, they account for less than 3% of people’s differences in reading ability

• But twin studies have shown that genetic variants account for 60% of people’s differences in reading ability; this is the ‘missing’ heritability

• ie the genetic background to dyslexia is highly complex and likely involves non-linear interactions between many genes with small effects, conferring vulnerability only if other genetic and also adverse environmental factors are present.

• So genetic diagnosis of dyslexia is not likely to be possible ever?• Instead the main reason for genetic studies in dyslexia is to help

work out the basic mechanisms at work, not for diagnosis, still less to plan in utero abortion

Improved Cognitive Testing?

• Most cognitive tests are set at too high a level and merely retest aspects of reading itself; we need to focus on the underlying biological factors

• Already hundreds of potential tests• Summary IQ formulae, eg ‘performance’, ‘non-verbal’,

‘verbal’, ’full scale’, IQ should not be used with dyslexics; they lump too many different skills together – in particular rate of processing with holistic skills

• Summaries are only appropriate for ‘flat’, not with spiky dyslexic, profiles, eg non verbal IQ includes speed of processing on which dyslexics perform poorly

• In the future cognitive testing needs to be replaced by more objective ‘biomarkers’ that will identify dyslexia reliably

Improved Cognitive tests? Spiky Dyslexia Profile- you must use tests that don’t penalise dyslexics

Oral Non verbal

Reading & spelling

SpeedSTMDecoding

Lateral thinking

Left hemisphere language areas that activate less in dyslexics

Cell migration gene variants cause under-activation in the LH language network

Neuroimaging?

Neuroimaging

• Results very variable- not much agreement

• Good for research, but not yet diagnostic

• Highly expensive

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Improved Psychophysical Tests

• Psychophysical tests measure lower level physiological functions, visual and auditory temporal processing,

• Eg Visual motion sensitivity• Rapid auditory processing • Eye movement control• These tests have now been shown to be

reliable biomarkers of true developmental dyslexia Coherent Motion at Threshold (%)

0 10 20 30 40 50 60 70 80

Orth

ogra

phic

Dis

crim

inat

ion

(% C

orre

ct)

0

20

40

60

80

100

n = 792; r = - 0.38

Improved psychophysical tests? Visual motion sensitivity predicts orthographic reading skill in

everyone

Physiological EEG measures?

• Rapid visual and auditory processing stimuli set up brain waves which can easily be recorded from the scalp at low cost.

• Moving visual stimulus: signal reaches the brain more slowly in dyslexics

• In future auditory & visual EEG biomarkers will probably be the most practical way of diagnosing true dyslexia

Visual cortex brain waves responding to a moving visual stimulus

Conclusions• Dyslexia can indeed be distinguished from other causes of reading failure

using Pringle Morgan’s original criteria: a) poor reading; b) discrepancywith normal or high other cognitive skills; c) hereditary/genetic basis

• Modern techniques have revived these criteria and have revealed specific neurological biomarkers in dyslexic brains involving magnocellular timing systems

• These cause slower auditory and visual sequencing which impairs reading

• These differences can be measured to provide reliable biomarkers to detect dyslexia

• Understanding these mechanisms is enabling us to develop simple techniques to help dyslexics speed up their visual and auditory processing, hence to improve their reading

Dyslexia does exist!It is due to Sensorimotor

Processing Problems

John Stein, MagdalenCollege,

Oxford University, UK

Supported by The Dyslexia Research (www.dyslexic.org.uk), EsmeeFairbairn, Garfield Weston, Tolkien and Wellcome Trusts, BBC

Children in Need

DRT