Dyslexia theory

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Dyslexia theory

• Biological substrates genes, hormones and visual
  theories

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R. DAWKINS (1989) The Selfish Gene.

• We, that is our brains, are separate and
  independent enough from our genes to rebel
  against them.

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Genetic factors

• Nowadays, there is a wide consensus that
  developmental dyslexia is a neurological disorder
  with a genetic origin (e.g. Ramus, 2003
  Grigorenko et al., 2007).
• Twin studies have revealed higher concordance
  rates for reading disability in monozygotic MZ
  (84-100) compared to dizygotic DZ (20-35)
  twins (Zerbin-Rüdin, 1967 Bakwin, 1973)

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DYX1C1 on chromosome 15q21

• The risk of a son of a dyslexic father
  manifesting dyslexia is approximately 40 per
  cent, with the same rate being reported among
  siblings of affected persons (Pennington and
  Gilger, 1996).
• Linkage studies had provided seven reliable
  chromosomal sites suspected to harbour genes
  associated with dyslexia (Ramus, 2006 Saviour
  Ramachandra, 2006 Grigorenko et al., 2007).

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From genes to brains

• DCDC2 and KIAA0319 have been found to be
  crucially implicated in cell migration (Ramus,
  2006).
• The former is a member of the proteins in the DCX
  family, involved in neuronal migration to the
  neocortex and it may also be involved in the
  development of the corpus callosum (Galaburda et
  al., 2006).

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Brain morphology

• The post mortem findings of Geschwind and
  Levitsky (1968) directed interest towards the
  asymmetries between the plana temporale (PT),
  part of the superior surface of the temporal
  lobe, which is thought to be involved in language
  function.

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plana temporale

• PT is also regarded as the site where auditory
  phonemes are mapped onto visual graphemes,
  therefore being a site of interest in dyslexia
  research (Shapleske et al., 1999).
• Geschwind and Levitsky found the two plana to be
  asymmetrical (left gt right) in 65 per cent of the
  cases.
• This asymmetry was thought to reflect the
  functional linguistic predominance of the left
  hemisphere in normal populations
• Symmetrical in DD possibly due to the lack of a
  specialised left hemisphere (Gazzaniga, Ivry,
  Mangun, 2002

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Lateralisation

• Dyslexics fail to complete the normal
  developmental progression from rightward to
  leftward cerebral lateralisation processes
  (Orton, 1937 Bakker, 1990 2006).
• (as do 35 of normals!)
• The right hemisphere specialises in holistic,
  global information processing, as opposed to the
  left hemisphere, which is primarily engaged in
  the processing at a local level.

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bed
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Shifts from RH to LH

• Too late/ fail P-type (P for perceptual)
• Too early L-type (L for linguistic).
• Mixed

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P-type dyslexia

• is thought to develop when the beginning reader
  correctly processes text by visuo-spatial (i.e.
  right-hemisphere) mediated strategies but fails
  to switch to more subtle linguistic strategies in
  the more advanced stages of reading acquisition.
  Therefore, P-type dyslexics or spellers
  according to Bakker (1992 2006), read in a slow,
  fragmented style, and generally perform
  time-consuming errors (self-corrections, syllabic
  reading, fragmentations, stuttering, and
  repetitions Lorusso, Facoetti Molteni, 2004
  Masutto, Bravar Fabbro, 1994), which suggests
  that they must sound out words carefully in order
  to read them and, therefore, exhibit difficulties
  with irregular words.

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L-type dyslexics

• guessers exhibit a premature shift to the left
  hemisphere they read relatively quickly guessing
  words on the basis of context or structure,
  however, they also read inaccurately, performing
  substantive errors (omissions, substitutions and
  inversions Lorusso et al. 2004), which suggests
  a whole-word method of reading.

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• The reading performance criteria which
  distinguish the two groups are (i) speed, (ii)
  accuracy, and (iii) types of errors.
• Mixed The M-subtype describes readers who have
  characteristics of both types that is, slow
  reading and quite some substantive errors

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Geschwind and Galaburda (1987)
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Expanded
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Lateralisation

• Prenatal testosterone
• Digit ratio to identify ASD and Dyslexia in
  new-borns (Manning and Bundred, 2000)

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But

• No evidence (van Gelder et al., 2005)
• Diverse sample (Manning, 2005)
• Brosnan and Pneuman (2008)

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• More boys in families with Dyslexia (James, 2008)
  
• Sex ratio in DD (0.537) that is significantly
  higher (?24.3, p0.038) than the US live birth
  sex ratio (0.512).
• DD lower scores on GEFT (Brosnan et al., 2001)

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James (2008)

• Hypothesis DD is associated with (caused by?)
  high intrauterine testosterone concentrations.
• There is now very substantial evidence to support
  the hypothesis that the sex of mammalian
  (including human) offspring is partially
  determined by the hormone levels of both parents
  around the time of conception.
• High parental levels of testosterone are
  associated with the subsequent production of male
  offspring.
• It follows, therefore, that if a congenital
  disorder were at least partially caused by a high
  maternal intrauterine testosterone level, then
  that disorder would be expected to occur more
  frequently in males.

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Boys

• There have been studies reporting familial trends
  and an unequal gender prevalence of the disorder
  (males/females 3.2/1 Lewis et al., 1994)
• Some genetic studies suggest that this higher
  incidence of dyslexia in males than females
  implicates the involvement of a locus on the sex
  chromosome Xq26 (Grigorenko et al., 2007).

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But

• The gender ratio in family samples is
  considerably lower, about 1.5-1.8 to one
  (DeFries, 1989).
• Similar male to female gender ratios (i.e. 1.6 to
  1) have been reported in language groups other
  than English, such as Chinese (Chan et al.,
  2007).
• Other studies indicate similar numbers of
  affected boys and girls suggesting differences
  in reported sex ratios may be attributable to
  referral bias due to social factors (Shaywitz et
  al., 1990).

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The Posterior Parietal Cortex (PPC) and Attention

• All of the parietal cortex, behind the primary
  and secondary somatosensory cortex (Culham
  Valyear, 2006).
• Area controlling multimodal spatial attention
  (Facoetti, Lorusso, Cattaneo, Galli, Molteni,
  2005).
• Involved in integration, especially of that
  information relating to sensorimotor functions,
  such as the processing of spatial relations,
  visually guided movements and eye movements
  (Jaskowski Rusiak, 2005 Walsh Cowey, 2006
  Wolbers et al. 2006).

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Eye control

• Unstable binocular fixation
• Letters can appear to move
• Can make visual reading errors
• Large prink can help (Cornelissen etal., 1991)
• Closing one eye can help (Stein and Fowler, 1985)

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Saccadic Eye movements(7 letters)
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The PPC and the Visual Mini-Neglect Hypothesis

• Facoetti and Turatto (2000)
• Ignore distracter arrows in RVF or LVF
• Congruent arrows speed recognition
• RVF OK but not LVF (right PPC)
• Incongruent arrows slow recognition
• RVF over-distractibility

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Neglect
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task

• ? ? ? ? ? ? ? ? ? ?

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The PPC and the Visual Mini-Neglect Hypothesis

• Facoetti and Turatto (2000)
• Ignore distracter arrows in RVF or LVF
• Congruent arrows speed recognition
• RVF OK but not LVF (right PPC)
• Incongruent arrows slow recognition
• RVF over-distractibility
• DD more distracted on Digit recall (WAIS)
  (Brosnan et al., 2001)

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Lateral Geniculate Nucleus (LGN)
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LGN
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• Magnocellular
• Parvocellular
• (Koniowellular)

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Magnocellular pathway

• 2 ventral layers sensitive to
• Low spatial frequency
• Low luminance
• Fast
• High temporal sensitivity
• achromatic
• transient
• Periphery of vision
• Parvo, 4 dorsal layers opposite, sustained
  colour, shape, size, texture

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Retina LGN Visual Cortex
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• PPC is dominated by magno-like properties and
  relatively insensitive to parvo-like properties.

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Acquired damage
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Visual problems in reading
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Magnocellular theory of Dyslexia

• Stein Walsh (1997) M deficit theory
• Dyslexia as a dysfunction of higher-order
  processing of visual information, as manifested
  by deficits (i) in contrast thresholds for
  low-spatial-frequency, achromatic stimuli and
  (ii) in impairments of the transient system, such
  as impaired visual motion sensitivity,
  performance on which some claim remains deficient
  even for stimuli of high contrast and
  illumination.

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www.ucl.ac.uk/smgxscd/MotionResearch.html

• Many dyslexics complain words and letters move
  around
• Motion coherence
• Elevated thresholds in DD due to reduced
  sensitivity in M-System
• Post mortem evidence (Livingstone et al., 1980
  Geschwind and Galaburda, 1987 Lovegrove et al,
  1990)
• 20 smaller

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The auditory temporal hypothesis

• Tallal (1980) demonstrated that children with
  language learning impairments and dyslexic
  children have significantly more difficulty than
  age-matched controls in making temporal order
  judgments (TOJ) when the inter-stimulus intervals
  (ISIs) are short, and postulated that this may be
  related to their problems with phonological
  decoding.

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Tallal (1980)

• If a processing deficit of specific aspects of
  acoustic information was directly linked to
  reading impairment, then correlations might be
  expected between nonverbal auditory perception
  (performance on the TOJ) and the use of
  phonological skills in reading.
• r 0.81 between performance on these non-verbal
  signals and phonological skills (nonword reading)
  
• An underlying auditory perceptual dysfunction
  affected the processing of phonetic material and,
  eventually, hindered reading development.

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Multisensory Integration

• Broader window for integration
• Hairston et al. (2005)
• Normal 250ms
• Dyslexia larger
• McGurk?
• Anna Polemicou

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TOJ Visual/ Auditory
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But

• Coherent motion deficiencies also identified in
  ASD
• Skottun and Skoyles (2008)
• (1) M deficit does not cause DD
• (2) Motion coherence does not test M
• (or everyone with ASD is dyslexic!)

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Cerebellum

• The Cerebellar Deficit Hypothesis posits
  abnormalities in the cerebellum as an underlying
  causal factor of dyslexia (Nicolson, Fawcett,
  Dean, 2001).
• Traditionally the cerebellum has been associated
  with the control of coordinated movement.
• Mild cerebellar deficit leads to difficulties in
  any skill dependent on the cerebellum for
  acquisition, automatisation or execution, which
  may be taken to directly account for some
  dyslexia symptoms such as poor balance and
  posture, coordination, and handwriting (Brookes,
  Nicolson, Fawcett, 2007).

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Nutrition

• LCPUFA (include omega-3 and omega-6) have been
  linked with brain growth and improved vision
  (Richardson, 2004)
• Deficiency may result in problems such as
  retarded visual acuity, cognitive impairment, and
  cerebellar dysfunction (Haag, 2003).
• Cannot be synthesized de novo in humans and must
  therefore be provided by dietary sources (Haag,
  2003 Richardson, 2004 Cyhlarova, Bell, Dick,
  MacKinlay, Stein et al. 2007).

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Flynn Effect

• Over the last hundred years, the IQ of every
  generation has increased by about 20 per cent
  partly, it is thought, because fatty food -once
  the preserve of the rich- is now widely available
  and, consequently, few babies suffer from a lack
  of fat intake (Livingstone, 2005 Haag, 2003).

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Dyslexia

• Cyhlarova et al. (2007), reported that higher
  omega-3 concentrations were directly related to
  better reading performance. Moreover, the authors
  suggest that it is the omega-3/omega-6 balance
  that is of particular relevance to dyslexia.
• Low concentrations of LCPUFAs are likely to
  restrict the size of large magno neurons, causing
  them to resemble the smaller parvo cells (Taylor
  and Richardson, 2000)