Development

Question 1

eye movement responses

methods for studying infant vision

Answer 1

• forced-choice preferential looking
• optokinetic nystagmus

Question 2

electrophysiological responses

methods for studying infant vision

Answer 2

• visual evoked potential
• electroretinogram

Question 3

forced choice preferential looking

teller (1977)

Answer 3

• infants looks at a reference and test stimuli randomly positioned on left or right
• presented with 2 stimuli (grating or luminance grey of gratings summed). If they can’t see the grating, they won’t look at it
• observer decides whether infant is looking at left or right stimulus
• significant result if infant looks at one stimulus more than the other (more than 75% of time)
• depends on infant preferentially looking at an “interesting” stimulus

Question 4

optokinetic nystagmus

Answer 4

• oscillation of the eyes back and forth when looking at a slowly moving stimulus
• spin the striped pattern to determined the thinnest stripes that elicits optokinetic nystagmus (spin drum with stripes)
• change the spatial frequency of the stripes until reach limit of infants visual system
• depends on primarily subcortical neural mechanisms and needs large stimulus

Question 5

visual evoked potential

Answer 5

• electrical potential induced by visual stimulus and recorded from scalp over visual cortex
• measures performance of visual pathways from retina to visual cortex
• amplitude of waveform decreases until starts to look like baseline activity
• depends on infant fixating and accommodating
• newborn infants do not always make conjugate eye movements which can make it hard to interpret results – works best when have more control

Question 6

electroretinogram

Answer 6

• electrical potential recorded between front of the eye and the skin near the eye
• electrode placed at front
• measures the combined activity of cells in the retina
• depends only on properties of the retina, not later stages of visual processing
• highly relative to stimulus

Question 7

brain activity before birth

Answer 7

• before birth there is neural activity in the visual pathways
• spontaneous waves of action potentials are present in the retina weeks before any vision is present
• before birth – retina generating activity which will be needed during life. Only RGCs, rods and cones haven’t yet developed
• these waves consist of domains of activity that form a mosaic pattern over the entire ganglion cell layer in the retina (part of the brain)

Question 8

synaptogenesis

Answer 8

• several processes take place after young neurons have reached their final target location (pathfinding)
  1. Cell loss through death of some cells – genetic control. Apoptosis
  2. Pruning of axon terminals and/or growth of new ones
  3. Differentiation of dendrites – ramification and retraction of spines
  4. Formation/loss of synapses

• Each process above occurs during the development of the visual system
• 2-4 are dependent on sensory input and occur after eye opening (post-natal)
• Early blind patients often have a thicker cortical sheet – this is thought to be caused by a failure of axonal pruning and retraction of processes (Jiang et al., 2009)
• Number of synapses peaks at time when visual system is most susceptible to changes in sensory input
• Thicker cortical sheet thought to be due to stages 2 and 3

Question 9

newborn’s can

Answer 9

• See large objects (visual acuity 6x worse than adults)
• Distinguish shades of grey (contrast sensitivity 25x worse than adults)
• Distinguish large differences in colours (e.g. red and green) but not subtle colour differences (reddish-orange)
• Distinguish large differences in the tilt, direction and speed of an object
• Move their eyes and track large objects but eyes are not well coordinated

Question 10

newborn’s cannot

Answer 10

• See in depth (no stereo acuity, no 3d vision)
• Distinguish mother’s face from other faces (poor face recognition)

Question 11

development of visual acuity

Answer 11

• Visual acuity improves with age – remarkable agreement between studies using different techniques to measure acuity (data from 3 studies using different measures have agreement in trends)
• Large improvement in visual acuity between birth and nine months of age (1 cycle/deg to ~10 cycles/deg or 6/80 to 6/18) and further improvement thereafter

Question 12

development of photoreceptors in retina

Answer 12

• Large part of development of acuity explained by changes in size, shape and distribution of photoreceptors in retina (Banks & Bennett, 1988)
• Cones in fovea wider in newborn (> 6 microns) than adult (1.9 microns) and spaced further apart
• Outer segment of infant cone shorter and absorbs less light than adult cone
• Acuity improves substantially with age because cones become thinner, closer together, and outer segment lengthens
• Larger inner segment – cannot pack cones as close together
• Packing mosaic down allows you to see finer spatial detail
• More light is absorbed by cones and width of an object covered by single cone is reduced

Question 13

development of the fovea

yuodelis & henrickson (1986)

Answer 13

• Development of the fovea (pit) in retina responsible for high resolution, sensitive, central vision
• Birth – foveal depression wide and continues to deepen after birth until 15 months
• 45 months – foveola width and cone diameter at adult levels. Ganglion cells dispersed off to the side, photons have unobstructed access
• Gives more gradual change in acuity over time

Question 14

development of contrast sensitivity

Answer 14

All parts of the contrast sensitivity curve change with age (Atkinson et al., 1977)
* Not equally sensitive to different spatial frequencies (inverted U-shaped graph)
* Over time, need to move diagonally to superimpose to match adult

Question 15

3 processes in development of contrast sensitivity with different time courses

Answer 15

1. Improves at all spatial frequencies (birth – 10 weeks)
2. Rapid improvement at high spatial frequencies (until 4 years of age)
3. Slower improvement at low spatial frequencies (until 9 years of age)

Question 16

development of colour vision (spectral sensitivity)

Answer 16

• Newborns have some (limited) ability to distinguish colours from grey (Adams et al., 1986)
• Immature long wavelength (L or red), medium wavelength (M or green) and short wavelength (S or blue) cones are present at birth
• Infants as young as 2 weeks of age have colour vision (Peeples & Teller, 1975), but colour discrimination and sensitivity is poorer than adults because of shorter cones that absorb less light
• By 6 months of age, colour vision (and discrimination) is essentially adult-like

Question 17

development of sensitivity to form

braddick & attkinson (2011)

Answer 17

• Infants have the cortical apparatus to detect and distinguish large changes in orientation, but the cortex needs to mature before fine discrimination of orientation develops
• Orientation detected by single cells in visual cortex
• Tuning curve – preference for orientations
  o Broad in infants so limited orientation discrimination
• The ability to discriminate the form of a stimulus in noise is present by 2-3 months of age, but the amount of noise that can tolerated is poor compared to adults
• Global form measurements claimed to tap ventral stream processing and develop at different rate to global motion measurements (which tap dorsal stream processing)

Question 18

development of sensitivity to motion

Answer 18

• Very soon after local motion signals are first available in the developing brain (7-12 weeks of age; Wattam-Bell, 1991), infants can integrate local motion into a global representation of motion (Braddick & Attkinson, 2011)
• The ability to discriminate the direction of dot motion develops rapidly up until 24 weeks (Wattam-Bell, 1994), but the amount of noise that can be tolerated has still not reached adult levels

Question 19

development of depth perception

Answer 19

• Visual cliff experiment
• 9-12mos
• Table that has pattern immediately under or with an illusory cliff
• All crawled to shallow end when encouraged but almost none did to deep end
• Depth perception isn’t available to infants until 9-12m

Question 20

development of binocular vision

Answer 20

• For binocular vision, the two eyes must converge or diverge so that two images fall on corresponding parts of the retinas
• Must be good acuity in both eyes and good control of eye movements
• Binocular function matures as acuity in the retina matures and vergence movements become more accurate
• In humans, earliest evidence of binocular function at about 3mos (Held et al., 1980; Birch et al., 1982, 1996)
• Earlier than visual cliff would suggest

Question 21

development of stereopsis

Answer 21

• Stereoscopic depth perception – the ability to use the differences in the images caused by each eye viewing the world from a slightly different viewpoint
• Earliest evidence of stereoscopic depth discrimination at 3mo (Held et al., 1980; Birch et al., 1982, 1996)
• Stereo acuity improves gradually and close to adult levels by 6 months of age (Held et al., 1980; Birch et al., 1982, 1996)
• Retinal disparity – used to judge depth
• Crossed vs uncrossed disparity
  o Where in relation to horopter
  o Both adult-like by 6mos

Question 22

the developed visual system has

Answer 22

• 20/20 (6/6) visual acuity
• Detect 1% change in contrast
• Distinguish subtle changes in colour
• Distinguish 0.5-1 deg change in the tilt of a stimulus and direction of movement
• Accurately move their eyes to a target and accurately track an object
• Distinguish depths of 0.0005 degrees (~2s of arc)
• Recognise and discriminate faces and facial expression

Question 23

imprinting

Answer 23

• Any kind of phase-sensitive learning (occurring at a particular age or life stage) that is rapid & appears independent of the consequence of behaviour
• Under genetic control
• Filial imprinting – form strong and exclusive attachments to particular types of objects/animals after relatively brief exposure early in life
  o Most common form
  o Exclusive social bond infants form with an adult
  o Only really seen in animals who are somewhat self-sufficient at birth
• Spalding (1872): reported “stamping in” domestic chics
• Heinroth: first used the German term Pragung (translated as imprinting)
• Lorenz (1935): followed up and popularised Heinroth’s work

Question 24

filial imprinting

Answer 24

• Lorenz demonstrated imprinting behaviours of geese soon after hatching by dividing eggs laid by graylag goose into two groups:
  1. Hatched by mother goose
  2. Hatched by Lorenz in incubator
• Incubator-hatched geese imprinted on first moving stimulus within what Lorenz called a “critical period” (13-16hrs after hatching)
• Strong and exclusive bond

Question 25

when does imprinting happen in young birds? | hess (1959)

Answer 25

* Some imprinting occurs after hatching * Imprinting is more consistently achieved in all animals 13-16hrs after hatching * Clear evidence for a critical period for imprinting behaviour

Question 26

critical periods

Answer 26

* Imprinting led to the notion that there are critical periods in the development of brain and behaviour * CP: a period during the early life of an animal when some property develops rapidly, and is most susceptible to alteration by the environment * For sensory analysis: critical period is early in life where visual function can be shaped Three waves of learning during the critical period * Without the appropriate stimulus during a critical period, it may be difficult, or impossible, to develop some functions later in life * Critical periods for cortical regions devoted to vision and other senses open in infancy, then tightly close * Critical periods for language and higher cognition open later and never entirely close (plasticity in these)

Question 27

lifespan and critical periods

Answer 27

* The critical period is a definite portion of an animal’s life devoted to shaping the neural connections * The longer the lifespan the longer the critical period (Berardi et al., 2000) * Critical period shows linear relationship with the lifespan of the species, it is a finite portion of the lifespan

Question 28

critical periods and the visual system

Answer 28

* Critical periods have been most extensively studied in the visual system * Wiesel & Hubel (1963) – critical period to describe the period during which ocular (eye) dominance can be disrupted by monocular deprivation * Critical period is not a single entity – particular to: different visual functions, parts of brain and visual histories * Distinguish between critical periods for development, disruption, and recovery

Question 29

critical periods and monocular deprivation

Answer 29

* Hubel and Wiesel classified cells primary visual cortex in terms of the balance of input they received from each eye * When one eye is closed during the critical periods of visual development neurons in primary visual cortex stop responding to input from that eye and start responding to input from the other eye * Classification system based on input preference * Outside layer 4 – might still have a preference, more effective with one eye * Binocular not nearly as bad for you as monocular * Deprive early = shift in cortex, not if deprive late

Question 30

general principles of critical periods

Answer 30

1. The visual system is plastic between eye opening and puberty 2. More severe visual deprivations have larger effects 3. Higher levels of the visual system have later critical periods 4. Different properties have different critical periods 5. Critical periods depend on the history of visual experiences 6. Critical periods for disruption and recovery may be different

Question 31

the visual system is plastic between eye opening and puberty

Answer 31

Effects of monocular deprivation in different species suggest critical period starts after eye opening and ends around puberty is broadly true

Question 32

more severe visual deprivations have larger effects

Answer 32

* Cases of unilateral cataract in humans – start and end of deprivation are well defined * Horizontal bars span the period of deprivation at different ages * Same length of deprivation has dramatically different effects on visual acuity at different ages * The severity of the deficit in visual acuity depends upon both the length of monocular deprivation and the time during the critical period at which it is applied * Subjects who gained cataract & removal during the visual critical period, left with poor visual acuity afterwards. This was not the case for those whose onset was around the end of the critical period onwards to after critical period

Question 33

higher levels of the visual system have later critical periods | wiesel & hubel (1963)

Answer 33

* Monocular deprivation has very little effect in the retina * Monocular deprivation has little effect on the LGN cells, except deprived cells are smaller (small morphological but not functional changes) * Responses of cells in primary visual cortex are dominated by open eye and cannot be driven by closed eye after long deprivation * In higher visual areas (e.g. inferotemporal cortex), early critical period and later more protracted period of development and plasticity * Dorsal stream visual functions may be more vulnerable to disruption than ventral stream functions during development

Question 34

different properties have different critical periods

Answer 34

* Effects of monocular deprivation at different ages on the balance of visual sensitivity between the two eyes in macaque monkeys * Monocular deprivation only disrupts a- Dark adapted light sensitivity before 3mo b- Light adapted light sensitivity before 6mo c- Contrast sensitivity before 20mo * Demonstrates there are different critical periods for different visual functions

Question 35

LeVay et al (1980) | different properties have different critical periods

Answer 35

* Different critical periods for the development of the parvocellular (P) pathway and magnocellular (M) pathway * Used reverse suture in the macaque: monocular deprivation and changing the eye closed from right to left at 3 weeks of age * Monocular deprivation reduces extent of LGN axons (width of ocular dominance columns) innervating visual cortex * Reverse deprivation/suturing: open eye that had been closed and close eye that had been open * Layer 4C(alpha) (M) dominated by axons from left eye that was open first * Layer 4C(beta) (P) dominated by axons from right eye that was open second * Critical period for M axons innervating cortex ends before critical period for P axons

Question 36

critical periods depend on the history of visual experiences

Answer 36

* Rearing an animal in the dark delays both the start and end of the critical period (Cynader & Mitchell, 1980; Mower, 1991) * Mower (1991): dark reared cats are less plastic than light-reared cats at 5-6 weeks of age, equally plastic at 8-9 weeks, and more plastic at 12-20 weeks. Sensitivities later in dark reared cats * History of visual experiences (e.g. no exposure to light during early development) shifts the critical period to a later age. Push critical period window back in time, visual history of experience is important

Question 37

critical periods for development, disruption and recovery may be different

Answer 37

* Critical period for disruption of acuity may last longer than its initial period of development * Strabismus and anisometropia change the critical period in humans (like dark rearing) * The critical period for disruption in strabismus and anisometropia different from deprivation * The critical period for recovering visual acuity is hugely different to its development and disruption (Astle et al., 2011) * Different techniques have been used to reopen juvenile-like critical periods of heightened brain plasticity in adult brains * Reopening critical periods in an adult brain is thought to work by removing structural and functional brakes on brain plasticity (Bavelier et al., 2010)

Question 38

what is amblyopia

Answer 38

* “Lazy eye” * Poor (blunt) vision in one eye * Difference in visual acuity between the two eyes * Developmental disorder that affects 2-4% of the population * Associated with abnormal visual experience during the critical periods * No pathology in the eye itself – “lazy brain”. Problem lies in the visual cortex rather than eye or optic nerve * Defined inn terms of the deficit in visual acuity * Leads to inability to combine visual input from the two eyes * Deficit in binocular and stereoscopic vision. Serious consequences for binocular visioni as foveas are not looking at same object

Question 39

diagnosis of amblyopia

Answer 39

* At least a two-line difference in acuity between the two eyes on a letter chart, despite full optical correction * No pathology or damage to the eye itself – no damage to axons

Question 40

strabismus

Answer 40

misalignment of visual axes in the two eyes. Neuromuscular anomaly of vision, strength of deficit based on angular deviation

Question 41

anisometropia

Answer 41

unequal refractive error in the two eyes. Difference in spectacle prescription in each eye

Question 42

inter-oculular suppression and amblyopia

Answer 42

* Normal vision: object of interest is imaged on corresponding points on the two retinas and fused for binocular vision * Amblyopic vision: suppression ‘switches off’ vision in the deviating eye preventing signals reaching conscious awareness * In amblyopia (with strabismus), object of interest is imaged on non-corresponding points on the retinas in the two eyes 1. Confusion: something other than object of interest is imaged on fovea of deviating eye 2. Diplopia: object of interest imaged on non-foveal part of retina in deviating eye * Images on foveas in deviating and non-deviating eyes are dissimilar and cannot be fused * Space mapped across image * With strabismus we deviate from the idea of corresponding points

Question 43

amblyopia with strabismus

Answer 43

* Deviations of the eye may cause rearrangements of connections between retina and cortex * Sometimes a new point of fixation is created away from the fovea and new connections are formed from new point of fixation to cortex * Different rearrangements of the connections between retinas and cortex can occur to compensate for strabismus * Rearrangement of connections between retina and cortex can lead to complex array of visual (acuity, sensitivity, stereo, perceived distortions) deficits * Reworking connections to generate essentially a surrogate fovea * Type of cortical compensation to deal with confusion

Question 44

classical model of amblyopia etiology

Answer 44

* The terms ‘strabismic amblyopia’ and ‘anisometropic amblyopia’ are in common use and strongly imply a causal relationship in the development of amblyopia * Lose high spatial frequency information in anisometropia

Question 45

amblyopia is more than an acuity deficit

Answer 45

The perceptual consequences of amblyopia can be manifested as changes to different combinations of * Limits of central vision (at threshold) 1. Visual acuity (and crowding) 2. Contrast sensitivity 3. Stereo acuity * Supra-threshold vision (patterns readily available to you) 1. Perceived distortions The particular combinations of perceptual consequences appears to depend upon the abnormal visual experiences during visual development (e.g. strabismus, anisometropia, cataract)

Question 46

acuity deficit in amblyopia | levi & klein (1982)

Answer 46

* Anisometropia (A): the letter acuity, grating acuity and Vernier acuity deficits are proportional to each other in the amblyopic eye of an individual with anisometropia * Strabismus (S): Vernier acuity deficits are proportionally worse than letter acuity and grating acuity in the amblyopic eye of an individual with strabismus. Extra loss with extra in positional acuity

Question 47

crowding in peripheral vision and a crowding deficit in amblyopia

Answer 47

* Crowding affects visual acuity * Crowding: flanked letter acuity is poorer than isolated acuity in amblyopia (Levi et al., 2007) * Critical letter spacing for reading equals the critical spacing for crowding * Central amblyopic vision is crowded * Fixate on spot * Somewhere in visual field ad ask to identify letter * More difficult with flanker letters (R is crowded) * As you have strabismus – have more crowding that is seen earlier in development. Past the critical period for this crowding effect

Question 48

contrast sensitivity deficit in amblyopia

Answer 48

Bradley & Freeman (1981): contrast sensitivity curve measured in the amblyopic eye shows substantial loss of sensitivity at high spatial frequencies, but not much loss at low spatial frequencies

Question 49

stereo acuity deficit in amblyopia

Answer 49

Stereo acuity task: is the central disk in front or behind the surrounding disk? * Stereo acuity is the smallest detectable depth difference that can be seen in binocular vision * Amblyopia produces a deficit in stereo acuity, the severity of which depends upon the nature of the visual disruption during development * Random dot stimulus * Oney eye to see one population of dots, other eye to see other population of dots * In front or behind background? * ~70% of people w/ anisometropia retain some stereopsis * Vast majority of strabismic anisometropes are stereoblind

Question 50

amblyopia (with small angle strabismus) is like anisometropia

Answer 50

* When the angle of deviation in the amblyopic eye is small (<5deg), the acuity and contrast sensitivity deficits are similar to anisometropic amblyopia * A particular form of retinal correspondence (harmonious ARC) is usually present * Show high spatial frequency loss and some perceptual depth perception

Question 51

perceived visual distortions

Answer 51

Barrett et al. (2003) * Perceived distortions are most apparent when you ask amblyopes with strabismus to reproduce a stimulus * Heterogeneous types of perceptual distortions of the position, orientation and spatial frequency of visual patterns * These perceived distortions do not correlate with the acuity and contrast sensitivity deficits in amblyopia * This is a subjective estimate of the distortions experienced by amblyopic observers * Distortion not marked at low frequencies * Increasing, appears e.g. wavy lines Hussain et al. (2015) * Developed an objective estimate of perceptual distortions * Task was to position the response probe in the diagonally opposite position to the target * All probed locations produces a coarse map of visual space * Mirror visual space through different eyes * Type of maps technique produces

Question 52

pattern of visual deficits in amblyopia | McKee et al. (2003)

Answer 52

* Measured acuity and sensitivity * Used factor analysis to classify amblyopic subjects into four groups 1. High acuity and moderate sensitivity (visually normal) 2. Moderate acuity and high sensitivity (strabismics) 3. Moderate acuity and high sensitivity (anisometropes) 4. Low acuity and moderate sensitivity (strabismic anisometropes) * Letter acuity, contrast sensitivity and other tasks… * 2 factors that explain around 80% of differences: visual acuity and contrast sensitivity * Reduced resolution and loss of binocularity determine pattern of visual deficits in amblyopia * Amblyopes with no binocular vision typically have poorer visual acuity (but better monocular contrast sensitivity) than those with binocular vision

Question 53

typical diagnostic criteria of dev dyslexia

Answer 53

* Severe and persistent difficulty in reading skill acquisition * Absence of intellectual, physical or emotional impairment * Despite normal motivation & educational opportunity

Question 54

epidemiology of dev dyslexia

Answer 54

* Estimates of prevalence ~5% of population * More prevalent in boys * Substantial genetic component

Question 55

etiology of dev dyslexia

Answer 55

* As reading is complex, understanding cause could be dysfunction of any of a number of requisite cognitive and perceptual skills. Lots of things working in conjunction in order to read * Dominant current theory = phonological deficit hypothesis

Question 56

phonological deficit hypothesis | theory of dev dyslexia

Answer 56

* Nothing to do with vision * Learning to read in an alphabetic language requires mapping between letters (graphemes) and mental representations of speech sounds (phonemes) * Associations between these

Question 57

process hindered in dyslexia due to problems with

Answer 57

* Understanding phonological structure of speech: rhyme detection, word onset detection * Retaining and retrieving speech sounds: rapid automatised naming (e.g. rapid colour naming), letter and word repetition

Question 58

parallel processing model of early vision

Answer 58

* Visual information initially processed by a set of independent mechanisms with complementary tuning properties (Kulikowski & Tolhurst, 1973) * Specialised for flicker/motion processing * Characterised by sensitivity to low spatial frequencies and high temporal frequencies

Question 59

transient channel deficit hypothesis

Answer 59

* In 1980’s Lovegrove et al published a series of papers comparing contrast sensitivity in dyslexia and normal readers * Findings of selective impairment at low spatial frequencies and high temporal frequencies interpreted as evidence for a transient channel deficit in dyslexia * Specialised for form/pattern processing * Characterised by sensitivity to high spatial frequency and low temporal frequencies

Question 60

magnocellular deficit hypothesis

Answer 60

* Psychophysical research & sustained mechanisms recast in term of underlying anatomical pathways: o Magnocellular (M) – brief response; spatial-temporal tuning is low spatial frequencies and high temporal frequencies; no colour opponency o Parvocellular (P) – prolonged response; spatial-temporal tuning is high spatial frequencies and low temporal frequencies; colour opponency * Physiological response properties of individual neurons in M & P pathways mirror the attributes of the psychophysically defined transient and sustained systems * Impaired contrast sensitivity for low spatial frequency and high temporal frequency stimuli interpreted as evidence for abnormal processing in M pathway * Evidence from lesion studies in macaque monkeys is mixed o Lesioning M layers of LGN does impair contrast sensitivity at high temporal frequencies o But M lesions have no effect on static contrast sensitivity, even at low spatial frequencies ## Footnote merigan & maunsell (1993)

Question 61

dorsal stream | cortical processing pathways

Answer 61

* Projects into parietal cortex and thought to support spatial and motion analysis * Receives greater input from M pathway than P pathway (though segregation is incomplete) * Damage to dorsal stream areas is associated with selective impairments in visual motion processing (e.g. bilateral damage to MT can result in inability to perceive visual motion, akinetopsia) and visual attention (e.g. lesions to the right posterior parietal cortex, area 7, can result in a deficit in attention to and awareness of regions of space, neglect)

Question 62

visual motion processing deficit? | dev dyslexia

Answer 62

Poor performance by dyslexic groups on a range of visual motion tasks has been interpreted evidence for deficient magnocellular/dorsal stream processing, including * Speed discrimination – Demb et al. (1998) * Global dot motion detection – Cornelissen et al. (1995) * Thresholds tend to be higher in dyslexic groups

Question 63

visual attention deficit? | dev dyslexia

Answer 63

Visual search: dyslexic children slower at difficult search tasks, such as finding a target defined by a unique conjunction of orientation and colour * Vidyasagar & Pammer (1999) * Find horizontal green bar * Time it takes to find target increases with distractors * More so in those with difficulties Spatial cueing: dyslexic individuals fail to use spatial cues to optimise visual task performance * Roach & Hogben (2007) * Dyslexic individuals were not able to use a cue in the same way as those without

Question 64

magnocellular/dorsal stream deficit? | dev dyslexia

Answer 64

* Poor performance of dyslexic groups on contrast sensitivity, motion discrimination & visual attention tasks often cited as converging evidence for a M/dorsal stream deficit * Appears to be difficulty with contrast selectivity

Question 65

reading level-matched designs | dev dyslexia

Answer 65

* Most studies use CA matched * But could use MA matched – compare dyslexic readers to younger children matched at the same reading level * If visual deficits causal to dyslexia, differences between dyslexia & control groups should be maintained * Olulade et al. (2013), Gori et al. (2015)

Question 66

intervention designs | dev dyslexia

Answer 66

* If visual deficits are causal to dyslexia, can interventions that improve vision also lead to improvements in reading * Franceschini et al. (2013), Luniewska et al. (2018)

Question 67

typical diagnostic criteria ASD

Answer 67

* Difficulties with social interaction * Difficulties with communication * Restricted range of activities & interests

Question 68

epidemiology ASD

Answer 68

* Prevalence ~1% * Male to female ration ~4:1 * More prevalent in MZ than DZ twins – genetic component

Question 69

weak central coherence theory | frith (1989)

Answer 69

* Propose that non-social features of autism may follow from a tendency to process local rather than global information * Individuals w/ ASD good at analysing local featural detail, but relatively poor at extracting overall gist or meaning * General cognitive theory seeking to address both deficits and assets in ASD across domains e.g. visual perception, memory etc.

Question 70

embedded figures | superior performance in ASD

Answer 70

* Autistic children faster and more accurate at finding simple figure within a more complicated pattern * e.g. Shah & Frith (1983)

Question 71

block design | superior performance in ASD

Answer 71

* Autistic children correctly construct complex two-tone pattern using individual blocks faster than matched controls * e.g. Shah & Frith (1993)

Question 72

navon task | superior performance in ASD

Answer 72

* Typically observers find it easier to identify the larger letter than the smaller letters (global superiority effect) * In contrast, ASD children have been shown to show a preference for identifying the small letters (local advantage) * e.g. Plaistead et al. (1999)

Question 73

interpretations of superior performance in ASD

Answer 73

* Different cognitive processing ‘style’ (e.g. Happe & Frith, 1996) * Enhanced low-level visual processing of local detail (e.g. Mottron et al., 2006) * Impaired high-level visual processing of global structure (e.g. Behrmann et al., 2006)

Question 74

ashwin et al. (2009) | enhanced visual acuity in ASD?

Answer 74

* Measured visual acuity in 15 individuals w/ ASD and 15 controls using Freiburg Visual acuity * “Individuals with ASC have significantly better visual acuity compared with control subjects – acuity so superior that it lies in the region reported for birds of prey” * Criticised by Bach & Dakin (2009) on the basis that display screen resolution was not high enough to support accurate measurement of resolution thresholds – computerised version, issues for measuring visual acuity, measurements below 1 pixel cannot count * Claimed to find enhanced visual acuity in individuals with ASD * Where the gap in the ‘C’ is: reducing the size of gap, harder * Significantly better acuity than control group – birds of prey bullet point ## Footnote Tavassoli et al. (2011) * No difference in visual acuity between adults with and without ASD under appropriate testing conditions * Redid previous experiment but found no differences

Question 75

de Jonge et al. (2007) | enhanced contrast sensitivity in ASD?

Answer 75

no significant differences in static contrast sensitivity between ASD and matched control group across a range of spatial frequencies (1.5 c/deg to 18 c/deg)

Question 76

berton et al. (2005) | enhanced constrast sensitivity in ASD?

Answer 76

* Compared contrast sensitivity at low spatial frequencies (0.75 c/deg) in high functioning ASD ppts (HFA) and typically developing (TD) controls * HFA group were significantly better at detecting first order (luminance-modulated) gratings * But significantly worse at detecting second-order (contrast modulated) gratings

Question 77

dickinson et al. (2014) | enhanced orientation discrimination in ASD?

Answer 77

* Measured thresholds for discriminating small changes in orientation from 45 deg * Performance correlated with autistic traits in sample of 38 UG students * How orientation discrimination varies in general population * How this correlates with AQ scores

Question 78

glass pattern | impaired global form processing in ASD?

Answer 78

* Image composed of randomly positioned dot pairings (dipoles) with orientations arranged according to some global form (e.g. circular structure) * Strength of global form signal can be manipulated by adding in randomly oriented dipoles

Question 79

tsermentseli et al. (2008) | impaired global form processing in ASD?

Answer 79

poor form coherence thresholds in high functioning autistic individuals (HFA)

Question 80

impaired face processing? | ASD

Answer 80

* ASD individuals less able to identify complex emotions from faces * Spend less time fixating on critical areas of the face such as the eyes when judging emotion * Pelphrey et al. (2002):

Question 81

discrimination of non-emotional attributes | ASD

Answer 81

* Some reports of impaired ability to discriminate gender and identify of faces in ASD * However, other studies have failed to find any differences (Simmons et al., 2009) * Behrmann et al. (2006)

Question 82

poor global motion integration? | ASD

Answer 82

A number of studies have shown that autistic children have higher motion coherence thresholds than age-matched controls (e.g. Spencer et al., 2000; Pelicano & Gibson, 2008) * Pellicano & Gibson (2008) * Global motion thresholds * Poor performance = lower threshold * Worse performance in ASD & dyslexic groups

Question 83

is poor global motion perception a common features of neurodevelopmental disorders?

Answer 83

* Similar patterns of high motion coherence thresholds across a range of disorders * ASD, dyslexia, Williams syndrome, Fragile-X Syndrome, cerebral palsy etc.

Question 84

dorsal stream vulnerability hypothesis | braddick et al. (2003), ASD

Answer 84

Propose that because neural systems that subserving global motion perception emerge relatively late in development, they may be particularly susceptible to impairment

Question 85

could poor performance on global dot motion tasks reflect non-sensory factors? | roach et al. (2004)

Answer 85

* Patterns of performance similar to that seen in neurodevelopmental disorder groups can be simulated by assuming that individuals are simply more prone to giving random responses * Predicts that significant differences will only occur when there is greater variability in the neurodevelopmental disorder group than the control group (consistent with meta-analysis of dyslexia studies)