‫کارگاه تخصصی‬ Learning

Disorder
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‫اختالالت یادگیری‬ How Learning
Disorders
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Develop?
1396 ‫پاییز‬
Farhangdoost

PhD in Cognitive Neuroscience

How Learning
Disorders
Develop?
learning disorder

– any neurodevelopmental disorder that interferes with the learning

of academic and/or social skills

– learning disabilities, such as dyslexia or reading disability (RD) and

mathematics disorder (MD), a subset of learning disorders

– congenital, genetically influenced variations in brain development

learning disorder

– Autism spectrum disorder (ASD),

– Intellectual disability (ID, formerly called “mental retardation”),
– Developmental coordination disorder (DCD),
– Speech sound disorder (SSD),
– Language impairment (LI)
– Attention-deficit/hyperactivity disorder (ADHD)
– Dyslexia or reading disability (RD)
– Mathematics disorder(MD)
– congenital, genetically influenced variations in brain development
– Their origins in genetic and environmental risk factors
– generally act early in development and change the developmental trajectory
– Encounter different developmental tasks, different symptoms emerge,
– there is only heterotypic continuity in the symptoms of a disorder across ages
– a child at family risk for dyslexia
– By kindergarten : speech problems, as well as some delays in vocabulary
development and expressive syntax
– In preschool: trouble in learning letter names and color names
– In first grade: phoneme awareness ,learning to decode new printed words
– later elementary grades : Problems in reading fluency and comprehension,
memorizing math facts
Models of causation
Models of causation

– Etiology
– distal causes of disorders
– genetic and environmental risk
– distal causes act on brain development, often in utero,
– changing the wiring and/or the neurotransmitter systems of the brain
Models of causation

– structural and neurochemical changes in the alter its functions

– functions can detected with neuropsychological tests

– alterations in neuropsychological functions affect behaviors observable by

teachers, parents, and peers

– changes in behavior are the symptoms that define various learning disorders
Models of causation

– brain development is an open process continues throughout the lifespan

– the environment, including the social environment, affects brain development

– model is probabilistic rather than deterministic

– the causal influences are bidirectional

– multiple-deficit model versus modular single-deficit model
– cognitive modules
– brain regions specialized for processing certain kinds of input, such as language or faces
– are not innate,
– are the products of a developmental process that shows considerable plasticity
– the function of these developed modules is not encapsulated
– depends on their connections and interactions with other brain structures
– it is too simplistic to completely localize such a complex cognitive operation as recognizing
faces or spoken words in just one part of the brain
The single-deficit

– a single cognitive deficit is sufficient to explain the symptoms of disorder

– different disorders have different single deficits

– disorders cooccur (“comorbidity”) abandon the single-deficit model

– frequent phenomenon of comorbidity is often explained by partially shared

etiological and cognitive risk factors

multiple cognitive
deficits
– RD and ADHD have a partial genetic overlap, as do RD and SSD
– multifactorial model, multiple genetic and environmental risk factors combine
to produce a given disorder
– If a cognitive deficit is shared by two distinct disorders, it cannot be sufficient to
– produce either one,
– it may act as a cofactor with other cognitive deficits not shared by the two
comorbid disorders
multiple-deficit model

– (1) the etiology of complex behavioral disorders is multifactorial and involves

the interaction of multiple risk and protective factors, which can be either
genetic or environmental;

– (2) these risk and protective factors alter the development of the neural
systems that mediate cognitive functions necessary for normal development,
thus producing the behavioral symptoms that define these disorders;

– (3) no single etiological factor is sufficient for a disorder, and few may be
necessary;
multiple-deficit model

– (4) comorbidity among complex behavioral disorders is to be expected because

of shared etiological and cognitive risk factors;
– (5) the liability distribution for a given disease is often continuous and
quantitative rather than discrete and categorical, so that the threshold for
having the disorder is somewhat arbitrary.
– Applying the model to two comorbidities (RD + ADHD and RD + SSD), we can
see that each individual disorder will have its own profile of risk factors (both
etiological and cognitive),
– but that some of these risk factors will be shared by another disorder, resulting
in comorbidity
‫تصویر همبودی اختالالت رشدی‬
 An Example

– dyslexia or RD, a deficit in phoneme awareness was the single cognitive deficit
– children with SSD can have a similar deficit in phoneme awareness and not develop
RD
– whether this single deficit is sufficient to produce RD?
– children with RD, compared to children with SSD but not RD (SSD only), have deficits
in processing speed;
– intact processing speed is a protective factor for children with SSD
– deficits in processing speed are shared by RD and ADHD (Shanahan et al., 2006),
helping to explain their comorbidity
Neuropsychological
Constructs
Constructivism versus modular models

– three different kinds of processing performed by the real neural networks

– (1) the slow learning of overlapping distributed representations of the environment,
performed by the posterior cortex;
– (2) active maintenance by the prefrontal cortex of limited amounts of information
over short time intervals, to enable problem solving; and
– (3) rapid acquisition of unique conjunctions of novel information by the hippocampus
and related structures.
executive functions

– Planning

– Working memory

– Inhibition

– shifting
Neuropsychological
Constructs
Theoretical areas
related
to Dyslexia
Theories at the biological level

– loci on chromosomes 2, 4, 6, 9, 13 and 18 in developmental dyslexia

– Magnocellular deficit

– reading problems are a consequence of impaired development of

a system of large neurons in the brain (magnocells)

– responsible for timing sensory and motor events,

Magnocellular deficit

– Most dyslexic children have

– unstable vision leading to orthographic weakness and
– difficulties with sequencing sounds leading to phonological problems.
– problems with focusing visual and auditory attention.
– have poor sequencing
– be uncoordinated and clumsy
Magnocellular deficit

– dyslexia overlaps with

– developmental dysphasia (specific language impairment),
– developmental dyspraxia,
– attention deficit
– disorder (ADD),
– Asperger syndrome
– neurodevelopmental syndrome
 Magnocellular deficit

– may result from impaired development of magnocellular neurons throughout the

brain,
– perhaps as a consequence of immunological attack (Galaburda and Livingstone, 1993)
– transient responses required of magnocellular neurons demand rapid membrane
dynamics
– rapid conformational changes in their channel proteins
– flexibility requires a high content of polyunsaturated essential fatty acids
 Magnocellular deficit

– two partially independent mechanisms for reading

– Lexical : familiar words

– sub-lexical: unfamiliar words

– role of vision is probably greater for the faster whole-word, lexical route compared

with the sublexical route,

Visual fixation for reading

– linguistic information conveyed by print is obtained during brief (300 ms)

fixations on words
– The eyes are then advanced by a rapid saccade to the next word
– Thus successful reading depends greatly upon achieving stable visual perception
during each fixation on the word to be read and rapid shifts of visual attention
to the next
Visual fixation for reading
The visual magnocellular system

– visual attention and of eye movements generated by the visual magnocellular

system
– 90% of retinal ganglion cells are small parvo cells
– that signal the fine detail and color of objects,
– 10% are much larger magnocells
– That signal the timing of visual events, not their form
The visual magnocellular system

– Their dendritic area, hence receptive field size, is some 500 times that of parvo
cells
– they have rapid membrane dynamics so that they can signal sharply the onset
and offset of stimuli
– They have heavily myelinated axons, which conduct signals to the cerebral
cortex some 10 ms faster than parvo cells
– They project to the magnocellular layers of the thalamic visual relay nucleus
(the lateral geniculate nucleus – LGN) and from there onwards to layer IV C
The visual magnocellular system

– The ventral stream is devoted to identifying objects on the basis of

their fine detail and coloring.

– This pathway is therefore often called the ‘what’ pathway.

– It culminates in the inferior temporal cortex;

– it receives almost equal quantities of magno and parvo input

The visual magnocellular system

– The dorsal pathway passes via the middle temporal motion area to the posterior
parietal cortex
– It is dominated by magnocellular input
– signals provide information about the timing of visual events and of the motion of
visual targets,
– the dorsal system is important for the guidance of both eye and limb movement
– ‘where’ system are to motor structures including the frontal eye fields,
– The superior colliculus;
– provides a very large input to the cerebellum
The visual magnocellular system
– All these areas then project to the ocularmotor nuclei,
– which controls the movements of the eyes
– magnocellular system is crucial for controlling eye movements
during reading,
– The magnocellular layers were clearly separate from the
parvocellular layers in control brains,
– but parvo and magno layers were seen to merge together in the
dyslexic brains
– the size of the magnocellular neurons was reduced by 30% in the
dyslexic brains compared to the controls (Livingstone et al., 1991)
The visual magnocellular system

– Needed greater contrast between stationary black and white bars separated by a
1˚visual angle (a low spatial frequency grating – 1 cycle per degree),
– they were actually slightly more sensitive than controls at high spatial
– frequencies (10 cycles/degree).
– These findings are consistent with a mild weakness of the peripheral
magnocellular system
The visual magnocellular system

– they had lower sensitivity at both high and low spatial frequencies, again as
expected of a magnocellular deficit
Cortical magnocellular system

– dorsal ‘where’ pathway from the primary visual cortex to the temporal motion
area (MT) and to the posterior parietal cortex (PPC) is dominated by
magnocellular input
– random dot kinematogram (RDK) stimuli
– consist of dots moving around randomly. If enough of the dots are moved together in
the same direction, ‘coherently’ rather than randomly,
– we see a cloud of dots moving in that direction
random dot kinematogram
(RDK) stimuli
Cortical magnocellular system

– the density of the dots that have to be moved together for a subject to see the
coherent motion gives the sensitivity of that subject’s magnocellular system

– So when the number of dots moving together has been reduced to such an extent
that the subject can no longer reliably determine which of two side by side panels
contains the coherent motion,
– we define this as the subject’s threshold and his sensitivity is the reciprocal of this
– two-thirds of dyslexics have higher than normal thresholds for perceiving coherent
motion – they have reduced magnocellular sensitivity
Cortical magnocellular system

– one of the main functions of the visual magnocellular system is known to be to

guide eye movements and in particular to mediate stable eye fixation
– poor motion sensitivity leads to poor fixation;
– this causes unsteady visual perceptions;
– this in turn interferes with children’s ability to acquire orthographic skills
Auditory/phonological
requirements for reading
– The acoustic cues that distinguish letter sounds
– changes in frequency and changes in amplitude
– sensitivity to the changes in sound frequency (frequency modulations) that
signal phonemic distinctions
– vary the frequency of a tone, and measure by how much the frequency has to
change for the person to hear the change compared with a pure tone
– dyslexics and poor readers in general are significantly worse than good readers
at detecting frequency modulations
Auditory/phonological
requirements for reading
– Tracking frequencies in real time seems to be one function of large cells in the
auditory system that may be analogous to the magnocellular neurons in the
visual system

– If poor readers are worse at detecting frequency change then they should also
be worse at detecting the cues that distinguish letter sounds which depend on
such frequency changes
Auditory/phonological
requirements for reading
– dyslexics’ sensitivity to amplitude modulations as well. Again we have been able to
show that they have lower sensitivity to AM

– frequency changes, one function of large neurons throughout the auditory system

– Studying dyslexic brains post mortem, Galaburda and colleagues (1994) found that
large neurons in the magnocellular division of the left medial geniculate nucleus (the
auditory thalamic relay) are smaller than those on the right side or in control brains
Theories at the cognitive level

– automatization deficit

– phonological deficit

– double deficit’ hypothesis

– phonological processing but also in central processing speed

Theories at the cognitive level

– ‘square root rule’,

– Dyslexic people may take longer to acquire a skill in proportion to the

square root of the time normally taken to acquire it.

– If a skill takes 4 practice sessions to master, it would take a dyslexic

child 8 sessions to reach the same standard.

learning to read

– Uta Frith’s analysis

– the logographic stage (recognizing a whole word as an integral
shape)
– ‘alphabetic’ stage, where one picks out the individual letters in
an unfamiliar word, and, using the principles of grapheme–
phoneme translation, blends them together into the
corresponding spoken form
– ‘orthographic’ stage, strings of letters are recognized as a unit
and recognizes the word corresponding to the spoken sound
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