How Learning Disorders Develop?

Learning

Disorder

How Learning

Disorders

Develop?

Farhangdoost

PhD in Cognitive Neuroscience

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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

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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 developRD

– 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


– dyslexia overlaps with

– developmental dysphasia (specific language impairment),

– developmental dyspraxia,

– attention deficit

– disorder (ADD),

– Asperger syndrome

– neurodevelopmental syndrome


– 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


– 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


– 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 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 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


– 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)


– 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


– 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


– 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


– 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



– 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



– 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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How Learning Disorders Develop?

Health & Medicine

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