3. Structure of causes of specific learning disabilities

Etiology of SLD - history and current concepts in our country and in the world
basic premise: the intellect is not affected

Traditional division in modern form:
 - internal influences: damage, heredity (autosomal dominant transmission, 35–45%) 60–70% heredity 30–40% of damage
 - external influences: inappropriate teaching, family

  • Traditional model of SLD etiology according to O. Kučera (1961)
  • Minor brain damage (MBD, formerly encephalopathy) - a neurological finding mentions more minor conspicuousness, the anamnesis points to possible brain damage in the prenatal, perinatal or postnatal period - 50% of individuals with SLD
  • Hereditary etiology - history of typical occurrence of communication disorders in relatives - 20% of individuals with SLD
  • Hereditary encephalopathic etiology - a combination of both previous types - 15% of individuals with SLD
  • Neurotic or unclear etiology - 15% of individuals with SLD. Neurosis as a cause is incomparably rarer than neurosis as a consequence of SLD
1980s: neurological-biological etiology

Etiological factors
  • interacting internal and external factors
  • development of views on the causes of failures
  • genetic factors ---> partial deficits
  • Current etiological models: e.g.
  - phonological
  - visual
  - magnocellular
  - cerebellar
  - neurobiological
  • common significant etiological context
    • deficits of partial functions
      • risk types of laterality
      • perceptual, motor, memory
      • within MBD/ HKD/ ADHD
Neurobiological approach
  • demonstrated the difference in the brain of dyslexics
  • enabled by the development of imaging techniques since the 1980s.
  • monitoring of normal and diseased structures and performance, especially in the left hemisphere
    •  post-mortem analysis (dead brains) - prof. Galaburda
    •  dyslexia as a disorder of neuronal migration
    •  analysis by imaging methods - detected metabolic changes in various parts of the brain, identification of nerve circuits involved in reading, especially in the left hemisphere
    • analysis of evoked potentials - monitoring of electrical reactions of the brain to a stimulus (word or picture), detection of intermodal deficit, good possibilities of prediction of dyslexic difficulties
Phonological model
significant mainly in the Anglo-Saxon language environment
I. Libermanová
  • inverse concept replaced by language concept
  • key concept of phoneme awareness
 = ability to recognize in the overall sound form of a word its parts - phonemes (the smallest, indivisible units of language), are achievable by analysis
  • the child needs phonemic awareness (segmentation) only in connection with reading,
  • phoneme-grapheme relationship: complex process of character identification and sounding = grapheme - phoneme correspondence (disturbed in dyslexics)
  • revealing the importance of short-term memory for reading and deviations in dyslexics (mainly in verbal memory)
  • Libermanová: timely search for children at risk of reading according to differences in phoneme awareness and verbal short-term memory
  • phonological skills: analysis, synthesis and short-term phonological memory
      - factors stable over time, with a high predictive connection with reading
      - manifested in phonological decoding - recognition of words and their parts (easier in transparent orthographies)

Double deficit theory (N. Geschwind)
  • originated in the solution to phonological reeducation of resistant cases of dyslexia
  • dyslexia is caused by two deficits: phonological awareness and rapid automated processing of stimuli
  • problems in the sound processing itself and the resulting inability to create a link between the grapheme and the phoneme
  • dyslexics are unable to perceive short or rapidly changing sounds.
  • use of the quick naming test - detects visual-verbal discontinuity
  • Norman Geschwind: founder of behavioral neurology
Theory of visual deficit
  • pointed out the deficits, which were subsequently explained by magnocellular theory
  • deals with the share of visual disorders in reading problems
  • monitors deficits in the analysis and differentiation of visual perceptions
  • emphasizes in particular unstable binocular fixations and incorrect perception of object boundaries, which leads to difficulties with processing letters and words on the text page, a specific deficit is the so-called iconic persistence (visual persistence)
  • related mainly to abnormalities in the right hemisphere
Magnocellular theory
  • in the brain there are two different nervous systems related to reading: magnocellular and parvocellular, controlled from the subcortical (thalamus) - transfers information to superior structures in the cerebral cortex
  • magnocellular system (magnus = large, cellular = cellular) - strongly myelinated cells that transfer excitations well
  • responsible for the speed and timeliness of information processing, allows vision in low light and low contrast, the system is sensitive to changes in time, predominates in peripheral vision
  • parvocellular system (parvus = small)
  • small cells capable of processing even small distances between stimuli
  • specialized in color perception and detailed object viewing
  • handles short words accurately when reading
  • dyslexics are not able to process a large number of short visual stimuli in a small area, there is a merging of characters
Cerebellar theory
  • seeks the cause of dyslexia in mild cerebellar dysfunction ensuring motor coordination
  • Disruption of the cerebellum leads to reduced ability