Learning Disabilities

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Learning Disabilities

  • First observations and studies focused on reading disorders, as early as 100 years ago.
    • No diagnostic category of “LD” until 1960’s.
    • Original label was minimal brain damage/dysfunction.
    • Ongoing etiological debate: biological nature of disorder vs. failure of educational system (nature vs. nurture).
  • 1987 definition (is there a more recent one?):
    • a generic term that refers to a heterogeneous group of disorders manifested by significant difficulties in the acquisition and use of listening, speaking, reading, writing, reasoning or mathematical abilities, or of social skills.
    • These disorders are intrinsic to the individual and presumed to be due to central nervous system dysfunction.
    • Even though a LD may occur concomitantly with other handicapping condition (e.g., sensory impairment, mental retardation, social and emotional disturbance) with socioenvironmental influences (e.g., cultural differences, insufficient or inappropriate instruction, psychogenic factors) and especially with attention deficit disorder, all of which may cause learning problems, a LD is not the direct result of those conditions or influences.
    • LD is based on a discrepancy between “ought” (e.g., IQ score) and “is” (e.g., academic performance score). MUCH controversy exists over cut-offs.
  • No single etiology; may be due to genetic influences, congenital factors, prenatal injury, perinatal distress, early brain injury; range from no observable evidence to some objective evidence to frank CT evidence
    • Duffy’s BEAM studies showed bilateral abnormalities, mostly in frontal regions, patients with dyslexia
    • Hynd and Semrud-Clikeman have also shown morphological markers of ADHD and dyslexia on imaging studies
    • Geschwind noted a higher incidence of autoimmune disorders (e.g., SLE) in family members of LD individuals, LD is more common in males, and higher proportion of left-handed individual in LD population. Therefore, hypothesized that that LD may be linked to hormonal (testosterone) influences on the brain in utero, which serve to delay the development of the left hemisphere, leading to dyslexia and other language processing disorders and to the change to left-handedness. Higher autoimmune d/o frequency reflects concomitant influence of testosterone on development of immune system. Galaburda has followed up.

PENNINGTON’S NEUROPSYCHOLOGICAL MODEL OF LDs

  • Brain functions are modular
    • which means that brain systems are specialized for processing specific kinds of information and that these modules are autonomous in function and neural representation
  • These modules are differentially vulnerable
    • if all brain systems were equally vulnerable we should find equal numbers of developmental disorders for each brain system – but we don’t. Some areas are more vulnerable than others
  • Exception – executive functions aren’t completely distinct from other modules; they can affect how well modules function, partly because they control attention
  • Symptoms are divided into 4 categories:
    • Primary – core symptoms, universal, specific and persistent
    • Correlated – same etiology/affect different brain systems (e.g., autism and mental retardation – many have MR, but it is not universal or specific to the disorder)
    • Secondary – consequences of primary or correlated symptoms
    • Artifactual – appear associated/not causally related

PENNINGTON’S FIVE FUNCTIONAL DOMAINS

Domain Location Disorder
Phonological Processing Left perisylvian region Dyslexia
Executive Functions Prefrontal Region ADD
Spatial Reasoning Posterior Right Hemisphere Math/Handwriting
Social Cognition Limbic, Orbital, Right hemisphere Autism spectrum
Long-term Memory Hippocampus, Amygdala Memory disorder / Amnesia

According to Pennington, these domains account for nearly all the learning disorders.

  • PHONOLOGICAL PROCESSING
    • The perisylvian region includes Wernicke’s area in the posterior left temporal lobe and Broca’s area in the premotor portion of the frontal lobe.
  • SPATIAL COGNITION
    • This is modality specific, so blind children can still develop spatial cognition.
    • Functions in this domain include
      • object localization;
      • spatial or visual memory;
      • attention to extrapersonal space;
      • mental rotations;
      • spatial construction
    • There are several brain regions which subserve this funtion
      • generation of visual information has a left posterior localization
      • transfer of info. to long-term memory involves the limbic system especially in the rt. hem.
      • Although verbal knowledge shows continuing increases into the later decades of life, spatial reasoning peaks in adolescence and then slowly declines thereafter.
      • dyslexia – traditional beliefs feel it represents some kind of visual or spatial problem, but recent research has strongly shown that most dyslexics have impaired phonological processing skills
  • EXECUTIVE FUNCTIONS
    • Developmentally – traditionally seen as occurring quite late in normal brain development, but studies have shown there are some important changes which occur during the second half of the 1st year.
    • Development seems to roughly correspond to the Piagetian stages of cognitive development.
    • Thus the WCST will be harder for preschoolers and early elementary children because “number” is much less salient a dimension than form or color.
    • Pathologies which can involve executive functioning:
      • ADHD
      • Schizophrenia
      • Tourette’s syndrome; since children can delay tics they are sometimes viewed as a failure of inhibition. Some evidence suggests basal ganglia involvement (w/c has strong connections w/frontal lobe)
      • Autism
      • Early treated PKU – children will have normal IQ’s but a higher rate of learning and cognitive problems than controls (especially on measures of executive fxning)

ROURKE’S NEUROPSYCHOLOGICAL MODEL OF LDS

  • Treats LD as a disorder of information processing (so does Denckla, Weintraub, et. al.)
  • This system can also account for ADHD, conduct disorder, savant, special talents, etc.
  • LD results from dysfunction in one of three possible neural systems:
    • Phylogenetically lower to higher centers
    • Posterior cortex to anterior cortex
    • Right-left dysfunction
  • ROURKE’S FOUR MAJOR SYNDROMES OF DEVELOPMENTAL NEUROCOGNITIVE PROCESSING DISORDERS:
    • Verbal Processing Disorder
      • Disruption of language skills in auditory or visual modality
      • Includes developmental dysphasia, dyslexia, dysgraphia, spelling disorders, and some types of dyscalculia
      • Associated with dysfunction or frank damage to language networks in left hemisphere
  • Nonverbal Processing Disorder
    • Disruption of ability to perceive or produce nonverbal information
    • Most notable in development of social-interpersonal skills
    • Well-developed language skills, but with poor mathematical abilities, nonverbal and visuospatial functions, and attention. May also have affective disorders.
    • Reflective of dysfunction in neurocognitive networks in right hemisphere
  • Attention Deficits Disorder (with or without hyperactivity)
    • Disruption of arousal-attention-concentration
    • May or may not have associated LD, or may do well or poorly across board
    • Associated with dysfunction in right hemisphere and/or bifrontal dysfunction and/or reticular activating system (i.e., neurocognitive network for attention)
  • Insight/Judgment/Comportment Disorder
    • Disruption of insight, judgment, comportment (“conduct disorder”)
    • Can’t learn rules of socially acceptable behavior and decision-making strategies
    • Stimulus-bound, concrete
    • May reflect deficient development of frontal networks

AUTISM SPECTRUM DISORDER

  • Autism vs. Asperger’s
    • in Autism VIQ is relatively depressed, whereas the opposite is true for Asperger’s (in this respect Asperger’s is more like a NVLD)
    • Basic Defining Characteristics – developmental disorders in w/c the main symptom is a severe deficit in social contact w/c emerges early in life and persists into adulthood (2/3 of autistic samples are MR, but most Asperger’s have nonretarded IQ’s)
    • Sex ratio for Autism is approximately 3:1 (males:females)
    • Often impaired on executive fxn tasks (e.g., WCST)
    • Etiology – possibly heritable; it is specifically associated w/fragile X syndrome, and untreated PKU; but environmental factors have also been implicated
    • Brain mechanisms – the neurological basis still unknown partly b/c of the debate over which deficit is the “core symptom”. Current evidence suggests that a dysfxn in the limbic systems and frontal lobes reduce appropriate social fxning and cause the primary symptom.
      • Studies have shown these children have enlarged ventricles (suggesting cortical atrophy)
      • Atrophy of the cerebellum
      • Theory of mind – is believed to be disrupted in autistic children. That is they have difficulty predicting other people’s beliefs or feelings
      • Treatment – re: that stimulant medication is contraindicated in some cases of autism as stimulant medications may worsen some autistic symptoms (such as stereotypies) in some patients

DYSLEXIA

  • Basic definition – an unexpected difficulty in learning to read and spell (i.e., no obvious reasons for difficulty such as inadequate schooling, sensory handicap, ABI, or low FSIQ)
  • Reading involves:
    • visual perceptual processes
    • word recognition
    • comprehension
  • Dyslexia involves the word recognition component due to deficit in the use of phonological codes to recognize words.
  • Kinds of Reading Errors:
    • Dysfluency – slow and halting reading due to decreased automatic decoding skills
    • Errors on fxn words – i.e., substitutions on “little” words such as articles and propositions (e.g., interchange a and the and misread propositions)
    • Visual words (whole word guesses) – e.g., reading “car” for “cat”
    • Lexicalization errors when reading nonwords – misreading nonword as real word (e.g., “boy” for “bim”)
  • Kinds of Dyslexia
    • Surface dyslexia – read by well established phonological rules, short words easier than long, difficulty with semantic access; trouble with nonwords, and with visual aspects of word recognition; good phonological skills, but comprehension is seriously affected
      • I.e., normal language skills but poor visual-perceptual abilities; may have features of Gerstmann’s syndrome
    • Deep dyslexia – read familiar words well (esp. nouns), but make many semantic paralexias in oral reading (see “mutton”, say “sheep”); rely on imageability, concreteness, and word frequency
      • I.e., superior perceptual skills but marked language disabilities
  • Kinds of Spelling Errors
    • Phonetically inaccurate errors (e.g., errors in consonants are added, omitted, or substituted)
    • “Reversal errors” e.g., spelling “bog” for “dog” – much rarer than used to be thought (used to believe these were “trademark” signs)
  • Both genetic and environmental factors can cause dyslexia
  • Common characteristics: difficulty learning letter names, generally good at math and spatial tasks, deficit persists into adulthood
  • May be associated with slow reading or writing speed, letter and number reversals, problems memorizing basic math facts and unusual reading and spelling errors
  • Higher rate of spoken language problems (e.g., early articulation disorders, problems finding names or remembering sequences (e.g., phone numbers, or months of the year)
  • Also associated with difficulty following directions, reduced speech or difficulty expressing themselves and problems with peer relations; language problems interfere with their ability to express their feelings so may be more likely to act out or withdraw into themselves
  • Deficit is due to difficulties in phonological coding – since dyslexics have difficulty sounding out words, reading is much slower and less automatic w/c detracts considerably from comprehension
    • Brain mechanisms – a developmental anomaly of the left hemisphere (re: literature re: symmetry of planum temporale (superior posterior portion of the temporal lobe/Wernicke’s area on left hem.) also seen when measuring the whole temporal lobe)
      • There is another neuroanatomical theory of dyslexia (w/less empirical support) that suggests that there is a deficit in the corpus callosum, so info. is transferred less efficiently b/t the two hemispheres
    • Developmental course – may have mild speech delay, articulation difficulties, problems learning letter names or color names, and problem remembering phone numbers/verbal sequences as early as preschool. Children do not typically “catch up”, but remain slower than their peers (incl. adulthood). Most are capable of going to college, but on average complete fewer years of formal education.
      • Some can learn to compensate for their difficulties so they are no longer diagnosable in adulthood (seen more often in females) – but they still report some dyslexic difficulties
    • History – high familial risk; should be evident by 1st or 2nd grade (may even be noticeable by kindergarten due to difficulty learning the alphabet)
    • Treatment – drilling in phonics-based approach to reading; whole word approaches do not help dyslexics; older dyslexics may need help with reading comprehension strategies and study skills; spelling is difficult to remediate, often better to use compensatory devices
      • also benefit from extra time on written exams, by not downgrading spelling errors.

NONVERBAL LEARNING DISABILITIES (Rt. hem LD’s)

Problems with math, handwriting, and social cognition (all believed to be rt. hemisphere fxns)

  • Math deficits – fundamental conceptual problems in understanding mathematics (w/c may be secondary to deficits in spatial cognition); difficulties with visuo-spatial problems makes it hard for kids to understand complex visual-spatial concepts
  • Dyslexia and “rt. hem LD’s” – re: there is a frequent co-occurrence of math and handwriting problems with dyslexia, but their symptoms generally differ from those seen in children with only math and/or handwriting deficits
    • Handwriting deficits linked to linguistic or motor sequencing problems, not spatial processing
    • Presenting symptoms – initial presentation may suggest an emotional or motivational problem (e.g., not turning in homework, power struggle); may be late in acquiring a good grip of the pencil (may still hold it awkwardly), may be less adept on the jungle gym; eye-hand coordination tends to be weak and difficulty finding their way in new places.
    • Etiology – some genetic syndromes w/c produces these symptoms (e.g., Turner syndrome and fragile X in females (most males with fragile X are MR so do not exhibit the LD’s); Rourke feels there is quite an overlap between NVLD and Asperger’s, but considers Autism to be a separate entity due to its greater language pathology)

ATTENTION DEFICIT DISORDER

  • ADD – developmentally inappropriate levels of inattention, impulsivity, and, often, overactivity
  • Associated neurochemical defect may involve dopaminergic system or noradrenergic system
  • Epidemiological surveys suggest as many as 49% of boys and 27% of girls are described as inattentive by their teachers (i.e., relatively common in normal children)
    • Serious deficits occur in 3-10% of school-age children (i.e., most prevalent of all childhood neuropsychological disorders) – most diagnosed ADD
    • Attention deficits also common in, e.g., autism, PDD, depression, conduct disorder, LD, as well as CHI, leukemia (plus tx for), epilepsy (and tx for), anoxia/hypoxia, tic disorders (up to 70% of Tourette’s), lead/toxin poisoning, exposure to biological hazards during perinatal period

ASSESSMENT OF LEARNING DISABILITIES

  • History, including
    • prenatal/perinatal stress factors
    • early development and milestones,
    • medical history (child and family)
    • neurological hx
    • psychiatric hx,
    • psychosocial factors,
    • family h/o learning, neurological, medical, or psychiatric problems
    • Exclude possibility that “LD” is due to sensorimotor deficits, primary psychiatric illness, social or educational deprivation, or MR
    • Determine profile of strengths and weaknesses, and describe each deficit as primary or secondary
    • Qualitative description of disability and its limits – critical for recommendations
    • Recommendations for tx
      • meds
      • therapy (group, individual, family)
      • instructional strategies (improve deficit or compensate for it)
  • After neuropsych assmt (above), continue with neurological exam, diagnostic educational assmt, and psychosocial assmt