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Neuropsych Diagnoses > Childhood Learning and Neuropsychiatric Disorders > Flashcards

Childhood Learning and Neuropsychiatric Disorders Flashcards

1
Q

Stats on Dyslexia

A
  • 4-9% of school aged kids
  • 3:2;M:F
  • Genetic component
  • Acquired or developed
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2
Q

Visual processing model

A

Impaired whole word reading but words can be sounded out, implying an impairment of orthographic skills

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3
Q

Phonological model

A

Intact whole word readings but impaired ability to sound out words, implying an impairment of auditory/language skills

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4
Q

What is phonological processing?

A

Translating letters into speech and sound

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5
Q

What is word-decoding?

A

Translating letter strings into word sounds

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6
Q

What is naming-speed?

A

The rate of retrieval for digits, letters etc.

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7
Q

Symptoms of dyslexia

A
  • Difficulty with word decoding
  • Slow and non-automatic reading
  • Disrupted indentifying and comprehending words
  • Deficits in phonological processing and naming speed
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8
Q

What components are spared in Dyslexia?

A

Listening comprehension, intelligence, reasoning, vocab and syntax

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9
Q

Double deficit hypothesis

A

Cause-effect issue: reading disabilities can be caused by phonological processing and naming speed deficits

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10
Q

Two components of working memory implicated in dyslexia

A
  1. Articulatory phonological loop, buffer for manipulating verbal + auditory info
  2. Visuospatial sketchpad, buffer for manipulating visual + visuospatial info
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11
Q

Neuropathogenesis of dyslexia

A

Phonological processing = planum temporale of the left posterior temporal lobe.
Regional abnormality = less activation of the left posterior temporal + tempero-parietal cortices
Reading performance = rate of CBF to the region aroynd the planum temporale

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12
Q

Three systems involved in reading

A
  1. Left dorsal parietal-temporal: visual print to phonological, requires attention
  2. Left ventral occipital-temporal: visual word recognition, no attention required
  3. Broca’s
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13
Q

Stats of non-verbal learning disability

A
  • 0.1-1% of learning disability population
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14
Q

Neuropsychological pathology of NVLD

A
  • Posterior RH: associated with diffuse organization and inter-regional integration of info
  • Integrity of white matter: affects communication within the brain
  • Anterior RH: conceptual thinking and mental flexibility
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15
Q

Treatment of NVLD

A

Improving verbal and non-verbal communication skills + social skills

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16
Q

Pervasive Developmental Disorder areas of impairment

A
  1. Social interactions
  2. Verbal + non-verbal language
  3. Range of interests and activities
  4. Flexibility of behaviour
17
Q

Stats about autism

A
  • 1/1000 children
  • Across culture and race
  • 2:1/6:1 - M:F
18
Q

Impairments in autism

A
  • Social relatedness
  • Language development
  • Unusual, repetitive patterns of behaviour
19
Q

3 Core deficits in autism

A
  1. Ability to relate to others
  2. Deficits in communication
  3. Unusual behavioural patterns
20
Q

Ability to relate to others, expanded

A

Limited awareness of others, emotional aloofness and lack of understanding for social convention

21
Q

Deficits in communication, expanded

A

Delayed/failure to develop spoken language, impairment of expression and comprehension.

22
Q

Unusual behaviour patterns, expanded

A

Preoccupation with specific areas of interest: objects, tasks etc.

23
Q

How does Aspergers’ differ from high functioning autism?

A

Normal IQ and onset of language, difference between not wanting to do something and not being able to,

24
Q

Pathogenesis of autism

A
  • Environmental: perinatal conditions
  • Genetics: 20 genes implicayed
  • Greater head circumference at birth, increased brain grown in months 1-2 and 6-14.
25
Q

Disruptive Behavioural Disorder

ADHD, ODD, CD

A

Psychiatric: presence of developmentally inappropriate behaviour or violations of socially dictated acceptable behaviour

26
Q

Clinical presentation of ADHD

A

Age inapproporiate inattention, impulsivity and hyperactivity

27
Q

Stats on ADHD

A
  • Over half of childhood disorders
  • 3-9% of population
  • 3:1/9:1-M:F
  • 30-60% continues into adulthood
28
Q

Comorbidity for ADHD

A
  • 40-65% CD and ODD
  • 25-50% Tourettes
  • 18-50% Anxiety and Depression
  • 15-20% Learning Disabilities
29
Q

Neuropsychological pathogenesis of ADHD

A
  • Genetic
  • Family context
  • Neural substrates: Most major cortical + subcortical regions implicated, asymmetrical smaller frontal lobes, smaller cerebellum and disruption in frontal BG.
30
Q

Developmental course of ADHD

A

Infant: overactive, sensitive to stimuli, slow adaptation to change
Toddler: doesn’t consider consequences, difficult, doesn’t listen to orders, accident prone
Teen: learning difficulties, frustration
Adult: hyperactivity, inattention and impulsivity persist

31
Q

Treatment for ADHD

A

Multimodal: tailored to each individual, targets core components, centred around caretakers and teachers.. Usually a hybrid of behavioural intervention and psychopharmacology

32
Q

Clinical categories of tics

A

Transient: motor OR vocal, -12 months
Chronic: motor OR vocal, 12+ months
Tourette’s: motor AND vocal, 12+ months, significant clinical impairment

33
Q

4 different tics

A
  1. Copropraxia: obscene gestures
  2. Echopraxia: repeated movements of others
  3. Coprolalia: obscene/inappropriate speech
  4. Echolalia: repeating words of others
34
Q

Prevalence of Tourettes

A
  • 1-8/1000 children
  • 4:1 - M:F
  • Across ethnic groups

Neuropsych Diagnoses (3 decks)

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