Neurodevelopmental Disorders Flashcards

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1
Q

Neurodevelopmental disorders

A
  • Problems that emerge in early childhood, affecting intellectual, social & motor development
  • Life-long conditions, present from birth but only manifest when person fails to emit an expected behavior
  • While there’s no cure, adequate support can mediate negative outcome
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2
Q

2 broad categories in DSM V

A
  1. specific learning disorder = difficulty acquiring and using academic skill
  2. Communication disorders = deficits in language, speech and communication
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3
Q

DSM 5 definition for specific learning disorder

A
  • difficulties in learning & using academic skills in 1 or more areas
  • Problems in learning & using academic skills marked by at least one of ff over a 6 month period:
    1. Inaccurate or slow and struggling to read
    2. Diff understanding meaning of words
    3. Spelling difficulties
    4. Difficulties in expressing self through writing
    5. Difficulty understanding numbers
    6. Difficulties working with numbers
  • Affected skills below what’s expected for age and intellectual capacity
  • Not better accounted for by ID, visual/hearing problems or other neuro or mental disorder
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4
Q

Comorbitity of specific learning disorder

A

71% of kids with bipolar
67% of ASD kids
71% of ADHD
Anxiety & depression;

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5
Q

Language disorder

A

problems with acquiring & using language, both written and spoken, including:

  • Reduced vocabulary, comprehension & production
  • Limited sentence structure ability
  • Difficulties in dialogue
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6
Q

Speech sound disorder

A

problems with speech sound production that interfere with speech intelligibility & impact on social, academic and occupational achievement

  • Sound substitution, e.g. wabbit
  • May be associated with physical problems (cleft palate, hearing problems, cerebral palsy) but problems must exceed what’s expected even with these problems for additional diagnosis
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7
Q

Childhood-onset fluency disorder

A

problems with fluency & speech patterning, involving:

  • Frequent repetitions or prolongation of words
  • Pauses within words
  • Filled or unfilled pauses in speech
  • Word substitutions to avoid pronouncing problematic words
  • Word pronunciation with excessive physical tension
  • Monosyllabic word repetitions
  • May be accompanied by tics, eye blinks, jerking of head
  • Causes anxiety about speaking
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8
Q

Genetic factors for dyslexia

A

80% or more kids with dyslexia have a relative with the disorder; research implicates genes on many chromosomes that cause abnormalities in brain development

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9
Q

cognitive factors for dyslexia

A

reading difficulties due to problems differentiating phonemes & associating these sounds to letters in written word, which is independent of other abilities

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10
Q

neurological factors for dyslexia

A

Brain abnormalities: in various regions of brain

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11
Q

aetiology for dyscalculia

A
  • Genetic links

- Brain anomalies in left parieto-temporal & inferior prefrontal cortex

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12
Q

aetiology for communication disorders

A

familial links & genetic component

Brain anomalies in circuits that mess with basal ganglia

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13
Q

treatment for communication disorders and dyscalculia/dyslexia

A

Remedial & compensatory support

Speech & OT

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14
Q

Intellectual Disability

A
  • Characterized by below average cognitive/intellectual functioning (less than 2 standard deviations below average) on standardized IQ measures
  • focus on current rather than predicted performance
  • IQ = ratio of mental age (MA) to chronological age (CA);
  • Deficits that limit at least 2 areas of adaptive functioning /independent living
  • Deficits creates vulnerability
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15
Q

mild disability

A
  • IQ: 50-55 to approx 70
  • 85% of ID population
  • More likely to be hereditary than the other levels, thus family history NB in assessment;
  • Association with the combination of heredity (low intelligence), some organic problems and a markedly below average environment (poverty, nutrition, low stimulation etc.). Some evidence that most in this category come from low SES backgrounds
  • Environmental factors, e.g. trauma, prenatal insults.
  • Interplay between behavioral & scholastic problems
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16
Q

Adaptive functioning in Mild range

A
  1. Can develop social & communication skills; have minimal sensorimotor deficits and only distinguishable from typically developing kids in school;
  2. Can learn skills of up to Gr 6 by late teens but generally need special educational provision to enable learning in relatively “non-academic” way;
  3. Capable of living/performing adequately in social and work situations as adults but may need more guidance, esp. when under serious social stress
  4. Current educational provisioning in SA = mainstream school with support
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17
Q

Moderate ID

A
  • 35-40 to 50-55
  • 10% of ID population
  • More likely to have an organic basis
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18
Q

Adaptive functioning in moderate range

A
  • Can talk or learn to communicate, fair motor development, poor social awareness in early childhood but can be managed with moderate supervision
  • School years: functional academic skills up to Gr 4 level by late teens if they get special education
  • As adults can self-maintain in semi- or unskilled work & need support for mild stress
  • SA: placement in Special School where skills taught
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19
Q

Severe ID

A
  • IQ: 20-25 to 35-40
  • 3-4% of ID population
  • Poor motor development, minimal speech, unable to profit from training in self-help as kids
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20
Q

Adaptive functioning in severe range

A
  • Learn to talk or communicate by school age, can be trained in basic hygiene & health habits; unable to learn functional academic skills during school age
  • As adults can contribute a bit to self-support but under high levels of supervision & can develop some self-protection skills (limited)
  • SA = often placed in school of skills or sheltered employment
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21
Q

Profound ID

A

IQ below 20-25

  • 1-2% of ID population
  • Gross disability in almost all areas, with tendency to have severe physical deficits as well; little sensorimotor functioning
  • Higher incidence of seizures & high pain thresholds, pica, self-biting, feacal smearing; lack of social skills
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22
Q

Adaptive functioning in profound range

A

May learn some motor skills and some self-care (e.g. be toilet-trained; feed or able to request)

23
Q

Some key issues to keep in mind with intellectual disability

A
  • Traditional assessments focus on deficits (as shown in definitions) but current thinking tends towards describing how to maximize person’s functioning & providing the best support for that indiv:
  • -Need to identify person’s strengths, psychological, emotional & physical health, current environmental situation
  • -Use information about person to identify type and intensity of support required to empower the person
24
Q

Borderline Intellectual functioning

A
  • DSM-IV defines borderline as IQ between 71-84
  • Not listed with as disorder but necessary to keep it in mind because cognitive problems not as obvious as in ID
  • Low parental involvement rather than open hostility or negative problem
  • Problems with affect regulation and increased chances of acting out behaviors
  • Self-esteem issues as increasing complexity of school work becomes difficult for this group to manage
25
Q

Causes of ID biological

A

chromosomal abnormalities:

  • down syndrome
  • fragile x syndrome
  • klinefelter syndrome
26
Q

Down Syndrome

A
  • 1 in 700 – 800 births; related to extra chromosome when 21st in ovum or sperm doesn’t divide normally, resulting in 47 vs 46 chromosomes;
  • More likely with increasing maternal age
  • Multiple health challenges, including heart & respiratory problems, ADHD, expressive language problems & aggressive behaviour
  • Learning and development problems: nearly all have ID but levels are variable, with most in moderate range
27
Q

Fragile X syndrome

A
  • most commonly identified genetic cause of ID after Down Syndrome
  • 1 in 1000-1500 males & 1 in 2000-2500 females affected; 1 in 1000 females = carriers
  • More profound ID ranges in males (thus more in severe to profound range); females affected more mildly disabled
  • Often only recognised in adolescence
28
Q

Klinefelter syndrome

A

Only in males, results of XXY chromosome pattern —> under developed secondary sex characteristics and possible ID

29
Q

Turner’s syndrome

A

single X chromosome in females

30
Q

Pregnancy, birth & postnatal factors of ID

A
  • Maternal infections, e.g. rubella, syphilis
  • Maternal substance use, e.g. FAS
  • Birth complications, e.g. anoxia, head injuries, prematurity
  • Postnatal: encephalitis, meningitis, lead poisoning
  • Environmental deprivation
31
Q

Interventions for ID: prevention

A

e.g. educating potential parents about risk factors like substance use & generating strategies to avoid alcohol cravings; genetic testing & counselling for syndromes; support for low socioeconimic status mothers to facilitate development of a stimulating environment

32
Q

Interventions for ID: training

A

basic training to develop needed adaptive skills, minimize challenging, aggressive and/or self-mutilating behaviours; ABA approach best

33
Q

Interventions for ID: Inclusioni

A

need to make education accessible:

  • mainstreaming (good in theory for mild ID but requires individualized support, which is resource-intensive);
  • LSEN schools – specialized learning environment that uses individual’s strength
34
Q

Autism Spectrum Disorder

A
  • Early onset disorder, not easily detected until age-appropriate behaviours don’t emerge or acquired skills are lost; parents sometimes report tell-tale signs
  • Lifelong: presentation may change over lifespan
35
Q

ASD communication problems

A
  • range from few difficulties in Asperger’s to profound impairments in many cases where child learns only a few words and/or loses language ability
  • some children acquire language but rate of acquisition slower
  • difficulties not due to sensory deficits or difficulties with mechanics of speech – more about inability to imitate or engage in reciprocal communications
36
Q

ASD Speech oddities

A
  • Dysprosody = ‘unusual’/atypical rate, rhythm & intonation in speech
  • Echolalia  repeating phrases
  • Reversals in use of ‘you’ & ‘I’
  • Poor use of gestures for communication
37
Q

ASD Impaired social interaction

A
  • Lack of social or emotional reciprocity;
  • lack of motivation for attachment to others, e.g. not seeking parental comfort or attention; gaze aversion
  • little interest in peers;
  • Lack of theory of mind
  • Others = objects
38
Q

ASD Stereotyped behaviours, interests & activities

A
  • Odd behaviours/activities (flapping, switching lights on 7 off)
  • Odd, often circumscribed interests (e.g. trains, dinosaurs
  • Rigidity, e.g. around routines & food
  • Stereotypies = self stimulation because of too little sensory input but current theories suggests they help shut out unwanted sensory input
39
Q

ASD Sensory deficits

A
  • Hypersensitivity to types of inputs, e.g. certain sounds (singing) whilst they can easily shut out others; theorised to be due to sub-cortical anomaly that impairs ability to integrate sensory data
  • Hyposensitivity to others, e.g. pain
  • Self-injury = minor to severe damage can occur; self-stimulation
40
Q

ASD Savant performance/splinter skills:

A
  • exceptional ability in a specific/specialized area of functioning
  • Not indicator of high IQ – only about 25% of kids with autism have IQs above 70
41
Q
  1. Autistic Disorder: diagnostic triad
A
  • Qualitative impairment in social interaction
  • Qualitative impairment in communication
  • Restricted repetitive and stereotyped patterns of behaviour
42
Q

Asperger’s

A
  • Qualitative impairment in social interaction
  • Restricted repetitive and stereotyped patterns of behaviour
  • NO IMPAIRED COMMUNICATION
43
Q

Childhood Disintegrative Disorder:

A
  • Loss of previously acquired skills before age 10 yrs.
  • Abnormalities of functioning in 2 of:
    1. impaired social functioning
    2. Impaired communication
    3. Restricted repetitive & stereotyped patterns of behavor.
    4. Onset after 2 years of normal development, with loss of acquired skills
44
Q

PDD-NOS: Pervasive Developmental Disorder-Not Otherwise Specified

A

Presence of severe & pervasive impairment in development of reciprocal social interaction or verbal & nonverbal communication or presence of stereotyped beh. but criteria not met for specific PDD

45
Q

Rett’s Disorder:

A

genetic disorder found exclusively in girls NOT included in DSM 5 as ASD

46
Q

DSM 5 diagnostic criteria ASD

A

A. Persistent deficits in social communication AND social interaction, manifest as:
-Deficits in social-emotional reciprocity
-Deficits in nonverbal communicative behaviours (e.g. non-understanding & use of gestures; poor eye contact)
-Deficits in developing, maintaining & understanding relationships (e.g. sharing in imaginative play, adjusting to various contexts)
B. Restricted, repetitive patterns of behaviour, interests or activities manifest by at least 2 of ff. (current or by history):
-Restricted repetitive motor movements, use of objects or speech (e.g. motor stereotypies; lining up cars or idiosyncratic phrases or echolalia)
-Insistence on sameness, inflexible adherence to routines or ritualized patterns of verbal or nonverbal beh
-Highly restricted, fixated interests, abnormal in intensity or focus
-Hyper- or hypo-reactivity to sensory input or unusual interest in sensory aspects of environment

47
Q

ASD prevalence

A

-Fewer comorbid ID diagnosis than previously, suggesting more less-disabled/disturbed kids are also -being diagnosed
3 to 4 times more boys than girls diagnosed
-More common among siblings of a diagnosed child  genetic causes

48
Q

ASD causes

A

Increasing numbers of diagnosed children, possibly due to:

  • Broadened diagnostic criteria lead to more cases diagnosed
  • Earlier detection
  • Increased awareness & more thorough assessment
  • NO evidence of vaccines or chemicals (e.g. anti-depressants) or particular environmental toxins (e.g. lead, mercury) being cause
49
Q

Psychological & social factors:

ASD

A
  • Psychoanalytic theorising about cold, distant and rejecting refrigerator parents  NOT true
  • Possible misinterpretation of parental response to what seem like child’s indifference
50
Q

Biological factors: ASD

A
  • many disorders/syndromes have features of autism
  • Genetics: evidence of higher concordance among MZ than DZ twins suggests strong genetic link
  • Neuroscience: focus on which structures of the brain are implicated; functioning of mirror neurons; neuro-transmitters
51
Q

ASD Treatment

A
  • No cure but interventions can alter course and outcomes
  • More community than institutional care
  • Medication: no cure but possible medication to assist behaviour management (e.g. risperidone)
52
Q

ABA treatment for ASD (Applied behavior analysis)

A

Focus on treating specific symptoms and teaching functional skills by:
1. identifying specific behaviours to be targeted
2. gain control over these
3. extinguish unwanted behaviours
Treatment very individualized:
1. thorough assessment,
2. treatment plan with clear goals
3. specified steps towards the goals,
4. track changes
Implementation: use of behavioural principles such as reinforcement (e.g. praise) & punishment; chaining;
Works well for self-care but not social interaction

53
Q

Treatment issues to consider in SA ASD

A
  • Multiple skills affected in ASD, requiring input from different disciplines (e.g. OT, speech and physio-therapy)
  • Cost and resource availability
  • Need for cheap, parent-led interventions that target all or most skill deficits: the “ESDM” project
54
Q

“ESDM” project

A
  • The Early Start Denver Model (ESDM) is a comprehensive behavioral early intervention approach for children with autism, ages 12 to 48 months.
  • The program encompasses a developmental curriculum that defines the skills to be taught at any given time and a set of teaching procedures used to deliver this content.
  • It is not tied to a specific delivery setting, but can be delivered by therapy teams and/or parents in group programs or individual therapy sessions in either a clinic setting or the child’s home.