Neurodevelopmental Disorders Flashcards

1
Q

Intellectual Disability: DSM-IV Degrees of Severity

A
Mild: IQ 50-55 to ~70
Moderate: IQ 35-40 to 50-55
Severe: IQ 20-25 to 35-40
Profound: IQ <20 to 25
*shift away from the 70 cutoff in DSM-5...
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2
Q

Intellectual Disability: DSM-5 Criteria

A
  • 3 criteria:
    A) Deficits in intellectual functions (e.g., reasoning, problem solving) confirmed by clinical assessment and intelligence testing
    B) Deficits in adaptive functioning; Without ongoing support, deficits limit functioning in one or more ADLs like communication, social participation, and independent living, across multiple environments.
    C) Onset of intellectual and adaptive deficits during the developmental period
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3
Q

ID: DSM-5 Severity Specifiers

A

Defined on basis of adaptive functioning and not IQ

  • Mild ID: similar to typically developing peers, often diagnosed later in school years, often minority or low SES, 6th grade academic skills, able to be independent adults
  • Moderate ID: usually preschool years, usually develop communication skills, 2nd grade academic skills, moderate supervision for self-care, often unskilled labor/supervised workshop
  • Severe ID: most cases organic causes, often physical/ambulatory problems, simple communication & self-care can be learned, require assistance throughout life, often live in supervised group homes & employed in workshop settings
  • Profound ID: almost always identifiable organic cause, often nonverbal, intensive training needed for self-care, lifelong 24-hour care, usually residential facilities or group homes
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4
Q

Global Developmental Delay

A
  • Under age 5
  • Fails to meet developmental milestones in several areas
  • Severity level cannot be reliably determined
  • Can be given because IQ often not valid before age 5 so hard to give ID diagnosis
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5
Q

Unspecified Intellectual Disorder

A
  • Over age 5
  • When obtaining an accurate assessment is difficult or impossible due to child characteristics
  • Use only in exceptional circumstances; acts as a placeholder for ID if hard to get diagnosis
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6
Q

ID Associated Features

A
  • Can have similar personality and behavioral features found in others (but may have unique features based on ID etiology)
  • Communication deficits may often explain aggression (can’t communicate distress & discomfort)
  • Can have full range of mental disorders, but often difficult to identify
  • Comorbid mental disorders common (3-4 x greater prevalence)
  • ID may influence how anxiety, depression, etc. manifests
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7
Q

ID: Culture, Age, and Gender

A
  • Must consider culture when assessing intellectual functioning
  • Must consider developmental factors when evaluating adaptive skills
  • Slightly more common in males (1.6:1 mild, 1.2:1 severe)
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8
Q

Prevalence and Course of ID

A
  • About 1% gen population
  • More severe levels associated with genetic syndromes
  • Severe level often has acute onset
  • Lifelong impairment is typical, but supports can improve ADLs and QoL
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9
Q

Developmental vs Acquired ID

A
  • Dx not dependent on specific etiology
  • Dx depends on developmental level: during childhood diagnosed with ID but during adulthood diagnosed with neurocognitive d/o (if already have ID, then acquire head injury you can diagnose both)
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10
Q

ID: Differential Diagnosis

A
  • Major & Mild Neurocognitive Disorder
  • Specific LD
  • Communication Disorders
  • Autism Spectrum Disorder
  • Deafness
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11
Q

Ethical Considerations with Diagnosis of ID

A
  • School referral-to-placement decisions based on state interpretations of IDEA
  • Diagnosis affects eligibility for services
  • Impacts prognosis and life course
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12
Q

Etiology of ID

A
  • 30% unknown
  • 40% genetic disorder
  • 10% metabolic disorders
  • 10% teratogens
  • 10% perinatal problems or injury
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13
Q

Hereditary and Chromosomal Disorders

A

Tay Sach’s Disease (errors in metabolism), Phenylketonuria (errors in metabolism), Tuberous Sclerosis (single-gene), Neurofibromatosis (single-gene), Fragile X syndrome (chromosomal aberrations), Down’s syndrome (trisomy 21), Cri-du-Chat (chromosomal deletion), Prader-Willi Syndrome (chromosomal deletion)

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14
Q

ID: Prenatal Events

A
  • Nutritional deficiencies
  • Congenital infections
  • Exposure to toxins (e.g., FAS)
  • Neural tube defects
  • Iodine deficiency disease
  • Rhesus incompatibility
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15
Q

ID: Perinatal Events

A
  • Hypoxia
  • Hypoglycemia
  • Cerebral hemorrhage
  • Gross trauma
  • Fetal malnutrition
  • Prematurity
  • Low birth weight
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16
Q

ID: Postnatal Events

A
  • Infections/illness: encephalitis/meningitis
  • Trauma/accidents: TBI, near drowning
  • Malnutrition
  • Toxins & poisons: lead poisoning, mercury exposure
  • Environmental deprivation
  • Child abuse
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17
Q

Dual-Diagnosis

A

ID + another mental disorder

  • full range of psychiatric disorders can emerge
  • rates much higher (30-50%)
  • lower functioning = higher rates
  • difficult to assess
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18
Q

Einfeld article

A

Collectively, these studies demonstrate rates of comorbidity for children and adolescents between 30 and 50% with a relative risk of mental disorder associated with intellectual disability ranging from 2.8–4.5.

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19
Q

Stereotypy

A

Repetitive motor movements that are nonfunctional (e.g., body rocking, hand flapping)

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20
Q

Self-injurious behavior

A

Repetitive behaviors which may result in self-inflicted bodily injury (e.g., head banging, self-biting, face slapping)

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21
Q

Stereotypic Movement Disorder DSM-5 Criteria

A
  • Repetitive, apparently purposeless motor behavior
  • Interferes with social, academic, or other activities that may result in self-injury
  • Onset in early developmental period
  • Not attributable to substance, neuro condition, or another disorder
    Specify if: with or without self-injurious behavior, associated with a known medical or genetic condition, neurodevelopmental disorder, or environmental factor
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22
Q

Stereotypic Movement Disorder: Epidemiology/Prevalence/Course

A
  • Most commonly seen in ID (4-16%)
  • SIB more common with certain GMCs
  • Sometimes seen with severe sensory deficits
  • More common in institutional settings
  • Gender difference (head banging more common in males, self-biting more common in females)
  • 3-4% children/adol in community
  • Onset typically by age 3; can persist for years but typography may change
  • Note: not Tic Disorders, ASD, OCD, etc.
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23
Q

History of ASDs

A
  • 1943 Kanner (U.S.)
  • —- 11 cases of “early infantile autism;” 3 problem areas
  • —- 3 problem areas: social isolation, peculiar language, insistence on sameness
  • 1944 Asperger (Austria)
  • —- 4 cases of “autistic psychopathy”
  • —- Impairments in pragmatic language, social interaction, circumscribed interests, clumsiness
  • —- Unknown until 1981, when described as Asperger Syndrome
  • 1980 DSM-III: Infantile autism
  • 1994 DSM-IV: Asperger Syndrome added
  • 2013 DSM-5: Autism Spectrum Disorder
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24
Q

ASD Controversies

A
  • Is Asperger’s a separate disorder/valid diagnostic category?
  • Are actual rates of ASD increasing or is it just rate of diagnosis increasing?
  • Do the DSM-5 criteria under-identify children?
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25
Q

DSM-IV Pervasive Developmental Disorders

A
  • Autistic Disorder
  • Asperger’s Disorder
  • Rett’s disorder (genetic disorder taken out in DSM-5)
  • Childhood disintegrative disorder
  • Pervasive Developmental Disorder, NOS
  • Above are now lumped under “Autism Spectrum Disorder” in DSM-5
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26
Q

Autism Clinical Presentation

A
  • Chief complaint: no language and lack of social responsiveness
  • Concerns that child is deaf, neurologically impaired, or ID
  • Often concerns have been present 2-3 years
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27
Q

Autism DSM-IV Criteria

A
  • Qualitative impairment in social interaction, communication, and RBRIs
  • Onset prior to age 3
28
Q

Asperger’s Disorder DSM-IV

A
  • Autistic disorder without early language delay

- No cognitive or adaptive delays

29
Q

ASD Key Changes to DSM-5

A
  • 3 categories of impairment to 2 (social and language combined into Social-Communication)
  • Changed from categorical to dimensional
  • 2 RBRIs required instead of 1 (added atypical sensory process symptom)
  • Specifiers and modifiers
  • Severity level
30
Q

Lai et al. article

A

Describes way of conceptualizing the spectrum

31
Q

ASD Criteria DSM-5

A
  • Deficits in social communication across contexts in all 3 of following:
    1) Deficits in social-emotional reciprocity (e.g., failure of normal back and forth conversation, reduced sharing of interest)
    2) Deficits in nonverbal communicative behaviors (e.g., eye contact, body language, etc.)
    3) Deficits in developing/maintaining relationships (e.g., difficulty adjusting behavior for different contexts, lack of friendships)
  • Restricted/repetitive behaviors in at least 2 categories:
    1) Stereotyped/repetitive movements
    2) Insistence on sameness/adherence to routine
    3) Restricted interests abnormal in intensity of focus
    4) Atypical sensory reactivity and/or focus
  • Symptoms present in early developmental period
  • Clinically significant impairment in functioning
  • Not better explained by ID or global dev delay
32
Q

ID & ASD co-occurence

A
  • ID and ASD frequently co-occur

- To make comorbid dx, social communication should be below that expected for general dev level

33
Q

DSM-5 ASD Specifiers

A

Specify if accompanying intellectual impairment, accompanying language impairment, if known medical or genetic condition or environmental factor, associated with a neurodevelopmental, mental, or behavioral disorder, or with catatonia

34
Q

DSM-5 ASD Severity Levels

A

Level 1: requiring support
Level 2: requiring substantial support
Level 3: requiring very substantial support
- Away from # symptoms and towards QoL

35
Q

Epidemiology of ASDs

A
  • In 1990s: was 2-5 per 10,000 for autism
  • Now as high as 5.7-21.9/1,000
  • Debate: Increase in autism or increase in diagnosis?
  • Increases leveling off recently; maybe due to awareness?
  • Onset prior to age 3, but symptoms hard to identify before expectations of language etc.
  • Lifelong impairment but better outcomes if earlier age for treatment
36
Q

Age/Gender Features ASD

A
  • Nature of social impairment may change over time
  • Approx 5:1 boys
  • Girls more severely affected/more likely to have comorbid ID
37
Q

Mandel & Lecavalier article

A
  • CDC came up with rates using a records review

- Even if child didn’t have diagnosis, they could give it during review if enough red flags.

38
Q

ASD Associated Features

A
  • Intellectual disabilities
  • Splinter skills/savants (rare)
  • Behavioral symptoms: hyperactivity, impulsivity, inattention, aggression, self-injurious behaviors, tantrums, elopement
  • Sleep disturbances
  • Seizures
  • Eating Disorders
  • GI disorders
  • Motor delays/clumsiness
39
Q

ASD Differential Diagnosis

A
  • Rett Syndrome
  • Selective Mutism
  • Language disorders and Social Communication Disorder
  • ID
  • Stereotypic Movement Disorder
  • ADHD
  • Reactive Attachment Disorder
  • OCD
  • Schizophrenia
40
Q

ASD Comorbidity

A
  • 70% have 1 comorbid condition
  • 40% have 2+ comorbid conditions
  • ID: 31%
  • ADHD: 33-78%
  • Anxiety: 40-50%
  • Depression: 17-27%
41
Q

ASD Etiological Models: Psychological

A
  • Psychodynamic/psychogenic: “refrigerator mother”; theory not supported
  • Poor theory of mind, lack of joint attention/poor social processing, social orientation, weak central tendency, poor executive function
42
Q

ASD Etiological Models: Biological

A
  • Genetic factors: heritability 90%, high twin concordance rate, family aggregation, BAP: broader autism phenotype
  • Neuroanatomical: abnormal cell growth/pruning, atypical brain structure
  • Neurochemical: increased serotonin, dopamine, norepinephrine, endogenous opioids?
43
Q

ASD Etiological Models: Environmental

A
  • Pre & perinatal risk factor: maternal infections, maternal medical conditions, obstetric complications at birth, prenatal exposure to certain medications
  • Seasons of birth: mothers with flu during pregnancy
  • Advanced parental age (particularly older fathers)
  • Environmental toxins: pollutants/pesticides
44
Q

Dawson and colleagues on ASD

A

Hypothesize that social impairments stem from abnormality in social reward neural circuitry influencing motivation to attend to people

45
Q

ADHD History

A
  • 1800s: Fidgety Phil as 1st case study
  • Early 1900s: “explosive will,” “volitional inhibition,” “defect in moral control”
  • Encephalitis epidemic of 1917-18: brain-injured child syndrome
  • 1950s: minimal brain damage/dysfunction, hyperkinetic impulse disorder
  • 1960s: hyperkinetic reaction of childhood (Freud influenced this description)
  • 1970s: ADD with and without hyperactivity
  • 1980s: ADHD
  • 1990s: ADHD predominantly inattentive, hyperactive-impulsive, and combined types
  • 2010s: ADHD predominantly inattentive, hyperactive-impulsive, and combined presentations
46
Q

ADHD DSM-5 Criteria

A

Persistent pattern of:

  • Inattention (at least 6 symptoms for 6+ months): fails to give close attention to detail, difficulty sustaining attention, does not seem to listen, doesn’t follow through on instructions, difficulty organizing tasks, avoids/dislikes tasks that require sustained mental effort, loses things, distractible, forgetful
  • And/or hyperactivity-impulsivity (at least 6 symptoms for 6+ months): fidgets/squirms, leaves seat when not supposed to, runs/climbs when inappropriate, unable to play quietly, acts “as if driven by a motor,” talks excessively, blurts out answer before question completed, difficulty waiting their turn, interrupts/intrudes on others
  • Symptoms before age 12; present in two or more settings
  • Subtypes: combined, predominantly inattentive, predominantly hyperactive/impulsive presentation
  • Mild, moderate, severe
47
Q

Other Specified ADHD

A
  • Symptoms of ADHD with distress/impairment
  • Do not meet full criteria
  • Clinician chooses to communicate reason for not meeting criteria
48
Q

Unspecified ADHD

A
  • Symptoms of ADHD with distress/impairment
  • Do not meet full criteria
  • Clinician chooses NOT to communicate reason for not meeting criteria OR insufficient information to make more specific dx
49
Q

Differences in Subtypes?

A
  • Is there a pure hyperactive/impulsive subtype?
  • Changes over time (e.g., move from hyperactive to inattentive)
  • Sluggish cognitive tempo: purely inattentive type (daydreaming, not hyperactive)
  • Differences in attention problems and family factors
50
Q

ADHD Epidemiology

A
  • Prevalence: 3-7%
  • Risk Factors: temperament; environment, genetic & physiological, & course modifiers
  • Age 4-5 can be reliably diagnosed
  • 2:1 male children, 6:1 clinical
  • Females more likely primarily inattentive
  • Culture: increased rates in lower SES; rating scales may be biased and over-identify some minorities
51
Q

Developmental Course of ADHD

A

2-3: excessive motor activity (hard to distinguish)
3-4: continued disinhibition
5-7: inattention; 40-70% oppositional/aggressive
6-12: executive functioning px more prominent
8-12: approx. 25-45% may develop conduct disorder
Adolescence: decline in disinhibition; 50-80% maintain attentional problems
Adulthood: 30-50% maintain symptoms of inattention and restlessness

52
Q

ADHD Associated Features

A
  • Health Risks: accident prone, driving risks, sleep problems
  • Motor incoordination
  • Impaired academic functioning
  • Reduced intelligence
  • Social problems
53
Q

ADHD: Comorbid Disorders

A

LD, ODD, Conduct Disorder, Antisocial PD, Substance Use Disorder, Anxiety, Mood Disorder, Tics/Tourette’s (lead to increased chance ADHD), ASD

54
Q

ADHD Differential Diagnosis

A

Oppositional behavior, Intermittent Explosive Disorder, other neurodevelopmental disorders (SMD, ASD, Tourette’s), Specific Learning Disorder, ID, ASD, Reactive Attachment Disorder, Anxiety, Depressive disorders, Bipolar, DMDD, Substance Use Disorder, PD’s, Psychotic disorders, Medication-induced symptoms of ADHD, Neurocognitive Disorders

55
Q

Barkley’s Etiological Model of ADHD

A
  • Prepotent responses: responses for which immediate reinforcement is available or has been given in the past
  • Behavioral inhibition (deficits largely organic)
    1) Response inhibition: resistance to temptation; delay in prepotent response (children with ADHD struggle with this)
    2) Interference control: protection of this delay
    Struggles with inhibition can affect…
  • Working memory: ability to keep mental information mind and use it to direct behavior
  • Self-regulation: self-control; ability to modify emotional response in pursuit of goal-directed behavior
  • Internalization of speech: self-directed speech (e.g., voice in head that says “maybe I shouldn’t do that”)
  • Reconstitution: ability to mentally analyze and take apart and put events back together before generating a response
    These all lead to ADHD symptoms
56
Q

Other ADHD Etiological Models

A
  • Genetic: family aggregation, adoption studies, twin studies
  • Neurological factors: prefrontal lobe dysfunction, abnormal neurotransmitter levels
  • Pregnancy/birth related (premature) - mixed findings
  • Toxins (lead, pesticides)
  • Psychosocial (no good causal evidence, but may exacerbate symptoms)
  • Gene x environment interaction
57
Q

Federal definition of Specific Learning Disorder

A
  • Born out of education, not medical field
  • Disorder in basic psychological processes involved in understanding or using language; imperfect ability to listen, speak, read, write, spell, or do mathematical calculations
58
Q

LDs from DSM-IV to DSM-5

A
  • DSM-IV: split into separate diagnoses for reading, math, written expression, and NOS
  • DSM-5: all under one diagnosis with specifiers for reading, written expression, and math
59
Q

SLD DSM-5 Criteria

A
  • Difficulty learning or using academic skills despite interventions to improve skills. At least one of following for at least 6 months: slow or effortful reading, difficulty understanding word meanings, poor spelling, poor writing, difficulty with math calculations, difficulty with math reasoning
  • Skills substantially and quantifiably below levels expected for child’s age
  • Difficulties began during school-age years
  • Not due to ID or inadequate instruction
  • Specifier (reading, written expression, math) and severity (mild, moderate, severe)
60
Q

Epidemiology of SLD

A
  • Prevalence: 5-15% overall
  • Gender: more common in males
  • Course: typically begins early elementary but can’t be diagnosed until adequate instruction & poor performance
  • Associated features: low self esteem, poor social skills, school drop-out, birth-related complications, GMCs
61
Q

4 Main Models of SLD

A

1) IQ-Achievement Discrepancy: research not very supportive
2) Intra-individual discrepancy (subtest scatter): useful in some cases, but make many assumptions
3) Low achievement: doesn’t differentiate LD from non-LD low achievers
4) Response to intervention: some evidence of validity and improved reliability
- questions: how much improvement needed? should interventions be switched if no results? were interventions completed with integrity?

62
Q

Bell article

A
  • Research on what changes should be made in DSM-5 for ADHD criteria
  • Adjusting or eradicating age of onset criteria well-supported; DSM-IV said some symptoms must be present before age 7
  • Adjusting symptoms for adult populations necessary (ex - symptoms written for children like “often squirms in seat”); hard to ask adults to recall the age of onset
  • ADHD can also influence adults in ways that reduce their executive functioning
  • Should there be subtypes or should it be more fluid? (some research showing people move between subtypes)
63
Q

Einfeld article

A
  • 9 studies collectively demonstrate rates of comorbidity for children and adolescents with ID between 30 and 50% (compared to 8-18% for children without ID)
  • The risks for this comorbidity (ID & mental disorder) associated with age, gender, severity of intellectual disability, and socioeconomic status remain uncertain.
64
Q

Lai et al. article

A
  • Spectrum nature of ASD new to DSM-5
  • Two issues to address: 1) clarification of the meaning of “spectrum” and 2) the need for subgrouping
  • Three possible definitions of spectrum: 1) differences in severity and presentation of symptoms among those with ASD, 2) continuity between the general population and the clinical population (“autistic traits”), and 3) subgroups
  • Specifiers used in DSM-5: article suggests expanding the list of specifiers towards the identification of clear subgroups
  • Suggested specifiers: developmental pattern (age and pattern of onset), sex/gender, clinical phenotype (behavioral/clinical presentation), genetic correlates, and potential environmental factors (e.g. exposure to teratogens)
65
Q

Mandell & Lecavalier article

A
  • Dramatic increase in ASD prevalence rates according to the CDC
  • Rates are determined by a diagnosis in medical or education records, and if there are “red flags” a child can be put in the ASD category without an official diagnosis
  • A lot of cross-site variation in rates
    • Due to differences in local policies, resources, awareness
    • Not true prevalence rates as advertised
  • In a “true” prevalence study, researchers clinically assess individuals in person; CDC didn’t do this
66
Q

Scanlon article

A
  • DSM-5 LD definition: retains presumption that LD is an academic-based disorder originating in the CNS
  • The theory that LD could be measured via an aptitude-achievement discrepancy has been soundly disputed
  • Changes from DSM-IV: no discrepancy cut score (look at academic performance instead), elimination of NOS, severity levels now recognized
  • LD can exist across the lifespan
  • APA intends to categorize LD as a neurodevelopmental disorder (has origin in developmental period); however, it may need to also be regarded as a neurocognitive disorder (includes cognitive decline)