ADHD and Autism Flashcards

1
Q

What is autistic disorder?

A
  • Autism is a lifelong condition affecting approximately 1.1% of the population
  • It is a spectrum condition meaning that it affects people differently and to varying degrees
     Combined with Asperger’s disorder and pervasive developmental disorder not otherwise specified in DSM V into autism spectrum disorder
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2
Q

What do you need for a diagnosis of Autism?

A
  • DSM-5 key diagnostic criteria
     Persistent deficits in social communication and social interaction
     Restricted, repetitive patterns of behaviour, interests or activities
  • In addition
     Symptoms must be present in the early developmental period
     Symptoms cause clinically significant impairment in social, occupational, or other important areas of current functioning
     These disturbances are not better explained by intellectual disability (intellectual developmental disorder) or global development delay
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3
Q

How does social impairment present itself in people with Autism?

A
  • Usually the first symptoms identified
  • Infants with autistic disorder usually do not want to be held and may arch their backs when picked up
  • Can have difficulty entering into social relationships and predicting other’s behaviour or understanding their motivations
  • Deficit in theory of mind – representing other’s mental state (Baron-Coen et al., 1985; Ward, 2010)
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4
Q

What is communication impairment in autism?

A
  • General consensus that language is commonly impaired or absent in people with autism
  • Tends to be used for instrumental rather than social purposes
  • Content tends to be repetitive and egocentric
  • Nonverbal communication impairments, e.g. comprehension and use of facial expressions and gestures
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5
Q

what is restricted, repetitive patterns of behaviour, interests or activities in autism?

A
  • Stereotypes or repetitive motor movements, use of objects, or speech
  • Insistence on sameness, inflexible adherence to routines, or ritualised patterns of verbal or nonverbal behaviour
  • Highly restricted, fixated interests that are abnormal in intensity or focus
  • Hyper or hypo reactivity to sensory input or unusual interest in sensory aspects on the environment
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6
Q

Give features of what autism spectrum disorder is

A
  • A range of different attributes, any of which may, or may not occur in any one person, to a greater or lesser extent
  • Don’t reflect discrete entities
  • Able/high functioning autism – severe; with/ without cognitive impairments
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7
Q

What is Asperger’s syndrome?

A

 Considered part of the spectrum by many (e.g. DSM-5), others see it as a sub-group or distinct condition
 No delay in language development in Asperger’s syndrome
 Frequently social interaction difficulties, repetitive or stereotyped behaviours, and/or obsessional interest in narrow subjects

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8
Q

What is Colver et al’s twin study that gives evidence for heritability of autistic spectrum disorders?

A

 Twin pairs born in 1994-1996 in England and Wales
 5 different measures with 203 – 6,423 twin pairs per measure
 Concordance of 77% to 99% for monozygotic twins
 22-65% concordance for dizygotic twins
 Variance across tools but significantly higher across all assessment tools for monozygotic twins

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9
Q

What defined biological causes may cause autism?

A

rubella, prenatal thalidomide, encephalitis caused by the herpes virus, tuberous sclerosis

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10
Q

What are the differences in brain growth of people with autism?

A

 People with autism appear to have a slightly smaller brain at birth
 Their brain then undergoes abnormally quick growth in infancy (10% larger)
 Before growth slows significantly by adolescence

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11
Q

What is Zielinski’s longitudinal study?

A

 97 males with autism and 60 males with typical development
 Accelerated expansion in early childhood
 Accelerated cortical thinning (cutting back of extra neuronal connections) in adolescence
 Decelerated cortical thinning in early adulthood
 Region specific and variation by IQ and age

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12
Q

What was Castelli’s study on brain pathology on autism (to do with triangles and functional imaging)

A

 Showed animations of two triangles interacting in different goal-directed ways to people with high functioning ASD and people with typical development
 People with ASD had difficulty describing the intentions of a triangle trying to trick or coax the other
 Functional imaging showed similar cerebral blood flow in the visual association cortex but lower levels of cerebral blood flow in the superior temporal sulcus (STS) and the medial prefrontal cortex (usually activates when considering the intentions, thoughts or beliefs of others)

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13
Q

What has been thought about the Fusiform Gyrus (face area) and autism?

A

 Part of the visual association cortex that is involved in the recognition of individual faces
 Traditionally thought to be impaired or underdeveloped in people with autism
 However, recent evidence from an event-related potentials (ERP) study disagreed
 Suggested the effect may not be due to specific impairment of the FFA but rather dysfunction of neural mechanisms and networks involved in driving and integrating the social information conveyed by faces

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14
Q

What did Sultz and colleagues find when looking at the fusiform area in people with autism and what may this be a consequence of?

A
  • Shultz and colleagues found little or no activity in the fusiform face area in people with autism when they were viewing pictures of human faces
     Decreased fusiform gyrus activity repeatedly reported in ASD might be a developmental consequence of early dysfunction of the amygdala and thus reduced salience of facial stimuli in ASD
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15
Q

What is the role of oxytocin in autism (and generally)

A

 Oxytocin – peptide that facilitates pair bonding and increases trust and closeness to others
 Modahl and colleagues (1998) reported lower levels of oxytocin in children with autism
 Administration of oxytocin has been shown to increase performance on tests of emotion recognition
 Administration of oxytocin increased amygdala activity in response to facial stimuli in people with Asperger’s syndrome (Domes and colleagues)

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16
Q

What was Baron-Cohen’s extreme male brain theory and what support is there for and against it?

A

 Baron-Cohen (2002) suggested that ASD may be a reflection of an ‘extreme male brain’
 Support:
 ASD more prevalent in males
 Higher prenatal exposure to testosterone
 Against
 Several researchers suggest that ASD is down to sexual differentiation (physical and in functional brain connectivity)
 Females with ASD exhibit more masculine traits
 Males with ASD exhibiting more feminine traits

17
Q

What is Attention deficit (hyperactivity) disorder and what must you need to be diagnosed with it??

A

• DSM V – a persistent pattern of inattention and/or hyperactivity – impulsivity that interferes with functioning or development
 6 or more symptoms of inattention/ hyperactivity – impulsivity (5 or more if aged 17+) that have persisted for at least 6 months
 Several symptoms were present before age 12
 Symptoms occur in two or more settings
 Symptoms interfere with, or reduce the quality of social, school or work functioning
 The symptoms are not better explained by another mental disorder
- look at notes for inattention symptoms and hyperactivity symptoms

18
Q

What is ADHD often associated with?

A

aggression, conduct disorder, learning disabilities, anxiety, and low self-esteem

19
Q

What did Larsson et al’s study shown about heritability and autism?

A
  • One twin study with 59, 514 twins indicated a lifetime heritability of 88% (Larsson et al., 2014)
  • Larsson and colleagues also showed that shared environment was not that important
20
Q

What are the symptoms of ADHD similar to those produced by? What are these symptoms?

A
- The symptoms of ADHD are similar to those that are produced by damage to the prefrontal cortex 
 Distractibility 
 Forgetfulness 
 Impulsivity 
 Poor planning
 Hyperactivity
21
Q

What did a meta-analysis show about ADHD and brain structures?

A
  • Meta-analysis reported that people with ADHD have consistent functional abnormalities in brain areas related to inhibition and attention
  • Inferior frontal cortex, supplementary motor area, and anterior cingulate cortex for inhibition
  • Dorsolateral prefrontal cortex, parietal and cerebellar areas for attention
22
Q

How is the corpus callosum affected in ADHD?

A
  • Research has consistently indicated that those with ADHD have a significantly smaller corpus callosum
  • Others suggest that in adulthood the corpus callosum is still implicated but volume is similar to those without ADHD, rather the white matter integrity is compromised
  • Different findings as to the exact abnormalities, but consistent evidence the corpus callosum is involved
  • Corpus callosum connects the two hemispheres of the brain
23
Q

How is dopaminergic transmission involved in ADHD?

A
  • Under activity of dopaminergic transmission has bene implicated in ADHD
  • Low levels of dopamine receptor stimulation impairs functioning of the prefrontal cortex
  • Aarts et al. (1015) reported that striatal dopamine plays an important role in the abnormal cognitive-task related processing in ADHD
  • Genetic studies have implicated dopamine receptor genes in the aetiology of ADHD
24
Q

How is ADHD treated?

A
  • The most common treatment for ADHD is methylphenidate (Ritalin)
  • This drug inhibits the reuptake of dopamine
  • Lends additional support for a role of dopamine transmission in ADHD
  • Dosage is important, too low and there is no effect, too high a dose results in increases in activity levels disrupting children’s attention and cognition