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Brain & behaviour > Lecture 6 - Autism, Asperger's, ADD, ADHD > Flashcards

Lecture 6 - Autism, Asperger's, ADD, ADHD Flashcards

1
Q

What is the heritability of autism?

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A

5%

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2
Q

What are the proposed causes of Autism?

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A

•Maternal infections

  • Rubella, Herpes, TBC, PKU
  • might cause other disorders too, like adhd

• Mirror cells are either absent or non-functional
- enlarged brain size in childhood

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3
Q

What is the prevelance of ADHD?

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A
  • 4-5% of children, more common in boys
  • 60% keep it as adults: leads to them being antisocial and doing drugs
  • Common to see in adult prisoners
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4
Q

Outline the ‘A: Deficitis in social communication and social interaction across multiple context’ Diagnostic criteria for autism
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A

A: Deficits in Social Communication and Social Interaction across multiple contexts

  1. Deficits in social-emotional reciprocity
    - back-and-forth, sharing interests, sarcasm, responding to others
  2. Deficits in non-verbal communication
    - eye contact/ body language incorrect
  3. Deficits in developing, maintaining and understanding relationships
    - problems adjusting behaviour to context
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5
Q

What are the 4 Diagnostic Criteria for Autism

A

A: Deficits in social communication and social interaction across multiple contexts
B: Restrictive Behaviour
C: Must be present early on in developmental period
D: Symptoms cause significant impairment in areas of functioning

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6
Q

Outline ‘B: Restrictive Behaviour’ Diagnostic criteria for Autism
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A

B: Restrictive Behaviour

  • Stereotyped or repetitive moments, use of objects, speech
  • Preference for sameness, adherence to routines, ritualised patterns
  • Restricted, fixated interests
  • Sensory overload
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7
Q

If you meet all 4 criteria what are you diagnosed with?

A

Autism Spectrum Disorder

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8
Q

If you mainly meet the A criteria what are you diagnosed with?

A

Social (pragmatic) communication disorder

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9
Q

What are the 4 diagnostic criteria for Social (pragmatic) communication disorder?
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A

A: persistant difficulties in the social use of verbal and nonverbal communication
B: This causes limitations in effective communication, social participantion and relationships
C: Onset is in early development
D: Not caused by any other disorder (incl ASD) or low abilities in word structure/ grammar etc

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10
Q

Outline “A: Persistant difficulties in the social use of verbal and nonverbal communication”
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A

A: Persistant difficulties in the social use of verbal and nonverbal communication

  1. Deficits in using communication for social purposes
    - e.g. greeting/ sharing info
  2. Inability to match communication to context/ needs of listener
  3. Trouble following conversational rules
    - e.g. turn taking, gesticulation, rephrasing if confused
  4. Difficulties understanding what is not explicitly stated
    - inferences, nonliteral/ ambiguous language
    - take things very literally

Culturally varying depending on rules of conversation in that culture

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11
Q

Outline Mirror Cells

A
  • Mirror Cells in the premotor cortex
  • Learning how to do things (hence: motor areas)
  • also necessary in doing the thing
  • Might be implicated in ASD & Pragmatic Communication Disorders
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12
Q

Outline how we change our facial expression to empathise with other person
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A
  • We will change our own facial expression when someone else is crying and share their pain
  • Corregator Muscle (between eyebrows) contracts when you’re sad - necessary for empathy as you mirror their facial expression
  • Those with Botox cant mirror this facial expression - feel less empathic
  • research has found that they experience less depression
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13
Q

Whats the DSM criteria for ADHD?

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A

Persistant Pattern of inattention and/ or hyperactivity

  • has to be present before 12
  • has to be in more than one setting
  • generally not focused unless hyper-focus (if really interested)
  • persistant pattern over many areas
  • Cant be better explained by Sz, or another psychotic disorder: mood, anxiety, dissociative, personality disorders etc - substance abuse
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14
Q

What are gender differences in ADHD roughly?

A

Girls tend to deal with more attention problems

Boys tend to deal with more hyperactivity problems

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15
Q

What does DSM-5 say ADHD has to interfere with?

A
  • Interefere with or reduce quality of social, academic, or occupational functioning
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16
Q

How many of the symptoms to adults vs children need?

A

•Adults require 5 or more symptoms
• Children require 6 or more symptoms
- cant be defiance/ reactive - has to be impulsive and hyperactive

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17
Q

What are broad symptoms of inattention (ADD)

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A
  • cant sustain or give close attention
  • doesnt listen when spoken to
  • cant follow instructions
  • loses things
  • very easily distractable
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18
Q

What are broad symptoms of Hyperactivity & Impulsivity (ADHD)
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A
  • Fidgets
  • Leaves seat when inappropriate
  • Cant play quietly
  • Excessive energy, talks, blurts out, cant wait turn
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19
Q

Which Neuropsychological tests do those with ADHD struggle with?
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A
  1. Spatial working memory - drawing from memory
  2. Planning & Inhibition - Stroop, mazes,
  3. Wisconcison card sorting task a bit
  4. Tower of London test
  5. Trail making test b (shifting from numbers to letters)

Indicates clear frontal Basal Ganglia issues

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20
Q

What are some potential brain abnormalities in ADHD?

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A
  1. Enlarged Occipital Lobes
  2. Smaller Anterior Frontal Regions
  3. Smaller Caudate Nuclues (In BG)
  4. Smaller Corpus Callosum
  5. Higher Density of Dopamine receptors in Caudate and Globus Pallidus (BG) - associated with Dopamine deficit (try and catch it all?)
21
Q

What do fMRI scans show about brain abnormalities in ADHD?

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A
  1. Hypoactivation in frontostriatal neurons (basal ganglia)
  2. Ventral PFC and inferior parietal causes issues with motor inhibition and task switching
    - can be corrected through DA stimulants
22
Q

How can Ritalin help ADHD symptoms?

A

Because people ADHD children are really active, people thought they had too much dopamine, but they actually have a deficit (indicated by the increase of receptors in Caudate and Globus Pallidus

  • So ritalin increases amount of dopamine
  • this can regulate symptoms
23
Q

What is SPECT?

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A

single photon emission computed tomography

- looks at metabolism

24
Q

What has SPECT found in ADHD

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A
  1. Reduced Cerebral Blood Flow in Frontal lobe and Basal Ganglia
  2. Increased CBF in occipital
    - why they are easily distracted by visual stimuli
  3. Reduced Glucose metabolism during attention tasks in frontal lobes
25
What is the combination Hypothesis about ADHD? | ***************
- the abnormalities in frontal and striatal dopamine is party due to genetics and partly due to environment Environment + Genes = atypical brain development
26
What is going wrong at the synpase for those with ADHD?
The problem occurs during reuptake | - Excess dopamine is being reuptaken by DAT - the Dopamine transporter - reuptakes dopamine too much
27
What was the initial theory about why stimulants work for ADHD patients
- People thought they worked because: If you are stimulating even more, it means you will swing back like a pendulum and will become calmer - if they are hyperactive, give them a stimulant, it will make them swing back and become calm
28
Whats the actual reason why stimulants work for ADHD patients? ***************
- Stimulants work by sitting on the DAT receptor and preventing it from reuptaking dopamine - They block DAT by 60% = more dopamine in synapse - sitting on D1 receptor, helps inhibition of behaviour - helps them focus and stop being hyperactive
29
How does cocaine increase dopamine?
Blocks reuptake - acts on the D1 receptor - influences reward system (VTA/ PFC) - Amphetamines do the same thing
30
Which neurotransmitters does cocaine and amphetamine also effect ***************
Impacts on D1 - Also has effects on Norepinephrine, serotonin, glutamate and acetylcholine - all associated with reward
31
What are the effects of inhibiting Dopamine | ***************
Euphoria, energy, confidence, libido | - libido can get too high and cause sexual dysfunction
32
What are short term side effects of blocking dopamine receptors? ***************
- insomnia - impulsivity - tachycardia: when heart goes too fast - anxiety - Psychosis - tweaking - confusion - panic attacks - sexual dysfunction
33
What are long term side effects of blocking dopamine receptors?
- Tolerance increases - paranoia and aggression as effects start wearing off - Fewer DA neurons in Substantia Nigra - parkinson symptoms - Overdose = convulsion, strokes
34
What is the treatment for ADHD? | ***************
Methylphenidate (MPH) - also known as Ritalin - Works like cocaine - Blocks 60% of DAT receptors - causes DA to stay in the synapse much longer
35
Whats the difference between treated and untreated kids? | ***************
Treated: - more DAT in striatum (is this because of treatment?) Untreated: - Low DAT density in mesencephalon - Low DAT in striatal Complex/ caudate Others: - no difference in DAT in putamen
36
How can you argue that DAT is plastic?
DAT is lowered in response to low DA levels - if low DA, DAT goes down as its not needed DAT is increased in response to high DA levels - therefore, if DA is increased via drugs, DAT will go up
37
What are the 2 genetics tests?
1. Candidate Gene approach - investigate a specific gene on the known chromose location to test their genotype and relate it to a disorder - know of a specific gene and see if they have it 2. Genome scan - do statistics on genetic markers to locate chromosomal regions - see what they have
38
What are the 2 possible candidate genes | ***************
1. Dopamine Transport gene - DAT Gene 2. Dopamine receptor type 4/5 - DRD4/5 Gene Might be a combination of the two causing hypodopaminergic state - related to lack of frontal inhibition, - pleasure seeking/ stimuli seeking - cant inhibit pleasure seeking behaviour
39
What are the similarities between ADHD and Parksinsons? | ***************
Those with ADHD may have higher risk of Lewy Body disease - associated with Parkinsons - both associated with low levels of DA in SN Similarities: • Parksinsons score high on attention deficit and hyperactivity than controls • But not on impulsivity, oppositional disorder or social adaptation Link between parkinsons, lewy body and ADHD is probably not genetic - might implicate similar DA areas/ receptors
40
Why do Antipsychotics have such a global impact on the brain?
Because they impact the D2 receptors, which are all over the brain - hence they help motor control as well as disordered thoughts
41
What are the proposed Heritability causes of ADHD
You inherit a vulnerability to: • Dopamine receptor genotypes • Dopamine transporter genotypes
42
What are the proposed environmental factors causing ADHD?
- Food colouring (debated) - Sugar (increases hyperactivity - more so in ADHD?) - Heavy metals (lead = 2-4X higher in ADHD) - Smoking Mother (2-4X risk during pregnancy) - Low birthweight/ premature - causes lots of issues - TBI as children - Need the genetic vulnerability too - and these are not exclusive to ADHD as they all often cause other issues
43
What are tics in tourettes?
Can be: - Motor: repeitive/ rapid - Vocal: utterances/ noises Urge arises, cannot be repressed/ inhibited
44
What is prevelance of tourettes syndrome?
Rare - 3-9 in 1000 Boys are 3/4 X more common to get it Usually gone by adulthood
45
What is tourettes related to? | ***************
Maternal stress, smoking, infections, fetal hypoxia | - note exclusive again
46
What is Tourettes overlapped with?
Tics can also be seen in ADHD and OCD - may be related to DA hyperinnervation of striatum - Used to calm the system down, which is why they increase when they are stressed - No inhibition from frontal lobes - basal ganglia starts up to calm system down, e.g. via a tic or a checking behaviour
47
Whats a treatment for Tourettes?
Haldol - an anti-psychotic, a dopamine antagonist or Behavioural intervention - teach them to repress the tics etc
48
How is serotonin involved?
Serotonin inhibts basal ganglia/ PFC - why prozac helps for OCD - might help with ADHD or tourettes

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