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Mental health edited > Lecture - Neurodevelopmental psychiatry > Flashcards

Lecture - Neurodevelopmental psychiatry Flashcards

1
Q

Give two psychiatric childhood conditions which have a strong environmental component. What about those with a strong biological component?

A

Environmental:

  1. Oppositional defiant disorder
  2. Conduct Disorder

Biological:

  1. ADHD
  2. Autism
  3. Psychosis
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2
Q

How do we know that some psychiatric conditions are largely genetic?

A
  1. Family studies - relatives of affected individuals vs controls BUT this doesn’t get rid of environmental factors
  2. Adoption studies - e.g. take adopted children with a disorder and examine rate of disorder in biological vs adopted parents.
  3. Twin studies – Calculate correlation between twin pairs, and compare results for MZ vs DZ twins. Can estimate contribution of:
    • Genes (illustrated by “heritability” concept)
    • Shared environment
    • Non-shared environment
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3
Q

What is the heritability of autism, ADHD and schizophrenia?

A

Autism – 90%

ADHD – 60-90%

Schizophrenia – 80%

Therefore, they are neurodevelopmental conditions as there is much evidence into biological risk factors for these conditions.

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4
Q

What is the triad of ADHD?

A

Impulsivity

Inattention

Hyperactivity

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5
Q

What is the ICD-10 criteria for ADHD?

A
  • >6 months
  • Inattention +/- hyperactivity-impulsivity
  • Pervasive across different situations
  • Onset <7 years - e.g. milestone delays
  • Significant distress or social impairment
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6
Q

How common is ADHD? Who is ADHD more common in?

A
  • 1% hyperkinetic disorder
  • 5% ADHD
  • M>F 3:1
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7
Q

What comorbidities may occur in ADHD?

A

Comobidities may occur:

  • Oppositional defiant disorder 50%
  • Conduct disorder 25%
  • Anxiety 25%
  • Depressive disorders 15%
  • Learning difficulties 30% including reading difficulties
  • Soft neurological signs
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8
Q

What is the ADHD spiral?

A

ADHD symptoms may cause learning difficulties and oppositional beahviour

—> failure at school academically and socially

low self-esteem, isolation and delinquent peer group

—> ADHD symptom…. etc etc

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9
Q

What is the FH association with ADHD?

A

20% of children with ADHD have parents reporting childhood hyperactivity

Biological parents of adopted-away child with ADHA have higher frequenct of childhood hyperactivity and current antisocial traits, alcohol, poor attention.

Concordance rate are 80% in monozygotic twins, 30% in DZ

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10
Q

What is the underlying cause of ADHD in terms of candidate proteins/genes?

A

?Underfunctioning of dopamine system - DRD4 receptor and DAT1 transporter

?Deficit in prefrontal cortex - responsible for executive function (EF); ‘top-down’ control of behaviour … (i.e. the things that kids with ADHD have difficulty in)

  • planning & flexible strategy
  • impulse control
  • orient to salient stimuli & adjust action
  • suppress inappropriate actions in favour of appropriate ones
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11
Q

What evidence is there that the prefrontal cortex may be implicated in ADHD?

A

Prefontal Cortex dysfunction in ADHD

  • MRI: reduced size
  • Functional Imaging: reduced blood flow

Poor performance on EF tasks in ADHD

  • Wisconsin Card Sorting Test
  • Stroop - tests distractibility by other stimuli
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12
Q

What does the Stroop test involve? What would you expect to find in normal vs AHDH brain?

A

If you have ADHD there will be a large discrepancy between the first and second list of words as there would be a major struggle to ignore the distarction in the first list (i.e. incongruence)

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13
Q

What are the non-genetic biological aetiologies of ADHD?

A
  • Prematurity
  • Very low birth weight
  • Foetal alcohol syndrome
  • Association between some food additives and childhood hyperactivity - although they may cause hyperactivity it is not necesarily ADHD.
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14
Q

What parental factors may be associated with ADHD in a child?

A
  • Parental high criticism/ maltreatment/ physical discipline
  • Low sensitivity to child’s needs
  • Maternal depression

But not sure what is causing what… ADHD could be affecting parental responses or genes could be causing both parental and child ADHD.

Research on Romanian orphans: lack of social boundaries and of specific attachments could cause ADHD-type symptoms.

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15
Q

What is the management of ADHD?

A
  1. Cognitive assessment
  2. Pscyho-education - explain that disorder which is no-one’s fault, give info leaflets, support groups
  3. Diet - individual sensitivities may be present
  4. Parental skills training - individual or group (e.g. Webster Stratton)
  5. Medication - readdresses prefrontal underactivity
    1. Stimulants e.g. methyphenidate (‘Ritalin’) , immediate or sustained release, block pre-synaptic DAT + agonist at postsynaptic DrD4
    2. Non-stimulants e.g. atomoxetine (noradrenaline reuptake inhibitor)
    3. SE include: effects on height, weight, sleep and mood
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16
Q

What is the MOA of methyphenidate in ADHD?

A
  • Stimulant
  • AKA ‘Ritalin’
  • immediate or sustained release
  • block pre-synaptic DAT + agonist at postsynaptic DRD4
17
Q

What is the MOA of Atomoxetine in ADHD?

A
  • Non-stimulants
  • Noradrenlaine reuptake inhibitor
18
Q

What is the prognosis with ADHD?

A

~ 90% Conduct Disorder if untreated

Hyperactivity & impulsivity improve with age but 2/3 continue to have symptoms such as inattention, restlessness or disorganisation as adults.

15% continue to have ADHD as adults

19
Q

What is the triad of autism and ASD?

A
  1. Reciprocal social intercation difficulties
  2. Communication difficulties
  3. Repetitive/restrictive behaviour
20
Q

What kind of reciprocal social interaction difficulties do people with ASD have?

A
  • Poor appreciation of social cues
  • Difficulty reciprocating in social interactions – reduced sharing interest / enjoyment with others; reduced proto-declarative pointing
  • Poor non-verbal communication - eye contact, social smiling, facial expression range
  • Failure to develop peer relationships
21
Q

What kind of communication difficulties occur in ASD?

A

Non verbal – reduced gestures, reduced variety / spontaneity of pretend play

Verbal –

  • delay in language development although language is often normal in Asperger’s Syndrome, which is also associated with a higher IQ cf. autism;
  • stereotyped / repetitive speech;
  • lack of chit-chat / to-&-fro conversation;
  • unusual tone
22
Q

What kind of restricted/repetitive behaviours occur in ASD?

A
  • Unusual or repetitive play / use of objects
  • Unusual sensory interests
  • Stereotyped motor mannerisms
  • Adherence to routines / rituals
  • Unusual pre-occupations or circumscribed interests
23
Q

What other difficulties may occur in ASD?

A
  • Usually lower IQ
  • Fears & phobias, OCD
  • ADHD, aggression, self-injury
  • Epilepsy in 20% – suggestive of underlying biological disorder

NOTE: ASD abnormalities evident < 3yrs old, although manifestations change as child develops.

24
Q

What is the aetiology/genetics of ASD?

A

Genetics

  • MZ:DZ = 60:5
  • Heritability = 90%
  • Cf. in 1950-80s: ASD thought 2° ‘refrigerator parents’

6-10% due to medical conditions

25
Q

What medical conditions can cause ASD?

A
  • Tuberous Sclerosis
  • Fragile X
  • Downs Syndrome
26
Q

How common is ASD?

A

Autism 0.25%

ASD 1% (more diverse spectrum)

Rates increasing although probably due to increased awareness and deveopment of specialist services

27
Q

Explain why MMR does not cause autism.

A

Wakefield in Lancet’98: found a link btn MMR and ASD as he found measles antigens in GI tract in small sample of children with ASD

BUT subsequent research including a large MRC review found:

  • no increased rates of ASD in vaccinated populations.
  • no clustering of cases in 6 months after vaccination.
  • no differences in pathology between children that regressed & those that didn’t.

BUT still reduced MMR uptake and hence measles incidence so has been detrimental.

28
Q

What psychological tests/theories are available for ASD?

A

Executive dysfunction theory

  • Explains poor flexibility of behaviour to context.
  • Patients with autism do poorly on EF tests and reduced prefrontal activity on neuroimaging.

Theory of Mind theory

  • Difficulty to conceive of others as having thoughts or feelings different to their own.
  • Patients with autism do poorly on ‘Sally Anne’ tests (below)
29
Q

What is the management of ASD?

A
  1. Cognitive assessment
  2. Psycho-education
  3. Explain disorder – ‘no-one at fault’ and give info leaflets / www / support groups ( National Autistic Society)
  4. Multi-disciplinary –
    • Education: Extra / specialist support, specialist schools;
    • May also need Paediatrics, SALT, OT
  5. If emotional / behaviour problems:
    • Behavioural management,
    • Medication for some co-morbid psychiatric disorders
30
Q

What is the prognosis with ASD?

A
  • Variable outcome
  • Predicted by level of language and generalised cognitive impairment
  • Severe social / language deficits tend to remain
  • 10% achieve independent lives, work, relationships
31
Q

True or False: The following are necessary features of Hyperkinetic disorder:

  • A) Inattention
  • B) Pervasive symptoms
  • C) Oppositional behaviour
  • D) Symptoms manifest before 7 yrs old
  • E) Communication difficulties
A
  1. True
  2. True
  3. False
  4. True
  5. False
32
Q

True or False: The following are known pathological factors associated with autism:

  1. A) Genetic factors
  2. B) Poor parenting skills
  3. C) ‘Theory of Mind’ deficits
  4. D) MMR vaccination
  5. E) Tuberous Sclerosis
A
  1. True
  2. False
  3. True
  4. False
  5. True

Mental health edited (53 decks)

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