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MD4001 Week 7 > 1. ADHD and autism > Flashcards

1. ADHD and autism Flashcards

1
Q

ADHD?

A

Attention Deficit Hyperactivity disorder

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2
Q

What are the co-occuring disorders of ADHD?

A 
Emotional and Behavioural disorders
Learning difficulties: reading/writing disorder, asperger's
Tourette’s Syndrome: Tic
Sleep problems
Oppositional defiant disorder (ODD)
Developmental co-ordination disorder
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3
Q

What is ASD?

A

What is autism spectrum disorder

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4
Q

What defines ASD?

A
  • Marked genetic predisposition, and a wide range of aetiologies
  • Marked phenotypical heterogeneity
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5
Q

Co-occuring problems/disorders of ASD?

A

e.g. :-
•Learning Disability •Epilepsy
•ADHD (!)
•Sleep Disorders •Motor Difficulties •Sensory sensitivities

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6
Q

Definition of ADHD?

A

Developmentally inappropriate hyperactivity, Impulsivity, and/or inattention, leading to impairment in social, behavioural and/or academic function

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7
Q

Subtypes of ADHD

A
  • Hyperactive/impulsive •Inattentive

* “Combined”

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8
Q

Classic inattention symptoms on ADHD

A 
Does not attend
Fails to finish tasks
Can’t organise
Avoids sustained effort
Loses things, ‘forgetful’
Easily distracted
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9
Q

Classic hyperactivity symptoms on ADHD

A 
Fidgets
Leaves seat in class
Runs/climbs excessively
Cannot play/work quietly
Always ‘on the go’
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10
Q

Classic inattention symptoms on impulsivity

A 
Talks excessively 
Blurts out answers 
Cannot await turn 
Interrupts others 
Intrudes on others
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11
Q

What is meant by Tic disorder?

A

Tics are defined as repeated, sudden, rapid, nonrhythmic muscle movements including sounds or vocalizations. Tourette syndrome is diagnosed when people have had both motor and vocal tics for > 1 yr.

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12
Q

What is the course of ADHD in the psychosocial impairments?

Hint:
Symptoms domains + psychiatric comorbities -> Functional impairments (Self, school/work, home, social)

A 
Symptom domains 
 Inattention
 Hyperactivity
 Impulsivity
 \+
Psychiatric comorbidities 
  Disruptive behavioural disorders (conduct disorder and oppositional defiant disorder)
 Anxiety and mood disorders
----> Functional impairments
Self:
 Low self-esteem
 Accidents and injuries
 Smoking/ substance abuse 
 Delinquency

School/ work:
 Academic difficulties/
underachievement
 Employment difficulties

Home:
 Family stress
 Parenting difficulties

Social:
 Poor peer relationships
 Socialisation deficit
 Relationship difficulties

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13
Q

Prevalence of ADHD

A

•The Global prevalence is around 5%

•“Administrative prevalence” in Scotland average is 0.5% (i.e. Underdiagnosed * )
Of those diagnosed… Hyperactive/impulsive c. 15% of total
Inattentive c. 20-30%
“Severe-Combined” c.75%

Male/female ratio c. 3:1 in population studies and c. 10:1 in clinics!

•Increased prevalence is associated with lower socioeconomic status.

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14
Q

Genetic cause of ADHD?

A

Core symptoms are highly heritable. 75% mean heritability

(Evidence: from Family, adoption, twin studies.)

ADHD is associated with widely distributed markers e.g. at chromosomes 4, 5, 6, 8, 11, 16, and 17.
Analysis shows linkage with various dopamine receptor and transporter
genes, serotonin transport genes and others the role of which is unclear

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15
Q

Contribution factors to ADHD causation?
Anti/peri natal….
Postnatal…

A

Ante/peri-natal:-
•Pre-term delivery.
•Smoking
•Alcohol. (Note Fetal alcohol spectrum disorders and potential role of epigenetic
effects (**) plus the quantity, frequency, and timing of alcohol exposure) •Maternal stress
Intrapartum asphyxia

Postnatal:-
•Brain trauma
•Epilepsy •Deprivation/attachment

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16
Q

Pathophysiology of ADHD

at which structures of the anterior/posterior attentional pathways and in the cortex?

A

“Anterior attentional pathways” :
•Frontal Lobes
•Cingulate Gyrus
•Basal ganglia ( “Corpus striatum”, particularly the caudate nucleus)

“Posterior attentional pathways” :
•Locus Caeruleus
•Cerebellum

Cortex:
Ventral prefrontal cortex
Premotor cortex
Anterior cingulate gyrus
Dorsolateral prefrontal cortex (DLPFC)
Orbitofrontal cortex (OFC)
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17
Q

What is the evidence based via imaging, neuropharmacology and neuropsychology to support disordered frontal lobe function and altered Dop and NA flux in ADHD?

A

IMAGING
•Volumetric CT and MRI studies – reduced volume of key structures
•Pet scanning, SPECT scanning Functional MRI – reduced activation of key brain areas,
particularly frontostriatal pathways

NEUROPHARMACOLOGY
•Improvement in core ADHD symptoms in response to medications which modify the release and reuptake of key neurotransmitters (Dopamine and Noradrenaline), which are region specific for key brain pathways concerned with self regulation and attention.

NEUROPSYCHOLOGY
•Identifiable alterations and deficiencies in frontal lobe mediated functions such as working memory, executive function, focus, distractibility.

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18
Q

Key structures of basal ganglia involved in ADHD?

A

Globus pallidus
Caudate nucleus
Putamen

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19
Q

What makes up the dopamine pathways relevant to ADHD?

A
  1. Reward system (mesolimbic pathway)
    - From ventral tegmental area and nucleus accumbens
  2. Control of cerebral motor output (nigostriatal pathways)
    - From substantia nigra
    - To the GP, Striatum (putamnen + caudate nucleus)
    - To nucleus accumbens
  3. Tuberoinfundibular
  4. Mesocortical pathways
    o This tract is made up of dopaminergic neurons that project from the ventral tegmental area to the prefrontal cortex.
    Relevant to the physiology of:
    o Cognition and executive function @ dorsolateral prefrontal cortex
    o Emotions and affect @ ventromedial prefrontal cortex
20
Q

What are the NA pathways relevant to ADHD?

A 
Release from the pons
--> 
To cerebellum
Thalamus
Hippocampus
Amygdala
Hypothalamus
Neocortex
Spinal cord
21
Q

Anterior cingulate gyrus links what structures…

A

Frontal cortex and amygdala

22
Q

Which loop of the basal ganglia concerns ADHD?

A

Executive loop
i.e.

Dorsolateral prefrontal cortex 
--> Dorsolateral caudate nucleus 
-->GPi
--> Medial dorsal and ventral anterior nuclei
(then loops back to start)
23
Q

• ADHD linked to malfunctioning _______ cortex
• Classic symptoms associated with specific prefrontal regions
– _______ = orbital frontal cortex
– Hyperactivity = prefrontal motor cortex
– Inattention = dorsal anterior _______ and dorsolateral prefrontal
• Specific regional cortico-striatal-______ circuit disruption contributes to specific ADHD symptoms

A

• ADHD linked to malfunctioning prefrontal cortex
• Classic symptoms associated with specific prefrontal regions
– Impulsivity = orbital frontal cortex
– Hyperactivity = prefrontal motor cortex
– Inattention = dorsal anterior cingulate and dorsolateral prefrontal
• Specific regional cortico-striatal-thalamic circuit disruption contributes to specific ADHD symptoms

24
Q

Describe the neurochemistry and disturbed networks in ADHD patients?

A

Anterior attention system:
@ Prefrontal cortex **
@ Anterior cingulate gyrus
Dopamine selectively controls inputs to anterior attention system via D1 receptors inhibition of excitatory NMDA inputs

Posterior attention system:
@ Posterior parietal cortex
@ Pulvinar nucleus of thalamus
@ Superior colliculus
NA enhances the signal-to-noise ratio of target cells by inhibiting basal neuronal firing
25
Q

Role of Dopamine and Norepinephrine (Noradrenaline) in Information Processing

A
  • Optimum information processing requires distinguishing signals from noise
  • DA and NE tune the prefrontal cortex to make information processing more efficient
  • Too much DA or NE input can be as disruptive as too little input in regulating cortical information processing
26
Q

Examples of how ADHD persists into adulthood

A

School failure, underachievement —> Job failure, under- employment

Multiple injuries —-> Fatal car wrecks, risk taking, accidental injuries

27
Q

Definition of Autism spectrum disorders?

A

Highly variable and heterogeneous condition, with a wide range of aetiologies and phenotypes

28
Q

What are the Triad of impairments of ASD?

A
  • Social communication
  • Social interaction
  • Social “imagination”
29
Q

What are the 3 social communication impairments of ASD?

A
  1. Difficulties in verbal and non verbal communication e.g appropriate use of…
    - eye contact
    - facial expression
    - gesture
    - prosody (rhythm and tone of speech)
  2. Reciprocal aspects of communication e.g.
    - initiating and turn taking in conversation
    - negotiating a shared topics
    - topic maintenance
    - readily recognising what the listener knows.
  3. Those with good language skills may interpret language in a literal manner, and may struggle to understand idiom, metaphor or sarcasm.
30
Q

What are the 5 social “imagination” impairments of ASD?

A

1Difficulties with thinking and behaviour

  1. Poor imaginative skills may lead to restricted repetitive, stereotyped patterns of behaviour.
  2. Lack of a capacity to appreciate and integrate the “bigger picture” (central coherence).
  3. Interests tend to be circumscribed and intense, often not reflecting cultural norms.
  4. A preoccupation with routine and structure is also common.
31
Q

What are the social interaction impairments of ASD?

A
  1. Social development is different, delayed or atypical with interaction difficulties
  2. Struggle with reciprocity, shown by lack of empathy or failure to adapt their behaviour according to others perspectives and social context.
32
Q

Prevalence of ADS

A

At least 1% of children have ASD; some studies report a prevalence of around 2%.
•Around 50% or more children with ASD have an intellectual disability (Baird et al. 2006

33
Q

Aetiology of ASD

A

Highly heritable
10% sibling recurrence
Twin studies show high concordance
Male:female 4:1

In a minority of cases (approximately 10%) ASD occurs in association with cytogenetically detectable chromosomal abnormalities and recognised genetic conditions, such as Fragile X Syndrome, Tuberous Sclerosis, Down’s syndrome, and Angelman’s Syndrome.

34
Q

Clinical signs of ASD

A

Tuberous schlerosis
Brain tumours –> Seizures
Angelmans syndrome (maternal allele deletion)
Fragile X syndrome from males (big ears and testes*)

35
Q

S/S of fragile x syndrome?

A 
Long ears
long face
delayed speech
large testes
hyperactive
tactile defensiveness
gross motor delay
austic-like behaviour
36
Q

Clinically important other considerations in ASD

A
  1. Association with Childhood Onset Epilepsy *
    - Brain disorder
    - EEG is WILD
  2. Prevalence of Sleep Disorders**
    - 6/10 on spectrum don’t sleep
    - Melatonin treatment
  3. Altered Motor Function***
    - Low tone
    - Low co-ordination
    - Repetitive action
    - Ataxia
  4. Altered Sensory Function**
    - Hypo/hyper responsiveness
    - Some stimuli can be upsetting
    - Can affect vision, smell, taste, hearing, vestibular/ proprioceptive function and kinaesthetic sensitivity.
37
Q

Pathophysiology of ASD

A

•Total brain volume enlarged in early infancy in 90% (subsequently slows) ALWAYS MEASURE HEAD SIZE
•Macrocephaly (Occiptofrontal circumference >97th centile) - 20% cases overall
•Histology – reduced size and distortion of neurones and intrinsic neuronal connectivity e.g. Purkinje cells of cerebellum, neurones in fusiform gyrus.
•Widespread reduction in white matter volume and connectivity, - demonstrated by MRI , Diffusion tensor imaging, Functional MRI, - described as “global extrinsic hypoconnectivity”
PUTATIVE LINKS BEWEEN BRAIN REGIONS AND ASD RELATED SEQUELAE?

38
Q 
In ASD for the following what is the dysfunction...
Brain region: Frontal
Putative area:
Prefrontal
Inferior frontal
Primary motor
Orbitofrontal
A

Dysfunction:
Prefrontal **: Executive function, attention, working memory

Inf frontal: Expressive language
Primary motor: Motor skills
Orbitotemporal: Repetitive ritualistic behaviours

39
Q 
In ASD for the following what is the dysfunction...
Brain region: Temporal
Putative area:
Sup temporal
Fusiform gyrus
Hippocampus
A

Dysfunction…
Sup temporal: Auditory processing ; language comprehension
Fusiform gyrus: Facial recognition
Hippocampus: Short term memory ; verbal/spatial learning

40
Q

In ASD for the following what is the dysfunction…
Brain region: Parietal
Putative area: Post-central gyrus

A

Dysfunction:

Somatosensory perception ; body image, spatial perception

41
Q

In ASD for the following what is the dysfunction…Brain region: Insula
Putative area:
Insula cortex

A

Dysfunction: Pain, smell, taste and autonomic perceptions

42
Q 
In ASD for the following what is the dysfunction...
Brain region: Limbic system
Putative area:
Cingulate gyrus
Amygdala/hypothalamus
A

Dysfunction..
Cingulate gyrus: Emotion ; fear
Amygdala/hypothalamus: Affect ; aggression

43
Q

In ASD for the following what is the dysfunction…
Brain region: Cerebellum
Putative area:
Vermis and hemispheres

A

Dysfunction…
Vermis: Balance, gait, motor co-ordination
Hemispheres: Learning, language, cognition

44
Q

In ASD for the following what is the dysfunction..
Brain region: Occipital
Putative area: Visual cortex

A

Dysfunction in vision

45
Q

However, A single “neurological” explanation
for the presenting signs of ASD is not yet possible.

Suggested deficits in psychological processing and function have included:-

A

1.Impairments in frontal lobe mediated “executive functioning” and working memory .
(difficulties with problem solving and forward planning in order to achieve a goal)
2.Deficiencies in “theory of mind”
(difficulties in the consideration of how other people might think and
react to a particular situation)
3.Problems in achieving “central coherence”
(the failure to integrate information into meaningful wholes)

46
Q

ASD Postscript/Resume:
•_____ heritable and now well recognised neurodevelopmental disorder
•Brain abnormalities described but no unitary explanation for core symptoms
•Lifelong disability with prognosis dependant on coexisting ______ impairment
•Strong capacity to engender ______ and secondary psychiatric morbidity
•Wide variability in phenotypical _______
•Important associations with disorders including sleep disruption, epilepsy, motor and sensory problems
•ASD and ADHD used to be mutually exclusive diagnoses but it is now recognised you can have both!

A

ASD Postscript/Resume
•Highly heritable and now well recognised neurodevelopmental disorder
•Brain abnormalities described but no unitary explanation for core symptoms
•Lifelong disability with prognosis dependant on coexisting cognitive impairment
•Strong capacity to engender anxiety and secondary psychiatric morbidity
•Wide variability in phenotypical expression
•Important associations with disorders including sleep disruption, epilepsy, motor and sensory problems
•ASD and ADHD used to be mutually exclusive diagnoses but it is now recognised you can have both!

MD4001 Week 7 (8 decks)

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