Exam 3 - ADHD

Question 1

What is the most frequently diagnosed childhood disorder?

Answer 1

ADHD

Question 2

What is the (Approx) prevalence of ADHD ?

What is the gender ratio? AND What is the mean age of onset?

Answer 2

prevalence: 4-7%
gender: M:F 3:1
mean onset: 3-7 years - but features are usually apparent earlier in life.

Question 3

Why might the Dx of ADHD be delayed despite signs in early life?

Answer 3

Prior to 3-7, the ADHD behaviour may be mistake for normal toddler variability. Around age 3-7 there is more opportunity for comparisons with non-ADHD children, and thus the ADHD symptoms are more obvious and cannot be discounted by reference to toddler behavioural variability.

Question 4

What is the primary aetiology of ADHD?

What else may contribute to the aertiology of ADHD?

Answer 4

Primarily genetic (~76% variance) [twin studies 92% monozygotic and 33% dizygotic

Environmental influences

Most likely interactions between both.

Question 5

Describe the environment aetiologies/contributors to ADHD?

What is there consistent empirical evidence for? inconsistent evidence for? no empirical evidence for?

Answer 5

Consistent empirical evidence:

• prenatal tobacco exposure
• prematurity and low birth weight, birth complications
• zinc deficiency (emerging evidence; requires more studies)

Inconsistent/conflicting empirical evidence:

• prenatal alcohol exposure
• refined sugar
• iron deficiency
• food additive
• deficiency in essential fatty acids (omega3/6)

No empirical evidence
- food sensitivity (e.g., specific intolerance, allergy - e.g., gluten)

Question 6

Neurobiology of ADHD?

i.e., brain areas affected
and

Answer 6

• decreased volume of frontal lobe, striatum (caudate, putamen & globus pallidus) and cerebellum.
• [other studies] frontal white matter and increased grey matter in posterior temporal and inferior parietal cortices.
• hypoperfusion in frontal-striatal region of the prefrontal cortex whilst performing executive tasks. Perfusion increases when child is treated with methylphenidate (i.e., Ritalin)
• fMRI - reduced global activation, reduced local activation in basal ganglia and anterior frontal lobe

Precise mechanism affects activation in these areas - precise mechanism yet to be specified.

Question 7

Neurotransmitters in ADHD and how ritalin (Methyphenidate might help!)

Answer 7

The exact action of stimulants in ADHD is unknown (Krull, 2014). There are two proposed mechanisms. Catecholamine metabolism and neurobiological mechanism.

CATECHOLAMINE
It has been suggest that ADHD is due to an imbalance between norephinerphrine and dopamine in the prefrontal cortex. Kids with ADHD found to have increased dopamine transporter density meaning that dopamine is removed too quickly from the synapses; reduced inhibitory dopaminergic activity results in increased norepinephrine activity (modualtes higher-cog functions and flight/flight system). Treatment with Methylphenidate (ritalin) (ritalin) increases extracellular dopamine in the brain

NEUROBIOLOGICAL

• ADHD represents a functional hypoperfusion in frontal lobes (due to structural or biochemical changes in prefrontal cortex, subcortical regions and cerebellum)
• Stimulant meds increase blood flow to prefrontal cortex, and decrease blood flow to motor cortex and primary sensory cortex
• CLINICALLY - seen as less distractable and decreased motor activity.

ADDITIONAL DETAILS

[reduced dorsolateral prefrontal cortex activity = difficulties with working memory, problem solving, self-monitoring, planning, cognitive flexibility, organisation of information
Reduced orbital prefrontal cortex activity - difficulties with response inhibition and regulation of emotions.]

—Catecholamine metabolism

• Most abundant catecholamines: epinephrine, norepinephrine, dopamine (all neurotransmitters)
• noradrenergic system involved in modulation of higher cortical functions including attention, alertness, vigilance, “fight/flight”
• Animal models suggest that an imbalence between norepinephrine & dopamine systems in prefrontal cortex contributes to pathogenesis of ADHD (reduce inhibitory dopaminergic activity & increased norepinephrine activity)
• findings in human studies showing pts with ADHD have an increase in dopamine transported density (dopamine is cleared from synapse too quickly)
• Methylphenidate (ritalin) increases extracellular dopamine in the brain

Question 8

outline the diagnostic criteria of ADHD (DSM-5) (not specific symptoms, just the main criteria)

Answer 8

• 6 or more symptoms of hyperactivity/impulsitivity and/or inattention (adolescents and greater than 17 years require only 5 symptoms); persisting for at least 6 months. Several symptoms were present before age 12. and several symptoms must be observable in at least 2 settings.
• Clearly interferes with, or reduces, quality of social/occupational/academic function.
• Hyper/impulse symptoms cannot be account for by mood, psychotic or other disorder
• Inattentive symptoms are not due to oppositional behaviour, defiance, hostility or failure to understand tasks or instructions.

Question 9

Give some examples of hyperactive/impulsive symptoms of ADHD?

Answer 9

HYPERACTIVE
•often fidgets, squirms in seat
• often leaves seat when seating expected
• often runs about, climbs in situations where
inappropriate (adolescents: restlessness)
• often unable to play or engage in leisure activities
quietly
• often “on the go” as if “driven by a motor” (e.g.,
difficulty being still, hard to keep up with)
• often talks excessively

IMPULSIVE
• often blurts out answers
• often has difficulty awaiting turn
• often interrupts or intrudes on others (e.g., butts
into games/activities, starts using other people’s
things without permission, may “take over”)

Question 10

Describe some inattentive symptoms of ADHD

Answer 10

•Often fails to give close attention to details, makes careless errors (e.g., overlooks or misses details, work is inaccurate)
• often has difficulty sustaining attention in tasks or play activities
• often does not seem to listen when spoken to directly (e.g., mind seems elsewhere, even in absence of any obvious distraction)
• Often does not follow through on instructions and fails to finish
schoolwork, chores (e.g., starts tasks but quickly loses focus and is easily sidetracked)
• Often has difficulty organising tasks (e.g., difficulty managing
sequential tasks, keeping materials & belongings in order,
messy/disorganised work, poor time management)
• Often avoids, dislikes or is reluctant to engage in tasks that
require sustained mental effort (e.g., schoolwork or homework)
• Often loses things necessary for tasks or activities
• Often easily distracted by extraneous stimuli (for older
adolescents: may include unrelated thoughts)
• Often forgetful in daily activities (e.g., doing chores, running errands)

Question 11

What criteria would exclude ADHD?

Answer 11

• Secondary ADHD (secondary to TBI or epilepsy etc)
• Other disorders that share ADHD features: int disability, learning disability, oppositional behaviour, under-stimulation, or be better explained by anxiety, bipolar or ASD.
• Pediatrician and psychologist should work to exclude underlying medical or psychological factors for symptoms (e.g., sleep disturbance, anxiety, bipolar, psychotic disorder, medication-related).

Question 12

How likely are comorbid disorder in ADHD?

Answer 12

80-90% presence of comorbid disorder

67% have 2 comorbid disorders

Hyperactive type more likely to have externalizing behaviour problems

Question 13

What is the most common comorbid disorder?

Answer 13

• Most common comorbid disorder is oppositional defiant disorder (~30-50%)

[DETAILS]
OPPOSITIONAL DEFIANT DISORDER - recurrent pattern of angry/irritable mood, argumentative/defiant behaviour, or vindictiveness.
Aproxx 30-50% comorbidity

CONDUCT DISORDER - repetitive and persistent pattern of behaviour in which basic rights of others or major societal rules are violated.
Approx 25% comorbidity.

Question 14

Comment on the prognosis of ADHD - what happens with symptoms with age?

What factors predict function in adolescents?

Answer 14

Age-dependent decline of symptoms of ADHD. Between 1/3 - 2/3 of children with ADHD will contine to manifest symptoms in adulthood (consensus ~50%).

DSM-5 states 2.5% prevalence in adults; compared to 4-7% in children.

Adolescence functioning predicted by

• initial clinical presentation (including severity of symptoms, comorbid conduct problems)
• intellect
• social advantage
• strength of ADHD response to any mode of treatment

Question 15

Outline the neuropsychological profile of ADHD. (Overall and general deficits on testing)

Answer 15

• Research broadly suggests executive dysfunction (in line with frontal dysfunction) - but not ALL executive tests.
• Also deficits on Attention and processing speed.
• Inconsistent performance (high variability) in IQ, due to fluctuating attention.
• Difficulty with independent retrieval of information form memory (this is a frontal function) –> reasonable immediate recall, poorer delayed recall, intact recog
• Poor immediate memory span in contrast to good recall after repeated presentations

Question 16

What are some areas of executive dysfunction that kids with ADHD have been shown to have difficulty with?

Answer 16

• response inhibition
• initiation
• working memory
• planning & organisational skills
• independent goal-directed activity
• self-monitoring
• mental flexibility
• emotional regulation
• selective attention
• sustained attention
• speed of processing

Question 17

Outline deficits in attention in ADHD?

What other factors might contribute to impaired attention (other than ADHD directly)?

Answer 17

• Main impairments in attention in ADHD are
– Sustained attention (both types)
– Selective attention (especially inattentive type)

• Other factors causing impaired attention:
– Sleep disorders
– Learning disorders
– Anxiety
– Depression (& other mood
disorders)
– Seizures
– Hunger
– Hearing/vision impairments
– Family conflict/crisis e.g, parental separation, bereavement

Question 18

What cognitive domains should be assessed in a neuropsychological assessment?

Answer 18

• Intellectual functioning (WISC-IV, DAS)
• Academic achievement (WIAT-IV, WRAT-3, Neale)
• Attention (CPT, TeaCh, Stroop)
• Working Memory (Digit Span, LNS(?), AWM)
• Immediate Memory span (Digits fwd, trial 1 of verbal
list learning e.g., CAVLT)
• Executive (D-KEFS, TOL, Rey figure, Trails, WCST)
• Speed of processing (Coding, Trails A)
• Learning & Memory (CMS, WRAML2, CAVLT, NEPSY)

• As well as the psychometric data, you need:
• Parent & teacher questionnaires
• Conners Rating Scale- Long Form / CBCL
• Behaviour Rating Inventory of Executive Function
• Detailed history
• Behavioural observations

Question 19

How can ADHD affect academic outcomes?

Answer 19

• Overall, significantly lower scores on literacy and
numeracy tests
• Executive deficits impact on general learning in
classroom, e.g., working memory (next slide)
• More likely to be suspended/expelled, repeat a
grade, special education placement
• 4 to 5 times more likely to use specialised
education services

Question 20

How might working memory impact a child in the classroom?

Answer 20

• Typical classroom tasks relying on working
memory:
– Carrying out multi-step activities (e.g., maths)
– Following complex instructions
– Keeping track of work
– Remembering/following rules & routines
– Reading comprehension (books, texts, written
instructions, written questions)
– Decoding new words (by breaking into
components)

Question 21

How might ADHD affect social outcomes?

Answer 21

• Executive deficits impact on social functioning
• Behaviours immediately apparent to new age peers
• Impaired social outcomes usually evident early on.
• Less well-liked, fewer dyad friendships
• Less than 1% rated as ‘popular’ status
• Irrespective of gender or age
• Attributed to ADHD and not
comorbid disorder
• Social & academic problems
contribute to low self-esteem.

Question 22

Why conduct a neuropsychological assessment for ADHD?

Answer 22

• Establish individual pattern of cognitive strengths &
weaknesses
– Explain & predict areas of academic and/or behavioural difficulty

• Establish baseline level of cognitive functioning
– For comparisons with future assessments to monitor cognitive
development & track efficacy of interventions

• Standardised questionnaires aid with diagnosis
– Less subjective than observation alone
– Standardised measures enable direct comparison across settings and
across different times

• Guide interventions
—Targeted strategies for both school and home based on pattern of
cognitive deficits & building on personal strengths

Question 23

What are some interventions for ADHD? what is the best choice?

Answer 23

• Psychosocial treatments for home & school (social
skills training, behaviour management)
• Environmental strategies (e.g., modified learning
environment, educational support)
• Stimulant medication
• Best outcome is a combination of above

• Preschool (4-5 years): parent and/or teacher behaviour therapy, Ritalin in severe cases (risk analysis required;
amphetamines not recommended)

• Primary school (6-11 years): medication (stimulants)
+ behaviour therapy combination (treatment must
include school environment)
• Secondary school/adolescents (12-18years): medication definitely, + behaviour therapy may be prescribed; “preferably both”

Question 24

What are some DISCREDITED TREATMENTS of ADHD?

Answer 24

• Diet supplements with essential fatty acids
(eg fish oil)
• Chiropractic treatment
• Behavioural optometry
• Neurofeedback
• Homeopathy
• Acupuncture
• Physical activity
• Massage
• Sensory integration therapies

Question 25

What are some behavioural and environmental interventions that can be implemented at school?

Answer 25

• Small class size, seat child near front/teacher
• Clear and consistent rules and expectations, ,
rehearsing rules for that environment
• Structure and routine
• Remove distracting stimuli e.g., cluttered desk
• Repetition of task instructions & redirection
• Increase physical activity, esp hyperactive children
• social skills training
• Novel & stimulating tasks
• Frequent shifts in tasks, incorporate breaks
• simplifying tasks
• assistance to complete tasks on time (eg. Timer)
• Generally less effective than stimulants in reducing
core symptoms (such as processing speed, impulse
inhibition, hypermotor activity)

Question 26

What are some parent training/parent based/home based interventions for ADHD?

Answer 26

• Focuses on:
• Establishing a routine
• Calm, consistent discipline
strategies
• Teaching parents to notice and
praise/reward good behaviours
• Reward system e.g., token economy /
star chart
• Clear, consistent consequences for behaviour
• Time out
• “positive parenting” principles
• Children with additional behaviour problems
and/or severe symptoms that may endanger
themselves or others require specialised input
from clinical psychologists and/or psychiatrists

Question 27

Describe the effectiveness of ritalin

Answer 27

• Ritalin- 77% success
• Dexamphetamine 74% success
• Work across all age groups
• Take effect within 20-30 mins, with peak clinical effect
1-2 hours after administration, effects last 2-5 hours
• Effects less apparent after 3 years
• Behavioural effects
• increased attention span & concentration
• Increased productivity
• reduced impulsivity
• increased task-focused activity
• reduced aggressiveness
• improved handwriting and fine motor skill
• improved peer relations & social status???

SIDE EFFECTS
• insomnia & reduced appetite (both common)
• headaches & stomach aches (transient)
• prone to crying
• Tics (rare – 1-2%)
• Mild to moderate weight loss associated with
reduced appetite
• Lower seizure threshold (minimal at therapeutic
doses)
• Stunted growth by 1-2cm with more than 3 years
of high dose, no rebound effect with cessation of
medication

Myths
• leads to aggressive/assaultive behaviour
• tics and Tourette’s is common
• sedates children
• addictive
• increased risk of later substance abuse

Truth:
– the prescribing rate for stimulant medications
has soared in the US from 600,000 children in
1990 to 3.5 million in 2013
(source: USA Centres for Disease Prevention and Control, 2013)

Question 28

Comment on the ADHD ‘epidemic’

Answer 28

The disorder is now the second most frequent long-term diagnosis made in children, narrowly trailing asthma, according to a recent New York Times analysis of C.D.C data.

• increased profits for ADHD drug companies
• ADHD drugs marketed as a benign solution to ‘symptoms’ of ADHD (even if not full ADHD).
• Health professionals feel pressured into making a diagnosis of ADHD in a child who is struggling at school (often with LD) who had a behavioural issue in order to legitimise a trial of stimulant medication.
• Many parents will ‘shop’ around for an ADHD-friendly health proffessional in order to obtain a ‘quick fix’

NEVERTHELESS - ADHD is a legitimate disorder of ~5% of children.

• impacts sig on day-to-day academic and social functioning
• has high-rates of comorbidity
• requires comprehensive assessment
• persists into adulthood, though symptoms typically reduce in number and severity
• is often helped by stimulant medication
• has generated many myths, misconceptions and sensationalistic journalism; SO treat information with caution.

Question 29

How can we as health professionals counter the ADHD ‘epidemic’

Answer 29

• Need to be careful how Dx is phrased e.g., “having a few symptoms” may be interpreted as a diagnosis of mild ADHD - which is INCORRECT as DSM-5 clearly defines mild-ADHD as still having all the criteria with ADHD.

• We have a responsibility as neuropsychologists to be able to
accurately diagnose and differentiate ADHD from other
disorders; and to accurately identify comorbid disorders so
that children can receive appropriate medical, psychological
and/or educational intervention.
• If not sure: refer on (e.g., to Clinical Psychologist)