ADHD Flashcards

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1
Q

Prevalence of ADHD in children

A

Prevalence of ADHD in children
Not enough child psychiatrists to diagnose and treat ADHD

As a group these children have well-known risk factors and show abnormal neuro-psychological functioning and neurobiological correlates

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2
Q

History

A

Der Struwwelpeter, an illustrated book portraying children misbehaving (“Impulsive Insanity/Defective Inhibition”) by Heinrich Hoffman (1854).

ADHD has long been described in the medical literature. Heinrich Hoffmann (1809-1894), a German psychiatrist, was the first to describe children whose behavior was marked by impulsivity and hyperactivity. He named this behavioral problem “impulsive insanity” or “defective inhibition”.

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3
Q

History

A
1902 Lancet article
1920’s “minimal brain damage”
1930’s “hyperkinetische Erkrankung”
1960’s “minimal brain dysfunction”
1937 Benzedrine discovered
Hyperkinetic Syndrome of Childhood” in ICD-9
1980 inattention recognized
DSM-III Attention-Deficit Disorder with or without Hyperactivity
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4
Q

ADHD

A

common in all cultures

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5
Q

ADHD can be serious:

A

untreated it can lead to educational failure, accidents and unfair harsh punishments that may worsen the behaviour and outcome.

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6
Q

Severe ADHD can persist into adulthood with risk of :

A

marriage breakdowns, unemployment, accidents, other psychiatric disorders

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7
Q

ADHD is stigmatizing:

A

Patients or their families may be blamed for the behaviours, suffering social exclusion

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8
Q

ADHD is treatable with:

A

several evidence based treatments

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9
Q

Core Symptoms

A

Inattention, hyperactivity, impulsivity
Present in more than one context
Leading to functional impairment

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10
Q

Subtypes in DSM

A

Combined subtype
Predominantly hyperactive
Predominantly inattentive

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11
Q

Changes to ADHD Dx in DSM-V

A

Symptoms must be present < 12 years old
(not 7 years old)

Adult symptoms similar to child symptoms, but lower threshold
(e.g. 5+ symptoms needed, not 6+)

No exclusion criteria for autism spectrum disorders, now considering ADHD as a co-morbid disorder

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12
Q

Prevalence

A

6% for children
3% for adolescents

Male > Female

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13
Q

Clinical Pictures Across Ages

Pre-school:

A

play < 3minutes, not listening “whirlwind”, no sense of danger

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14
Q

Clinical Pictures Across Ages

Primary school:

A

activities < 10minutes, forgetful, distracted, restless, intrusive, disruptive

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15
Q

Clinical Pictures Across Ages

Adolescence:

A

attention< 30 mins, no focus/planning, fidgety, reckless

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16
Q

Clinical Pictures Across Ages

Adults:

A

incomplete details, restless, forgetful, impatient, accidents

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17
Q

Associations with Durability of Symptoms

A
Lower academic achievement
Marital problems and dissatisfaction
Divorce
Difficulties dealing with offspring
Lower job performance
Unemployment
Employment below potential
Traffic accidents
Other psychiatric disorders
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18
Q

Etiology & Risk Factors

A

Strong genetic component (76%)

Perinatal factors – some evidence

Neurobiological deficits – growing evidence

Deprivation and family factors – important for course and outcome (maybe not causation)

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19
Q

Neurobiology

A

Frontal-striatal dysfunction
mediated by GABA
modulated by catecholamines
(DA, NE)

Catecholaminergic dysregulation

Delay in cortical maturation

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20
Q

Associated Features

A
Defiant, aggressive antisocial behaviors
Problems with social relationships
IQ tends to be lower than in the general population
Specific learning problems
Co-ordination problems
Specific developmental delay
Poor emotional self-regulation
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21
Q

Genetics:

A

proportion of variance attributed to additive genetic factors 76%

Negative results in genome wide association studies and most associated candidate genes only responsible for small increase in risk.

Most genes implied related to catecholaminergic system (DAT 1 – dopamine transporter gene)

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22
Q

Perinatal Factors

A

most evidence for association with prematurity, low birth weight and Intra-uterine tobacco exposure

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23
Q

Neurobiological deficits

A

(slight differences in mean values not brain damage)
Fronto-striatal dysfunction (executive function and inhibitory control)
Catecholaminic dysregulation
Delay in cortical maturation

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24
Q

Deprivation and family factors:

A

implied by epidemiological studies: more common in low SES, institutions etc. but may also be related to course and outcome rather than causation

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25
Q

Popular explanations that students may be confronted with by parents (e.g. through newspaper and internet articles) should be explored and discussed

A

i.g. food allergies (some evidence for some cases) computer games (no evidence) environmental toxins (inconclusive) but also any other culturally relevant explanatory models

26
Q

Comorbid Disorders in Brazilian Community Samples

A

Children with ADHD often suffer from other psychiatric conditions; systematic screening for the presence of other mental disorders is essential. Figure D.1.4 shows the prevalence of comorbid disorders in two Brazilian cohorts of children with ADHD; oppositional defiant disorder, anxiety disorders, conduct disorders and depression are among the most frequent (Souza et al, 2004).

27
Q

Oppositional Defiant Disorder

A

Three categories of symptoms

Includes both emotional & behavioral symptomatology – 6 months

No longer exclusion criteria for conduct disorder

28
Q

Three categories of symptoms

A

Angry/irritable mood
Argumentative/defiant behavior
Vindictiveness

29
Q

Angry/Irritable Mood

A

Often loses temper.
Is often touchy or easily annoyed.
Is often angry and resentful.

30
Q

Argumentative/Defiant Behavior

A

Often argues with authority figures or, for children and adolescents, with adults.
Often actively defies or refuses to comply with requests from authority figures or with rules.
Often deliberately annoys others.
Often blames others for his or her mistakes or misbehavior.

31
Q

Vindictiveness

A

Has been spiteful or vindictive at least twice within the past 6 months.

32
Q

Oppositional Defiant Disorder

A

A pattern of angry/irritable mood, argumentative/defiant behavior, or vindictiveness lasting at least 6 months as evidenced by at least four symptoms from any of the following categories, and exhibited during interaction with at least one individual who is not a sibling.

33
Q

Specify current severity:

A

Mild: Symptoms are confined to only one setting (e.g., at home, at school, at work, with peers).
Moderate: Some symptoms are present in at least two settings.
Severe: Some symptoms are present in three or more settings.

34
Q

ADHD Clinical Presentation & Diagnosis

A
Inattention 
Hyperactivity
Impulsivity
Pervasive symptoms 
Duration/age of onset
Impairment or distress
35
Q

Inattention:

A

Distractibility, forgetfulness, inability to finish what they start etc.

36
Q

Hyperactivity:

A

On the go all the time, restlessness, fidgeting, talking too much, inability to play quietly etc.

37
Q

Impulsivity:

A

Difficulty in delaying gratification, taking turns in play, acting without thinking

38
Q

Pervasive symptoms

A

Symptoms need to be pervasive

need for multiple informants! School!

39
Q

Clinical Assessment

A

Always obtain information from at least two contexts (e.g., home, school)
Perform medical and psychiatric assessment
History, family functioning, parenting style etc.
Patient might be well behaved during the clinical interview
Assess medical and psychiatric DD/co-morbidity
No additional tests necessary for diagnosis.

40
Q

Neuropsychological Testing

A

Only for research use

The majority of neuropsychological tests are copyrighted and expensive, which restricts their use, although specific tests can be of help. Intelligence tests (e.g., Wechsler) can be useful in clarifying intellectual deficits or IQ level and its implications. The Continuous Performance Test (CPT-II), Wisconsin Cart- Sorting test, STROOP test, and “Go/no go” tests are useful for research.

41
Q

Stroop test

A

The stroop test is used to measure attention. It takes advantage of our ability to read words more quickly and automatically than naming colors. The cognitive mechanism involved in this task is called directed attention: one has to manage one’s attention, inhibit or stop one response in order to say or do something else. It is one of the tests that, despite not being diagnostic, provides data about attentional ability.

42
Q

Differential Diagnosis

A
Situational hyperactivity 
Behavioral disorders (ODD/CD)
Emotional disorders
Tics, chorea or other dyskinesias
Misuse of substances
Autism Spectrum Disorder
Intellectual Disability
43
Q

Further Differential Considerations

A
Parental mental health issues
Severe marital discord or recent divorce
Domestic violence
Child abuse or neglect
Severe bullying or exclusion by peers
Severe deprivation or poverty
44
Q

Rating Scales

A

SNAP IV: http://www.adhd.net/snap-iv-form.pdf
SDQ : http://www.sdqinfo.org
SWAN: http://www.adhd.net/SWAN_SCALE.pdf
Vanderbilt: http://www.nichq.org/childrens-health/adhd/resources/vanderbilt-assessment-scales
Many other proprietary (not free) scales

45
Q

Rating Scales

Cont.

A

Not necessary for diagnosis but very useful for monitoring symptoms during treatment

While diagnosis cannot be made on the basis of rating scale data alone, using rating scales is good clinical practice for screening purposes, to measure symptom severity and to monitor response to treatment and outcome. There are numerous rating scales that can be either specific for ADHD or for general psychopathology, most have a child, parent and teacher versions.

46
Q

Aims of Treatment

A

Individually tailored
Reduce symptoms
Improve educational outcomes
Reduce family and school-based problems

47
Q

What works?

A

Evidence Based Treatments:
Best evidence for stimulant medication
Behavior treatments also effective in mild to moderate cases
Psycho-education for parents and school

48
Q

Psychosocial Treatments

A

Behavior therapy

Generally effective, but smaller effect size than medication

First line treatment in younger children or milder cases

49
Q

Behavior therapy

A

Individual, not always generalize
Parent management training: particularly useful in younger children and for associated behavior problems
School based: child in front of class, short tasks etc.

50
Q

Stimulant Medications

A
Methylphenidate or Amphetamines
Efficacy and safety well-established 
ES 0.8-1.1; clinical response in 70%
Dose: titrate for optimum response
Short/long acting (sustained release) available
51
Q

Stimulant Medications

cont.

A

Methylphenidate or Amphetamines
Common side effects: nausea, weight loss, insomnia, agitation
More serious side effects: tics, psychotic symptoms, raised blood pressure, growth retardation
Concern raised for risk of sudden cardiac death – raised in 2005, but has not panned out in the bigger studies. No EKG required for cases, but it is reasonable to get one if your history and physical exam suggests one.

52
Q

Atomoxetine (Strattera)

A
Noradrenergic reuptake inhibitor
Can be given once or twice daily
Less pronounced effects on appetite and sleep than stimulants
May have more nausea / sedation
Takes about 6 weeks to work
53
Q

Indications for Atomoxetine

A

Helps with patients with co-morbid anxiety but recommendation is still 1st line stimulant with added SSRI
Consider if active substance abuse problems, co-morbid anxiety or tics, and severe side effects to stimulants

54
Q

Atomoxetine Side Effects

A

Appetite suppression, nausea, sedation
Rare hepatotoxicity
Rare suicidality

55
Q

Meds used Off-label

A

Antidepressants

Alpha-2 agonists

56
Q

Antidepressants

A

Buproprion (Wellbutrin)
Imipramine
Nortriptyline

57
Q

Alpha-2 agonists

A

Clonidine / Kapvay (extended-release)

Guanfacine / Intuniv (extended-release)

58
Q

When to Refer

A

If no response and severe impairment after pharmacological treatment combined with behavioral approaches
Re-evaluate diagnosis and co-morbidity
Check for undetected social adversity or abuse
If still no response after 6 months consult with specialist

59
Q

Clonidine and guanfacine are

A

alpha-2 agonists with demonstrated efficacy in the treatment of ADHD

These medications can also be used for patients with comorbid tic disorders or Tourette’s syndrome, in which its efficacy seems to be higher. There are now long-acting formulations for both clonidine and guanfacine available.

60
Q

Guanfacine

A

is more selective than clonidine causing fewer adverse effects such as somnolence.

61
Q

Tricyclic antidepressants such as

A

imipramine, have also been shown to reduce ADHD symptoms.

Nevertheless tricyclic antidepressants are associated with significant side effects, are less effective than stimulant medications and should be used only after failure to respond to two or three stimulants and
atomoxetine (AAP, 2011).

Tricyclic antidepressants can interfere with cardiac conduction and can cause sudden death; it is important that patients are monitored with electrocardiogram before and during treatment.

62
Q

Bupropion

A

Bupropion is considered a third line treatment for ADHD; it can be tried in case of failure of stimulants, atomoxetine and alpha-2 agonists.

Bupropion lowers seizure threshold in a dose dependent fashion.