ADHD Flashcards

1
Q

what are externalising disorders?

A

 problem behaviours that includes several clinically recognised disorders such as attention-deficit/hyperactivity disorder (ADHD), conduct disorder (CD), and oppositional defiant disorder (ODD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

issue with externalising orders grouping?

A

 By grouping ADHD, CD, and ODD under one label as externalising disorders, the commonalities of these disorders are highlighted, however, some of their important differences are usually de-emphasised (Mullin & Hinshaw, 2007).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what does ADHD stand for?

A

 Attention-deficit/hyperactivity disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is ADHD characterised by

A

pervasive behavioural symptoms of hyperactivity, impulsivity and inattention, beginning in childhood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

rates of ADHD

A

 In the UK it is reported that 8% of children are diagnosed with ADHD (Alloway et al., 2010).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

gender occurance of ADHD

A

 The disorder commonly occurs amongst boys than girls; boys are 6-9% more likely to be diagnosed with ADHD.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

who made the first account of ADHD and what did they call it?

A

= Crichton (1798)
Called it mental restlessness described as “the incapacity of attending with a necessary degree of constancy to any one object”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

DMS-V diagnosis of ADHD changes

A
  • Adults and teenagers can officially be diagnosed
  • Earliest symptoms identified at age 12 years (instead of 7)
  • Subtypes are now referred to as ‘presentations’
  • Mild, moderate and severe levels of ADHD, depending on symptoms
  • Main difference from DSM IV-TR - Can be diagnosed with Autism Spectrum Disorder (ASD)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

different presentations of ADHD

A

Predominantly inattentive presentation- struggle with impulse control
Predominantly hyperactive/impulsive presentation- often unofficially referred to as ADD- have difficulty paying attention
Combined presentation- significant problems in both areas.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

severity of ADHD differences

A
  • Mild: Few, if any, symptoms in excess of those required to make the diagnosis are present, and symptoms result in only minor functional impairments.
  • Moderate: Symptoms or functional impairment between “mild” and “severe” are present.
  • Severe: Many symptoms in excess of those required to make the diagnosis, or several symptoms that are particularly severe, are present, or the symptoms result in marked impairment in social or occupational functioning.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is inattention according to DSM-V

A

Inattention according to DSM-V= things such as ‘often does not listen when spoken to directly’ ‘often has difficulty in organising tasks and activities’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is hyperactivity according to DSM-V

A

Hyperactivity according the DSM-V= things such as ‘often leaves seat in situations when remaining in seat is expected’ ‘often talks excessively’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

who found the following: Found that adolescents with ADHD had a higher percentage of behaviours such as getting distracted easily, not following instructions, fidgets than those without ADHD.

A

Barkley et al., 1990

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are cognitive deficits of ADHD

A

Impairments in all aspects of executive function (Martinussen et al., 2005; Willcutt et al., 2005)
Executive functions are a set of process involved in the strategic and deliberate allocation of attention and response i.e., this allows us to develop goals and plan.

Executive process are ( Diamond, 2001):
• Inhibition
• Working memory
• Cognitive flexibility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

general effects of ADHD

A

cognitive deficits

longitudinal effects–> academic and schooling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

academic impairment and ADHD study

A

Kent et al., 2010- studies male high school students with ADHD- dolescents with ADHD experienced significant academic impairment in high school relative to comparison adolescents, including lower overall and main academic subject grade point averages (GPA), lower levels of class placement (e.g. remedial vs. honors), and higher rates of course failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

school findings in ADHD (not intellectual)

A

Loe and Feldman 2007- ADHD is also associated with increased use of school-based services, increased rates of detention and expulsion, and ultimately with relatively low rates of high school graduation and postsecondary education

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are risk factors of ADHD

A

genetic

neuroatomical:

  • frontal cortex
  • basal ganglia
  • cerebellum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

overall size of brain in ADHD

A

Consistent evidence that the brains of children with ADHD are on average smaller than the brains of healthy comparison children throughout childhood and adolescence (Castellanos et al., 2002; Durston et al., 2002; 2004)
Total brain size in ADHD subjects is approximately 5% smaller than in age and gender matched controls CASTELLANOS et al., 1996

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what does the cortex play a key role in?

A

memory, attention thought and language gradually increases in thickness before reaching a peak during teenage years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what have fMRI scans of the corte revealed

A

Shaw et al., 2007- Cortex- in normal development the cortex- gradually increases in thickness before reaching a peak during teenage years. fMRI scans have shown than in children with ADHD the cortex generally develops more slowly particularly in frontal and temporal lobe regions (important for memory and controlling behaviour).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

PFC size in ADHD

A

More specifically, the prefrontal cortex (PFC) has been shown to be significantly smaller in ADHD children than controls (Castellanos et al., 1996; Durston et al., 2004; Mostofsky et al., 2002) and in their unaffected siblings (Durston et al., 2004).

but effect in siblings shows cant be full cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

differences in symmetry of prefrontal regions in ADHD

A

In normal participants there is normally right greater than left asymmetry of the prefrontal cortex. This asymmetry is reduced in ADHD children due to a significant decrease in right prefrontal regions (Castellanos et al., 1996; Reiss et al., 1996;).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

basal ganglia and ADHD

A

Caudate nucleus and putamen serve as the entry point to the basal ganglia and abnormalities of both structures have been shown in ADHD (Pontius 1973; Hill et al., 2003).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

caudate volume and ADHD

A

otal caudate volume was analysed in a mixed longitudinal design- decreased volumes were detected in the ADHD group but only in ages under 16 (castellanos et al., 2002). Around 16 caudate volume seems to normalize. This may provide an explanation to the diminishment of motoric symptoms in ADHD with increasing age.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

ADHD and brain injury

A

ADHD is the most common psychiatric disorder to develop after brain injury (Max et al., 1997) or stroke (Max et al., 2002) in childhood and its occurrence is correlated with severity of injury (Max et al., 1998). Lesions of the right putamen and posterior ventral putamen have been associated with higher incidence of ADHD (max et al., 2002). Another study followed 99 children from 4-19 yrs who suffered closed head injury over the course of a year. During this time odds of developing secondary development ADHD were 3.6x higher in those with basal ganglia injury (Gerring et al., 2000).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is the role of the basal ganglia

A

Role of basal ganglia primary function is likely to control and regulate activities of the motor and premotor cortical areas so that voluntary movements can be performed smoothly.(Stocco et al., 2010; Doya, 2000). Limbic sector of the basal ganglia includes various components (caudate nucleus, putamen, nucleus accumbens). Considerable evidence that this limbic part plays a central role in reward learning Schultz 2016.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is the cerebellum associated with

A

Associated with coordination of motor movements but also known to be involved with non-motor functions e.g. timing (Allen et al., 1997; Tracy et al., 2000).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

cerebellum in ADHD

A

(Berquin et al., 1998).

Reduced volume by 6% compared to controls (Hill et al., 2003)

30
Q

what are different models of ADHD

A

Executive function account of ADHD- Brown 2001

Behavioural inhibition model- Barkley 1997

Motivationally based accounts of ADHD:

The Dual Pathway Model of AD/HD- Sonuga-Barke 2002/2003

31
Q

what is executive function?

A

Executive functions, then, manage the brain’s cognitive functions; they provide the mechanism for “self-regulation” (Baumeister et al., 2004).
• Executive function is things such as being able to: Manage time, pay attention and Switch focus

32
Q

what does the executive function account of ADHD argue?

A

Argues that people with ADHD have week executive function and it is this that is the source of all problems.

33
Q

who developed the executive function account of ADHD

A

Brown 2001

34
Q

where was the model of Executive function derived from

A

derived from intensive clinical interviews with individuals diagnosed with ADHD and with their families, in which I inquired about specifics of the cognitive and behavioural activities in which these children, adolescents, and adults were impaired relative to others of the same age and developmental level- Brown 2001

35
Q

what does the executive function model include?

A

six clusters of cognitive functions which constitute a way of conceptualising executive functions for all individuals. None of these clusters is a unitary variable e.g. height/ weight each cluster is more like a basket containing a variety of related cognitive functions. These clusters are

  1. Activation; : Organising, prioritising and activating to work.
  2. Focus: Focusing, sustaining, and shifting attention to tasks.
  3. Effort: Regulating alertness, sustaining effort, and processing speed.
  4. Emotion: Managing frustration and regulating emotions.
  5. Memory: Utilising working memory and accessing recall.
  6. Action: Monitoring and self-regulating action.

Freds Adhd Annoys EM Efficiently

36
Q

what is a second important notion of the executive function account of ADHD

A

Another primary emphasis of my model is the situational variability of the impairments of ADHD.

Clinical studies by Brown have indicated that all individuals with ADHD seem to have some specific domains of activity in which they have no difficulty in performing various functions that are for them impaired in virtually every other area of life. This situational variability of the symptoms can be viewed as symptoms of the evidence that the impairments of the brain involved in ADHD are not with these fundamental cognitive functions themselves, but with the central management networks that turn them on and off. (Brown 2005)

ADHD is not an all-or-nothing syndrome like cancer where either one has dyslexia or they do not instead it is more like depression where all individuals experience low and high moods from time to time but only those significantly impaired over long periods of time are diagnosed as being depressed. ADHD might therefore be considered the extreme end of the normal range in impairments in executive function.

These clusters can turn specific things off meaning that individuals may show reduced ADHD symptoms in some tasks than others rather than one thing being constantly impaired as in other models

37
Q

support for executive function account of ADHD

A

studies have found that executive function is controlled by the frontal lobes (
Alvarez & Emory 2006) while ADHD children differed significantly from Normal Controls on measures of Frontal Lobe function, but not on tests of temporal lobe functions. ADHDs performed like 6- to 7-year-olds, despite their mean age of 10 years and minimum age of 8 years. (Shue and Douglas 1992).

38
Q

issues with executive function account of ADHD

A
  • doesn’t include motivational delay which has been found in individuals with ADHD
39
Q

who developed the Behavioural inhibition model of ADHD?

A

Barkley proposed a comprehensive theory of ADHD with deficient inhibitory control as the core deficit that secondarily disrupts other Executive Function processes

40
Q

outline the behavioural inbibition model

A

Barkley proposed a comprehensive theory of ADHD with deficient inhibitory control as the core deficit that secondarily disrupts other Executive Function processes

A theoretical model is constructed that links inhibition to 4 executive neuropsychological functions that appear to depend on it for their effective execution: (a) working memory, (b) self-regulation of affect-motivation-arousal, (c) internalization of speech, and (d) reconstitution (behavioral analysis and synthesis).

41
Q

support for behavioural inhibition model of ADHD

A

Konrad et al., 2009 children with ADHD engaged in two inhibition tasks stop-signal task and a delayed response task children with ADHD showed a pervasive deficit in their inhibitory control processes with respect to inhibition of both pre-potent and on-going responses.

Campbell et al., 2009
measures of delay capacity, inhibitory control, planning, and attention (assessed prior to 1st grade) were seen to what degree they predicted symptoms of attention deficit hyperactivity disorder (ADHD) assessed in third grade
poorer performance on earlier measures of resistance to temptation, delay of gratification, response inhibition, attention, and planning obtained from 36 months to 1st grade predicted membership in the two symptom groups relative to the comparison group in 3rd grade

42
Q

Problems of Behavioural inhibition model

A

Extended to ADHD, the model predicts that ADHD should be associated with secondary impairments in these 4 executive abilities and the motor control they afford. The author reviews evidence for each of these domains of functioning and finds it to be strongest for deficits in behavioral inhibition, working memory, regulation of motivation, and motor control in those with ADHD. Although the model is promising as a potential theory of self-control and ADHD, far more research is required to evaluate its merits and the many predictions it makes about ADHD.

43
Q

Who proposed the motivation account of ADHD

A

Sagvolden et al., 1998

44
Q

what does the motivation based account of ADHD propose?

A

AD/HD as the result of hypersensitivity to reward-related delay

45
Q

support for motivation based account of ADHD

A

Evidence for this model comes primarily from choice studies where children with AD/HD display a greater sensitivity to delay than their peers, choosing smaller sooner (SS) over larger later (LL) rewards (Kuntsi et al., 2001; Tripp & Alsop, 2001). This tendency appears most pronounced when the SS choices reduce overall delay rather than only increasing reward immediacy. As a result, children with AD/HD have been described as ’delay averse’ rather than ’impulsive’ (Sonuga-Barke, 1994; Sonuga-Barke et al., 1992).

46
Q

what is the dual pathway model of AD/HD

A

AD/HD is seen as the outcome of two dissociable psycho-patho-physiological pathways, mediated by distinctly different psychological process and rooted in functionally segregated, though conceptually related, brain circuits.
Proposes the existence of separate and neurobiologically distinct cognitive (executive disfunction) and motivational (delay aversion) developmental routes to AD/HD.
Neurobiological basis which leads to faults in the 1) executive circuit and 2) the reward circuit. These abnormalities then influence psychological processes however these are down two distinct paths. Firstly the executive circuit leads to inhibitory deficits which in turn lead to executive dysfunction.

47
Q

who proposed the dual pathway model of ADHD

A
  • Sonuga-Barke 2002/2003
48
Q

where does initial idea for dual pathway model of ADHD come from

A

We know however that there are two subgroups of ADHD as defined by DSM-V and even in the past there has been a distinction made between ADHD and ADD. These changes in the diagnostic criteria and the current differences in the subgroups hint towards the heterogeneity of ADHD.

49
Q

support for dual pathway model of ADHD

A

Solanto 2001:
The stop signal paradigm is premised upon a primary deficit in inhibitory control in AD/HD, whereas the delay aversion hypothesis, by contrast conceptualises impulsivity in ADHD not as an inability to inhibit a response but rather as a chance to avoid delay.
Study compared ecological validity of stop signal task and choice delay task, with respect to their utility in discriminating AD/HD children from normal controls. Although inhibitory deficits and delay sensitivity were uncorrelated, performance on both tasks was strongly associated with AD/HD group membership. In combination, the two measures allowed just under 90 percent of the AD/HD children to be correctly classified. The results of this study raised the possibility of distinct motivational and cognitive bases for AD/HD, which is therefore consistent with a dual developmental pathway model of AD/HD.

50
Q

describe the full dual pathway model of ADHD

A

In the reward circuit, abnormalities lead to a shortened delay reward gratification- these are also influenced by parental response (Whereby parental intolerance of ‘impulsiveness’ if it is associated with a subsequent harsh response, leads, over time, to ‘impulsive children’ associating delay in general with negative consequences. In turn this leads to the development of a negative emotional response to delay (i.e. delay aversion). In this way what starts off as being a potentially benign impulsiveness (e.g. a child favouring immediacy) becomes transformed into the more clinically significant general pattern of AD/HD behaviours). These both lead to delay aversion. Both this delay aversion paired with executive dysfunction leads to ADHD behavioural expression while executive dysfunction leads to a lack of engagement specifically.

51
Q

what does the dual pathway model allow ADHD to be explained in terms of?

A

Explains neuro-psychological heterogeneity in Attention Deficit/Hyperactivity Disorder (ADHD) in terms of dissociable cognitive and motivational deficits each affecting some but not other patients.

executive dysfunction–> attention deficit

delay aversion–>hyperactivity

52
Q

support for dual path model of ADHD in terms of correlations

A

Sonuga-Barke et al., 2010
Nine tasks designed to tap into the domains of inhibitory control, delay aversion and temporal processing were administered to ADHD children and adolescents

Found no correlation between temporal processing, inhibitory control and delay related deficits and these all represented independent neuropsychological components in ADHD group. ADHD subjects differed from controls on all factors. CONC- illustrates the heterogeneity in ADHD and in fact even provides initial support for a triple pathway.

53
Q

adoption study to show genetic element to ADHD

A

Faraone et al., 2000
6% of adoptive parents of adopted ADHD probands had ADHD compared to 18% of the biological parents of nonadopted ADHD probands and 3% of biological parents in control probands. Suggests that ADHD has a genetic component.

54
Q

twin study to show genetic element to ADHD

A

Rietveld et al., 2004
Mothers were asked to complete the Child Behavior Checklist (CBCL) for their twin offspring when the children were 3, 7, 10 and 12 years old. Focus on the Overactivity scale and on the attentional problem scale within the CBCL.
Results: broad heritability of overactivity and attentional problems are estimated at nearly 75% at each age thus these are both highly heritable at all ages.

55
Q

main genome study for ADHD & which genes specifically identified

A

meta-analysis Gizer et al., 2009 identified the following:

1) Dopamine transporter gene DAT1
2) Dopamine receptor gene (DRD4)
3) serotonine 1b receptor gene

56
Q

what does the dopamine transporter gene DAT1 code for

A

codes for a solute carrier protein responsible for the reuptake of dopamine from the synaptic cleft back to the pre-synaptic neuron.

57
Q

what lines of research justify DAT1 revelance in ADHD

A
  • Stimulant medications- e.g. methylphenidate- which are most widely prescribed and among most effective treatments available for ADHD symptoms have been shown to inhibit the function of the dopamine transporter and therefore increase levels of available dopamine in the synapse (Ritz et al., 1987; Volkow et al., 1995).
  • Mice that were bred lacking both copies of the DAT1 gene exhibited behaviours analogous to ADHD such as greater motor activity compared to ‘wild type’ controls and mice bred with a single intact copy of the gene (Giros et al., 1996)
  • Cook et al., 1995- found that the 10-repeat allele polymorphism in the 3’ untranslated region for DAT1 was preferentially transmitted to ADHD probands.
58
Q

what are reasons behind identifying Dopamine receptor gene DRD4 as a candidate gene for ADHD

A

Given that abnormalities in the dopamine neurotransmitter system have been hypothesised to underlie ADHD (levy 1991), the genes that code for dopamine receptors have been identified as candidate loci for ADHD.
Moreover DRD4 is predominantly expressed in frontal lobe regions which are thought to be involved in the aetiology of the disorder

59
Q

DRD4 polymorphism studies in ADHD

A

DRD4 polymorphism – LaHoste et al., 1996- reported increased prevalence of the 7-repeat allele of this polymorphism in ADHD cases compared to controls.
Several meta-analyses have confirmed this DRD4 association (Faraone et al., 2001, 2005; Li et al., 2006)

60
Q

justification between serotonin 1b receptor and ADHD

A

Serotonin dysregulation has been related to impulsive and aggressive behaviour in children (Spivak et al., 1997) and thus been hypothesised to play a causal role in ADHD.

61
Q

what does the serotonin 1b receptor do?

A

inhibits cyclic AMP formation (Murphy et al., 1998).

62
Q

support for serotonin 1b receptor

A

Mice who have been bred to have no copies of the Serotonin 1b receptor showed increased aggression and impulsive behaviour (Brunner and Hen 1997) and display an increased response to novel stimuli (Malleret et al., 1999)- both apparent in ADHD
Thus several studies have tested for association between serotonin 1b receptor and ADHD.
The polymorphism of guanine to cytosine at position 816 on the serotonin 1b receptor gene show a significant association to ADHD risk in a meta-analysis by Gizer et al., 2009

63
Q

according to Gizer et al., 2009 what are issues with genome studies

A

Limitations:
Individually tested – likelihood of false positives
Single genes identified – may not always be causal
Different genetic risk association – harder to identify single risk factor in

64
Q

what environmental risk factors are associated with ADHD?

A
  • low birth weight
  • premature birth
  • maternal smoking
  • social class
65
Q

low birth weight and ADHD

A

Low birth weight- Breslau & Chilcoat, 2000
Parents interviewed on inattentive and hyperactive-impulsive ADHD symptoms. There is an independent association between low birth weight and all forms of ADHD symptoms, even after controlling for all environmental and genetic confounds shared within twin pairs. These results indicate that fetal growth restriction (as reflected in birth weight differences within twin pairs is in the casual pathway leading to ADHD. Twin study used to control environmental and genetic factors.

66
Q

premature birth and ADHD

A

Bhutta et al., 2002 Meta-analysis of 227 studies included case-control studies reporting cognitive and/or behavioural data of children who were born preterm and who were evaluated after their fifth birthday. Premature children also show an increased incidence of ADHD

67
Q

Maternal Smoking and ADHD

A

Knopik 2009- notes that smoking in mothers is associated with many behavioral abnormalities, including increased evidence of attentional deficits, impaired learning and memory, lowered IQ, and cognitive dysfunction.
Milberger et al., 1996 Twenty-two percent of the ADHD children had a maternal history of smoking during pregnancy, compared with 8% of the normal subjects. This positive association remained significant after adjustment for socioeconomic status, parental IQ, and parental ADHD status. Significant differences in IQ were found between those children whose mothers smoked during pregnancy and those whose mothers did not smoke.

Linnet et al. 2003- reviewed 24 studies published between 1975 and 2002 investigating the relationship between prenatal maternal smoking and ADHD or ADHD symptoms in the children. The authors concluded that most studies reported an increased risk for the development of such problems in children of smoking mothers, some even showing a dose–response effect in the association

68
Q

interesting smoking birth rate correlation

A

Although interestingly…. Offspring of women who smoke during pregnancy show low birth weight (e.g., Ricketts, et al, 2005)

69
Q

effects of nicotine pre-natal

A

The effects of nicotine are thought to occur via its action on nicotinic acetylcholine receptors receptor proteins that respond to the neurotransmitter acetylcholine. Nicotine is an agonist of Acetylcholine, able to bind to receptor proteins and mimics the action of ACh [Dwyer 2009]. Suggested that ACh through its action on nAChRs plays an important role in brain maturation in foetuses and infants up to adolescence (Dwyer 2009]. These processes modulated by ACh can thus be perturbed by nicotine

70
Q

Social Class and ADHD

A
Langley et al., 2007 greater hyperactive-impulsive symptom severity was significantly associated with social class
Hjern 2009- socioeconomic indicators such as education, lone parenthood and reception of social welfare are associated with medicated ADHD in a Swedish context. Low maternal education alone predicted 33% of cases with medicated ADHD, single parenthood 14% and social welfare 10%, while psychiatric or addictive disorder in the parents predicted less than 4%.